EMERGENCY
STATION. ORGANIZATION OF WORK, FUNCTIONS, STRUCTURE. THE URGENT HELP AT ACUTE
MYOCARDIAL INFARCTION ON PRECLINICAL STAGE. THE URGENT HELP AT ACUTE HEART
FAILURE ON PREHOSPITAL STAGE (BY EMERGENCY & FAMILY DOCTORS)
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Diagram of
a myocardial infarction (2) of the tip of the anterior
wall of the heart (an apical infarct) after
occlusion (1) of a branch of the left
coronary artery (LCA, right
coronary artery = RCA). |
A heart attack, known in medicine
as an (acute) myocardial infarction (AMI or MI),
occurs when the blood supply to part of the heart is interrupted. This is
most commonly due to occlusion (blockage) of a coronary
artery following the rupture of a vulnerable
atherosclerotic plaque, which is an unstable collection of lipids (like cholesterol)
and white blood cells (especially macrophages)
in the wall of an artery.
The resulting ischemia
(restriction in blood supply) and oxygen
shortage, if left untreated for a sufficient period, can cause
damage and/or death (infarction) of heart muscle tissue (myocardium).
Classical symptoms of acute myocardial infarction include sudden chest pain
(typically radiating to the left arm or left side of the neck), shortness of
breath, nausea,
vomiting,
palpitations,
sweating,
and anxiety
(often described as a sense of impending doom). Women may
experience fewer typical symptoms than men, most commonly shortness of breath,
weakness, a feeling of indigestion, and fatigue. Approximately one quarter of all
myocardial infarctions are silent, without chest pain or other symptoms. A
heart attack is a medical emergency, and people experiencing
chest pain are advised to alert their emergency medical services, because prompt
treatment is beneficial.
Heart attacks are the leading
cause of death for both men and women all over the world. Important risk factors
are previous cardiovascular disease (such as angina,
a previous heart attack or stroke), older age (especially men over 40 and women over 50),
tobacco
smoking, high blood levels of certain lipids (triglycerides,
low-density lipoprotein or "bad
cholesterol") and low high density lipoprotein (HDL, "good
cholesterol"), diabetes, high blood
pressure, obesity, chronic kidney disease, heart failure,
excessive alcohol consumption,
the abuse of certain drugs (such as cocaine),
and chronic high stress levels.
Immediate treatment for suspected acute myocardial infarction includes oxygen,
aspirin,
and sublingual glyceryl trinitrate
(colloquially referred to as nitroglycerin
and abbreviated as NTG or GTN). Pain relief is also often given, classically morphine
sulfate.
The patient will receive a number
of diagnostic tests, such as an electrocardiogram
(ECG, EKG), a chest X-ray
and blood tests
to detect elevations in cardiac markers (blood tests to detect heart
muscle damage). The most often used markers are the creatine
kinase-MB (CK-MB) fraction and the troponin
I (TnI) or troponin
T (TnT) levels. On the basis of the ECG, a distinction is made between ST
elevation MI (STEMI) or non-ST elevation MI (NSTEMI). Most cases of
STEMI are treated with thrombolysis or if possible with percutaneous coronary intervention
(PCI, angioplasty and stent insertion), provided the hospital has facilities
for coronary angiography. NSTEMI is managed
with medication, although PCI is often performed during hospital admission. In
patients who have multiple blockages and who are relatively stable, or in a few
extraordinary emergency cases, bypass surgery of the
blocked coronary artery is an option.
The phrase "heart
attack" is sometimes used incorrectly to describe sudden cardiac death, which may or may not
be the result of acute myocardial infarction. A heart attack is different from,
but can be the cause of cardiac arrest, which is the stopping of the
heartbeat, and cardiac arrhythmia, an abnormal heartbeat. It
is also distinct from heart failure, in which the pumping action of
the heart is impaired; severe myocardial infarction may lead to heart failure,
but not necessarily.
Classification
Classification
of acute coronary syndromes.
Acute myocardial infarction is a type of acute coronary syndrome, which is most
frequently (but not always) a manifestation of coronary artery disease. The acute
coronary syndromes include ST segment elevation myocardial infarction (STEMI),
non-ST segment elevation myocardial infarction (NSTEMI), and unstable
angina (UA).
By zone
Depending on the location of the
obstruction in the coronary circulation, different zones of
the heart can become injured. Using the anatomical terms of location corresponding
to areas perfused by major coronary arteries, one can describe anterior,
inferior, lateral, apical, septal, posterior, and right-ventricular infarctions
(and combinations, such as anteroinferior, anterolateral, and so on).[42]
- For example, an occlusion of the left anterior descending
coronary artery(LAD) will result in an anterior wall
myocardial infarct.[43]
- Infarcts of the lateral wall are caused by
occlusion of the left circumflex coronary artery(LCx)
or its oblique marginal branches (or even large diagonal branches from the
LAD.)
- Both inferior wall and posterior wall
infarctions may be caused by occlusion of either the right coronary artery or the left
circumflex artery, depending on which feeds the posterior descending artery.
- Right ventricular wall infarcts are also
caused by right coronary artery occlusion.
Signs and symptoms
The cardinal sign of decreased
blood flow to the heart is chest pain experienced as tightness around the chest
and radiating to the left arm and the left angle of the jaw. This may be
associated with diaphoresis (sweating), nausea and vomiting,
as well as shortness of
breath. In many cases, the sensation is "atypical", with
pain experienced in different ways or even being completely absent (which is
more likely in female patients and those with diabetes).
Some may report palpitations, anxiety or a sense of impending
doom and a feeling of being acutely ill.
Diagnosis
Classification
of acute coronary syndromes
A myocardial
infarction occurs when an atherosclerotic plaque
slowly builds up in the inner lining of a coronary
artery and then suddenly ruptures, totally occluding the artery and
preventing blood flow downstream.
Electrocardiogram
In the setting of acute chest pain, the electrocardiogram
is the investigation that most reliably distinguishes between various causes.
If this indicates acute heart damage (elevation in the ST segment, new left bundle branch block), treatment for a
heart attack in the form of angioplasty or thrombolysis
is indicated immediately (see below). In the absence of such changes, it is not
possible to immediately distinguish between unstable angina and NSTEMI.
Imaging
and blood tests
As it is only one of the many
potential causes of chest pain, the patient usually has a number of
tests in the emergency department, such as a chest X-ray,
blood tests
(including myocardial markers such as troponin
I or T, and a D-dimer
if a pulmonary embolism is suspected), and telemetry
(monitoring of the heart rhythm).
Prediction scores
The ACI-TIPI score can be used to
aid diagnosis; using 7 variables from the admission record, this score predicts
crudely which patients are likely to have myocardial ischemia. The TIMI risk score can
identify high risk patients and has been independently validated.
Biomarkers
for diagnosis
The aim of diagnostic markers is
to identify patients with ACS even when there is no evidence of myocyte
necrosis.
- Ischemia-Modified Albumin (IMA) - In cases of
Ischemia - Albumin undergoes a conformational change and loses its ability
to bind transitional metals (copper or cobalt). IMA can be used to assess
the proportion of modified albumin in ischemia. Its use is limited to
ruling out ischemia rather than a diagnostic test for the occurrence of
ischemia.
- Myeloperoxidase (MPO) - The levels of circulating
MPO, a leukocyte enzyme, elevate early after ACS and can be used as an
early marker for the condition.
- Glycogen Phosphorylase Isoenzyme BB-(GPBB)
is an early marker of cardiac ischemia and is one of three isoenzyme
of Glycogen Phosphorylase.
- Troponin is a late cardiac marker of ACS
STEMI
If the ECG confirms changes
suggestive of myocardial infarction (ST elevations in
specific leads, a new left bundle branch block or a true posterior MI pattern),
thrombolytics
may be administered or primary coronary angioplasty may be performed.
In the former, medication is injected that stimulates fibrinolysis,
destroying blood clots obstructing the coronary
arteries. In the latter, a flexible catheter is passed via the
femoral or radial arteries and advanced to the heart to identify blockages in
the coronaries. When occlusions are found, they can be intervened upon
mechanically with angioplasty and perhaps stent deployment if a
lesion, termed the culprit lesion, is thought to be causing myocardial
damage.
NSTEMI and NSTE-ACS
If the ECG does not show typical
changes, the term "non-ST segment elevation ACS" is applied. The
patient may still have suffered a "non-ST elevation MI" (NSTEMI). The
accepted management of unstable angina and acute coronary syndrome is therefore
empirical treatment with aspirin, heparin (usually a low-molecular weight heparin such as enoxaparin)
and clopidogrel,
with intravenous glyceryl trinitrate and opioids if the
pain persists.
A blood test is generally
performed for cardiac troponins twelve hours after onset of the pain. If this
is positive, coronary angiography is typically
performed on an urgent basis, as this is highly predictive of a heart attack in
the near-future. If the troponin is negative, a treadmill exercise test or a
thallium scintigram may be requested.
Prevention
Acute coronary syndrome often
reflects a degree of damage to the coronaries by atherosclerosis.
Primary prevention of atherosclerosis is controlling the risk factors: healthy
eating, exercise, treatment for hypertension
and diabetes, avoiding smoking
and controlling cholesterol levels); in patients with
significant risk factors, aspirin has been shown to reduce the risk of cardiovascular
events. Secondary prevention is discussed in myocardial infarction.
After a ban on smoking in all
enclosed public places was introduced in
Angina pectoris, commonly known as angina, is severe chest pain
due to ischemia
(a lack of blood and hence oxygen supply) of the heart muscle,
generally due to obstruction or spasm of the coronary arteries (the heart's blood
vessels). Coronary artery disease, the main cause of
angina, is due to atherosclerosis of the cardiac arteries. The
term derives from the Greek ankhon ("strangling")
and the Latin
pectus ("chest"), and can therefore be translated as "a
strangling feeling in the chest".
It is not common to equate
severity of angina with risk of fatal cardiac events. There is a weak
relationship between severity of pain and degree of oxygen deprivation in the
heart muscle (i.e. there can be severe pain with little or no risk of a heart
attack, and a heart attack can occur without pain).
Worsening ("crescendo")
angina attacks, sudden-onset angina at rest, and angina lasting more than 15
minutes are symptoms of unstable angina (usually grouped with similar
conditions as the acute coronary syndrome). As these may
herald myocardial infarction (a heart attack),
they require urgent medical attention and are generally treated as a presumed
heart attack.
Symptoms
Most patients with angina
complain of chest discomfort rather than actual pain: the discomfort is usually
described as a pressure, heaviness, tightness, squeezing, burning, or choking
sensation. Apart from chest discomfort, anginal pains may also be experienced
in the epigastrium
(upper central abdomen), back, neck, jaw, or shoulders. Typical locations for radiation of pain are arms (often inner
left arm), shoulders, and neck into the jaw. Angina is typically precipitated
by exertion or emotional stress. It is exacerbated by having a full stomach and
by cold temperatures. Pain may be accompanied by breathlessness, sweating and
nausea in some cases. It usually lasts for about 1 to 5 minutes, and is
relieved by rest or specific anti-angina medication. Chest pain lasting only a
few seconds is normally not angina.
Myocardial ischemia
comes about when the myocardia (the heart muscles) receive insufficient blood
and oxygen to function normally either because of increased oxygen demand by
the myocardia or by decreased supply to the myocardia. This inadequate perfusion
of blood and the resulting reduced delivery of oxygen and nutrients, is
directly correlated to blocked or narrowed blood vessels.
Some experience "autonomic
symptoms" (related to increased activity of the autonomic nervous system) such as nausea, vomiting
and pallor.
Major risk factors for angina
include cigarette smoking, diabetes,
high cholesterol, high blood
pressure, sedentary lifestyle and family history of premature heart disease.
A variant form of angina (Prinzmetal's angina) occurs in patients with
normal coronary arteries or insignificant atherosclerosis. It is thought to be
caused by spasms of the artery. It occurs more in younger women.
Subtypes
Stable angina
This refers to the more common
understanding of angina related to myocardial ischemia. Typical presentations
of stable angina is that of chest discomfort and associated symptoms
precipitated by some activity (running, walking, etc) with minimal or
non-existent symptoms at rest. Symptoms typically abate several minutes
following cessation of precipitating activities and resume when activity
resumes. In this way, stable angina may be thought of as being similar to claudication
symptoms.
Unstable angina
Unstable angina (UA)is defined as
angina pectoris or equivalent ischemic discomfort with at least one of three
features: (1) it occurs at rest (or with minimal exertion), usually lasting
>10 min; (2) it is severe and of new onset (i.e., within the prior 4–6
weeks); and/or (3) it occurs with a crescendo pattern (i.e., distinctly more
severe, prolonged, or frequent than previously).UA may occur unpredictably at
rest which may be a serious indicator of an impending heart attack. What
differentiates stable angina from unstable angina (other than symptoms) is the
pathophysiology of the atherosclerosis. In stable angina, the developing atheroma
is protected with a fibrous cap. This cap (atherosclerotic plaque) may rupture
in unstable angina, allowing blood clots to precipitate and further decrease
the lumen of the coronary vessel. This explains why angina appears to be
independent to activity.
Diagnosis
In angina patients who are
momentarily not feeling any chest pain, an electrocardiogram
(ECG) is typically normal, unless there have been other cardiac problems in the
past. During periods of pain, depression or elevation of the ST segment may be observed. To elicit these
changes, an exercise ECG test ("treadmill test")
may be performed, during which the patient exercises to their maximum ability
before fatigue, breathlessness or, importantly, pain supervenes; if
characteristic ECG changes are documented (typically more than
In patients in whom such
noninvasive testing is diagnostic, a coronary angiogram is typically performed
to identify the nature of the coronary lesion, and whether this would be a
candidate for angioplasty, coronary artery bypass graft
(CABG), treatment only with medication, or other treatments. In patients who
are in hospital with unstable angina (or the newer term of "high risk
acute coronary syndromes"), those with resting ischaemic ECG changes or
those with raised cardiac enzymes such as troponin may undergo coronary angiography
directly.
Pathophysiology
Increase in heart rate results in
increased oxygen demand by the heart. The heart has a limited ability to
increase its oxygen intake during episodes of increased demand. Therefore, an
increase in oxygen demand by the heart (eg, during exercise) has to be met by a
proportional increase in blood flow to the heart.
Myocardial ischemia can result
from:
1.
a reduction of blood flow to the heart
that can be caused by stenosis, spasm, or acute occlusion (by an embolus)
of the heart's arteries
2.
resistance of the blood vessels
3.
reduced oxygen-carrying capacity of the
blood.
Atherosclerosis
is the most common cause of stenosis (narrowing of the blood vessels) of the heart's
arteries and, hence, angina pectoris. Some people with chest pain have normal
or minimal narrowing of heart arteries; in these patients, vasospasm
is a more likely cause for the pain, sometimes in the context of Prinzmetal's angina and syndrome X.
Myocardial ischemia also can be
the result of factors affecting blood composition, such as reduced
oxygen-carrying capacity of blood, as seen with seven anemia (low
number of red blood cells), or long-term smoking.
