Essential hypertension and symptomatic arterial hypertension:

main symptoms and syndromes. Hypertonic crisis.

Ischemic heart disease: main symptoms and syndromes in angina pectoris and myocardial infarction.

Main symptoms and syndromes in dry pleurisy and pleurisy with effusion. Syndrome of respiratory insufficiency in respiratory system pathology.

 

 

Essential hypertension (morbus hypertonicus) is the condition in which elevated arterial pressure is the leading symptom. Essential hypertension (also called primary hypertension or idiopathic hypertension) is the form of hypertension that by definition, has no identifiable cause. It is the most common type of hypertension, affecting 95% of hypertensive patients, it tends to be familial and is likely to be the consequence of an interaction between environmental and genetic factors. Prevalence of essential hypertension increases with age, and individuals with relatively high blood pressure at younger ages are at increased risk for the subsequent development of hypertension. Hypertension can increase the risk of cerebral, cardiac, and renal events. The disease is provoked by nervous and functional disorders in the regulation of the vascular tone. Men and women, mostly over 40, are equally attacked by the disease.

Classification

According to Obrastsov and Strazesko three stages of the disease are classified: The  first stage is latent; it is characterized by elevated arterial pressure during a psychic stress, while under normal conditions arterial pressure is normal, objective changes are absent.

In the second stage, arterial pressure is elevated permanently and more significantlv.  Changes in internal target-organs develop. By inspection at least one among the following signs are revealed:

–    hypertrophy of the left ventricle;

–    proteinuria (or elevation of creatinine level till 0,177   mmol/l;

–    narrowing of retinal vessels;

–    ultrasonic or X-ray data of atherosclerosis (plaques);

In the 3rd stage complication develops:

–    the heart: left ventricular heart failure or myocardial infarction;

–    the brain: brain insult, transient hemodynamic disorders, hypertensive encephalopathy;

–    eyes: retinal hemorrhage or papiloedema;

–    kidneys: creatitine level more than 0,177 mmol/l, renal failure;

–    vessels: dissecting aneurism of the aorta, occlusions of arteries.

 

Classification of blood pressure for adults

Hypotension	< 100	< 60
Desired	100–119	60–79
Prehypertension	120–139	80–89
Stage 1 Hypertension	140–159	90–99
Stage 2 Hypertension	160–179	100–109
Hypertensive Crisis	≥ 180	≥ 110

 

Arterial hypertension is defined as rising of arterial blood pressure  excess of 140 mm Hg systolic one (SBP), and/or excess of 90 mm Hg diastolic blood pressure (DBP). Recommendations from the Joint National Committee on the Prevention, Detection, Evaluation and treatment of High Blood Pressure (JNC-VI report) now regard a BP of 140/90 mm Hg as high normal and 130/85 mm Hg as normal

Essential hypertension should accurately be differentiated from symptomatic hypertension in which arterial pressure rises as a symptom of some other disease, this symptom being far from the leading one. Symptomatic hypertension occurs in aortic coarctation, atherosclerosis of the aorta and its large branches, in endocrine dysfunction (e.g. Itsenko-Cushing disease, phaeochromocytoma, primary aldosteronism, or the Conn syndrome), af­fection of the renal parenchyma, occlusive affection of the main renal arteries, and in some other diseases.

Evaluation of Secondary Hypertension

The possibility that an underlying condition is causing hypertension must also be considered; secondary hypertension is often unmanageable until the underlying cause is treated. Among 4000 patients with resistant hypertension who were evaluated during an 18-year period at one tertiary center, secondary causes were found in 10 percent of patients overall and in 17 percent of patients over the age of 60 years.

Chronic renal parenchymal disease, usually resulting from diabetic nephropathy or hypertensive nephrosclerosis, may be the most common cause of secondary hypertension. High blood pressure caused by acute renal parenchymal damages is mainly due to water and sodium retention, therefore timely diuretic treatment often can lower the blood pressure.

While the pathogenesis of hypertension caused by chronic renal parenchymal disease is more complex and it can be caused by many factors. Activation of RAAS (rennin-angiotensin aldosterone system). Renal parenchymal diseases can cause ischemia and hypoxia in the kidneys which will activate the RAAS. Angiotensin II has direct stimulation to vasoconstriction and aldosterone can worsen water and sodium retention so as to further increase high blood pressure.

          Atherosclerotic renovascular disease, which is particularly prevalent among elderly smokers, is another possible cause. The presence of an abdominal bruit or hypokalemia or a recent increase in the severity of hypertension may suggest the diagnosis of atherosclerotic renovascular disease.

 Screening for renovascular disease may be warranted if other causes of resistant hypertension are not identified, since angioplasty and stenting may improve blood pressure. However, in cases of renovascular hypertension caused by atherosclerotic disease, blood pressure often remains high even after intervention, in contrast to hypertension caused by the much less common fibromuscular dysplasia.

Renal artery stenosis (RAS) is the major cause of renovascular hypertension and it accounts for about 1-10% of the 50 million people in the United States who have hypertension. The incidence is less than 1% of cases of mild to moderate HTN. However, it rises to 10 to 45 % in patients with acute (or superimposed upon a preexisting elevation in blood pressure), severe, or refractory hypertension.

Major causes of the renal arterial lesions are:

 Atherosclerosis —It is the cause of RAS in >2/3rd of the cases. This primarily affects men over the age of 45 and usually involves the aortic orifice or the proximal main renal artery. This disorder is particularly common in patients with diffuse atherosclerosis, but can occur as a relatively isolated renal lesion.

         Fibromuscular dysplasia — are uncommon angiopathies associated with heterogeneous histologic changes that may affect the carotid circulation as well as the visceral and peripheral arteries. In comparison to atherosclerosis, fibromuscular dysplasia most often affects younger women and typically involves the distal main renal artery or the intrarenal branches.

 Other less common causes of RAS include:

§  Vasculitis (Takayasu’s arteritis)

§  Dissection of the renal artery. 

§  Thromboembolic disease

§  Renal artery aneurysm

§  Renal artery coarctation

§  Extrinsic compression

§  Radiation injury

Summarizes features of and screening tests for these and other causes of secondary hypertension, such as primary aldosteronism (considered to be more common than previously recognized), pheochromocytoma, and sleep apnea (recently recognized to be associated with refractory hypertension). Generally, the decision to screen a patient for such disorders should depend on suggestive findings on history taking, physical examination, or basic laboratory testing. Interventions that are directed at these disorders (e.g., surgery or aldosterone-antagonist therapy for hyperaldosteronism, surgery for pheochromocytoma etc.

Primary aldosteronism (PA; synonym: Conn’s syndrome) is characterized by autonomous aldosterone excess with subsequent suppression of renin levels. The main causes of primary aldosteronism accounting for >95% of cases are aldosterone producing adenoma (APA) and idiopathic primary aldosteronism (IHA). The distinction between these 2 entities is clinically crucial. APA is a curable form of hypertension, and unilateral adrenalectomy results in correction of hypokalemia and blood pressure normalisation in the majority of patients.

Pheochromocytoma hypertensive crisis may manifest with impressively dramatic clinical features. The BP is markedly elevated during the paroxysm and the patient may have profound sweating, marked tachycardia, pallor, numbness, tingling, and coldness of the feet and hands. A single attack may last from a few minutes to hours and may occur as often as several times a day to once a month, or less.

Aetiology and pathogenesis.

Hypertension is one of the most common complex disorders. The etiology of hypertension differs widely amongst individuals within a large population. And by definition, essential hypertension has no identifiable cause. However, several risk factors have been identified.

Essential hypertension is four times more common in black than white people, accelerates more rapidly and is often more severe with higher mortality in black patients.

More than 50 genes have been examined in association studies with hypertension, and the number is constantly growing.

Hypertension can also be age related, and if this is the case, it is likely to be multifactorial. One possible mechanism involves a reduction in vascular compliance due to the stiffening of the arteries. This can build up due to isolated systolic hypertension with a widened pulse pressure. A decrease in glomerular filtration rate is related to aging and this results in decreasing efficiency of sodium excretion. The developing of certain diseases such as renal microvascular disease and capillary rarefaction may relate to this decrease in efficiency of sodium excretion. There is experimental evidence that suggests that renal microvascular disease is an important mechanism for inducing salt-sensitive hypertension.

Obesity can increase the risk of hypertension to fivefold as compared with normal weight, and up to two-thirds of hypertension cases can be attributed to excess weight. More than 85% of cases occur in those with a Body mass index greater than 25. A definitive link between obesity and hypertension has been found using animal and clinical studies; from these it has been realized that many mechanisms are potential causes of obesity-induced hypertension. These mechanisms include the activation of the sympathetic nervous system as well as the activation of the renin–angiotensin-aldosterone system.

Another risk factor is salt (sodium) sensitivity which is an environmental factor that has received the greatest attention. Approximately one third of the essential hypertensive population is responsive to sodium intake. When sodium intake exceeds the capacity of the body to excrete it through the kidneys, vascular volume expands secondary to movement of fluids into the intra-vascular compartment. This causes the arterial pressure to rise as the cardiac output increases. Local autoregulatory mechanisms counteract this by increasing vascular resistance to maintaiormotension in local vascular beds. As arterial pressure increases in response to high sodium chloride intake, urinary sodium excretion increases and the excretion of salt is maintained at expense of increased vascular pressures. The increased sodium ion concentration stimulates ADH and thirst mechanisms, leading to increased reabsorption of water in the kidneys, concentrated urine, and thirst with higher intake of water. Also, the water movement between cells and the interstitium plays a minor role compared to this. The relationship between sodium intake and blood pressure is controversial. Reducing sodium intake does reduce blood pressure, but the magnitude of the effect is insufficient to recommend a general reduction in salt intake.