Epidemiology
Roughly 6.3 million Americans are
estimated to experience angina. Angina is more often the presenting symptom of
coronary artery disease in women than in men. The prevalence of angina rises
with an increase in age. Similar figures apply in the remainder of the Western
world. All forms of coronary heart disease are much less-common in the Third World,
as its risk factors are much more common in Western and Westernized countries;
it could therefore be termed a disease of affluence. The increase of smoking,
obesity
and other risk factors has already led to an increase in angina and related
diseases in countries such as China.
Treatment
The main goals of treatment in angina pectoris are relief of symptoms,
slowing progression of the disease, and reduction of future events, especially heart attacks and of course death. An aspirin
(75 mg to 100 mg) per day has been shown to be beneficial for all patients with
stable angina that have no problems with its use. Beta blockers
(eg. carvedilol, propranolol, atenolol etc. are some few examples) have a large
body of evidence in morbidity and mortality benefits (fewer symptoms and
disability and live longer) and short-acting nitroglycerin
medications are used for symptomatic relief of angina. Calcium channel blockers (such as nifedipine
(Adalat) and amlodipine), Isosorbide mononitrate and nicorandil
are vasodilators commonly used in chronic stable angina. A new therapeutic
class, called If inhibitor, has recently been made available: ivabradine
provides pure heart rate reduction,.[1] leading to major anti-ischemic and antianginal
efficacy. ACE inhibitors are also vasodilators with both
symptomatic and prognostic benefit and lastly, statins
are the most frequently used lipid/cholesterol modifiers which probably also
stabilise existing atheromatous plaque.
Surprising perhaps is that
exercise is also a very good long term treatment for angina (but only
particular regimes - gentle and sustained exercise rather than dangerous
intense short bursts),[2] probably working by complex mechanisms such
improving blood pressure and promoting coronary artery collateralisation.
Identifying and treating risk
factors for further coronary heart disease is a priority in patients with
angina. This means testing for elevated cholesterol and other fats in the
blood, diabetes and hypertension
(high blood pressure), encouraging stopping
smoking and weight optimisation.
Ranolazine
(Ranexa) is a new class of anti anginal drug that was approved by the Food and
Drug Administration (FDA)
Recently,
The largest randomised trial of
an anti-anginal drug to date is the ACTION trial. It included 7,665 patients
with stable angina pectoris. ACTION demonstrated that the calcium channel
blocker nifedipine (Adalat) prolongs cardiovascular event- and procedure-free
survival in patients with coronary artery disease. For example new overt heart
failures were reduced by 29% compared to placebo. This finding confirms the
vascular-protective effects of nifedipine.
Symptoms
Rough diagram of
pain zones in myocardial infarction (dark red = most typical area, light red =
other possible areas, view of the chest).
Back view.
The onset of symptoms in
myocardial infarction (MI) is usually gradual, over several minutes, and rarely
instantaneous. Chest pain is the most common symptom of acute
myocardial infarction and is often described as a sensation of tightness,
pressure, or squeezing. Chest pain due to ischemia
(a lack of blood and hence oxygen supply) of the heart muscle is termed angina
pectoris. Pain radiates most often to the left arm, but may also radiate
to the lower jaw,
neck, right arm, back,
and epigastrium,
where it may mimic heartburn. Levine's sign,
in which the patient localizes the chest pain by clenching their fist over the
sternum, has classically been thought to be predictive of cardiac chest pain,
although a prospective observational study showed that it had a poor positive
predictive value.
Shortness of breath (dyspnea)
occurs when the damage to the heart limits the output
of the left ventricle, causing left ventricular failure and consequent pulmonary
edema. Other symptoms include diaphoresis
(an excessive form of sweating), weakness, light-headedness,
nausea,
vomiting,
and palpitations.
These symptoms are likely induced by a massive surge of catecholamines
from the sympathetic nervous system which occurs in
response to pain and the hemodynamic abnormalities that result from cardiac
dysfunction. Loss of consciousness (due to inadequate
cerebral perfusion and cardiogenic shock) and even sudden death (frequently due to the
development of ventricular fibrillation) can occur in myocardial infarctions.
Women and older patients
experience atypical symptoms more frequently than their male and younger
counterparts. Women also have more symptoms compared to men (2.6 on average vs
1.8 symptoms in men). The
most common symptoms of MI in women include dyspnea,
weakness, and fatigue. Fatigue, sleep disturbances,
and dyspnea have been reported as frequently occurring symptoms which may
manifest as long as one month before the actual clinically manifested ischemic
event. In women, chest pain may be less predictive of coronary ischemia
than in men.
Approximately half of all MI
patients have experienced warning symptoms such as chest pain prior to the
infarction.
Approximately one fourth of all
myocardial infarctions are silent, without chest pain or other symptoms. These
cases can be discovered later on electrocardiograms or at autopsy without a
prior history of related complaints. A silent course is more common in the elderly,
in patients with diabetes mellitus and after heart transplantation, probably because
the donor
heart is not connected to nerves of the host. In diabetics, differences in pain
threshold, autonomic neuropathy, and psychological
factors have been cited as possible explanations for the lack of symptoms.
Any group of symptoms compatible
with a sudden interruption of the blood flow to the heart are called an acute coronary syndrome.
The differential diagnosis includes other
catastrophic causes of chest pain, such as pulmonary embolism, aortic
dissection, pericardial effusion causing cardiac
tamponade, tension pneumothorax, and esophageal rupture.
Diagnosis
The diagnosis of myocardial
infarction is made by integrating the history of the presenting illness and
physical examination with electrocardiogram
findings and cardiac markers (blood tests
for heart muscle
cell
damage). A coronary angiogram allows visualization of
narrowings or obstructions on the heart vessels, and therapeutic measures can
follow immediately. At autopsy, a pathologist can diagnose a myocardial
infarction based on anatomopathological findings.
A chest
radiograph and routine blood tests may indicate complications or
precipitating causes and are often performed upon arrival to an emergency department. New regional wall
motion abnormalities on an echocardiogram are also suggestive of a
myocardial infarction. Echo may be performed in equivocal cases by the on-call
cardiologist. In stable patients whose symptoms have resolved by the time of
evaluation, technetium-99m
2-methoxyisobutylisonitrile (Tc99m MIBI) or thallium-201 chloride can
be used in nuclear medicine to visualize areas of reduced
blood flow in conjunction with physiologic or pharmocologic stress. Thallium
may also be used to determine viability of tissue, distinguishing whether
non-functional myocardium is actually dead or merely in a state of hibernation
or of being stunned.
Diagnostic
criteria
WHO criteria have classically been used to diagnose MI; a patient is
diagnosed with myocardial infarction if two (probable) or three (definite) of
the following criteria are satisfied:
1.
Clinical history of ischaemic type chest
pain lasting for more than 20 minutes
2.
Changes in serial ECG tracings
3.
Rise and fall of serum cardiac
biomarkers such as creatine kinase-MB fraction and troponin
The WHO criteria were refined in
2000 to give more prominence to cardiac biomarkers.[41] According to the new guidelines, a cardiac troponin
rise accompanied by either typical symptoms, pathological Q waves, ST elevation
or depression or coronary intervention are diagnostic of MI.
Physical examination
The general appearance of
patients may vary according to the experienced symptoms; the patient may be
comfortable, or restless and in severe distress with an increased respiratory
rate. A cool and pale skin is common and points to vasoconstriction.
Some patients have low-grade fever (38–39 °C). Blood
pressure may be elevated or decreased, and the pulse can be become irregular.
If heart failure ensues, elevated
jugular venous pressure and hepatojugular reflux, or swelling of the
legs due to peripheral edema may be found on inspection. Rarely, a cardiac bulge with
a pace different from the pulse rhythm can be felt on precordial examination. Various
abnormalities can be found on auscultation,
such as a third and fourth heart sound, systolic
murmurs, paradoxical splitting of the second heart sound, a pericardial
friction rub and rales
over the lung.
12-lead electrocardiogram
showing ST-segment elevation (orange) in I, aVL and V1-V5 with reciprocal
changes (blue) in the inferior leads, indicative of an anterior wall myocardial
infarction.
12-lead electrocardiogram
(ECG) showing acute inferior ST segment elevation MI (STEMI). Note the ST
segment elevation in leads II, III, and aVF along with reciprocal ST segment
depression in leads I and aVL.
Electrocardiogram
The primary purpose of the electrocardiogram
is to detect ischemia
or acute coronary injury in broad, symptomatic emergency department populations. However,
the standard 12 lead ECG has several limitations. An ECG
represents a brief sample in time. Because unstable ischemic syndromes have
rapidly changing supply versus demand characteristics, a single ECG may not
accurately represent the entire picture. It is therefore desirable to obtain serial
12 lead ECGs, particularly if the first ECG is obtained during a pain-free
episode. Alternatively, many emergency departments and chest pain centers use
computers capable of continuous ST segment monitoring. The standard 12 lead ECG
also does not directly examine the right
ventricle, and is relatively poor at examining the posterior basal
and lateral walls of the left ventricle. In particular, acute myocardial
infarction in the distribution of the circumflex artery is likely to produce a
nondiagnostic ECG. The use of additional ECG leads like right-sided leads V3R
and V4R and posterior leads V7, V8, and V9 may improve sensitivity for right
ventricular and posterior myocardial infarction. In spite of these limitations,
the 12 lead ECG stands at the center of risk stratification for the patient
with suspected acute myocardial infarction. Mistakes in interpretation are
relatively common, and the failure to identify high risk features has a negative
effect on the quality of patient care.
The 12 lead ECG is used to classify patients into one of three groups:
1. those with ST segment elevation or new bundle
branch block (suspicious for acute injury and a possible candidate for acute
reperfusion therapy with thrombolytics or primary PCI),
2. those with ST segment depression or T wave
inversion (suspicious for ischemia), and
3. those with a so-called non-diagnostic or normal
ECG.
A normal ECG does not rule out
acute myocardial infarction. Sometimes the earliest presentation of acute
myocardial infarction is the hyperacute T wave, which is treated the same as ST
segment elevation. In practice this is rarely seen, because it only exists for
2-30 minutes after the onset of infarction. Hyperacute T waves need to be
distinguished from the peaked T waves associated with hyperkalemia.
The current guidelines for the ECG diagnosis of acute myocardial infarction
require at least
Left bundle branch block and pacing interferes with the
electrocardiographic diagnosis of acute myocadial infarction. The GUSTO
investigators Sgarbossa et al. developed a set of criteria for identifying
acute myocardial infarction in the presence of left bundle branch block and
paced rhythm. They include concordant ST segment elevation >
The constellation of leads with
ST segment elevation enables the clinician to identify what area of the heart
is injured, which in turn helps predict the so-called culprit artery.
|
Wall Affected |
Leads |
Leads |
Suspected Culprit Artery |
|
Septal |
V1, V2 |
None |
|
|
Anterior |
V3, V4 |
None |
|
|
Anteroseptal |
V1, V2, V3, V4 |
None |
|
|
Anterolateral |
V3, V4, V5, V6, I, aVL |
II, III, aVF |
Left Anterior Descending (LAD), Circumflex (LCX), or Obtuse
Marginal |
|
Extensive anterior (Sometimes
called Anteroseptal with Lateral extension) |
V1,V2,V3,
V4, V5, V6, I, aVL |
II, III, aVF |
|
|
II, III, aVF |
I, aVL |
||
|
Lateral |
I, aVL, V5, V6 |
II, III, aVF |
|
|
Posterior (Usually associated
with Inferior or Lateral but can be isolated) |
V7, V8, V9 |
V1,V2,V3, V4 |
Posterior
Descending (PDA) (branch of the RCA or Circumflex
(LCX)) |
|
Right ventricular (Usually associated with
Inferior) |
II, III, aVF, V1, V4R |
I, aVL |
As the myocardial infarction
evolves, there may be loss of R wave height and development of pathological Q
waves (defined as Q waves deeper than
Cardiac markers
Cardiac markers or cardiac
enzymes are proteins from cardiac tissue found in the blood. These proteins are
released into the bloodstream when damage to the heart occurs, as in the case
of a myocardial infarction. Until the 1980s, the enzymes SGOT and LDH were used to assess cardiac injury.
Then it was found that disproportional elevation of the MB subtype of
the enzyme creatine kinase (CK) was very specific for
myocardial injury. Current guidelines are generally in favor of troponin
sub-units I or T, which are very specific for the heart muscle and are thought
to rise before permanent injury develops. Elevated troponins in the setting of
chest pain may accurately predict a high likelihood of a myocardial infarction
in the near future. New markers such as glycogen phosphorylase isoenzyme BB
are under investigation.
The diagnosis of myocardial
infarction requires two out of three components (history, ECG, and enzymes).
When damage to the heart occurs, levels of cardiac markers rise over time,
which is why blood tests for them are taken over a 24-hour
period. Because these enzyme levels are not elevated immediately following a
heart attack, patients presenting with chest pain are generally treated with
the assumption that a myocardial infarction has occurred and then evaluated for
a more precise diagnosis.
Angiography
Angiogram
of the coronary arteries.
In difficult cases or in
situations where intervention to restore blood flow is appropriate, coronary angiography
can be performed. A catheter is inserted into an artery (usually the femoral
artery) and pushed to the vessels supplying the heart. A
radio-opaque dye is administered through the catheter and a sequence of x-rays
(fluoroscopy) is performed. Obstructed or narrowed arteries can be identified,
and angioplasty
applied as a therapeutic measure (see below). Angioplasty requires extensive
skill, especially in emergency settings. It is performed by a physician trained
in interventional cardiology.
Histopathology
Microscopy image
(magn. ca 100x, H&E stain) from autopsy specimen of
myocardial infarct (7 days post-infarction).
Microscopy image
of myocardial infarction scar in the heart of a rat
Histopathological examination of the heart
may reveal infarction at autopsy. Under the microscope, myocardial infarction
presents as a circumscribed area of ischemic, coagulative necrosis
(cell death). On gross examination, the infarct is not identifiable within the
first 12 hours.
Although earlier changes can be
discerned using electron microscopy, one of the earliest
changes under a normal microscope are so-called wavy fibers.
Subsequently, the myocyte cytoplasm becomes more eosinophilic
(pink) and the cells lose their transversal striations, with typical changes
and eventually loss of the cell nucleus. The interstitium at the margin of
the infarcted area is initially infiltrated with neutrophils,
then with lymphocytes
and macrophages,
who phagocytose
("eat") the myocyte debris. The necrotic area is surrounded and
progressively invaded by granulation tissue, which will replace the
infarct with a fibrous (collagenous) scar (which are typical steps in wound healing).
The interstitial space (the space between cells outside of blood vessels) may
be infiltrated with red blood cells.
These features can be recognized
in cases where the perfusion was not restored; reperfused infarcts can have
other hallmarks, such as contraction band necrosis.
First
aid
As myocardial infarction is a
common medical emergency, the signs are often part of first aid
courses. The emergency action principles also apply in
the case of myocardial infarction.
Immediate care
When symptoms of myocardial
infarction occur, people wait an average of three hours, instead of doing what
is recommended: calling for help immediately. Acting
immediately by calling the emergency services can prevent sustained damage to
the heart ("time is muscle").
Certain positions allow the
patient to rest in a position which minimizes breathing difficulties. A
half-sitting position with knees bent is often recommended. Access to more
oxygen can be given by opening the window and widening the collar for easier
breathing.
Aspirin
can be given quickly (if the patient is not allergic
to aspirin); but taking aspirin before calling the emergency medical services may be
associated with unwanted delay. Aspirin has an antiplatelet
effect which inhibits formation of further thrombi
(blood clots) that clog arteries. Non-enteric
coated or soluble preparations are preferred. If chewed or
dissolved, respectively, they can be absorbed by the body even quicker. If the
patient cannot swallow, the aspirin can be used sublingually.
Glyceryl trinitrate
(nitroglycerin) sublingually (under the tongue) can be given if available.
If an Automated External
Defibrillator (AED) is available the rescuer should immediately bring the AED
to the patient's side and be prepared to follow its instructions, especially
should the victim lose consciousness.
If possible the rescuer should
obtain basic information from the victim, in case the patient is unable to
answer questions once emergency medical technicians arrive. The
victim's name and any information regarding the nature of the victim's pain
will be useful to health care providers. The exact time that these symptoms
started may be critical for determining what interventions can be safely
attempted once the victim reaches the medical center. Other useful pieces of
information include what the patient was doing at the onset of symptoms, and
anything else that might give clues to the pathology of the chest pain. It is
also very important to relay any actions that have been taken, such as the number
or dose of aspirin or nitroglycerin given, to the
Other general first aid
principles include monitoring pulse, breathing, level of consciousness and, if possible,
the blood pressure of the patient. In case of cardiac
arrest, cardiopulmonary resuscitation (CPR) can be
administered.
Automatic external defibrillation (AED)
Since the publication of data
showing that the availability of automated external defibrillators
(AEDs) in public places may significantly increase chances of survival, many of
these have been installed in public buildings, public
transport facilities, and in non-ambulance emergency vehicles (e.g. police cars
and fire engines).
AEDs analyze the heart's rhythm and determine whether the rhythm is amenable to
defibrillation
("shockable"), as in ventricular tachycardia and ventricular fibrillation.
Emergency services
Emergency Medical Services (EMS) Systems
vary considerably in their ability to evaluate and treat patients with
suspected acute myocardial infarction. Some provide as little as first aid and
early defibrillation. Others employ highly trained paramedics with
sophisticated technology and advanced protocols. Early access to EMS is promoted by a 9-1-1 system
currently available to 90% of the population in the
With primary PCI emerging as
the preferred therapy for ST segment elevation myocardial infarction, EMS can play a key role in reducing door to
balloon intervals (the time from presentation to a hospital ER to the restoration of coronary artery
blood flow) by performing a 12 lead ECG in the field and using this information to triage the
patient to the most appropriate medical facility. In addition, the 12 lead ECG
can be transmitted to the receiving hospital, which enables time saving
decisions to be made prior to the patient's arrival. This may include a
"cardiac alert" or "STEMI alert" that calls in off duty
personnel in areas where the cardiac cath lab is not staffed 24 hours a
day. Even in the absence of a formal alerting program, prehospital 12 lead ECGs
are independently associated with reduced door to treatment intervals in the
emergency department.
Wilderness first aid
In wilderness first aid, a possible heart
attack justifies evacuation by the fastest available means,
including MEDEVAC,
even in the earliest or precursor stages. The patient will rapidly be incapable
of further exertion and have to be carried out.
Air travel
Certified personnel traveling by
commercial aircraft may be able to assist an MI patient by using the on-board first aid kit,
which may contain some cardiac drugs (such as glyceryl trinitrate spray, aspirin,
or opioid
painkillers), an AED, and oxygen. Pilots may divert the flight to land at a nearby
airport. Cardiac monitors are being introduced by some
airlines, and they can be used by both on-board and ground-based physicians.
Treatment
A heart attack is a medical
emergency which demands both immediate attention and activation of
the emergency medical services. The ultimate
goal of the management in the acute phase of the disease is to salvage as much
myocardium as possible and prevent further complications. As time passes, the
risk of damage to the heart muscle increases; hence the phrase that in
myocardial infarction, "time is muscle," and time wasted is muscle
lost.
The treatments itself may have
complications. If attempts to restore the blood flow are initiated after a
critical period of only a few hours, the result is reperfusion injury instead of amelioration.
Other treatment modalities may also cause complications; the use of
antithrombotics for example carries an increased risk of bleeding.
First line
Oxygen,
aspirin,
glyceryl trinitrate
(nitroglycerin) and analgesia (usually morphine,
although experts often argue this point), hence the popular mnemonic
MONA, morphine, oxygen, nitro, aspirin) are administered as soon
as possible. In many areas, first responders can be trained to administer these
prior to arrival at the hospital. Morphine is classically the preferred pain
relief drug due to its ability to dilate blood vessels, which aids in blood
flow to the heart as well as its pain relief properties. However, morphine can
also cause hypotension (usually in the setting of hypovolemia), and should be
avoided in the case of right ventricular infarction. Moreover, the CRUSADE
trial also demonstrated an increase in mortality with administering morphine in
the setting of NSTEMI.
Of the first line agents, only
aspirin has been proven to decrease mortality.
Once the diagnosis of myocardial
infarction is confirmed, other pharmacologic agents are often given. These
include beta blockers,
anticoagulation (typically with heparin), and possibly additional antiplatelet agents such as clopidogrel.
These agents are typically not started until the patient is evaluated by an
emergency room physician or under the direction of a cardiologist. These agents
can be used regardless of the reperfusion strategy that is to be employed.
While these agents can decrease mortality in the setting of an acute myocardial
infarction, they can lead to complications and potentially death if used in the
wrong setting.
Reperfusion
The concept of reperfusion has
become so central to the modern treatment of acute myocardial infarction, that
we are said to be in the reperfusion era. Patients who present with suspected
acute myocardial infarction and ST segment elevation (STEMI) or new bundle
branch block on the 12 lead ECG are presumed to have an occlusive thrombosis in an
epicardial coronary artery. They are therefore candidates for immediate
reperfusion, either with thrombolytic therapy, percutaneous coronary intervention
(PCI) or when these therapies are unsuccessful, bypass surgery.
Individuals without ST segment
elevation are presumed to be experiencing either unstable angina (UA) or non-ST
segment elevation myocardial infarction (NSTEMI). They receive many of the same
initial therapies and are often stabilized with antiplatelet
drugs and anticoagulated. If their condition remains (hemodynamically)
stable, they can be offered either late coronary angiography with subsequent
restoration of blood flow (revascularization), or non-invasive stress testing to determine if there is
significant ischemia that would benefit from revascularization. If hemodynamic
instability develops in individuals with NSTEMIs, they may undergo urgent
coronary angiography and subsequent revascularization. The use of thrombolytic
agents is contraindicated in this patient subset, however.
The basis for this distinction in
treatment regimens is that ST segment elevations on an ECG are typically due to
complete occlusion of a coronary artery. On the other hand, in NSTEMIs there is
typically a sudden narrowing of a coronary artery with preserved (but
diminished) flow to the distal myocardium. Anticoagulation and antiplatelet
agents are given to prevent the narrowed artery from occluding.
At least 10% of patients with
STEMI don't develop myocardial necrosis (as evidenced by a rise in cardiac
markers) and subsequent Q waves on EKG after reperfusion therapy. Such a
successful restoration of flow to the infarct-related artery during an acute
myocardial infarction is known as "aborting" the myocardial
infarction. If treated within the hour, about 25% of STEMIs can be aborted.
Thrombolytic therapy
Thrombolytic therapy is indicated
for the treatment of STEMI if the drug can be administered within 12 hours of
the onset of symptoms, the patient is eligible based on exclusion criteria, and
primary PCI is not immediately available. The effectiveness of thrombolytic
therapy is highest in the first 2 hours. After 12 hours, the risk
associated with thrombolytic therapy outweighs any benefit. Because
irreversible injury occurs within 2–4 hours of the infarction, there is a
limited window of time available for reperfusion to work.
Thrombolytic drugs are
contraindicated for the treatment of unstable angina and NSTEMI and for the
treatment of individuals with evidence of cardiogenic
shock.
Although no perfect thrombolytic
agent exists, an ideal thrombolytic drug would lead to rapid reperfusion, have
a high sustained patency rate, be specific for recent thrombi, be easily and
rapidly administered, create a low risk for intra-cerebral and systemic
bleeding, have no antigenicity, adverse hemodynamic effects, or clinically
significant drug interactions, and be cost effective. Currently available
thrombolytic agents include streptokinase, urokinase,
and alteplase
(recombinant tissue plasminogen activator, rtPA). More
recently, thrombolytic agents similar in structure to rtPA such as reteplase
and tenecteplase
have been used. These newer agents boast efficacy at least as good as rtPA with
significantly easier administration. The thrombolytic agent used in a
particular individual is based on institution preference and the age of the
patient.
Depending on the thrombolytic
agent being used, adjuvant anticoagulation with heparin
or low molecular weight heparin may be of
benefit. With TPa and related agents (reteplase and tenecteplase), heparin is
needed to maintain coronary artery patency. Because of the anticoagulant effect
of fibrinogen depletion with streptokinase and urokinase treatment, it is less
necessary there.
Intracranial bleeding (ICB) and
subsequent cerebrovascular accident (CVA) is a
serious side effect of thrombolytic use. The risk of ICB is dependent on a
number of factors, including a previous episode of intracranial bleed, age of
the individual, and the thrombolytic regimen that is being used. In general,
the risk of ICB due to thrombolytic use for the treatment of an acute
myocardial infarction is between 0.5 and 1 percent.
Thrombolytic therapy to abort a
myocardial infarction is not always effective. The degree of effectiveness of a
thrombolytic agent is dependent on the time since the myocardial infarction
began, with the best results occurring if the thrombolytic agent is used within
two hours of the onset of symptoms. If the individual presents more than 12
hours after symptoms commenced, the risk of intracranial bleed are considered
higher than the benefits of the thrombolytic agent. Failure rates of thrombolytics
can be as high as 20% or higher. In cases of failure of the thrombolytic agent
to open the infarct-related coronary artery, the patient is then either treated
conservatively with anticoagulants and allowed to "complete the
infarction" or percutaneous coronary intervention
(PCI, see below) is then performed. Percutaneous coronary intervention in this
setting is known as "rescue PCI" or "salvage PCI".
Complications, particularly bleeding, are significantly higher with rescue PCI
than with primary PCI due to the action of the thrombolytic agent.
Monitoring for arrhythmias
Additional objectives are to
prevent life-threatening arrhythmias or conduction disturbances. This requires
monitoring in a coronary care unit and protocolised
administration of antiarrhythmic agents. Antiarrhythmic
agents are typically only given to individuals with life-threatening
arrhythmias after a myocardial infarction and not to suppress the ventricular ectopy that is
often seen after a myocardial infarction.
Rehabilitation
Cardiac rehabilitation
aims to optimize function and quality of
life in those afflicted with a heart disease. This can be with the
help of a physician, or in the form of a cardiac rehabilitation program.
Physical
exercise is an important part of rehabilitation after a
myocardial infarction, with beneficial effects on cholesterol levels, blood
pressure, weight, stress and mood.
Some patients become afraid of exercising because it might trigger another
infarct. Patients are stimulated to exercise, and should only avoid certain
exerting activities such as shovelling. Local authorities may place limitations
on driving
motorised
vehicles. Some people are afraid to have sex after a heart attack. Most people can
resume sexual activities after 3 to 4 weeks. The amount of activity needs to be
dosed to the patient's possibilities.
Secondary prevention
The risk of a recurrent
myocardial infarction decreases with strict blood pressure management and
lifestyle changes, chiefly smoking cessation,
regular exercise, a sensible diet for patients with heart disease, and limitation of
alcohol intake.
Patients are usually commenced on
several long-term medications post-MI, with the aim of preventing secondary
cardiovascular events such as further myocardial infarctions, congestive heart failure or cerebrovascular accident (CVA). Unless contraindicated, such
medications may include:
- Antiplatelet drug therapy such as aspirin
and/or clopidogrel should be continued to reduce
the risk of plaque rupture and recurrent myocardial infarction. Aspirin is
first-line, owing to its low cost and comparable efficacy, with
clopidogrel reserved for patients intolerant of aspirin. The combination
of clopidogrel and aspirin may further reduce risk of cardiovascular events,
however the risk of hemorrhage is increased.
- Beta blocker therapy such as metoprolol
or carvedilol
should be commenced. These have been particularly beneficial in high-risk
patients such as those with left
ventricular dysfunction and/or continuing cardiac ischaemia.
β-Blockers decrease mortality and morbidity. They also improve
symptoms of cardiac ischemia in NSTEMI.
- ACE inhibitor therapy should be commenced
24–48 hours post-MI in hemodynamically-stable patients, particularly in
patients with a history of MI, diabetes mellitus, hypertension,
anterior
location of infarct (as assessed by ECG), and/or evidence of left
ventricular dysfunction. ACE inhibitors reduce mortality, the development
of heart failure, and decrease ventricular
remodelling post-MI.
- Statin therapy has been shown to reduce
mortality and morbidity post-MI. The effects of statins may be more than
their LDL lowering effects. The general consensus is that statins have plaque
stabilization and multiple other ("pleiotropic") effects that
may prevent myocardial infarction in addition to their effects on blood
lipids.
- The aldosterone antagonist agent eplerenone
has been shown to further reduce risk of cardiovascular death post-MI in
patients with heart failure and left ventricular dysfunction, when used in
conjunction with standard therapies above.
- Omega-3 fatty acids, commonly found
in fish, have been shown to reduce mortality post-MI. While the mechanism
by which these fatty acids decrease mortality is unknown, it has been
postulated that the survival benefit is due to electrical stabilization
and the prevention of ventricular fibrillation.] However, further studies in a high-risk subset
have not shown a clear-cut decrease in potentially fatal arrhythmias due
to omega-3 fatty acids.
Complications
Complications may occur immediately
following the heart attack (in the acute
phase), or may need time to develop (a chronic problem). After an infarction, an
obvious complication is a second infarction, which may occur in the domain of
another atherosclerotic coronary artery, or in the same zone if there are any
live cells left in the infarct.
Congestive
heart failure
A myocardial infarction may
compromise the function of the heart as a pump for the circulation, a state called heart failure.
There are different types of heart failure; left- or right-sided (or bilateral)
heart failure may occur depending on the affected part of the heart, and it is
a low-output type of failure. If one of the heart valves is affected, this may
cause dysfunction, such as mitral regurgitation in the case of
left-sided coronary occlusion that disrupts the blood supply of the papillary
muscles. The incidence of heart failure is particularly high in patients with
diabetes and requires special management strategies.