Renin elevation is another risk factor. Renin is an enzyme secreted by the juxtaglomerular apparatus of the kidney and linked with aldosterone in a negative feedback loop. In consequence, some hypertensive patients have been defined as having low-renin and others as having essential hypertension. Low-renin hypertension is more common in African Americans than white Americans, and may explain why African Americans tend to respond better to diuretic therapy than drugs that interfere with the Renin-angiotensin system. High renin levels predispose to hypertension by causing sodium retention through the following mechanism: Increased renin → Increased angiotensin II → Increased vasoconstriction, thirst/ADH and aldosterone → Increased sodium reabsorption in the kidneys (DCT and CD) → Increased blood pressure.

Hypertension can also be caused by Insulin resistance and/or hyperinsulinemia, which are components of syndrome X, or the metabolic syndrome. Insulin is a polypeptide hormone secreted by cells in the islets of Langerhans, which are contained throughout the pancreas. Its main purpose is to regulate the levels of glucose in the body antagonistically with glucagon through negative feedback loops. Insulin also exhibits vasodilatory properties. Iormotensive individuals, insulin may stimulate sympathetic activity without elevating mean arterial pressure. However, in more extreme conditions such as that of the metabolic syndrome, the increased sympathetic neural activity may over-ride the vasodilatory effects of insulin.

It has been suggested that vitamin D deficiency is associated with cardiovascular risk factors. It has been observed that individuals with a vitamin D deficiency have higher systolic and diastolic blood pressures than average. Vitamin D inhibits renin secretion and its activity, it therefore acts as a “negative endocrine regulator of the renin-angiotensin system”. Hence a deficiency in vitamin D leads to an increase in renin secretion. This is one possible mechanism of explaining the observed link between hypertension and vitamin D levels in the blood plasma.

Cigarette smoking, a known risk factor for other cardiovascular disease, may also be a risk factor for the development of hypertension. It has long been identified as an independent risk factor for cardiovascular disease. Traditionally, emphasis has been placed on elevated DBP as a risk factor for the development of target organ damage. However, as early as 1971, the Framingham study showed that, although DBP was a major determinant of cardiovascular risk in men under 45 years of age, SBP was the stronger risk factor in older men and in women of all ages. Since then, several observational studies have suggested that the pulse pressure (PP) may be a better predictor of cardiovascular complications than SBP or mean arterial pressure.

Overstrain of the central nervous system, caused by prolonged and strong emotional stress and also mental overstrain, are believed to be the main cause of the disease. In some cases essential hypertension develops after brain concussion (concussion-commotion form).

 Development of the disease greatly depends on occupation: it occurs mostly in subjects whose occupation is associated with nervous and mental  overstrain, e.g. in scientific workers, engineers, physicians, drivers, etc. Familial predispostion is another important factor. The early stage of essential hypertension is characterized by nervous-functional disorder in regulation of the vascular tone. Vegetative-endocrine disorders and changes in the renal regulation of the vascular tone are later steps of the pathological process. Overstrain of the higher nervous activity causes vasopressor adrenal reaction by whivh arterioles of internal organs are narrowed. Next steps are  production of rennin, stimulation of rennin-angiotensin system  and  systemicf vasodilatation; activation of aldosterone secretion.

An assessment of dietary and lifestyle factors is also important. Excessive alcohol use (more than three or four drinks per day) and a high sodium intake (typically defined by a urinary sodium excretion of more than 150 mmol per day) may contribute to resistant hypertension; the frequency of salt sensitivity is increased among patients who are at least 60 years of age, patients who are black or obese, and patients with renal impairment. Studies indicate that more than 40 per cent of patients with resistant hypertension are obese, and obese patients may require higher doses of antihypertensive medications than do nonobese patients. Clonidine withdrawal syndrome can result from abrupt discontinuation of a high-dosage regimen of clonidine, causing a hyperadrenergic state that mimics pheochromocytoma. When clonidine is abruptly discontinued (especially at high dosages) or rapidly tapered, a syndrome consisting of nausea, palpitation, anxiety, sweating, nervousness, and headache, along with marked elevation of the BP has beeoted. Symptoms of clonidine withdrawal can be relieved by reinstituting the clonidine regimen. If there is marked elevation of BP and the patient is experiencing symptoms such as palpitations, chest discomfort, and epigastric discomfort, the IV administration of phentolamine or labetalol is recommended.

Cocaine-induced hypertensive crisis can cause an abrupt, sudden increase in the systemic BP, resulting in a hypertensive emergency. Neurohumoral factors triggered by cocaine likely cause intense vasoconstriction and thus increase the vascular resistance and the BP. Sudden rise of BP in a previously normotensive individual may result in a serious cardiovascular complication. The BP should be lowered to safe limits without much delay.

Clinical  pattern. During the early stage of the disease the patient would usually complain of neurotic disorders: general weakness, impaired work capacity, inability to concentrate during work, deranged sleep, trancient headache, e feeling of heaviness in the heart, vertigo, noise in the ears, and sometimes palpitation. Exertional dyspnoea develops later.

The main objective sign of the disease is elevated arterial pressure (over 140/90 mm Hg). Blood pressure is liable in early stage of the disease but later stabilizes. Examination of the heart reveals hypertrophy of the left ventricle: expanding apex beat, displacement of the cardiac dullness leftward. The second heart sound is accentuated over the aorta. The pulse becomes firm and tense. Patients should be asked routinely about the use of medications or other substances that can elevate blood pressure or antagonize the effects of antihypertensive drugs. These substances include sympathomimetic drugs (e.g., ephedra, phenylephrine, cocaine, and amphetamines), herbal supplements (e.g., ginseng and yohimbine), anabolic steroids, appetite suppressants, and erythropoietin, although all these drugs probably account for less than 2 percent of cases of resistant hypertension. Nonsteroidal antiinflammatory drugs and cyclooxygenase-2 inhibitors may raise both systolic and diastolic blood pressure by several mm Hg.

The physical examination should begin with an assessment of BP, with an appropriate-size cuff in both upper extremities and in a lower extremity if peripheral pulses are markedly reduced. Brachial, femoral, and carotid pulses should be assessed. A careful cardiovascular examination as well as a thorough neurologic examination, including mental status, should be conducted. This assessment will aid in establishing the degree of involvement of affected target organs and should provide clues to the possible existence of a secondary form of hypertension, such as renovascular hypertension.

Accurate measurement of blood pressure and verification of elevated pressure on multiple occasions over time are important. Ambulatory or home blood-pressure monitoring can identify “white-coat hypertension” (blood pressure that is elevated when measured during an office visit but that is otherwise normal) and prevent unnecessary treatment. White-coat hypertension, present in 20 percent of patients with elevated blood pressure, is associated with a lower cardiovascular risk than is sustained hypertension, but it may be a precursor of sustained hypertension and therefore warrants monitoring.

The diagnosis is based on the findings of at least two or three elevated blood-pressure measurements (in the physician’s office or at home), despite adherence to regimens containing three medications. However, if the blood pressure is above 160/100 mm Hg, additional readings are not necessary for diagnosis. Evaluation (including physical examination and laboratory testing) is routinely warranted to look for evidence of end-organ damage related to hypertension and for other cardiovascular risk factors. Volume overload and elevated sympathetic tone, which are common in patients with uncontrolled blood pressure, may occasionally be suggested by the presence of a rapid pulse rate. Renin levels have not been found to be useful in the prediction of excess volume, though they may be useful in the evaluation of possible secondary causes of hypertension.

Blood pressure should be measured after a patient has been seated quietly for five minutes, with his or her arm supported at heart level and with the use of a properly calibrated and sized cuff. If the cuff is too narrow or too short, readings may be erroneously high (typically by 5 to 15 mm Hg in the case of systolic pressure). The patient should be asked whether he or she has smoked a cigarette within the previous 15 to 30 minutes, since smoking can cause an elevation in systolic blood pressure of 5 to 20 mm Hg. Avoidance of coffee is also recommended, although the increase in systolic blood pressure after one cup of caffeinated coffee is usually only 1 to 2 mm Hg. Long-term smoking or coffee drinking does not cause persistently elevated blood pressure.

Ambulatory blood pressure monitoring (ABPM) is a method of taking regular blood pressure readings, usually over a 24-hour period, as patients conduct their normal activities. A special, automatic blood pressure monitor is used, and patients are asked to keep a diary or log of their activities during the day.

X-rays reveal “aortic” heart configuration. The aorta is elongared, consolidated and dilated.

ECG: left type with displacement of S-T segment, low, negative, or two-phase T wave in the Ist and 2^nd standart leads and chest leads V5-V6.

 

Aortic heart configuration in hypertension

 

ECG in hypertension (hypertrophy of the left ventricle)

        

 

 

Hypertrophy of the left ventricle as a result of hypertension

 

Hypertension

In addition to the history taking and physical examination, several tests are routinely indicated in patients with hypertension: urinalysis, complete blood count, blood chemical tests (measurements of potassium, sodium, creatinine, fasting glucose, total cholesterol, and high-density lipoprotein), and 12-lead electrocardiography. The evaluation should identify signs of cardiovascular, cerebrovascular, or peripheral vascular disease and other cardiovascular risk factors that are frequently present in patients with hypertension. Severe or resistant hypertension or clinical or laboratory findings suggesting the presence of renal disease, adrenal hypertension (due to abnormal mineralocorticoid secretion or pheochromocytoma), or renovascular hypertension should be further investigated. Essential, or primary, hypertension, the focus of this article, is the diagnosis in over 90 percent of cases.