Myocardial rupture
Myocardial rupture is most common three to five
days after myocardial infarction, commonly of small degree, but may occur one
day to three weeks later. In the modern era of early revascularization and
intensive pharmacotherapy as treatment for MI, the incidence of myocardial rupture
is about 1% of all MIs. This may occur in the free walls of the ventricles,
the septum
between them, the papillary muscles, or less commonly the atria. Rupture occurs
because of increased pressure against the weakened walls of the heart chambers
due to heart muscle that cannot pump blood out effectively. The weakness may
also lead to ventricular aneurysm, a localized dilation or ballooning of the heart
chamber.
Risk factors for myocardial
rupture include completion of infarction (no revascularization performed),
female sex, advanced age, and a lack of a previous history of myocardial
infarction. In addition, the risk of rupture is higher in individuals who are
revascularized with a thrombolytic agent than with PCI.[175][176] The shear stress between the infarcted segment and
the surrounding normal myocardium (which may be hypercontractile in the
post-infarction period) makes it a nidus for rupture.
Rupture is usually a catastrophic
event that may result a life-threatening process known as cardiac
tamponade, in which blood accumulates within the pericardium
or heart sac, and compresses the heart to the point where it cannot pump
effectively. Rupture of the intraventricular septum (the muscle separating the
left and right ventricles) causes a ventricular septal defect with shunting
of blood through the defect from the left side of the heart to the right side
of the heart, which can lead to right ventricular failure as well as pulmonary
overcirculation. Rupture of the papillary muscle may also lead to acute mitral regurgitation and subsequent pulmonary
edema and possibly even cardiogenic
shock.
Life-threatening
arrhythmia
A 12 lead electrocardiogram
showing ventricular tachycardia.
Since the electrical
characteristics of the infarcted tissue change (see pathophysiology section), arrhythmias
are a frequent complication. The re-entry phenomenon may cause rapid heart
rates (ventricular tachycardia and even ventricular fibrillation), and ischemia in
the electrical conduction system of the
heart may cause a complete heart block (when the impulse
from the sinoatrial node, the normal cardiac pacemaker,
does not reach the heart chambers).
Pericarditis
As a reaction to the damage of
the heart muscle, inflammatory cells are attracted. The
inflammation may reach out and affect the heart sac. This is called pericarditis.
In Dressler's syndrome, this occurs several weeks
after the initial event.
Cardiogenic shock
A complication that may occur in
the acute setting soon after a myocardial infarction or in the weeks following
it is cardiogenic shock. Cardiogenic shock is defined
as a hemodynamic state in which the heart cannot produce enough of a cardiac
output to supply an adequate amount of oxygenated blood to the
tissues of the body.
While the data on performing
interventions on individuals with cardiogenic shock is sparse, trial data suggests
a long-term mortality benefit in undergoing revascularization if the individual
is less than 75 years old and if the onset of the acute myocardial infarction
is less than 36 hours and the onset of cardiogenic shock is less than 18 hours.
If the patient with cardiogenic shock is not going to be revascularized,
aggressive hemodynamic support is warranted, with insertion of an intra-aortic balloon pump if not
contraindicated. If diagnostic coronary angiography does not reveal a culprit
blockage that is the cause of the cardiogenic shock, the prognosis is poor.
Prognosis The prognosis
for patients with myocardial infarction varies greatly, depending on the patient,
the condition itself and the given treatment. Using simple variables
which are immediately available in the emergency
room, patients with a higher risk of adverse outcome can be
identified. For example, one study found that 0.4% of patients with a low risk
profile had died after 90 days, whereas the mortality
rate in high risk patients was 21.1%.
Although studies differ in the
identified variables, some of the more reproduced
risk stratifiers include age, hemodynamic
parameters (such as heart failure, cardiac
arrest on admission, systolic blood
pressure, or Killip class of two or greater), ST-segment
deviation, diabetes, serum
creatinine
concentration, peripheral vascular disease
and elevation of cardiac markers.
Assessment of left
ventricular ejection fraction may increase the predictive
power of some risk stratification models. The prognostic importance of Q-waves
is debated. Prognosis is significantly worsened if a mechanical complication (papillary
muscle rupture, myocardial free wall rupture, and so on) were to
occur.
There is evidence that case
fatality of myocardial infarction has been improving over the years in all
ethnicities.
Legal
implications
At common law,
a myocardial infarction is generally a disease,
but may sometimes be an injury. This has implications for no-fault insurance schemes
such as workers' compensation. A heart attack is
generally not covered; however, it may be a work-related
injury if it results, for example, from unusual emotional stress or
unusual exertion. Additionally, in some jurisdictions, heart attacks suffered
by persons in particular occupations such as police
officers may be classified as line-of-duty injuries by statute or
policy. In some countries or states, a person who has suffered from a
myocardial infarction may be prevented from participating in activity that puts
other people's lives at risk, for example driving a car, taxi or airplane.
Theme:
Urgent help at acute heart failure on prehospital stage
Acute heart failure
Syndroms: acute heart failure, acute left ventricular heart failure, acute right
ventricular heart failure; acute left atrial heart failure, acute right atrial
heart failure; acute failure either heart and vessels; acute vessels
insufficiency.
Acute heart failure (AHF) is always an indication for referral to an
intensive care unit. In the widest sense, the term acute heart failure includes
the manifestation forms of pulmonary edema, cardiogenic shock or rapid-onset
decompensated cardiac insufficiency unaccompanied by shock or pulmonary edema
(low-output syndrome).
Epidemiology
and aetiology
Acute heart failure may occur in the absence of previously known heart
disease. Existing prior specific diseases that may end in acute cardiac
insufficiency include acute myocardial infarction, decompensated
cardiomyopathy, myocarditis, cardiac tamponade, endocarditis or arrhythmogenic
heart failure. Coronary heart disease is the aetiology of AHF in
60–70% of patients, particularly in the elderly population.
In younger subjects, AHF is frequently caused by dilated
cadiomyopathy, arrhythmia, congenital or valvular heart disease, or
myocarditis. The management of heart failure consumes 1–2% of health care
expenditure in European countries, with around 75% relating to
inpatient care. Advanced heart failure and related acute decompensation
have become the single most costly medical syndrome in cardiology.
About
45% of patients hospitalized with AHF will be rehospitalized at
least once (and 15% at least twice) within twelve months. Estimates
of the risk of death or rehospitalization within 60 days of
admission vary from 30 to 60%, depending on the population studied.
Patients with AHF have a very poor prognosis.
Mortality is particularly high in patients with acute myocardial
infarction (AMI) accompanied by severe heart failure, with a 30% 12
month mortality. Likewise, in acute pulmonary oedema a 12%
in-hospital and 40% 1 year mortality have been reported.
Table
1
Causes and precipitating factors
in
acute heart failure
|
PATHOPHYSIOLOGY
Myocardial contraction
Myocardial
cells (myocytes) are about 50-100 |im long; each cell branches and
interdigitates with adjacent cells. An intercalated disc permits electrical
conduction (via gap junctions) and mechanical conduction (via the fascia
adherens)
to adjacent cells. The basic unit of
contraction is the sarcomere (2 \m\ in length), which is aligned to
those of adjacent myofibrils, giving a striated appearance due to the Z-lines
(see Fig. 12.4). Actin filaments (molecular weight 47 000) are attached at
right angles to the Z-lines and interdigitate with thicker parallel myosin
filaments (molecular weight 500 000). The cross-links between actin and myosin
molecules contain myofibrillar ATPase, which breaks down adenosine triphosphate
(ATP) to provide the energy for contraction. Two chains of actin molecules form
a helical structure, with a second molecule, tropomyosin, in the grooves of the
actin helix, and a further molecule, troponin, attached to every seventh actin
molecule (see Fig. 12.5). During contraction, shortening of the sarcomere
results from the interdigitation of the actin and myosin molecules,
without altering the length of either
molecule. Contraction is initiated when calcium is made available during the
plateau phase of the action potential by calcium ions entering the cell and
being mobilised from the sarcoplasmic reticulum. As its concentration rises,
calcium binds to troponin, precipitating contraction. The force of cardiac
muscle contraction, or inotropic state, is regulated by the influx of calcium
ions through 'slow calcium channels'. The extent to which the sarcomere can
shorten determines stroke volume of the ventricle. It is maximally shortened in response to powerful
inotropic drugs or severe exercise.
Fig. 1.
Contraction process with the muscle fibre
Fig. 2. Normal heart structures
Factors
influencing cardiac output
Cardiac output is determined by the product of stroke
volume and heart rate. Stroke volume is dependent upon enddiastolic pressure
(preload) and peripheral vascular resistance (afterload). Stretch of cardiac
muscle (arising from an increment in end-diastolic volume or preload) results
in the increased force of contraction, producing an increase in stroke volume.
This relationship is known as Starling's Law of the heart. Afterload falls as
blood pressure is reduced and this
allows
greater shortening of the muscle fibres and hence increased stroke volume. The
contractile state of the myocardium is controlled, in part, by the
neuro-endocrine system; it is also influenced by various inotropic drugs and
their antagonists. Determination of the response to a physiological change or
to a drug can be predicted on the basis of its combined influence on preload,
afterload and contractility.
Factors
influencing resistance to systemic blood flow
Systemic blood flow is critically dependent upon
vascular resistance, which varies with the fourth power of the radius of the
resistance vessel. Thus small changes in calibre have a marked influence on
blood flow. Metabolic and mechanical factors control arteriolar tone.
Neurogenic constriction operates
via
oe-adrenoceptors on vascular smooth muscle, and dilatation via muscarinic and
f52-adrenoceptors. In addition, systemic and locally released vasoactive
substances influence tone; vasoconstrictors include noradrenaline, angiotensin
II and endothelin, whereas adenosine, bradykinin, prostaglandins and nitric
oxide are vasodilators. Resistance to blood flow rises with viscosity, and is
mainly influenced by red cell concentration (haematocrit).
Factors
influencing resistance to coronary blood flow
Coronary blood vessels receive sympathetic and
parasympathetic innervation. Stimulation of oc-adrenoceptors causes vasoconstriction;
stimulation of P2-adrenoceptors causes vasodilatation; the predominant effect
of sympathetic stimulation in coronary arteries is vasodilatation.
Parasympathetic stimulation also causes modest dilatation of normal coronary
arteries. Healthy coronary endothelium releases nitric oxide which promotes
vasodilatation, but if the endothelium is damaged by atheroma, vasoconstriction
may predominate.
Systemic
hormones, neuropeptides and other locally derived factors such as endothelins,
which are the most potent vasoconstrictors identified, also influence arterial
tone and coronary flow. A similar balance exists in the systemic circulation
and
influences peripheral vascular tone and blood pressure. As a result of vascular
regulation, an atheromatous narrowing (stenosis) in a coronary artery does not
limit flow, even during exercise, until the cross-sectional area of the vessel
is reduced by at least 70%.
The vicious circle in the
acute failing heart
The final common denominator in the
syndrome of AHF is a critical inability of the myocardium to
maintain a cardiac output sufficient to meet the demands of the
peripheral circulation. Irrespective of the underlying cause of AHF,
a vicious circle is activated that, if not appropriately treated,
leads to chronic heart failure and death. This is shown in Figure,
and is described in detail elsewhere.
Fig. 3. Pathophysiology of the syndrome of
acute heart failure.
Following acute critical events,
In
order for patients with AHF to respond to treatment the myocardial dysfunction
must be reversible. This is particularly important in AHF due to
ischaemia, stunning or hibernation, where a dysfunctional myocardium
can return to normal when appropriately treated.
Myocardial
stunning is the myocardial dysfunction that occurs following
prolonged ischaemia, which may persist in the short-term even when
normal blood flow is restored. The intensity and duration of
stunning is dependent on the severity and duration of the preceding
ischaemic insult.
Hibernation
Hibernation is defined as an impairment of myocardial function due
to severely reduced coronary blood flow although myocardial cells
are still intact. By improving blood flow and oxygenation, hibernating
myocardium can restore its normal function.
Hibernating
myocardium and stunning can co-exist. Hibernation improves in time
with reinstitution of blood flow and oxygenation, whilst stunned
myocardium retains inotropic reserve and can respond to inotropic
stimulation. Since these mechanisms depend on the duration of
myocardial damage, a rapid restoration of oxygenation and blood flow
is mandatory to reverse these pathophysiological alterations.
classification
The Killip classification was
designed to provide a clinical estimate of the severity of
myocardial derangement in the treatment of AMI:
- StageI—No heart failure. No clinical signs
of cardiac decompensation;
- StageII—Heart failure. Diagnostic criteria
include rales, S3 gallop and pulmonary venous hypertension.
Pulmonary congestion with wet rales in the lower half of
the lung fields;
- StageIII—Severe heart failure. Frank
pulmonary oedema with rales throughout the lung
fields;
- StageIV—Cardiogenic shock. Signs
include hypotension (SBP
90mmHg),
and evidence of peripheral vasoconstriction such as
oliguria, cyanosis and diaphoresis.
|
Killip Classification
System |
||
|
Killip Class |
Characteristics |
Patients (%) |
|
I |
No
evidence of congestive heart failure |
85 |
|
II |
Rales,
↑ JVD, or S3 gallop |
13 |
|
III |
Pulmonary edema |
1 |
|
IV |
Cardiogenic Shock |
|
Forrester classification
The
Forrester AHF classification was also developed in AMI patients, and
describes four groups according to clinical and haemodynamic status
(Figure). Patients are classified clinically on the basis of
peripheral hypoperfusion (filliform pulse, cold clammy skin,
peripheral cyanosis, hypotension, tachycardia, confusion, oliguria)
and pulmonary congestion (rales, abnormal chest X-ray), and
haemodynamically on the basis of a depressed cardiac index (2.2 L/min/m2)
and elevated pulmonary capillary pressure (>18 mmHg). The
original paper defined the treatment strategy according to the
clinical and haemodynamic status. Mortality was 2.2% in group I,
10.1% in group II, 22.4% in group III, and 55.5% in group IV.
Fig.4. Clinical classification of the mode of heart
failure (Forrester classification). H I-IV refers to haemodynamic severity,
with reference figures for CI and pulmonary capillary pressures shown on the
vertical and horizontal axes, respectively. C I-IV refers to clinical severity.
‘Clinical
severity’ classification
The clinical severity
classification is based on observation of the peripheral circulation
(perfusion) and on auscultation of the lungs (congestion). The
patients can be classified as Class I (Group A) (warm and dry),
Class II (Group B) (warm and wet), Class III (Group L) (cold and
dry), and Class IV (Group C) (cold and wet). This classification has
been validated prognostically in a cardiomyopathy service, and is
therefore applicable to patients with chronic heart failure, whether
hospitalized or outpatients.
clinical
The patient with acute heart failure
may present with one of several distinct clinical conditions (Table 2):
I.
Acute
decompensated heart failure (de novo or as decompensation of
chronic heart failure) with signs and symptoms of acute heart failure,
which are mild and
do not fulfil criteria for cardiogenic shock, pulmonary oedema
or hypertensive crisis.
II.
Hypertensive
AHF: Signs and symptoms of heart failure are accompanied by
high blood pressure and relatively preserved left ventricular function
with a chest radiograph compatible with acute pulmonary oedema.
III.
Pulmonary
oedema (verified by chest X-ray) accompanied by severe respiratory
distress, with crackles over the lung and orthopnoea, with O2
saturation usually <90% on room air prior to treatment.
IV.
Cardiogenic
shock: Cardiogenic shock is defined as evidence of tissue
hypoperfusion induced by heart failure after correction of
pre-load. There is no clear definition for haemodynamic parameters,
which explains the differences in prevalence and outcome
reported in studies (Table 3), but cardiogenic shock is usually characterized
by reduced blood pressure (systolic BP <90 mmHg or a
drop of mean arterial pressure>30 mmHg) and/or low
urine output (<0.5 ml/kg/h), with a pulse rate
>60 b.p.m. with or without evidence of organ congestion.
There is a continuum from low cardiac output syndrome to cardiogenic
shock.
V.
High
output failure is characterized by high cardiac output, usually
with high heart rate (caused by arrhythmias, thyrotoxicosis, anaemia,
Paget's disease, iatrogenic or by other mechanisms), with warm
peripheries, pulmonary congestion, and sometimes with low BP as in
septic shock.
VI.
Right
heart failure is characterized by low output syndrome with
increased
jugular
venous pressure, increased liver size and hypotension.
Table
3
Terminology and
common clinical and haemodynamic characteristics
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There
are exceptions; the above values in table are general rules.
*The
differentation from low cardiac output syndrome is subjective and the clinical
presentation may overlap these classifications.
SBP=systolic
blood pressure; CI=cardiac index; PCWP=pulmonary capillary wedge pressure;
CNS=central nervous system.
Various
other classifications of the acute heart failure syndrome are
utilized in coronary care and intensive care units. The Killip
classification is based on clinical signs and chest X-ray findings,
and the Forrester classification is based on clinical signs and
haemodynamic characteristics. These classifications have been
validated in acute heart failure after AMI and thus are best applied
to acute de novo heart failure. The third ‘clinical severity’
classification has been validated in a cardiomyopathy service and is
based on clinical findings. It is most applicable to chronic
decompensated heart failure.
AHF is a clinical syndrome, with reduced cardiac
output, tissue hypoperfusion, increase in the pulmonary capillary
wedge pressure (PCWP), and tissue congestion. The underlying
mechanism may be cardiac or extra-cardiac, and may be transient and
reversible with resolution of the acute syndrome, or may induce
permanent damage leading to chronic heart failure. The cardiac
dysfunction can be related to systolic or diastolic myocardial
dysfunction (mainly induced by ischaemia or infection), acute valvular
dysfunction, pericardial tamponade, abnormalities of cardiac
rhythm, or pre-load/after-load mismatch. Multiple extra-cardiac
pathologies may result in acute heart failure by changing the
cardiac loading conditions for example (I) increased after-load due
to systemic or pulmonary hypertension or massive pulmonary emboli,
(II) increased pre-load due to increased volume intake or reduced
excretion due to renal failure or endocrinopathy, or (II) high
output state due to infection, thyrotoxicosis, anaemia, Paget's
disease. Heart failure can be complicated by co-existing end-organ
disease. Severe heart failure can also induce multi-organ failure,
which may be lethal.
Appropriate
long-term medical therapy and, if possible, anatomical correction of
the underlying pathology may prevent further AHF syndrome ‘attacks’
and improve the poor long-term prognosis associated with this
syndrome.
The
clinical AHF syndrome may be classified as predominantly left or
right forward failure, left or right backward failure, or a
combination of these.
Forward acute heart failure may be mild-to-moderate with only effort
fatigue, up to severe with manifestations of reduced tissue
perfusion at rest with weakness, confusion, drowsiness, paleness
with peripheral cyanosis, cold clammy skin, low blood pressure,
filliform pulse, and oliguria, culminating in the full blown presentation
of cardiogenic shock.
This
syndrome may be induced by a large variety of pathologies. An
adequate history may indicate the main diagnosis for example (I)
acute coronary syndrome with the relevant risk factors, past
history, and suggestive symptoms; (II) acute myocarditis with a
recent history suggestive of acute viral infection; (III) acute
valvular dysfunction with a history of chronic valve disease or
valve surgery, infection with the possibility of bacterial endocarditis,
or chest trauma; (IV) pulmonary embolism with a relevant history and
suggestive symptoms; or (V) pericardial tamponade.
Physical
examination of the cardiovascular system may be indicative of the
main diagnosis, for example by distended neck veins and paradoxical
pulse (pericardial tamponade), muffled heart sounds related to
myocardial systolic dysfunction, or the disappearance of artificial
valve sounds or an appropriate murmur indicating a valvular problem.
In forward AHF immediate management should include
supportive treatment to improve cardiac output and tissue
oxygenation. This can be achieved with vasodilating agents, fluid
replacement to achieve an optimal pre-load, short-term inotropic
support and (sometimes) intra-aortic balloon counterpulsation.
Left-heart backward
failure may be related to left ventricular dysfunction with varying
degrees of severity, from mild-to-moderate with only exertional
dyspnoea, to pulmonary oedema presenting with shortness of breath
(dry cough, sometimes with frothy sputum), pallor or even cyanosis,
cold clammy skin, and normal or elevated blood pressure. Fine rales
are usually audible over the lung fields. Chest X-ray shows
pulmonary congestion/oedema.
Pathology
of the left heart may be responsible for this syndrome, including:
myocardial dysfunction related to chronic existing conditions; acute
insult such as myocardial ischaemia or infarction; aortic and mitral
valve dysfunction; cardiac rhythm disturbances; or tumours of the
left heart. Extra-cardiac pathologies may include severe
hypertension, high output states (anaemia, thyrotoxicosis) and
neurogenic states (brain tumours or trauma).
Physical
examination of the cardiovascular system, including the apex beat,
the quality of the heart sounds, the presence of murmurs, and
auscultation of the lungs for fine rales and expiratory wheezing
(‘cardiac asthma’) may be indicative of the main diagnosis.
In left heart backward failure patients should be
treated mainly with vasodilation and the addition of diuretics, bronchodilators
and narcotics, as required. Respiratory support may be necessary. This
can either be with continuous positive airway pressure (CPAP) or
non-invasive positive pressure ventilation, or in some circumstances
invasive ventilation may be required following endotracheal
intubation.
The syndrome of
acute right heart failure is related to pulmonary and right heart
dysfunction, including exacerbations of chronic lung disease with
pulmonary hypertension, or acute massive lung disease (e.g. massive
pneumonia or pulmonary embolism), acute right ventricular
infarction, tricuspid valve malfunction (traumatic or infectious),
and acute or sub-acute pericardial disease. Advanced
left heart disease progressing to right-sided failure should also be
considered, and similarly long-standing congenital heart disease
with evolving right ventricular failure should be taken into
account. Non-cardiopulmonary pathologies include nephritic/nephrotic
syndrome and end-stage liver disease. Various vasoactive
peptide-secreting tumours should also be considered.
The typical presentation is with fatigue, pitting
ankle oedema, tenderness in the upper abdomen (due to liver
congestion), shortness of breath (with pleural effusion) and
distension of the abdomen (with ascites). The full-blown syndrome
includes anasarca with liver dysfunction and oliguria.
History
and physical examination should confirm the syndrome of acute right
heart failure, indicate the suspected diagnosis and guide further
investigation, which is likely to include ECG, blood gases, D-dimer,
chest X-ray, cardiac Doppler-echocardiography, angiography or chest
CT scan.
In
right heart backward failure fluid overload is managed with diuretics,
including spironolactone, and sometimes with a short course of low
dose (‘diuretic dose’) of dopamine. Concomitant treatment may
include: antibiotics for pulmonary infection and bacterial
endocarditis; Ca++ channel blockers, nitric oxide, or
prostaglandins for primary pulmonary hypertension; and anticoagulants,
thrombolytics, or thrombectomy for acute pulmonary embolism.
The diagnosis
of AHF is based on the symptoms and clinical findings, supported by
appropriate investigations such as ECG, chest X-ray, biomarkers, and
Doppler-echocardiography (Fig. 5).
The patient should be classified according
to previously described criteria for systolic and/or diastolic
dysfunction (Fig. 6), and
by the characteristics of forward or backward left or right heart
failure.
Fig. 5. An abnormal echocardiogram.
Colors are used to represent the velocity and direction of blood flow
Fig. 6. Diastolic and systolic dysfunction
Fig. 7. Diagnosis
of AHF
Fig. 7. Assessment of
A normal ECG is uncommon in acute heart
failure. The ECG is able to identify the rhythm, and may help
determine the aetiology of AHF and assess the loading conditions of
the heart. It is essential in the assessment of acute coronary
syndromes. The ECG may also indicate acute right or left ventricular
or atrial strain, perimyocarditis and pre-existing conditions such
as left and right ventricular hypertrophy or dilated cardiomyopathy.
Cardiac arrhythmia should be assessed in the 12-lead ECG as well
as in continuous ECG monitoring.
Chest X-ray and imaging techniques
Chest X-ray and other imaging should be performed
early for all patients with AHF to evaluate pre-existing chest or
cardiac conditions (cardiac size and shape) and to assess pulmonary
congestion. It is used both for confirmation of the diagnosis, and
for follow-up of improvement or unsatisfactory response to therapy.
Chest X-ray allows the differential diagnosis of left heart failure
from inflammatory or infectious lung diseases. Chest CT scan with or
without contrast angiography and scintigraphy may be used to clarify
the pulmonary pathology and diagnose major pulmonary embolism. CT
scan or transesophageal echocardiography should be used in cases of
suspicion of aortic dissection.
A
number of laboratory tests should be performed in AHF patients (Table).
Arterial blood gas analysis (Astrup) enables assessment of
oxygenation (pO2), respiratory adequacy (pCO2), acid–base
balance (pH), and base deficit, and should be performed in all
patients with severe heart failure. Non-invasive measurement with
pulse oximetry and end-tidal CO2 can often replace Astrup
(Level of evidence C) but not in very low output, vasocontricted
shock states. Measurement of venous O2 saturation (i.e.
in the jugular vein) may be useful for an estimation of the total
body oxygen supply-demand balance.
Table 4
Laboratory tests in patients hospitalized with AHF
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Other
specific laboratory tests should be taken for differential diagnostic purposes
or in order to identify end-organ dysfunction.
INR=international
normalized ratio of thromboplastin time; TnI=troponin I; TnT=troponin T.
Plasma
B-type natriuretic peptide (BNP) is released from the cardiac
ventricles in response to increased wall stretch and volume overload
and has been used to exclude and/or identify congestive heart
failure (CHF) in patients admitted, for dyspnoea, to the emergency
department. Decision cut points of 300 pg/mL for NT-proBNP and
100 pg/mL for BNP have been proposed, but the older population
has been poorly studied. During ‘flash’ pulmonary oedema, BNP levels
may remain normal at the time of admission. Otherwise, BNP has a
good negative predictive value to exclude heart failure. Various
clinical conditions may affect the BNP concentration including renal
failure and septicaemia. If elevated concentrations are present,
further diagnostic tests are required. If AHF is confirmed,
increased levels of plasma BNP and NT-pro BNP carry important
prognostic information. The exact role of BNP remains to be fully
clarified.
Echocardiography
Echocardiography is an essential tool
for the evaluation of the functional and structural changes
underlying or associated with AHF, as well as in the assessment of
acute coronary syndromes.
Class
I recommendation, level of evidence C
Echocardiography with Doppler imaging should be used
to evaluate and monitor regional and global left and right
ventricular function, valvular structure and function, possible
pericardial pathology, mechanical complications of acute myocardial
infarction and—on rare occasions—space occupying lesions. Cardiac
output can be estimated by appropriate Doppler aortic or pulmonary
time velocity contour measurements. An appropriate echo-Doppler study
can also estimate pulmonary artery pressures (from the tricuspid
regurgitation jet) and has also been used for the monitoring of left
ventricular pre-load. Echocardiography has not been
validated with right heart catheterization in patients with AHF.
Fig. 8. Echocardiographic Images in a
Other investigations
In cases of coronary-artery-related complications such as unstable angina
or myocardial infarction, angiography is important and angiography-based
revascularization therapy has been shown to improve prognosis.
Class I recommendation,
level of evidence B
Coronary
arteriography is also often indicated in prolonged AHF, unexplained
by other investigations, as recommended in the guidelines for
diagnosis of CHF.
Insertion of
a pulmonary artery catheter (PAC) may assist in making the diagnosis
of AHF. See Section 7.2.3 for further details.
Table 5
Non-invasive monitoring
In all critically ill patients, BP measurements should
be made routinely; blood pressure, temperature, respiratory rate,
heart rate, the electrocardiogram and blood pressure is mandatory.
Some laboratory tests should be done repeatedly i.e. electrolytes, creatinine
and glucose or markers for infection or other metabolic disorders.
Hypo– or hyperkalaemia must be controlled. These can all be
monitored easily and accurately with modern automated equipment. If
the patient becomes more unwell, the frequency of these observations
will need to be increased.
ECG
monitoring (arrhythmias and ST segment) is necessary during the
acute decompensation phase, particularly if ischaemia or arrhythmia
is responsible for the acute event.
The immediate goals are to improve symptoms and to
stabilize the haemodynamic condition (Table 6). An improvement in haemodynamic parameters
only may be misleading, however, and a concomitant improvement in
symptoms (dyspnoea and/or fatigue) is generally required. These
short-term benefits must also be accompanied by favourable effects
on longer-term outcomes. This is likely to be achieved by avoidance,
or limitation, of myocardial damage.
Instrumentation and monitoring of patients in AHF
Monitoring of the patient with AHF should be initiated
as soon as possible after his/her arrival at the emergency unit,
concurrently with ongoing diagnostic measures addressed at
determining the primary aetiology. The types and level of monitoring
required for any individual patient vary widely depending on the
severity of the cardiac decompensation and the response to initial
therapy. Local logistic issues may also be relevant. The guidelines
on monitoring discussed here are based on expert opinion.
Table 6
Goals of treatment
of the patient with AHF
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BUN=blood urea nitrogen.
Best
results are achieved if patients with AHF are treated promptly by
expert staff in areas reserved for heart failure patients. An
experienced cardiologist and/or other suitably trained staff should
treat AHF patients. The diagnostic services should provide early
access to diagnostic procedures such as echocardiography and
coronary angiography, as needed.
Treatment
of patients with AHF requires a treatment plan in the hospital
system.
Class I recommendation, level of evidence B
Comparative
studies have shown shorter hospitalization time in patients treated
by staff trained in heart failure management. The treatment of AHF
should be followed by a subsequent HF clinic programme when
applicable and as recommended by ESC guidelines.