If a secondary cause of hypertension is suspected, appropriate blood and urine samples should be obtained before aggressive therapy is initiated. A careful funduscopic examination should be performed to detect the presence of hemorrhages, exudates, and/or papilledema

Some patients who have what appears to be resistant hypertension have a normal blood pressure at home. This phenomenon has been attributed to transitory, or “white-coat,” resistant hypertension in the physician’s office. Repeated home measurements or 24-hour ambulatory monitoring may differentiate this type of hypertension from truly resistant hypertension. Such measures are warranted in patients undergoing treatment who have consistently high blood-pressure levels in the physician’s office yet have no evidence of target-organ damage. In one study, as many as a third of patients with apparently resistant hypertension had average blood-pressure levels of less than 130/85 mm Hg on 24-hour or home measurement. Some data suggest that blood-pressure values obtained at home or during 24-hour ambulatory procedures correlate better with target-organ involvement, especially left ventricular hypertrophy, than do values obtained in the physician’s office. However, office, or white-coat, hypertension is not benign and should not be ignored.

Rarely, in older patients, what appears to be refractory hypertension may represent inaccurate measurement owing to severely sclerotic arteries (i.e., pseudohypertension). The condition is suggested if the radial pulse remains palpable despite occlusion of the brachial artery by the cuff (the Osler maneuver),¹⁶ although this sign is not specific. The presence of this condition can be confirmed by intra-arterial blood-pressure measurement.

Complications

Hypertension is a risk factor for stroke, myocardial infarction, renal failure, congestive heart failure, progressive atherosclerosis. There is a continuous, graded relation between blood pressure and the risk of cardiovascular disease; the level and duration of hypertension and the presence or absence of coexisting cardiovascular risk factors determine the outcome. Treatment of hypertension reduces the risk of stroke, coronary artery disease, and congestive heart failure, as well as overall cardiovascular morbidity and mortality from cardiovascular causes. However, only 54 percent of patients with hypertension receive treatment and only 28 percent have adequately controlled blood pressure

In hypertension heart, eye fundus, kidney and the brain are affected thet is why they are called “target organs”. Cardiovascular or other target-organ disease denotes left ventricular hypertrophy, angina or prior myocardial infarction, prior coronary revascularization, heart failure, stroke or transient ischemic attack, nephropathy, peripheral arterial disease, and retinopathy.

In the later period of the disease heart  failure  may develop due to fatigue of the heart muscle as a result of increased arterial pressure. Heart failure is often manifested by acute attaks  of cardiac asthma or oedema of the lungs; or chronic circulatory insufficiency may develop.

High arterial pressure in the affected cerebral vessels can derange cerebral circulation. This can cause paralysis, disorders in sensitivity. Cerebral circulation is deranged due to spasms of the vessels, their thrombotic obstruction, hemorrhage due to rupture of the vessel, or diapedetic discharge of erythrocytes.

The affected kidneys become unable to concentrate urine (nicturia or isohyposthenuria develops). Metabolites (otherwise excreted with urine) are retained to provoke uraemia.

Vision may be deteriorated in grave cases. Examination of the fundus occuli  reveals its general pallidness; the arteries are narrow and tortuous, the veins are mildly dilated; haemorrhage into the retina (angiospastic retinitis) sometimes observed.

 

Hypertensive retinopathy is a condition characterized by a spectrum of retinal vascular signs in people with elevated blood pressure. The detection of hypertensive retinopathy with the use of an ophthalmoscope has long been regarded as part of the standard evaluation of persons with hypertension. This clinical practice is supported by both previous and current reports of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC), which list retinopathy as one of several markers of target-organ damage in hypertension. On the basis of the JNC criteria, the presence of retinopathy may be an indication for initiating antihypertensive treatment, even in people with stage 1 hypertension (blood pressure, 140 to 159/90 to 99 mm Hg) who have no other evidence of target-organ damage.

 

Hypertensive retinopathy

Hypertensive retinopathy

Malignant Hypertensive Retinopathy. Multiple cotton-wool spots (white arrows), retinal hemorrhages (black arrows), and swelling of the optic disk are visible.

 

Hypertensive encephalopathy is a deadly complication of severe hypertension that should be recognized as an emergency and quickly treated. Although encephalopathy occurs mainly in patients with chronic or malignant hypertension, it can also complicate sudden hypertension of brief duration. The clinical manifestations are generated not only by the severity of BP elevation but also by the abrupt rise of BP in a previously normotensive individual. This condition occurs more frequently when the hypertension is complicated by renal insufficiency than when the renal function is normal. The full-blown clinical syndrome of hypertensive encephalopathy may take anywhere from 12 to 48 hours to develop.

A 41-year-old woman with hypertensive encephalopathy. Hypertensive crisis with pheochromcytoma. (A) Coronal FLAIR image shows multiple hyperintense lesions in the subcortical white matter (arrows) and cortex (arrowheads) in both parieto-occipital areas. (B) T2-weighted image shows hyperintense lesions in the cortical and subcortical white matter in the right frontal (arrow) and parieto-occipital areas (arrowheads). (C) DWI shows the left parieto-occipital cortical lesion as hyperintense (arrowheads) and the right frontal subcortical lesion as iso- or slightly hyperintense (arrow). (D) ADC map reveals decreased ADC of the left cortical lesion representing cytotoxic edema (arrowheads). A subcortical lesion in the right frontal lobe shows increased ADC representing vasogenic edema (arrow).

Severe generalized, sudden headache is a prominent clinical manifestation. Neurogenic symptoms consisting of confusion, somnolence, and stupor may appear simultaneous with or following the onset of headache. If untreated, progressive worsening of neurological damage occurs, culminating in coma and death. The patient may be restless and uncooperative during the initial stages of the syndrome. Other clinical features may include projectile vomiting, visual disturbances ranging from blurring to frank blindness, and transient focal neurologic deficits.

On physical examination of the patient, the BP is markedly elevated but there is no certain level of BP above which encephalopathy is likely to develop. The fundi reveal generalized arteriolar spasm with exudates or hemorrhages. Although papilledema is present in most patients with this complication, its absence does not exclude the diagnosis of hypertensive encephalopathy.

Acute left ventricular failure may be caused by severe and uncontrolled hypertension; the higher the BP, the harder the left ventricle must work. Decreasing the workload of the failing myocardium may improve the heart function. In acute left ventricular failure, myocardial oxygen requirements increase due to increased end-diastolic fiber length and left ventricular volume. This could be particularly unfavorable in patients with concomitant coronary artery disease (CAD).

 

Left ventricular failure with alveolar edema. This is a posteroanterior chest film in a 48-year-old man. Severe interstitial and alveolar edema exists. Left ventricular enlargement indicates pulmonary venous hypertension secondary to left ventricular failure. The cause of the failure is not apparent. Note the normal azygos vein (arrowheads) and right atrium.

The chest x-ray of a patient with heart failure showing fluid and an enlarged heart shadow.

A raised JVP in a patient with heart failure (used with permission from Wikpedia).

A heart failure patient with peripheral oedema being checked at an annual review.

Eclampsia is a potentially serious cardiovascular complication in a pregnant patient. Although the definitive therapy is delivery of the fetus, the BP should be reduced to prevent neurologic, cardiac, and renal damage.

         Although other antihypertensive drugs may be effective in reducing the BP, the agent of choice is hydralazine, which has a long record of safety. Animal studies have shown that nitroprusside can cause problems in the fetus; therefore, its use should be reserved for hypertension refractory to hydralazine or methyldopa. The ganglion-blocking drug trimethaphan should be avoided because of the risk of meconium ileus. In pregnancy-induced hypertension, volume depletion may be present and diuretics should be avoided. IV labetalol and hydralazine have been used to treat severe hypertension in pregnancy.⁹ ACE inhibitors and angiotensin-receptor blockers should be avoided due to possible fetal/placental toxicity. Magnesium sulfate is also used as adjunctive therapy to control the convulsions.

Hypertensive crisis

Essential hypertension is characterized by periodically recurring trancient elevations of arterial pressure (hypertensive crisis). Development of such crises is preceded by psychic traumas, nervous overstrain, variations in atmospheric pressure, etc.

Hypertensive crisis develops with a sudden elevation of the arterial pressure that can persist from a few hours to several days. The crisis is manifested by sharp headache, feeling of heat, perspiration, palpitation, giddiness, piercing pain in the heart, sometimes by deranged vision, nausea, aid vomiting. In severe crisis, the patient may lose consciousness. The patient is excited, haunted by fears, or is indifferent, somnolent, and in­hibited. Auscultation of the heart reveals accentuated second sound over the aorta, and also tachycardia. The pulse is accelerated but can remain un­changed or even decelerated; its tension increases. Arterial pressure in­creases significantly. ECG shows decreased S-T interval and flattening of the T wave. In the late stages of the disease, with organic changes in the vessels, cerebral circulation may be deranged during crisis; myocardial infarction and acute left-ventricular failure may also develop.

Definitions and probable causes of hypertensive crisis

Hypertensive urgencies can be defined as severe elevations in BP that do not exhibit evidence of target-organ (cardiovascular, renal, CNS) dysfunction or damage. Urgencies can be managed by the administration of oral medications, most often in the emergency department (ED), and follow-up on an outpatient basis. Hypertensive emergencies are severe elevations in systolic and diastolic BP associated with acute target-organ damage that require immediate management in a hospital setting.

Hypertensive crises encompass a spectrum of clinical situations that have in common blood pressure (BP) that is elevated, and progressive or impending target organ damage. Most hypertensive urgencies or emergencies are preventable and are the result of inadequate treatment of mild-to-moderate hypertension or nonadherence to antihypertensive therapy.

Traditionally, hypertensive crises have been divided into emergencies and urgencies. Hypertensive emergencies are severe elevations in blood pressure (BP) that are complicated by evidence of progressive target organ dysfunction, and will require immediate BP reduction (not necessarily to normal ranges) to prevent or limit target organ damage. Examples include: hypertensive encephalopathy, intracranial hemorrhage, unstable angina pectoris, or acute myocardial infarction, acute left ventricular failure with pulmonary edema, dissecting aneurysm, or eclampsia. While the level of BP at the time of presentation is usually very high (greater than 180/120 mm Hg), keep in mind that it is not the degree of BP elevation, but rather the clinical status of the patient that defines a hypertensive emergency. For example, a BP of 160/100 mm Hg in a 60-year-old patient who presents with acute pulmonary oedema represents a true hypertensive emergency.