The
care and information needs of the acutely ill patient and his/her
family will usually be addressed by expert nurses.
Heart
failure staff nurses and cardiology/heart failure/intensive care
specialists should be given the opportunity for continuing professional
education.
Recommendations
on the standard structure, nursing staff and equipment requirements
in intensive cardiology care units and relevant step-down care units
based on the expert opinion of the Working Group of Acute Cardiac
Care are under preparation.
Class I recommendation,
level of evidence C
Maintenance
of normal blood pressure is critical during the initiation of
therapy, and consequently it should be measured regularly (e.g.
every 5 minutes), until the dosage of vasodilators, diuretics or
inotropes has been stabilized. The reliability of non-invasive,
automatic plethysmographic measurement of blood pressure is good in
the absence of intense vasoconstriction and very high heart rate.
Class I recommendation, level of evidence C
The
pulse oximeter is a simple non-invasive device that estimates the
arterial saturation of haemoglobin with oxygen (SaO2). The estimate
of the SaO2 is usually within 2% of a measured value from
a co-oximeter, unless the patient is in cardiogenic shock. The pulse
oximeter should be used continuously on any unstable patient who is
being treated with a fraction of inspired oxygen (FiO2)
that is greater than in air. It should also be used at regular
intervals (every hour) on any patient receiving oxygen therapy for
an acute decompensation.
Class I recommendation, level of evidence C
Cardiac
output and pre-load can be monitored non-invasively with the use of
Doppler techniques. There is little to no evidence to help choose
which of these to monitor and it makes no difference as long as the
limitations of individual monitoring devices are understood and the
data are used appropriately.
Class
IIb recommendation, level of evidence C
Arterial
line.
The indications for the insertion of an in-dwelling arterial catheter
are the need for either continuous beat-to-beat analysis of arterial
blood pressure due to haemodynamic instability or the requirement
for multiple arterial blood analyses. The complication rate for the
insertion of a 20-gauge 2-inch radial artery catheter is low.
Class
IIb recommendation, level of evidence C
Central
venous pressure lines.
Central venous lines provide access to the central venous circulation and
are therefore useful for the delivery of fluids and drugs and can
also be used to monitor the CVP and venous oxygen saturation (SvO2)
in the superior vena cava (SVC) or right atrium, which provides an
estimate of oxygen transport.
Class
II b recommendation, level of evidence C
Caution
has to be advised, however, to avoid the over-interpretation of
right atrial pressure measurements, as these rarely correlate with
left atrial pressures, and therefore left ventricular (
Class
I recommendation, level of evidence C
Pulmonary
artery catheter.
The pulmonary artery catheter (PAC) is a balloon flotation catheter that
measures pressures in the superior vena cava (SVC), right atrium,
right ventricle and pulmonary artery as well as cardiac output.
Modern catheters can measure the cardiac output semi-continuously as
well as the mixed venous oxygen saturation and right ventricular end
diastolic volume and ejection fraction.
Although
the insertion of a PAC for the diagnosis of AHF is usually
unnecessary, it can be used to distinguish between a cardiogenic and
a non-cardiogenic mechanism in complex patients with concurrent
cardiac and pulmonary disease. The PAC is also frequently used to
estimate PCWP, cardiac output and other haemodynamic variables and
therefore guide therapy in the presence of severe diffuse pulmonary
pathology or ongoing haemodynamic compromise not resolved by initial
therapy. PCWP is not an accurate reflection of left ventricular
end–diastolic pressure (LVEDP) in patients with mitral stenosis (MS)
aortic regurgitation (AR), ventricular interdependence, high airway
pressure, or stiff LV, due to, for example, left ventricular
hypertrophy (LVH), diabetes, fibrosis, inotropes, obesity,
ischaemia. Severe tricuspid regurgitation, frequently found in
patients with AHF, can overestimate or underestimate cardiac output
measured by thermodilution.
Several
retrospective studies assessing the use of the PAC in acute
myocardial infarction demonstrated increased mortality with the
The
use of a PAC is recommended in haemodynamically unstable patients
who are not responding in a predictable fashion to traditional
treatments, and in patients with a combination of congestion and
hypoperfusion. In these cases it is inserted in order to ensure
optimal fluid loading of the ventricles and to guide vasoactive
therapies and inotropic agents. Because the complications increase
with the duration of its use, it is critical to insert the catheter
when specific data are needed (usually regarding the fluid status of
the patient) and to remove it as soon as it is of no further help
(i.e. when diuretic and vasodilating therapy have been optimized).
Table 7
Fig.
9. Immediate goals in treatment of the patients
with AHF.
In coronary patients mean blood pressure (mBP) should be higher to
ensure coronary perfusion, mBP >70, or systolic >90 mmHg.
Another objective of treatment is reduction in the clinical signs
of HF. A reduction in body weight, and/or an increase in diuresis,
are beneficial effects of therapy in congestive and oliguric
patients with AHF. Similarly, an improvement in oxygen saturation,
renal and/or hepatic function, and/or serum electrolytes are
meaningful goals of treatment. Plasma BNP concentration can reflect
haemodynamic improvement and decreased levels are beneficial.
Beneficial
effects of therapy on outcome include reductions in the duration of
intravenous vasoactive therapy, the length of stay, and the
readmission rate with an increase in the time to readmission. A
reduction in both in-hospital and long-term mortality is also a
major goal of treatment.
Lastly, a favourable safety and tolerability profile
is also necessary for any treatment used in patients with AHF. Any
agent used in this condition should be associated with a low
withdrawal rate with a relatively low incidence of untoward side
effects.
Organization of the treatment of AHF
Table 8
General
therapeutic approach in AHF by findings on invasive haemodynamic monitoring
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In AHF patients: Decreased CI:
<2.2 L/min/m2; PCWP: low if <14 mmHg, high if
>18–20 mmHg.
Class
IIb recommendation, level of evidence C
In
cardiogenic shock and prolonged severe low output syndrome it is
recommended that the mixed venous oxygen saturation from the
pulmonary artery be measured as an estimation of oxygen extraction
(SpO2–SvO2). The aim should be to maintain SvO2
above 65% in patients with AHF.
General medical issues in the treatment
of AHF
Infections:
Patients with advanced AHF are prone to infectious complications,
commonly respiratory or urinary tract infections, septicaemia, or
nosocomial infection with Gram positive bacteria. An increase in
C-reactive protein (CRP) and a decrease in general condition may be
the only signs of infection—fever may be absent. Meticulous
infection control and measures to maintain skin integrity are
mandatory. Routine cultures are recommended. Prompt antibiotic
therapy should be given when indicated.
Diabetes:
AHF is associated with impaired metabolic control. Hyperglycaemia
occurs commonly. Routine hypoglycaemic drugs should be stopped and
glycaemic control should be obtained by using short-acting insulin
titrated according to repeated blood glucose measurements.
Normoglycaemia improves survival in diabetic patients who are
critically ill.
Catabolic
state: negative caloric and nitrogen balance is a problem in ongoing
AHF. This is related to reduced caloric intake due to reduced
intestinal absorption. Care should be undertaken to maintain calorie
and nitrogen balance. Serum albumin concentration, as well as
nitrogen balance, may help to monitor metabolic status.
Renal
failure: a close interrelationship exists between AHF and renal
failure. Both may cause, aggravate, and influence, the outcome of
the other. Close monitoring of renal function is mandatory.
Preservation of renal function is a major consideration in the
selection of the appropriate therapeutic strategy for these
patients.
Oxygen and ventilatory assistance
Rationale for using oxygen in AHF
The maintenance of an SaO2 within the normal range (95–98%)
is important in order to maximize oxygen delivery to the tissues and
tissue oxygenation, thus helping to prevent end-organ dysfunction and
multiple organ failure.
Class
I recommendation, level of evidence C
This
is best achieved first by ensuring that there is a patent airway and
then by administration of an increased FiO2. Endotracheal intubation
is indicated if these measures fail to improve tissue oxygenation.
Class
IIa recommendation, level of evidence C
Despite
this intuitive approach to giving oxygen, there is little to no
evidence available that giving increasing doses of oxygen results in
an improved outcome. Studies have demonstrated that hyperoxia can be
associated with reduced coronary blood flow, reduced cardiac output,
increased blood pressure, increased systemic vascular resistance,
and a trend to higher mortality.
The
administration of increased concentrations of oxygen to hypoxaemic
patients with acute cardiac failure is unquestionably warranted.
Class
IIa recommendation, level of evidence C
The
use of increased concentrations of oxygen in patients without evidence
of hypoxaemia is more controversial and may cause harm.
Ventilatory support without endotracheal
intubation (non-invasive ventilation)
Two
techniques are used for ventilatory support: CPAP or non-invasive positive
pressure ventilation (NIPPV). NIPPV is a method of providing
mechanical ventilation to patients without the need for endotracheal
intubation. There is a strong consensus that one of these two
techniques should be used before endotracheal intubation and
mechanical ventilation. Utilization of non-invasive techniques
dramatically reduce the need for endotracheal intubation and
mechanical ventilation.
Rationale
Application of CPAP can cause pulmonary recruitment and is associated
with an increase in the functional residual capacity. The improved pulmonary
compliance, reduced transdiaphragmatic pressure swings, and
decreased diaphragmatic activity can lead to a decrease in the
overall work of breathing and therefore a decreased metabolic demand
from the body. NIPPV is a more sophisticated technique that requires
a ventilator. Addition of a PEEP to the inspiratory assistance
results in a CPAP mode (also known as bilevel positive pressure
support, BiPAP). The physiological benefits of this mode of
ventilation are the same as for CPAP but also include the
inspiratory assist which further reduces the work of breathing and
the overall metabolic demand.
Evidence for the use of CPAP and
NIPPV in left ventricular failure
CPAP
in patients with cardiogenic pulmonary oedema improves oxygenation,
decreases symptoms and signs of AHF, and results in a decreased need
for endotracheal intubation. The studies have been relatively small
and therefore have not reported a statistically significant
reduction in mortality. A systematic review following the first
three trials suggested that CPAP was associated with a decreased
need for intubation and a trend to decreased in-hospital mortality
compared to standard therapy alone. Evidence was lacking, however,
on the potential for CPAP to actually cause harm.
There
have been three randomized controlled trials of the use of NIPPV in
the setting of acute cardiogenic pulmonary oedema. NIPPV appears to
decrease the need for endotracheal intubation, but this does not
translate into a reduction in mortality or improvement in long-term
function.
Conclusions
The use of CPAP and NIPPV in acute cardiogenic
pulmonary oedema is associated with a significant reduction in the
need for tracheal intubation and mechanical ventilation.
Class IIa recommendation, level of evidence A
There
are insufficient data to demonstrate a significant reduction in
mortality; however, the data do not trend in that direction.
Mechanical ventilation with endotracheal intubation in AHF
Invasive
mechanical ventilation (with endotracheal intubation) should not be
used to reverse hypoxaemia that could be better restored by oxygen
therapy, CPAP, or NIPPV, but rather to reverse AHF-induced
respiratory muscle fatigue. The latter is the most frequent reason
for endotracheal intubation and mechanical ventilation. Respiratory
muscle fatigue may be diagnosed by a decrease in respiratory rate,
associated with hypercapnia and confused state of mind.
Invasive
mechanical ventilation should only be used if acute respiratory
failure does not respond to vasodilators, oxygen therapy, and/or
CPAP, or NIPPV. Another consideration should be the need for
immediate intervention in a patient with pulmonary oedema secondary
to ST-elevation acute coronary syndrome.
Morphine
and its analogues in AHF
Morphine is indicated in the
early stage of the treatment of a patient admitted with severe AHF,
especially if associated with restlessness and dyspnoea.
Class IIb recommendation, level of evidence B
Morphine
induces venodilatation and mild arterial dilatation, and reduces
heart rate. In most studies, iv boluses of morphine 3 mg were
administered as soon as the intravenous line was inserted. This
dosing can be repeated if required.
Anticoagulation
Anticoagulation is well
established in acute coronary syndrome with or without heart
failure. The same is true in atrial fibrillation.
There is less evidence for the initiation of unfractionated heparin
or low molecular weight heparin (LMWH) in AHF. A large
placebo-controlled trial of enoxaparine 40 mg subcutaneoulsy in
acutely ill and hospitalized patients, including a major group of
heart failure patients, showed no clinical improvement but less
venous thrombosis. There are no large comparative studies comparing
LMWH to unfractionated heparin (given as 5000 IU twice or thrice
daily). Careful monitoring of the coagulation system is mandatory in
AHF as there is often concomitant liver dysfunction. LMWH is
contraindicated if the creatinine clearance is below 30 mL/min
or should be used with extreme care with monitoring of the
anti-Factor Xa level.
Vasodilators in the treatment of AHF
Vasodilators are indicated in
most patients with acute heart failure as first line therapy, if
hypoperfusion is associated with an adequate blood pressure and
signs of congestion with low diuresis, to open the peripheral
circulation and to lower pre-load (Table 8).
Table 8
Indications
and dosing of vasodilators in AHF
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Nesiritide
Recently, nesiritide, a new class of vasodilator, has been developed for
the treatment of AHF. Nesiritide is a recombinant human brain or
B-type natriuretic peptide (BNP) that is identical to the endogenous
hormone. Nesiritide has venous, arterial, and coronary vasodilatory
properties that reduce pre-load and after-load, and increase cardiac
output without direct inotropic effects.
Systemic
infusion of nesiritide in patients with CHF has beneficial haemodynamic
actions, results in an enhanced sodium excretion, and suppression of
the renin–angiotensin–aldosterone and sympathetic nervous systems.79
Nesiritide was compared to intravenous nitroglycerin and resulted in
improvement in haemodynamics more effectively and with fewer adverse
effects, although this did not translate into improvement in
clinical outcome. Nesiritide may cause hypotension and some patients
are non-responders.
Nitrates
Nitrates relieve pulmonary congestion without compromising stroke volume
or increasing myocardial oxygen demand in acute left heart failure,
particularly in patients with acute coronary syndrome. At low doses
they only induce venodilation, but as the dose is gradually
increased they cause the arteries, including the coronary arteries,
to dilate. With appropriate doses, nitrates exert balanced
vasodilation of the venous and arterial sides of the circulation,
thereby reducing
Initially
nitrates may be given orally but intravenous nitrates are also well
tolerated in AMI. Two randomized trials in AHF have established the
efficacy of intravenous nitrates in combination with furosemide and
have demonstrated that titration to the highest haemodynamically
tolerable dose of nitrates with low dose furosemide is superior to
high dose diuretic treatment alone.
Class I recommendation, level of evidence B
In
one of these randomized studies furosemide and isosorbide dinitrate as
bolus injections were tested and it was reported that intravenous
high dose nitrate was more effective than furosemide treatment in
controlling severe pulmonary oedema.75
In
practical use nitrates have a U-shaped curve effect. If given in
sub-optimal doses vasodilators may have a limited effect in
preventing AHF recurrences. However, administration of high doses
may also reduce their effectiveness. One disadvantage of nitrates is
the rapid development of tolerance especially when given
intravenously in high doses, limiting their effectiveness to
16–24 h only. Nitrates should be given at doses aimed at
achieving optimal vasodilation, leading to an increase in cardiac
index (CI) and decrease in pulmonary wedge pressure. Inappropriate
vasodilation may induce a steep reduction in blood pressure, which
may result in haemodynamic instability.
Nitroglycerin
can be administered orally or by inhalation [glyceryl trinitrate
(GTN) spray 400 µg (2 puffs) every 5–10 min], or buccally
(isosorbide dinitrate 1 or 3 mg), while monitoring blood
pressure. The intravenous administration and dosing of nitrates
(glycerylnitrate 20 µg/min increasing dose to 200 µg/min,
or isosorbide dinitrate 1–10 mg/h) should be done with extreme
caution, under careful blood pressure monitoring, titrating the dose
administered against blood pressure decrease. One should be
particularly cautious when administering nitrates to a patient with
aortic stenosis, although this therapy may help in these complex
situations. The dose of nitrates should be reduced if systolic blood
pressure falls below 90–100 mmHg and discontinued permanently
if blood pressure drops further. From a practical point of view a
reduction of 10 mmHg in mean arterial pressure should be
achieved.
Sodium
nitroprusside (SNP) (0.3 µg/kg/min up-titrating carefully to
1 µg/kg/min up to 5 µg/kg/min) is recommended in patients
with severe heart failure, and in patients with predominantly
increased after-load such as hypertensive heart failure or mitral
regurgitation.
Class I recommendation, level of evidence C
SNP
should be titrated cautiously and usually requires invasive arterial
monitoring and close supervision. Prolonged administration may be
associated with toxicity from its metabolites, thiocyanide and
cyanide, and should be avoided especially in patients with severe
renal or hepatic failure. Controlled trials with SNP in AHF are
lacking and its administration in AMI has yielded equivocal results.
SNP should be tapered down to avoid rebound effects. In AHF caused
by acute coronary syndromes, nitrates are favoured over SNP as SNP
may cause ‘coronary steal syndrome’.
Calcium
antagonists are not recommended in the treatment of AHF. Diltiazem
and verapamil, and dihydropyridines, should be considered
contraindicated.
Angiotensin
converting enzyme (ACE)-inhibitors in AHF
ACE-inhibitors are not indicated
in the early stabilization of patients with AHF.
Class
IIb recommendation, level of evidence C
However,
as these patients are at high risk, ACE-inhibitors have a role in
early management of AHF patients and AMI. There is still debate on
the selection of patients and the timing of initiation of ACE-inhibitor
therapy.
Effects and
mechanism of action
The
haemodynamic effects of ACE-inhibitors result from decreased formation
of AII and increased levels of bradykinin, which in turn decreases
total peripheral vascular resistances and promotes natriuresis.
Short-term treatment is accompanied by a decrease in angiotensin II
(AII) and aldosterone and an increase in angiotensin I and plasma
renin activity.
There
have been no efficacy studies of ACE-inhibitors in AHF to date.
Studies with ACE-inhibitors in heart failure after myocardial
infarction have focused on long-term effects. A recent meta-analysis
found that mortality at 30 days was reduced from 7.6% in the placebo
group to 7.1% in the ACE-inhibitor group [relative risk reduction 7%
(95% CI 2–11%, P<0.004)]. This equates to about five fewer
deaths per 1000 patients treated for 4–6 weeks [number needed to
treat (NNT) to prevent one death=200]. The trials which selected
high-risk patients found that ACE-inhibitors led to large relative
and absolute reductions in mortality.
Intravenous ACE-inhibition should be
avoided. The initial dose of the ACE-inhibitor should be low and
increased progressively after early stabilization within 48 h
with monitoring of blood pressure and renal function. The duration
of therapy, when initiated, should be at least six weeks.
Class I recommendation, level of evidence A
ACE-inhibitors
should be used with caution in patients with marginal cardiac output
as they may significantly reduce glomerular filtration.The risk of
intolerance to the ACE-inhibitors is increased by the concomitant
administration of non-steroid anti-inflammatory agents, and in the
presence of bilateral renal artery stenosis.
Diuretics
Administration
of diuretics is indicated in patients with acute and acutely
decompensated heart failure in the presence of symptoms secondary to
fluid retention.
Class I recommendation, level of evidence B
The
symptomatic benefits and their universal clinical acceptance have
precluded a formal evaluation in large-scale randomized clinical
trials.
Effects and
mechanisms of action
Diuretics
increase the urine volume by enhancing the excretion of water,
sodium chloride and other ions, leading to a decrease in plasma and
extracellular fluid volume, total body water and sodium, a reduction
in right and left ventricular filling pressures and a decrease in
peripheral congestion and pulmonary oedema. Intravenous
administration of loop diuretics also exerts a vasodilating effect,
manifested by an early (5–30 min) decrease in right atrial and
pulmonary wedge pressure as well as pulmonary resistances. With high
bolus doses (>1 mg/kg) there is a risk of reflex
vasoconstriction. As opposed to chronic use of diuretics, in severe
decompensated heart failure the use of diuretics normalizes loading
conditions and may reduce neurohormonal activation in the short
term. Especially in acute coronary syndromes diuretics should be
used in low doses and preference given to vasodilator therapy.
Intravenous administration of loop
diuretics (furosemide, bumetanide, torasemide), with a strong and
brisk diuretic effect is the preferred choice in patients with AHF.
Therapy can safely be initiated before hospital admission and the
dose should be titrated according to the diuretic response and
relief of congestive symptoms. Administration of a loading dose
followed by continued infusion of furosemide or torasemide have been
shown to be more effective than bolus alone. Thiazides and
spironolactone can be used in association with loop diuretics, the
combination in low doses being more effective and having with fewer
secondary effects than the use of higher doses of a single drug.
Combination of loop diuretics with dobutamine, dopamineor nitrates is
also a therapeutic approach that is more effective and produces
fewer secondary effects than increasing the dose of the diuretic.
Class IIb recommendation, level of evidence C
Table
below lists the recommendations for the practical use
of diuretics. Table gives the recommended doses of commonly
used diuretics in heart failure.
Table 10
Practical
use of diuretics in AHF
|
Table 11
Diuretic
dosing and administration
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HCTZ=hydrochlorothiazide.
Diuretic resistance
Diuretic
resistance is defined as the clinical state in which diuretic
response is diminished or lost before the therapeutic goal of oedema
relief has been achieved. Such resistance is associated with a poor
prognosis. It is more frequent in patients with chronic, severe
heart failure on long-term diuretic therapy, although it has also
been reported with acute volume depletion after intravenous
administration of loop diuretics. Diuretic resistance can be
attributed to a number of factors. A number of therapeutic approaches to overcome
diuretic resistance have been explored, and in clinical practice
different strategies may be of value in a particular patient.
Continuous infusion of furosemide is more effective than individual
boluses.
Table 12
Causes of diuretic resistance
|
Table 13
Managing resistance to diuretics
|
Although diuretics can be used safely in the majority of patients, secondary
effects are frequent and may be life-threatening. They include
neurohormonal activation, especially of the angiotensin–aldosterone system
and the sympathetic nervous system, hypokalaemia, hypomagnesaemia, and
hypochloraemic alkalosis that may lead to severe arrhythmias, and
nephrotoxicity and aggravation of renal failure. Excessive diuresis
may reduce venous pressure, pulmonary wedge pressure and diastolic
filling excessively, leading to a reduction in stroke volume and
cardiac output, particularly in patients with severe heart failure
and predominant diastolic failure or ischaemic RV dysfunction.
Intravenous administration of acetazolamide (1 or 2 doses) may be
helpful for the correction of alkalosis.
Some new compounds with diuretic and
other effects are under investigation, including vasopressin V2
receptor antagonists, brain natriuretic peptides and adenosine receptor
antagonists.
There
has been no study with ß-blocker therapy in AHF targeted to
acutely improve the condition. On the contrary, AHF has been
considered a contraindication for this treatment. Patients with more
than basal pulmonary rales, or hypotension, have been excluded from
trials early after AMI. In patients with AMI who are not in overt
heart failure or hypotensive, ß-blockers limit infarct size,
reduce life-threatening arrhythmias and relieve pain.
Intravenous
administration should be considered in patients with ischaemic chest
pain resistant to opiates, recurrent ischaemia, hypertension,
tachycardia, or arrhythmia. In the Gothenburg metoprolol study,
intravenous metoprolol or placebo was initiated early after an AMI
and followed by oral therapy for three months. Fewer patients
developed heart failure in the metoprolol group. In patients with
signs of pulmonary congestion with basal rales and/or treatment with
intravenous furosemide, metoprolol therapy had even greater effects
and reduced mortality and morbidity. There is experience with the
short acting ß-blocker esmolol mainly in the setting of
cardiac surgery. One small study has compared celiprolol and esmolol
in severe heart failure. Celiprolol reduced CI less at similar heart
rate reduction, which was claimed to be due to differences in the
vasodilation effect. The clinical importance of this difference is
unclear. Invasive haemodynamic monitoring was carried out in the
In patients with overt AHF and more
than basal pulmonary rales, ß-blockers should be used
cautiously. Among such patients in whom ongoing ischaemia and
tachycardia are present, intravenous metoprolol can be considered.
Class IIb recommendation, level of evidence C
However,
in patients with an AMI who stabilize after developing AHF,
ß-blockers should be initiated early.
Class IIa recommendation, level of evidence B
In
patients with chronic heart failure, ß-blockers should be
initiated when the patient has stabilized after the acute episode
(usually after 4 days).
Class I recommendation, level of evidence A
The
initial oral dose of bisoprolol, carvedilol, or metoprolol should be
small and increased slowly and progressively to the target dose used
in the large clinical trials. Up-titration should be adapted to
individual response. ß-blockers may reduce blood pressure and
heart rate excessively. As a general rule, patients on
ß-blockers admitted to hospital due to worsening heart failure
should be continued on this therapy unless inotropic support is
needed but the dose could be reduced if signs of excessive dosage
are suspected (i.e. bradycardia and hypotension).
Inotropic
agents are indicated in the presence of peripheral hypoperfusion
(hypotension, decreased renal function) with or without congestion
or pulmonary oedema refractory to diuretics and vasodilators at
optimal doses (Figure)
Fig. 11. Rationale
for inotropic drugs in AHF
Class IIa recommendation, level of evidence C
Their
use is potentially harmful as they increase oxygen demand and
calcium loading and they should be used with caution.
In
patients with decompensated CHF the symptoms, clinical course, and
prognosis of the disease may become critically dependent on the
haemodynamics. Thus, improvements in the haemodynamic parameters may
become a goal of treatment and inotropic agents may be useful and
life-saving in this setting. The beneficial effects of an
improvement in the haemodynamic parameters is, however, partially
counteracted by the risks of arrhythmias and, in some cases,
myocardial ischaemia and by the possible long-term progression of
myocardial dysfunction caused by an excessive increase in energy
expenditure. The risk-benefit ratio may not, however, be the same
for all the inotropic agents. Those acting through the stimulation
of the ß1-adrenergic receptors which increase
cytoplasmic myocardial cell Ca++ concentration may be
associated with the greatest risk. Lastly, only a few controlled
trials with inotropic agents in patients with AHF have been
performed, and very few have assessed their effects on the symptoms
and signs of heart failure and their long-term effects on prognosis.
Dopamine
At low doses (<2 µg/kg/min i.v.) dopamine acts only on
peripheral dopaminergic receptors and lowers peripheral resistance
both directly and indirectly. Vasodilation occurs predominantly in
the renal, splanchnic, coronary, and cerebral vascular beds. At this
dosage, its action may cause an improvement in renal blood flow,
glomerular filtration rate, diuresis, and sodium excretion rate,
with an increased response to diuretic agents, in patients with
renal hypoperfusion and failure.
At
higher doses (>2 µg/kg/min i.v.) dopamine stimulates the
ß-adrenergic receptors both directly and indirectly with a
consequent increase in myocardial contractility and cardiac output.
At doses >5 µg/kg/min dopamine acts on 
-adrenergic
receptors with an increase in the peripheral vascular resistance
which, though potentially useful in hypotensive patients, may be
deleterious in patients with AHF, as it may augment the LV
after-load, pulmonary artery pressure, and pulmonary resistance.
Dobutamine
Dobutamine is a positive inotropic agent acting mainly
through stimulation of ß1-receptors and ß2-receptors
to produce dose-dependent positive inotropic and chronotropic effects,
and a reflex decrease in sympathetic tone, and thus vascular
resistance. The resultant benefit may therefore differ from patient
to patient. At low doses, dobutamine induces mild arterial
vasodilatation, which augments stroke volume by reductions in
after-load. At higher doses dobutamine causes vasoconstriction.
Heart
rate is generally increased in a dose-dependent manner to a lesser
extent than with other cathecholamines. However, in patients with
atrial fibrillation, heart rate may be increased to undesirable
rates, due to facilitation of atrioventricular (AV) conduction.
Systemic arterial pressure usually increases slightly, but may
remain stable, or decrease. Similarly pulmonary arterial pressure
and capillary wedge pressure usually decrease, but may remain stable
or even increase in some patients with heart failure.
The
improved diuresis observed during dobutamine infusion in patients
with heart failure is the result of increased renal blood flow in
response to improved cardiac output.
Dopamine may be used as an inotrope
(>2 µg/kg/min i.v.) in AHF with hypotension. Infusion
of low doses of dopamine (2–3 µg/kg/min)
may be used to improve renal blood flow and diuresis in decompensated
heart failure with hypotension and low urine output. However if
no response is seen the therapy should be terminated.
Table 14
Administration
of positive inotropic agents
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Class of recommendation IIb, level of evidence C
Dobutamine
is currently indicated when there is evidence of peripheral
hypoperfusion (hypotension, decreased renal function) with or
without congestion or pulmonary oedema refractory to diuretics and
vasodilators at optimal doses.
Class IIa recommendation, level of evidence C
Dobutamine
is used to increase the cardiac output. It is usually initiated with
a 2–3 µg/kg/min infusion rate without a loading dose. The
infusion rate may then be progressively modified according to
symptoms, diuretic response, or haemodynamic monitoring. Its
haemodynamic actions are proportional to its dosage, which can be
increased to 20 µg/kg/min. The elimination of the drug is rapid
after cessation of infusion, making it a very convenient inotropic
agent.
In
patients receiving ß-blocker therapy with metoprolol, dobutamine
doses have to be increased as high as 15–20 µg/kg/min to
restore its inotropic effect. The effect of dobutamine differs in
patients receiving carvedilol: it can lead to an increase in
pulmonary vascular resistance during the infusion of increasing
doses of dobutamine (5--20 µg/kg/min).