Treatment.

·        Risk factor modification and lifestyle changes

·        If you are overweight or obese, you should lose weight

·        Quit smoking

·        Be more physically active and less sedentary

·        Eat less salt

The primary goal of the treatment of hypertension is to prevent cardiovascular disease and death. Coexisting cardiovascular risk factors increase the risks associated with hypertension and warrant more aggressive treatment. The five-year risk of a major cardiovascular event in a 50-year-old man with a blood pressure of 160/110 mm Hg is 2.5 to 5.0 percent; the risk doubles if the man has a high cholesterol level and triples if he is also a smoker.

Trials involving patients with stage 1 or 2 hypertension showed that lowering systolic pressure by 10 to 12 mm Hg and diastolic pressure by 5 to 6 mm Hg reduces the risk of stroke by 40 percent, the risk of coronary disease by 16 percent, and the risk of death from any cardiovascular cause by 20 percent. The higher the blood pressure and the number of risk factors, the greater the reduction in absolute risk (and the smaller the number needed to treat).

Determination of the need for drug therapy is based on a combined assessment of the blood-pressure level and the absolute risk of cardiovascular disease. Patients with stage 1 hypertension can be treated with lifestyle modifications alone for up to one year, if they have no other risk factors, or for up to six months, if they have other risk factors. Drug treatment should be provided if blood pressure remains elevated after a trial of lifestyle modifications alone. Lifestyle modifications and antihypertensive therapy are indicated for patients with cardiovascular or other target-organ disease (renal, cardiac, cerebrovascular, or retinal disease) and for those with stage 2 or 3 hypertension. Patients with diabetes are at high risk, and drug therapy is indicated in such patients even if blood pressure is at the high end of the normal range.

Two or more blood-pressure readings separated by two minutes should be averaged. If the pressure is at the high end of the normal range, it should be rechecked yearly. Stage 1 hypertension should be confirmed within two months. Patients with stage 2 hypertension should be evaluated and referred for care within one month; those with stage 3 hypertension should be evaluated immediately or within one week. If systolic and diastolic values are in different categories, the recommendations for the higher reading should be followed.

For patients with multiple risk factors, clinicians should consider drugs as initial therapy along with lifestyle modifications. Clinically important risk factors include smoking, dyslipidemia, diabetes mellitus, an age of more than 60 years, male sex, postmenopausal status in women, and a family history of cardiovascular disease for women under the age of 65 years and men under the age of 55 years.

The Dietary Approaches to Stop Hypertension (DASH) study showed that eight weeks of a diet of fruits, vegetables, low-fat dairy products, whole grains, poultry, fish, and nuts, with limited fats, red meat, and sweets, reduced systolic pressure by 11.4 mm Hg and diastolic pressure by 5.5 mm Hg^. With sodium intake at a level below 100 mmol per day, systolic pressure was 3 mm Hg lower and diastolic pressure was 1.6 mm Hg lower than with the DASH diet and a higher level of sodium intake.

Restriction of sodium intake to 2 g per day lowers systolic pressure, on average, by 3.7 to 4.8 mm Hg and lowers diastolic pressure, on average, by 0.9 to 2.5 mm Hg. Moderate sodium restriction appears to be generally safe and effective and is particularly effective in elderly persons.

Most clinical trials of lifestyle modifications have been underpowered or of insufficient duration to evaluate the effect of these interventions on major cardiovascular outcomes. However, lifestyle modifications should be encouraged, since they are safe and inexpensive and, when combined with drug therapy, may result in better blood pressure control and an improved quality of life.

Patients should routinely be encouraged to reduce their intake of sodium, lose weight (if appropriate), engage in moderate exercise, and reduce their intake of alcohol (to no more than two to three drinks per day). The degree of blood-pressure lowering expected with each of these approaches is often modest but clinically important — for example, 2 to 8 mm Hg with dietary sodium restriction (with a goal of urinary sodium excretion of less than 100 mmol per day), 2 to 4 mm Hg with reduced alcohol consumption, and 4 to 9 mm Hg with regular physical activity (such as walking briskly for 30 to 45 minutes daily).

Adherence to therapy may be increased by the initiation of a system of follow-up reminders or telephone contacts. The involvement of nurses or nurse practitioners, who may have more time than a physician to discuss potential side effects of medications, has been shown to improve patients’ control of their blood pressure. The use of combination therapy (two medications in one pill) may also improve adherence and, in some cases, may reduce the cost of care.

Complex therapy is required. Reasonable work should be alternated with rest, sufficient sleep, and remedial exercises.

In early stage sedatives should be given to improve sleep and to normalize excitation and inhibition processes. Hypotensive preparations are prescribed to inhibit the increased activity of the vasomotor centers and the synthesis of noradrenaline.

Pharmacological agents. Most antihypertensive drugs reduce blood pressure by 10 to 15 percent. Monotherapy is effective in about 50 percent of unselected patients, and those with stage 2 or 3. hypertension ofteeed more than one drug.

Diuretics, beta-blockers, ACE inhibitors or angiotensin-receptor antagonists and calcium channel blockers are recommended for patients with hypertension.

Here are some of the side effects of commonly used blood pressure lowering medications:

Diuretics have a limited role in the management of hypertensive emergencies. Diuretics (saluretics) are given to decrease intracellular sodium; aldosterone blocking agents (spironolactone) and other preparations are also given. Diuretics are often the first choice if diet and exercise changes aren’t enough. Also called “water pills,” they help the body shed excess sodium and water to lower blood pressure. That means you’ll urinate more often. Some diuretics may deplete your body’s potassium, causing muscle weakness, leg cramps, and fatigue. Some can increase blood sugar levels in diabetics. Erectile dysfunction is a less common side effect

Beta-blockers work by slowing the heart rate, which means that the heart doesn’t have to work as hard. They are also used to treat other heart conditions, such as an abnormal heart rate called arrhythmia. They may be prescribed along with other medications. Side effects can include insomnia, dizziness, fatigue, cold hands and feet, and erectile dysfunction.

ACE inhibitors reduce your body’s supply of angiotensin II — a substance that makes blood vessels contract and narrow. The result is more relaxed, open (dilated) arteries, as well as lower blood pressure and less effort for your heart. Side effects can include a dry cough, skin rash, or dizziness, and high levels of potassium. Women should not become pregnant while taking an ACE inhibitor.

Combination therapy may improve compliance and achieve the target blood pressure more rapidly.

Ischemic heart disease: main symptoms and syndromes

in angina pectoralis and myocardial infarction

Ischaemic or ischemic heart disease (IHD), or myocardial ischaemia, is a disease characterized by ischaemia (reduced blood supply) of the heart muscle, usually due to coronary artery disease (atherosclerosis of the coronary arteries). Its risk increases with age, smoking, hypercholesterolaemia (high cholesterol levels), diabetes, and hypertension (high blood pressure), and is more common in men and those who have close relatives with ischaemic heart disease.

The blood vessels are narrowed or blocked due to the deposition of cholesterol plaques on their walls. This reduces the supply of oxygen and nutrients to the heart musculature, which is essential for proper functioning of the heart.

 

 This may eventually result in a portion of the heart being suddenly deprived of its blood supply leading to the death of that area of heart tissue, resulting in a heart attack. As the heart is the pump that supplies oxygenated blood to the various vital organs, any defect in the heart immediately affects the supply of oxygen to the vital organs like the brain, kidneys etc.

A multitude of factors are responsible for the development of IHD. The major risk factors are smoking, diabetes mellitusand cholesterol levels.

Those with Hypercholesterolaemia (elevated blood levels of cholesterol) have a much higher tendency to develop the disease. There is also the theory that Hypertension is a risk factor in the development of IHD, Genetic and hereditary factors may also be responsible for the disease. Males are more prone to IHD. However, in post-menopausal women, the risk is almost similar to that of men. Stress is also thought to be a risk factor, though there has been a great deal of debate on this factor of late.

The disease process occurs when an atheromatous plaque forms in the coronary vessels, leading to narrowing of the vessel walls and obstructing blood flow to the musculature of the heart. Complete blockage results in deficient oxygenation and nutrient supply to the heart tissues, leading to damage, death and necrosis of the tissue, which is known as Myocardial Infarction (heart attack).

Symptoms of stable ischemic heart disease include angina (characteristic chest pain on exertion) and decreased exercise tolerance. Unstable IHD presents itself as chest pain or other symptoms at rest, or rapidly worsening angina. Diagnosis of IHD is with an electrocardiogram, blood tests (cardiac markers), cardiac stress

testing or a coronary angiogram. Depending on the symptoms and risk, treatment may be with medication, percutaneous coronary intervention (angioplasty) or coronary artery bypass surgery (CABG).

It is the most common cause of death in most Western countries, and a major cause of hospital admissions. There is limited evidence for population screening, but prevention (with a healthy diet and sometimes medication for diabetes, cholesterol and high blood pressure) is used both to prevent IHD and to decrease the risk of complications.

Ischaemic heart disease may be present with any of the following problems:

Angina pectoris (chest pain on exertion, in cold weather or emotional situations);

Acute chest pain: acute coronary syndrome, unstable angina or myocardial infarction (“heart attack”, severe chest pain unrelieved by rest associated with evidence of acute heart damage);

Heart failure (difficulty in breathing or swelling of the extremities due to weakness of the heart muscle);

Heartburn.