Based
on haemodynamic data alone, the inotropic effect of dobutamine is
additive to that of phosphodieasterase inhibitors (PDEI); the
combination of PDEI and dobutamine produces a positive inotropic effect
greater than either drug alone.
Prolonged
infusion of dobutamine (above 24–48 h) is associated with tolerance
and partial loss of haemodynamic effects. Weaning from dobutamine
may be difficult because of recurrence of hypotension, congestion,
or renal insufficiency. This can sometimes be solved by very
progressive tapering of dobutamine (i.e. decrease in dosage by steps
of 2 µg/kg/min every other day) and optimization of oral
vasodilator therapy such as with hydralazine and/or an ACE-inhibitor.
It is sometimes necessary to tolerate some renal insufficiency or
hypotension during this phase.
Infusion
of dobutamine is accompanied by an increased incidence of arrhythmia
originating from both ventricles and atria. This effect is dose-related
and may be more prominent than with PDEI and should prompt strict
potassium compensation during intravenous diuretic use. Tachycardia
may also be a limiting parameter, and dobutamine infusion may
trigger chest pain in patients with coronary artery disease. In
patients with hibernating myocardium dobutamine appears to increase
contractility in the short term at the expense of myocyte necrosis
and loss in myocardial recovery. There are no controlled trials on
dobutamine in AHF patients and some trials show unfavourable effects
with increased untoward cardiovascular events.
Milrinone
and enoximone are the two Type III phosphodiesterase inhibitors
(PDEIs) used in clinical practice. In AHF, these agents have
significant inotropic, lusitropic, and peripheral vasodilating
effects with an increase in cardiac output and stroke volume, and a
concomitant decline in pulmonary artery pressure, pulmonary wedge
pressure, systemic and pulmonary vascular resistance. Their
haemodynamic profile is intermediate between that of a pure
vasodilator, like nitroprusside, and that of a predominant inotropic
agent, like dobutamine. As their site of action is distal to the
beta-adrenergic receptors, PDEIs maintain their effects even during
concomitant ß-blocker therapy.
Type
III PDEIs are indicated when there is evidence of peripheral hypoperfusion
with or without congestion refractory to diuretics and vasodilators
at optimal doses, and preserved systemic blood pressure.
Class of recommendation IIb, level of evidence C
These
agents may be preferred to dobutamine in patients on concomitant ß-blocker
therapy, and/or with an inadequate response to dobutamine.
Class of recommendation IIa, level of evidence C
In
practical use milrinone is administered as a 25 µg/kg bolus over
10–20 min, followed by a continuous infusion at
0.375–0.75 µg/kg/min. Similarly, enoximone is administered as a
bolus of 0.25–0.75 mg/kg followed by a continuous infusion at
1.25–7.5 µg/kg/min. Hypotension caused by excessive peripheral venodilation
is an untoward effect observed mainly in patients with low filling
pressures. It may be avoided by starting the infusion without any
bolus. Thrombocytopaenia is uncommon with both milrinone (0.4%) and
enoximone.
The
data regarding the effects of PDEI administration on the outcome of
patients with AHF are insufficient, but raise concerns about safety,
particularly in patients with ischaemic heart failure.
Levosimendan
Levosimendan has two main mechanisms of action: Ca++
sensitization of the contractile proteins responsible for a positive
inotropic action, and smooth muscle K+ channel opening
responsible for peripheral vasodilation. Some data suggest
levosimendan may also have a phosphodioesterase inhibition effect.
Levosimendan has a potent acetylated metabolite that is also a Ca++-concentration
dependent Ca++ sensitizer. Its half-life is 
80 h,
which probably explains the prolonged haemodynamic effects of a
24 h levosimendan infusion.
Levosimendan
is indicated in patients with symptomatic low cardiac output heart
failure secondary to cardiac systolic dysfunction without severe
hypotension (Table ).
Class of recommendation IIa, level of evidence B
Levosimendan
is generally administered as a continuous intravenous infusion at a
dose of 0.05–0.1 µg/kg/min preceded by a loading dose of
12–24 µg/kg, administered over 10 min. Its haemodynamic
effects are dose-dependent and the infusion rate may be up-titrated
to a maximal rate of 0.2 µg/kg/min. Most of the clinical data
have been obtained with intravenous infusions lasting from 6 hto
24 h, but the haemodynamic effects persist for >48 h
after the end of the infusion.
Levosimendan
infusion in patients with acutely decompensated heart failure caused
by left ventricular systolic dysfunction has been associated with a
dose-dependent increase in the cardiac output and stroke volume, a
decline in the pulmonary wedge pressure, systemic vascular
resistance, and pulmonary vascular resistance, and a slight increase
in the heart rate, and decrease in the blood pressure. An
improvement in symptoms of dyspnoea and fatigue and a favourable
outcome has been shown in randomized trials comparing levosimendan
with dobutamine. Differently from dobutamine, the haemodynamic
response to levosimendan is maintained, or even of greater
magnitude, in the patients on concomitant ß-blocker therapy.
Tachycardia
and hypotension are described with high-dose levosimendan infusion
and it is not currently recommended in patients with a systolic
blood pressure <85 mmHg. Levosimendan has not been
associated with an increased frequency of malignant arrhythmias in
comparative trials with either placebo, or dobutamine. Reductions in
the haematocrit, haemoglobin, and plasma potassium, likely secondary
to vasodilation and secondary neurohumoral activation, have been
described and seem to be dose-dependent.
Vasopressor
therapy in cardiogenic shock
When the combination of inotropic
agent and fluid challenge fails to restore adequate arterial and
organ perfusion despite an improvement in cardiac output, therapy
with vasopressors may be required. Vasopressors may also be used, in
emergencies, to sustain life and maintain perfusion in the face of
life-threatening hypotension. Since cardiogenic shock is associated
with high vascular resistances, any vasopressor should be used with
caution and only transiently, because it may increase the after-load
of a failing heart and further decrease end-organ blood flow.
Epinephrine
Epinephrine is a catecholamine with high affinity for
ß1, ß2, and receptors.
Epinephrine is used generally as an infusion at doses of 0.05 to
0.5 µg/kg/min when dobutamine refractoriness is present and the
blood pressure remains low. Direct arterial pressure monitoring and
monitoring of haemodynamic response by PAC is recommended.
Norepinephrine
Norepinehrine is a catecholamine with high affinity
for -receptors
and is generally used to increase systemic vascular resistance. Norepinephrine-induced
increases in heart rate are less than with epinephrine. The dosing
is similar to epinephrine. Norepinephrine (0.2 to 1 µg/kg/min)
is favoured in situations with low blood pressure related to reduced
systemic vascular resistance such as septic shock. Norepinephrine is
often combined with dobutamine to improve haemodynamics.
Norepinehrine may reduce end-organ perfusion.
Cardiac glycosides inhibit myocardial Na+/K+ ATPase,
thereby increasing Ca++/Na+ exchange
mechanisms, producing a positive inotropic effect. In heart failure
the positive inotropic effect following ß-adrenergic
stimulation is attenuated and the positive force–frequency relationship
is impaired. In contrast to ß-adrenoceptor agonists, the
positive inotropic effect of cardiac glycosides is unchanged in
failing hearts and the force–frequency relationship is partially
restored. In chronic heart failure, cardiac glycosides reduce symptoms
and improve clinical status, thereby decreasing the risk of
hospitalization for heart failure without effects on survival. In
AHF, cardiac glycosides produce a small increase in cardiac
outputand a reduction of filling pressures. In patients with severe
heart failure following episodes of acute decompensation, cardiac
glycosides have been shown to be efficacious in reducing the
re-occurrence of acute decompensation. Predictors for these
beneficial effects are a third heart sound, extensive
However,
in patients following myocardial infarction with heart failure, a
substudy of the AIRE-Investigation has shown adverse effects on
outcome after AMI accompanied by heart failure. Furthermore,
following AMI an increase of creatinine kinase was more pronounced
in patients receiving cardiac glycosides. In addition, for patients
with myocardial infarction and AHF, the use of digitalis was a
predictor for life-threatening pro-arrhythmic events. Therefore,
inotropic support with cardiac glycosides cannot be recommended in
AHF, in particular following myocardial infarction.
An
indication for cardiac glycosides in AHF may be tachycardia-induced heart
failure e.g. in atrial fibrillation with insufficient rate-control
by other agents such as ß-blockers. Rigorous control of heart
rate in tachyarrhythmia during the course of AHF can control heart
failure symptoms. Contraindications to the use of cardiac glycosides
include bradycardia, second and third degree AV-block, sick sinus
syndrome, carotid sinus syndrome, Wolff–Parkinson–White syndrome,
hypertrophic obstructive cardiomyopathy, hypokalaemia, and
hypercalcaemia.
Treatment
of arrhythmias in acute heart failure
|
Class IIa recommendation, level of evidence C
Supraventricular
tachycardia (SVT)
Supraventricular
tachyarrhythmias may complicate or cause AHF. On rare occasions
persistent atrial tachycardias may cause decompensated heart failure
requiring hospitalization. Similarly, atrial fibrillation with a
rapid ventricular response may be the cause for a dilated cardiomyopathy
and AHF.
Recommendations
for treatment of supraventricular tachyarrhythmias in AHF
The
control of the ventricular rate response is important in patients
with AF and AHF, particularly in patients with diastolic dysfunction.
Class IIa recommendation, level of evidence A
Patients
with restrictive physiology or tamponade, however, may suddenly
deteriorate with rapid heart rate reduction. Rapid rate control or
cardioversion on clinical demand should be achieved . The therapy of
AF depends on its duration.
Patients
with AHF and AF should be anticoagulated. When AF is paroxysmal,
medical or electrical cardioversion should be considered after
initial work-up and stabilization of the patient. If the duration of
the AF is more than 48 h the patient should be anticoagulated
and optimal rate control achieved medically for 3 weeks before
cardioversion. If the patient is haemodynamically unstable, urgent
cardioversion is clinically mandatory, but atrial thrombus should be
excluded by transoesophageal echocardiography prior to
cardioversion.
Verapamil
and diltiazem should be avoided in acute AF as they may worsen heart
failure and cause third degree AV block. Amiodarone and
ß-blocking agents have been successfully used in AF for rate
control and prevention of recurrence.
Class I recommendation, level of evidence A
Verapamil
can be considered in the treatment of AF or narrow complex SVT in
patients with only slightly reduced ventricular systolic function.
Class
I anti-arrhythmic agents should be avoided in patients with low
ejection fraction and particularly in patients who have a wide QRS
complex. Dofetilide is a new drug with promising results in medical
cardioversion and prevention of new AF, but further studies are
needed to evaluate its safety and efficacy in AHF.
ß-blocking
agents can be tried in SVTs when tolerated. In wide complex
tachycardia, intravenous adenosine can be used in an attempt to
terminate the arrhythmia. Electrical cardioversion of SVT with
sedation should be considered in AHF with hypotension. AHF patients
with AMI and heart failure, and patients with diastolic heart
failure, do not tolerate rapid supraventricular arrhythmias.
Plasma
potassium and magnesium levels should be normalized particularly in
patients with ventricular arrhythmia.
Class IIb recommendation, level of evidence B
Treatment of
life-threatening arrhythmias
Ventricular
fibrillation and ventricular tachyarrythmia require immediate
cardioversion, with ventilator assistance if required, and in the
case of a conscious patient, with sedation.
Amiodarone
and ß-blocking agents can prevent repetition of these
arrhythmias.
Class I recommendation, level of evidence A
In
the case of recurrent ventricular arrhythmias and haemodynamically unstable
patients, immediate angiography and electrophysiological testing
should be performed. In cases of a localized arrhythmic substrate,
radiofrequency ablation may eliminate the arrhythmic tendency
although the long-term effect cannot be ascertained.
AHF is a severe
complication of many cardiac disorders. In some of them surgical
therapy improves prognosis if performed urgently or immediately.
Surgical options include coronary revascularization, correction of
the anatomic lesions, valve replacement or reconstruction, as well
as temporary circulatory support by means of mechanical assist
devices. Echocardiography is the most important technique in the
diagnostic work-up.
Table 16
Cardiac disorders and AHF requiring surgical
treatment
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Summary comments
The clinical syndrome of
AHF may present as de novo AHF or as decompensated CHF with
forward, left (backward), or right (backward) dominance in the
clinical syndrome.
A patient with AHF requires
immediate diagnostic evaluation and care, and frequent resuscitative
measures to improve symptoms and survival.
Initial diagnostic assessment
should include clinical examination supported by the patient's
history, ECG, chest X-ray, plasma BNP/NT-proBNP, and other
laboratory tests. Echocardiography should be performed in all
patients as soon as possible (unless recently done and the result is
available).
The initial clinical assessment
should include evaluation of pre-load, after-load, and the presence
of mitral regurgitation (MR) and other complicating disorders
(including valvular complications, arrhythmia, and concomitant
co-morbidities such as infection, diabetes mellitus, respiratory, or
renal diseases). Acute coronary syndromes are a frequent cause of
AHF and coronary angiography is often required.
Following initial assessment, an
intravenous line should be inserted, and physical signs, ECG and SPO2
should be monitored. An arterial line should be inserted when
needed.
The initial treatment of AHF
consists of:
·
Oxygenation
with face-mask or by CPAP (SPO2 target of 94–96%)
·
Vasodilatation by nitrate or
nitroprusside
·
Diuretic
therapy by furosemide or other loop diuretic (initially intravenous
bolus followed by continuous intravenous infusion, when
needed)
·
Morphine
for relief of physical and psychological distress and to
improve haemodynamics
·
Intravenous
fluids should be given if the clinical condition is
pre-load-dependent and there are signs of low filling pressure.
This may require testing the response to an aliquot of fluid.
·
Other
complicating metabolic and organ-specific conditions should be
treated on their own merits.
·
Patients
with acute coronary syndrome or other complicated cardiac disorders
should undergo cardiac catheterization and angiography, with
a view to invasive intervention including surgery.
·
Appropriate
medical treatment by ß-blocking agents and other medical
therapy should be initiated as described in this report.
Further specific therapies should
be administered based on the clinical and haemodynamic characteristics
of the patient who does not respond to initial treatment. This may
include the use of inotropic agents or a calcium sensitizer for
severe decompensated heart failure, or inotropic agents for
cardiogenic shock.
The aim of therapy of AHF is to
correct hypoxia and increase cardiac output, renal perfusion, sodium
excretion, and urine output. Other therapies may be required e.g.
intravenous aminophylline or ß2-agonist for
bronchodilation. Ultrafiltration or dialysis may be prescribed for
refractory heart failure.
Patients with refractory AHF or
end-stage heart failure should be considered for further support,
where indicated including: intra-aortic balloon pump, artificial mechanical
ventilation, or circulatory assist devices as a temporary measure, or
as a ‘bridge’ to heart transplantation.
The patient with AHF may recover
extremely well, depending on the aetiology and the underlying
pathophysiology. Prolonged treatment on the ward and expert care are
required. This is best delivered by a specialist heart failure team
that can rapidly initiate medical management and attend to the information
needs of the patient and family.