Stable Angina Pectoris

The diagnosis of chronic stable angina pectoris includes predictable and reproducible left anterior chest discomfort after physical activity, emotional stress, or both; symptoms are typically worse in cold weather or after meals and are relieved by rest or sublingual nitroglycerin. The presence of one or more obstructions in major coronary arteries is likely; the severity of stenosis is usually greater than 70 percent.

Pathophysiology Angina occurs when there is regional myocardial ischemia caused by inadequate coronary perfusion and is usually but not always induced by increases in myocardial oxygen requirements. Cardinal features of chronic stable angina include complete reversibility of the symptoms and repetitiveness of the anginal attacks over time, typically months to years. New, prolonged, or recent-onset symptoms are characteristic of unstable angina. Coexisting conditions, such as poorly controlled hypertension, anemia, or thyrotoxicosis, can precipitate or accentuate angina.

As coronary atherosclerosis progresses, there is deposition of plaque external to the lumen of the artery; the plaque may extend eccentrically and outward without compromising the lumen. Thus, stress testing or angiography may not suggest coronary disease, even in the presence of significant atherosclerosis. As atherosclerosis worsens, encroachment of the plaque mass into the lumen can result in hemodynamic obstruction and angina. Disordered endothelial vasomotor function of the coronary arteries is common in patients with angina and results in diminished vasodilatation or even vasoconstriction in response to various stimuli, including exercise Occasionally, patients with severe aortic-valve disease or hypertrophic cardiomyopathy have angina-like chest pain in the absence of overt coronary disease.

Classification of Angina Pectoris

Chest pain is characterized as classic, or typical, angina; as atypical angina, which includes symptoms that have some but not all the features of angina; and as nonanginal chest pain, which has none of the features of angina. Chest pain that occurs during rest or at night⁸ is well described in persons with chronic stable angina, particularly women.

Atypical presentations of angina are more common in women than in men. Women with ischemia are more likely than men to report variable pain thresholds, inflammatory pain, palpitations, or sharp, stabbing pain. Overall, chest pain in women is quite common and usually is not due to coronary artery disease. Data from the Women’s Ischemia Syndrome Evaluation initiative of the National Heart, Lung, and Blood Institute indicate that many women with anginal symptoms have inducible ischemia and a reduced coronary flow reserve yet no significant obstruction on coronary angiography. Atypical presentations of angina are also more frequent in older patients (who often have exertional dyspnea, weakness, or sweating) than in younger patients and in patients with diabetes (who often have atypical or even silent ischemic episodes) than in those without diabetes; a high level of suspicion for coronary disease is needed in these groups. The severity of angina should be assessed to aid in management decisions. However, there is no direct correlation between the class of angina and the severity of coronary artery disease as determined on angiography.

Diagnostic Strategies  Stress Testing. Various diagnostic tests are available for the evaluation of suspected coronary disease. Summarizes common stress-testing methods. Adults with typical or atypical features of chest pain, especially those with major risk factors for coronary artery disease, should undergo stress testing. False positive and false negative exercise tests occur in up to 20 to 30 percent of persons (more commonly in women); coronary angiography is ofteecessary to resolve equivocal test results. Noninvasive testing may provide useful additional prognostic information, such as total exercise time, the inducibility of left ventricular dysfunction, blood-pressure and heart-rate responses, and, most important, the degree of myocardial ischemia. In general, poor aerobic performance and disordered heart-rate or blood-pressure responses increase the likelihood of subsequent clinical events.

Coronary Angiography

Coronary angiography remains the diagnostic gold standard for obstructive coronary artery disease, but it may miss extraluminal plaque related to coronary remodeling. Indications for angiography include poorly controlled symptoms; abnormal results on stress testing, particularly with a substantial burden of ischemia (e.g., 1 mm or more of ST-segment depression); ischemia at a low workload (below 5 to 6 metabolic equivalents); large, inducible single or multiple wall-motion abnormalities; and substantial nuclear-perfusion defects.

 

Invasive coronary angiography

Conventional invasive coronary angiographic image compared

Atypical chest pain or inconclusive or discordant test results occasionally warrant the use of angiography. Intermediate-grade coronary obstructions (e.g., 50 to 70 percent stenosis) may require additional evaluation, such as assessment of coronary flow reserve. Suspected vasospastic or microvascular angina requires additional specialized testing.

Cardiac Biomarkers

Elevated levels of high-sensitivity C-reactive protein and other markers, including braiatriuretic peptide, have prognostic value with respect to cardiovascular events in patients with stable angina or asymptomatic coronary artery disease. However, the clinical utility of such testing remains uncertain.

Treatment 

Lifestyle Modifications

Although obesity and sedentary lifestyles are not listed as CAD risk factors, their presence will increase the likelihood of other risk factors (e.g., diabetes, elevated LDL, low HDL, hypertension). In order to reduce the risk of CAD, interventions aimed at increasing exercise and weight reduction in obese patients should be employed. Even modest weight reduction will improve a patient’s lipid profile and reduce the risk of hypertension, dyslipidemia and diabetes. Exercise also has been shown to have a positive effect on lipid profile by increasing HDL. Smokers with dyslipidemia should be counseled on the added risk of cigarette smoking and referred to a smoking cessation program.

Diet therapy has been shown to lower total serum cholesterol between 5% and 10%.

         Regular exercise reduces the frequency of anginal symptoms, increases functional capacity, and improves endothelial function. Patients with chronic stable angina who are receiving medical therapy should exercise regularly, beginning at low levels for 20 to 30 minutes and increasing as symptoms allow. A recent randomized trial that compared the effects of daily exercise with those of angioplasty and stenting among patients with chronic stable angina and single-vessel coronary artery disease demonstrated better outcomes (in terms of major adverse events and improved exercise capacity) at one year in the exercise group than in the revascularization group.

Vigorous efforts at smoking cessation and weight control are mandatory in patients with chronic stable angina. For patients with diabetes, a multifactorial approach that includes lifestyle changes and medications for glycemic control and coronary risk factors substantially reduces the risk of cardiovascular events.³⁷

Chemotherapy

It is useful to classify therapeutic drugs into two categories: antianginal (anti-ischemic) agents and vasculoprotective agents. Although medications for angina are widely used, therapy to slow the progression of coronary artery disease, to induce the stabilization of plaque, or to do both is a newer concept, and these forms of treatment are underprescribed.

Antianginal Agents

All antianginal drugs — nitrates, beta-adrenergic blockers, and calcium-channel blockers — have been shown to prolong the duration of exercise before the onset of angina and ST-segment depression as well as to decrease the frequency of angina.

– Beta-blockers work primarily by decreasing myocardial oxygen consumption through reductions in heart rate, blood pressure, and myocardial contractility.

– Calcium antagonists dilate coronary and systemic arteries, increase coronary blood flow, and decrease myocardial oxygen consumption.

– Nitrates dilate systemic and coronary arteries, including some coronary stenoses, and particularly the systemic veins; venous pooling of blood decreases cardiac work and chamber size. Sublingual or oral spray nitroglycerin relieves acute episodes of angina within 5 to 10 minutes; prophylactic use before activity can be helpful in persons with frequent angina. Prevention of tolerance requires an intermittent dosing strategy, with a nitrate-free interval of 12 to 14 hours. Phosphodiesterase type 5 inhibitors (e.g., sildenafil, vardenafil, and tadalafil) and nitrates should not be used within 24 hours of one another because of the potential for serious hypotension.

^– The use of aspirin at a dose of 81 to 150 mg per day reduces cardiovascular morbidity and mortality by 20 to 25 percent among patients with coronary artery disease.

Inotropic agents (Dopamine, Dobutamine) 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

Revascularization

Revacularization includes either percutaneous coronary intervention (i.e., balloon angioplasty and stenting) or coronary-artery bypass surgery

MYOCARDIAL INFARCTION

 

Acute coronary syndromes (ACS) include “a broad spectrum of clinical presentations, spanning ST-segment-elevation myocardial infarction, through to an accelerated pattern of angina without evidence of myonecrosis”.

Myocardial infarction, commonly known as a heart attack, is the irreversible necrosis of heart muscle secondary to prolonged ischemia. This usually results from an imbalance in oxygen supply and demand, which is most often caused by plaque rupture with thrombus formation in a coronary vessel, resulting in an acute reduction of blood supply to a portion of the myocardium.

Myocardial infarction occurs most often in the early morning hours, perhaps partly because of the increase in catecholamine-induced platelet aggregation and increased serum concentrations of plasminogen activator inhibitor-1 (PAI-1) that occur after awakening. In general, the onset is not directly associated with severe exertion. Instead, it is concomitant with exertion. The immediate risk of myocardial infarction increases 6-fold on average and by as much as 30-fold in sedentary people. A high index of suspicion should be maintained for myocardial infarction especially when evaluating women, patients with diabetes, older patients, patients with dementia, patients with a history of heart failure, cocaine users, patients with hypercholesterolemia, and patients with a positive family history for early coronary disease. A positive family history includes any first-degree male relative aged 45 years or younger or any first-degree female relative aged 55 years or younger who experienced a myocardial infarction.

 

Physical Examination. For many patients, the first manifestation of coronary artery disease is sudden death likely from malignant ventricular dysrhythmia. Physical examination findings for myocardial infarction can vary; one patient may be comfortable in bed, with normal examination results, while another may be in severe pain, with significant respiratory distress and a need for ventilatory support.

Patients with ongoing symptoms usually lie quietly in bed and appear pale and diaphoretic. Hypertension may precipitate myocardial infarction, or it may reflect elevated catecholamine levels due to anxiety, pain, or exogenous sympathomimetics. Hypotension may indicate ventricular dysfunction due to ischemia. Hypotension in the setting of myocardial infarction usually indicates a large infarct secondary to either decreased global cardiac contractility or a right ventricular infarct. Acute valvular dysfunction may be present. Valvular dysfunction usually results from infarction that involves the papillary muscle. Mitral regurgitation due to papillary muscle ischemia or necrosis may be present.

The typical chest pain of acute myocardial infarction is intense and unremitting for 30-60 minutes. It is retrosternal and often radiates up to the neck, shoulder, and jaw and down to the ulnar aspect of the left arm. Chest pain is usually described as a substernal pressure sensation that also may be described as squeezing, aching, burning, or even sharp. In some patients, the symptom is epigastric, with a feeling of indigestion or of fullness and gas.

Atypical presentations are common and frequently lead to misdiagnoses. Moreover, any patient may present with atypical symptoms, which are considered the anginal equivalent for that patient. A patient, for example, may present with abdominal discomfort or jaw pain as his or her anginal equivalent. An elderly patient may present with altered mental status. Atypical chest pain is common, especially in elderly patients and patients with diabetes. A low threshold should be maintained when evaluating high- and moderate-risk patients, as their anginal equivalents may mimic other presentations. Women tend to present more commonly with atypical symptoms such as sharp pain, fatigue, weakness, and other nonspecific complaints.

Diaphoresis, weakness, a sense of impending doom, profound restlessness, confusion, presyncope, hiccupping (which presumably reflects irritation of the phrenic nerve or diaphragm), nausea and vomiting, and palpitations may be present. (Nausea and/or abdominal pain often are present in infarcts involving the inferior or posterior wall.)

Decreased systolic ventricular performance may lead to impaired perfusion of vital organs and reflex-mediated compensatory responses, such as restlessness, impaired mentation, pallor, peripheral vasoconstriction and sweating, tachycardia, and prerenal failure.

By contrast, impaired left ventricular diastolic function leads to pulmonary vascular congestion with shortness of breath and tachypnea and, eventually, pulmonary edema with orthopnea. Shortness of breath may be the patient’s anginal equivalent or a symptom of heart failure. In an elderly person or a patient with diabetes, shortness of breath may be the only complaint.

In patients with acute inferior-wall myocardial infarction with right ventricular involvement, distention of neck veins is commonly described as a sign of failure of the RV. (Central venous pressure is most properly estimated independently of venous distension on the basis of the height of the meniscus of venous pulsation above the mid atrium.) Impaired right ventricular diastolic function also leads to systemic venous hypertension, edema, and hepatomegaly with abdominojugular reflux, which may result in saline-response underfilling of the LV and a concomitant reduction in cardiac output.

Elderly patients and those with diabetes may have particularly subtle presentations and may complain of fatigue, syncope, or weakness. The elderly may also present with only altered mental status.

As many as half of myocardial infarctions are clinically silent in that they do not cause the classic symptoms described above and consequently go unrecognized by the patient. Myocardial infarction is clinically silent in as many as 25% of elderly patients, a population in whom 50% of myocardial infarctions occur; in such patients, the diagnosis is often established only retrospectively, by applying electrocardiographic criteria or by scanning the patients using 2-dimensional (2D) echocardiography or magnetic resonance imaging (MRI).

On clinical evaluation, ventricular aneurysms may be recognized late, with symptoms and signs of heart failure, recurrent ventricular arrhythmia, or recurrent embolization.

Vital signs

The patient’s heart rate is often increased secondary to sympathoadrenal discharge. The pulse may be irregular because of ventricular ectopy, an accelerated idioventricular rhythm (demonstrated below), ventricular tachycardia, atrial fibrillation or flutter, or other supraventricular arrhythmias. Bradyarrhythmias may be present; bradyarrhythmias may be attributable to impaired function of the sinus node. An AV nodal block or infranodal block may be evident.

In general , the patient’s blood pressure is initially elevated because of peripheral arterial vasoconstriction resulting from an adrenergic response to pain and ventricular dysfunction. However, with right ventricular myocardial infarction or severe left ventricular dysfunction, hypotension is seen.

The respiratory rate may be increased in response to pulmonary congestion or anxiety.

Coughing, wheezing, and the production of frothy sputum may occur.

Fever is usually present within 24-48 hours, with the temperature curve generally parallel to the time course of elevations of creatine kinase (CK) levels in the blood. Body temperature may occasionally exceed 102°F.

Arterial pulsations

Arterial pulsations may exhibit pulsus alternans, which reflects impaired left ventricular function and is characterized by strong and weak alternating pulse waves (the variation in systolic pressure is >20 mm Hg). Carotid pulsation may be thin (pulsus parvus) because of decreased amplitude and length of the pulse secondary to decreased stroke volume.

Pulsus bisferiens consists of 2 systolic peaks; it may be palpated in association with hypertrophic obstructive cardiomyopathy (HOCM) or mixed aortic stenosis and regurgitation. A dicrotic pulse is encountered in cases involving hypovolemic shock, severe heart failure, or cardiac tamponade. It manifests as a double pulse, produced by a combination of the systolic wave followed by an exaggerated dicrotic (diastolic) wave.

A bigeminal pulse is observed in the presence of ectopic beats or Wenckebach heart block; it is characterized by regular coupling of 2 beats with the interval between a pair of beats greater than that between the coupled beats themselves.

Pulsus paradoxus is defined as a decline in systolic blood pressure of 10 mm Hg or more on inspiration; it is seen in cases involving cardiac tamponade, constrictive pericarditis, restrictive cardiomyopathy, hypotensive shock, severe chronic lung disease, or pulmonary embolism.

In patients with associated aortic regurgitation, a pulse with sharp descent, or a water-hammer pulse, may be observed.

Venous pulsations

Jugular venous distention may accompany right ventricular myocardial infarction or right ventricular failure secondary to profound left ventricular dysfunction and pulmonary hypertension. It may also be elevated as a result of an increase in right atrial pressure in patients with heart failure, decreased right ventricular compliance, pericardial disease, fluid overload, or tricuspid or superior vena cava obstruction. The Kussmaul sign, characterized by a paradoxical increase in jugular venous pressure during inspiration, may occur in patients with constrictive pericarditis, congestive HF (CHF), or tricuspid stenosis.

Chest

Rales or wheezes may be auscultated; these occur secondary to pulmonary venous hypertension, which is associated with extensive acute left ventricular myocardial infarction. Unilateral or bilateral pleural effusions may produce egophony at the lung bases. On chest radiographs, they are evidenced by blunted costophrenic angles; on MRI, they are evidenced by dependent fluid signal intensity; on echocardiography, they are evidenced by echolucent zones adjacent to the heart.

Heart

On palpation, lateral displacement of the apical impulse, dyskinesis (seen in the image below), a palpable S4 gallop, and a soft S1 sound may be found. These indicate diminished contractility of the compromised LV.

Paradoxical splitting of S2 may reflect the presence of left bundle-branch block or prolongation of the preejection period with delayed closure of the aortic valve, despite decreased stroke volume.

Increased S4 and S3 gallops may suggest increased LV stiffness; they represent the rapid filling phase (S3) or atrial contraction (S4).

A mitral regurgitation murmur (typically holosystolic near the apex) indicates papillary muscle dysfunction or rupture or mitral annular dilatation; it may be audible even when cardiac output is substantially decreased.

A holosystolic systolic murmur that radiates to the midsternal border and not to the back, possibly with a palpable thrill, suggests a ventricular septal rupture; such a rupture may occur as a complication in some patients with full-thickness (or Q-wave) myocardial infarctions. With resistive flow and an enlarged pressure difference, the ventricular septal defect murmur becomes harsher, louder, and higher in pitch than before.

A pericardial friction rub may be audible as a to-and-fro rasping sound with 1-3 components; it is produced through sliding contact of inflammation-roughened surfaces.

Neck vein and pulse patterns, splitting of S2, or ECG findings may suggest premature ventricular beats, brief runs of ventricular tachycardia, accelerated idioventricular rhythm, atrial flutter or atrial fibrillation, or conduction delays.

Extremities

Peripheral cyanosis, edema, pallor, diminished pulse volume, delayed rise, and delayed capillary refill may indicate vasoconstriction, diminished cardiac output, and right ventricular dysfunction or failure. Pulse and neck-vein patterns may reveal other associated abnormalities, as previously discussed. Dependent edema may be graded 0-4 by assessing the depth of persistent pitting after thumb pressure is applied to the patient’s inner shin for more than 10 seconds or by evaluating the lower back if the patient has had his or her legs elevated.

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 diagnosis is based on the clinical presentation and the electrocardiogram (ECG) findings and, in particular, the presence or absence of ST-segment elevation. As the vast majority of patients who present with initial ST-segment elevation develop biochemical evidence of myonecrosis, the term “ST-segment-elevation myocardial infarction” (STEMI) is often used from the outset in these patients.

Electrocardiography

The ECG is the most important tool in the initial evaluation and triage of patients in whom an ACS is suspected. It is confirmatory of the diagnosis in approximately 80% of cases.

Electrocardiography is necessary to detect ischaemic changes or arrhythmias. It should be noted that the initial ECG has a low sensitivity for ACS, and a normal ECG does not rule out ACS. However, the ECG is the sole test required to select patients for emergency reperfusion (fibrinolytic therapy or direct PCI). Patients with STEMI who present within 12 hours of the onset of ischaemic symptoms should have a reperfusion strategy implemented promptly (grade A recommendation). Many people who have had a prior MI will have an ECG that appears normal. There may however be typical features of previous MI, and the most conspicuous of these is Q waves. A simplistic explanation of these prominent Q waves is that an appropriately placed lead “sees through” the dead tissue, and visualises the normal depolarisation of the viable myocardial wall directly opposite the infarcted area. Because, in the normal myocardium, depolarisation moves from the chamber outwards, this normal depolarisation is seen as a Q wave

Acute anterior myocardial infarction.

Another feature of previous MI is loss of R wave amplitude. It’s easy to imagine that if muscle is lost, amplitude must be diminished. (Having a pre-infarction ECG for comparison is invaluable).

One can get some idea of the site of infarction from the lead in which abnormalities are seen – inferior, lateral, or anterior.

Ischaemic heart disease – ST changes

One should always remember that more than a quarter of people presenting with an acute myocardial infarction will have no ECG evidence of ischaemia or infarction! The ECG on its own is a blunt-edged tool in the detection of coronary artery disease. Exercise testing to elicit ischaemia is also not very sensitive in detecting this common disease.

Acute myocardial infarction — the `hyperacute phase’

There are four main features of early myocardial infarction (as per Schamroth):

1.     increased VAT

2.     increased R wave amplitude (!)

3.     ST elevation which is sloped upwards!

4.     Tall, widened T waves (The ST segment often merges with these)

We now lay great emphasis on ST segment elevation in diagnosing acute MI (In the past, Q waves were remarked on, but as noted above, these are often absent, early on). The features of `full blown’ MI may be:

1.     prominent Q waves;

2.     elevated ST segments;

3.     Inverted `arrowhead’ T waves.

Remember our previous warning, that a significant proportion of people having an acute MI will have a normal ECG, so do not rely on any of these features to Posterior MI

The trick in diagnosing this is to realise that posterior wall changes will be mirrored in the leads opposite to the lesion — V1 and V2. S we’ll see a tall R (corresponding to a Q), ST depression, and upright arrowhead T waves:

Non-ST elevation MI

There are no reliable correlates of “subendocardial” or non-ST elevation MI, and the diagnosis is based on the combination of clinical and laboratory criteria (troponin elevation being important). There may be no ECG changes, or even ST segment depression and/or T wave abnormalities.

 

 

 

A) Shows the normal QRS complex in a lead.

B C) Within hours of the clinical onset of an MI, there is ST segment elevation. At this stage no QRS or T wave changes have occurred. This indicates myocardial damage only, not definitive evidence of infarction.

D) Within days, the R wave voltage falls and abnormal Q waves appear. This is sufficient evidence of an infarction. In addition, T wave inversion will also have appeared but the ST segment elevation may be less obvious than before.

E) Within one or more weeks, the ST segment changes revert completely to normal. The R wave voltage remains low and the abnormal Q waves persist. Deep, symmetrical T wave inversion may develop at this stage.

F) Months after the MI, the T waves may gradually return to normal. The abnormal Q waves and reduced R wave voltage persist.

Occasionally, all evidence of infarction may be lost with the passing of time; this is due to shrinkage of scar tissue.

 

Because primary ECG changes occur in leads overlying the infarct, the location of an infarct can be derived by looking at the primary changes occurring in such leads. This is depicted in the following table:

Location of infarction	Leads showing primary changes
	Typical changes
Anterior infarction
Antero-septal	V1, V2, V3
Anterior	Some of V1-V3 plus some of V4-V6
Anterior extensive	V1, V2, V3, V4, V5, V6,I, aVL
Antero-lateral	V4, V5, V6, I, aVL, possibly II
High lateral	aVL and/or I
Inferior infarction
Inferior	II, III, aVF
Infero-lateral (= apical)	II, III, aVF, V5, V6 & sometimes also I, aVL
Infero-septal	II, III, aVF, V1, V2, V3
	Other changes
Posterior infarction	V1, V2 (inverse of usual changes elsewhere)
Subendocardial infarction	Any lead (usually multiple leads)

Diagnostic criteria for MI

A definitive diagnosis of MI from the ECG can only be made on the basis of abnormalities in the QRS

complex. The following changes are seen:

1.                   q waves which are either 0.04 s or longer in duration (excluding aVR and lead III) or have a depth which is more than 25% of the height of the following R wave (excluding aVR and lead III).

2.                   qs or QS complexes (excluding aVR and lead III).

3.                   Local area of inappropriately low R wave voltage.

4.                   Additional changes frequently associated with MI are:

5.                       ST segment elevation (convex upwards) in leads facing the infarcted zone.

6.                       ST segment depression occurs as a reciprocal change in leads mutually opposite to the primary leads showing evidence of infarction.

7.                       Horizontal ST segment depression may occur as a primary change in subendocardial infarction.

 

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

 

The simple (and possibly even correct) explanation of why you see ST segment elevation with this variant form of angina is that the predominant area of ischaemia is epicardial. This disorder is thought to be related to vascular spasm, and angiography shows coronaries without a significant burden of atheroma. Many other morphological abnormalities have been described with this disorder.

         Posterior Myocardial Infarction

 Clinical Significance

v Posterior infarction accompanies 15-20% of STEMIs, usually occurring in the context of an inferior or lateral infarction.

v Isolated posterior MI is less common (3-11% of infarcts).

v Posterior extension of an inferior or lateral infarct implies a much larger area of myocardial damage, with an increased risk of left ventricular dysfunction and death.

v Isolated posterior infarction is an indication for emergent coronary reperfusion. However, the lack of obvious ST elevation in this condition means that the diagnosis is often missed.

Be vigilant for evidence of posterior MI in any patient with an inferior or lateral STEMI.

How to spot posterior infarction

As the posterior myocardium is not directly visualised by the standard 12-lead ECG, reciprocal changes of STEMI are sought in the anteroseptal leads V1-3:

v Posterior MI is suggested by the following changes in V1-3:

v Horizontal ST depression

v Tall, broad R waves (>30ms)

v Upright T waves

v Dominant R wave (R/S ratio > 1) in V2

In patients presenting with ischaemic symptoms, horizontal ST depression in the anteroseptal leads (V1-3) should raise the suspicion of posterior MI.

Typical appearance of posterior infarction in V2

v Posterior infarction is confirmed by the presence of ST elevation and Q waves in the posterior leads (V7-9).

Anterior-inferior STEMI

 

v ST elevation is present throughout the precordial and inferior leads.

v There are hyperacute T waves, most prominent in V1-3.

v Q waves are forming in V1-3, as well as leads III and aVF.

v This pattern is suggestive of occlusion occurring in “type III” or “wraparound” LAD (i.e. one that wraps around the cardiac apex to supply the inferior wall)

 

Early inferior STEMI:

v Hyperacute (peaked) T waves in II, III and aVF with relative loss of R wave height.

v Early ST elevation and Q-wave formation in lead III.

v Reciprocal ST depression and T wave inversion in aVL.

v ST elevation in lead III > lead II suggests an RCA occlusion; the subtle ST elevation in V4R would be consistent with this.

Note how the ST segment morphology in aVL is an exact mirror image of lead III. This reciprocal change occurs because these two leads are approximately opposite to one another (150 degrees apart).

The concept of reciprocal change can be further highlighted by taking lead aVL and inverting it… see how the ST morphology now looks identical to lead III.

 

 

Hyperacute inferior STEMI:

Ø Hyperacute T waves in II, III and aVF.

Ø Early ST elevation and loss of R wave height in II, III and aVF.

Ø Reciprocal change in aVL and lead I.

Anterior MI

The next 12 lead is an example of an anterior septal wall MI.

 Non-Q Wave MI

 Recognized by evolving ST-T changes over time without the formation of pathologic Q waves (in a patient with typical chest pain symptoms and/or elevation in myocardial-specific enzymes)

 Although it is tempting to localize the non-Q MI by the particular leads showing ST-T changes, this is probably only valid for the ST segment elevation pattern.

 Evolving ST-T changes may include any of the following patterns:

Ø  Convex downward ST segment depression only (common) 

Ø  Convex upwards or straight ST segment elevation only (uncommon)

Ø  Symmetrical T wave inversion only (common)

Ø  Combinations of above changes

 Example: Anterolateral ST-T wave changes

 

 

Blood tests

Measurements should include:

          Serum troponin I or T levels (or CK-MB if troponin is not available).

Troponin is a contractile protein that normally is not found in serum. It is released only when myocardial necrosis occurs.

Troponin levels are now considered to be the criterion standard for defining and diagnosing myocardial infarction, according to the American College of Cardiology (ACC)/American Heart Association (AHA) consensus statement on myocardial infarction. Positive troponin levels are considered virtually diagnostic of myocardial infarction, according to a revised version of the ACC/AHA consensus statement, as they are without equal in combined specificity and sensitivity in this diagnosis. Reichlan et al suggest that absolute changes in troponin levels have a significantly higher diagnostic accuracy for acute myocardial infarction than relative changes. Serum levels increase within 3-12 hours from the onset of chest pain, peak at 24-48 hours, and return to baseline over 5-14 days. Improved cardiac troponin assays offer even greater diagnostic accuracy than the standard assays do, according to a study by Reichlin et al. This is especially true for the early diagnosis of acute myocardial infarction, particularly in patients with a recent onset of chest pain, according to the investigators.

          Full blood count.

          Serum creatinine and electrolyte levels, particularly potassium concentration, as hypokalaemia is associated with an increased risk of arrhythmias, especially ventricular fibrillation (grade B recommendation). Knowledge of kidney function (expressed as estimated glomerular filtration rate) is strongly encouraged (grade B recommendation) given the association between renal impairment and adverse outcomes (evidence level III).

          Serum creatine kinase (CK) level.

Creatine Kinase Levels: The 3 CK isoenzymes are as follows:

CK with muscle subunits (CK-MM), which is found mainly in skeletal muscle

CK with brain subunits (CK-BB), which is found predominantly in the brain

CK-MB, which is found mainly in the heart

          Serial measurements of CK-MB isoenzyme levels were previously the standard criterion for the diagnosis of myocardial infarction. CK-MB levels increase within 3-12 hours of the onset of chest pain, reach peak values within 24 hours, and return to baseline after 48-72 hours. levels peak earlier (wash out) if reperfusion occurs. Sensitivity is approximately 95%, with high specificity. However, sensitivity and specificity are not as high as they are for troponin levels, and, as mentioned above, the trend has favored using troponins for the diagnosis of myocardial infarction.

          Serum lipid levels (fasting levels of total cholesterol, low-density-lipoprotein cholesterol, high-density-lipoprotein cholesterol and triglycerides) within 24 hours.

          Blood glucose level.

Myoglobin, a low-molecular-weight heme protein found in cardiac and skeletal muscle, is released more rapidly from infarcted myocardium than is troponin. Urine myoglobin levels rise within 1-4 hours from the onset of chest pain. Myoglobin levels are highly sensitive but not specific; they may be useful within the context of other studies and in the early detection of myocardial infarction in the emergency department (ED)

 

Principles of treatment

Patients without ST-segment elevation on the initial ECG should be further observed and investigated to promptly identify patients suitable for an emergency reperfusion strategy (based on ECG changes) and/or determine the best management protocol for NSTEACS based on risk stratification

Reperfusion may be obtained with fibrinolytic therapy or PCI. A combination of fibrinolysis and PCI may also be used (facilitated or rescue PCI). Coronary artery bypass graft (CABG) surgery may occasionally be more appropriate — particularly in patients who have suitable anatomy and are not candidates for fibrinolysis or PCI. CABG surgery may also be considered in patients with cardiogenic shock or in association with mechanical repair.

Aspirin (300 mg) should be given to all patients with STEMI unless contraindicated and, in the absence of significant side effects, low-dose therapy should be continued in the long term (grade A recommendation).

There is evidence that clopidogrel (300–600 mg loading dose) should be prescribed in addition to aspirin for patients undergoing PCI with a stent. In patients selected for fibrinolytic therapy, clopidogrel (300 mg) should be given in addition to aspirin, unless contraindicated (grade B recommendation). Note, however, that if it is thought that the patient is likely to require CABG acutely, clopidogrel should be withheld.

Clopidogrel (75 mg daily) should be continued for at least a month after fibrinolytic therapy, and for up to 12 months after stent implantation, depending on the type of stent and circumstances of implantation (level II evidence; grade B recommendation).

Antithrombin therapy. Antithrombin therapy should be used The aim should be to obtain an activated clotting time (ACT) between 200 and 300 seconds if using GP IIb/IIIa inhibitors, or between 300 and 350 seconds if these drugs are not used (grade B recommendation). It may be advisable to give a bolus of heparin while the patient is in transit to the catheterisation laboratory (grade D recommendation).

Antithrombin therapy should be used with fibrin-specific fibrinolytic agents (grade A recommendation).

Enoxaparin may be used in conjunction with fibrin-specific fibrinolytic agents

 

Main symptoms and syndromes in dry pleurisy and pleurisy with effusion.

 Syndrome of respiratory insufficiency in respiratory system pathology

Pleurisy, also called pleuritis, is an inflammation of the pleura membranes lining the inside of the chest cavity and coating the lungs. Normally these membranes are very slippery, aiding in breathing, but when they become infected, they don’t slide over each other as well. The condition can make breathing extremely painful. Sometimes it is associated with another condition called pleural effusion, where excess fluid fills the area between the membrane’s layers.

Dry pleurisy (pleuritis sicca) and pleurisy with effusion (pleuritis exudativa) are distinguished.

The double-layered pleura protects and lubricates the surface of the lungs as they inflate and deflate within the rib cage. Normally, a thin, fluid-filled gap – the pleural space – allows the two layers of the pleural membrane to slide gently past each other. But when these layers become inflamed, with every breath, sneeze or cough their roughened surfaces rub painfully together like two pieces of sandpaper.

In some cases of pleurisy, excess fluid seeps into the pleural space, resulting in pleural effusion. This fluid build-up usually has a lubricating effect, relieving the pain associated with pleurisy as it reduces friction between the membrane’s layers. But at the same time, the added fluid puts pressure on the lungs, reducing their ability to move freely. A large amount of fluid may cause shortness of breath. In some cases of pleural effusion, this excess liquid can become infected.

Causes of pleurisy

Viral infection is probably the most common cause of pleurisy. Other causes include the following:

Lung infections, such as pneumonia and tuberculosis. Diseases such as systemic lupus erythematosus (lupus), rheumatoid arthritis, cancer, liver diseases and pulmonary embolism. Chest injuries. Drug reactions. Pleurisy and pleural effusion are generally only as serious as the underlying disease causing it. If you have either of these conditions, you may already be undergoing treatment for the underlying disease; if not, seek medical attention immediately.

DRY PLEURISY

Clinical picture. A characteristic symptom of dry pleurisy is pain in the chest which becomes stronger during breathing and coughing. Cough is usually dry, the patient complains of general indisposition; the temperature is subfebrile. Respiration is superficial (deep breathing intensifies friction of the pleural membranes to cause pain). Lying on the affected side lessens the pain. Inspection of the patient can reveal unilateral thoracic lagging during respiration. Percussion fails to detect any changes except decreased mobility of the lung border on the affected side. Auscultation determines pleural friction sound over the inflamed site. The blood picture remains unchanged but moderate leucocytosis is observed in some cases. X-ray picture shows limited mobility of the diaphragm because the patient spares the affected side of his chest.

Course. Dry pleurisy has a favourable course and the patient recovers, completely in one or three weeks.

 

PLEURISY WITH EFFUSION

Clinical picture. Patients suffering from pleurisy with effusion usually complain of fever, pain or the feeling of heaviness in the side, and dyspnoea (which develops due to respiratory insufficiency caused by com­pression of the lung). Cough is usually mild (or absent in some cases). The patient’s general condition is grave, especially in purulent pleurisy, which is attended by high temperature with pronounced circadian fluctuations, chills, and signs of general toxicosis. Inspection of the patient reveals asymmetry of the chest due to enlargement of the side where the effusion accumulated; the affected side of the chest usually lags behind respiratory movements. Vocal fremitus is not transmitted at the area fluid accumulation.

 

Percussion auscultation in pleuricy with effusion

Pleurisy with effusion: a-anterior view; b—posterior view:

1—Damoiseau’s curve; 2—Garland’s triangle;

3—Rauchfuss-Grocco triangle.

The most characteristic symptom is severe pain in the chest, which increases when patient cough and breathing, and is due to rubbing of the inflaed pleural layers. When there is a pleural effusion of a certain size, the pain is reduced because the liquid prevents rubbing. If the fluid becomes abundant crushes the lungs, causing shortness of breath and tightness. Other frequent symptoms are dry cough and fever. Pleurisy can be discovered by careful examination. To understand the cause can sometimes be useful ultrasound, CT scan and some blood tests. Sometimes, finally, it may be necessary to examine a small sample of the fluid inside the pleural space through the thoracentesis

Percussion over the area of fluid accumulation produces dullness. The upper limit of dullness is usually the S-shaped curve (Damoiseau’s curve) whose upper point is in the posterior axillary line. The effusion thus occupies the area, which is a triangle both anteriorly am posteriorly. The Damoiseau curve is formed because exudate pleurisy with effusion more freely accumulates in the lateral portions of the pleural cavity, mostly in the costal-diaphragmatic sinus.

More difficult is radiographic diagnostics of encysted pleurisy, which shadow can have the different localizations. Encysted pleurisy can get encysted due to the presence of pleural adhesions. According to localization, pleurisy:differ into:

ô costal-diaphragmatic;

ô diaphragmatic;

ô costal;

ô interlobe;

ô paramedistinal;

ô apical.

As distinct from effusion, which is restricted by adhesions, transudate more freely presses lung and the Damoiseau curve is not therefore determined. In addition  to the Damoiseau curve, two triangles can be determined by percussion in pleurisy with effusion. The Garland triangle is found on the affected side is characterized by a dulled tympanic sound. It corresponds to the lung pressed by the effusion, and is located between the spine and the Damoiseau curve. The Rauchfuss-Grocco triangle is found on the healthy and is a kind of extension of dullness determined on the affected side, sides of the triangle are formed by the diaphragm and the spine, while the continued Damoiseau curve is the hypotenuse. The triangle is mainly  displacement of the mediastinum to the healthy_side. Mobility of the  border of the lung on the affected side is not usually determined in pleurisy with effusion. Left-sided pleurisy with effusion is characterized by absence of the Traube space (the left pleural sinus is filled with effusion  and a dulled percussion sound is heard over the gastric air bubble instead of tympany).

Respiration in the region of accumulated effusion is not auscultated, or it can be very weak. Respiration auscultated slightly above the effusion level is usually bronchial which is due to compression of the lung and displacement of air from it. Vocal fremitus and bronchophony over the effusion are not determined because the vibrating walls over the bronchi that conduct voice are separated from the chest wall by the fluid. The heart is usually displaced by the effusion toward the healthy side. Tachycardia isobserved. Arterial pressure may be decreased. Dizziness, faints, etc., sometimes occur because of the marked toxicosis.

X-ray of the thoracic organs shows a homogeneous density whose area corresponds to the area of dullness. If effusion is scarce, it accumulates in the outer sinus. Large volumes of effusion cover the entire lung to its apex and displace the mediastinum toward the intact lo lower the diaphragm. The encapsulated parietal pleurisy gives the picture of parietal density. The medial border is usually sharply outlined, Density of the interlobar pleurisy extends along the interlobar sulcus in the form of a triangle or a spindle. Diaphragmatic pleurisy is characterized either by a limited mobility of the diaphragm or its complete absence. The upper border of the effusion is convex (upward) to follow the curvature of diaphragm.

Exploratory puncture is necessary in order to determine the properties of the  exudate for accurate diagnosis. The fluid obtained by pleural punctire is studied at the laboratory.

  The character of the inflammatory effusion may be different: serous, serofibrinous, purulent, and haemorrhagic.

Serous and serofibrinous pleurisy attend tuberculosis (in 70-90 per cent of cases), and pneumonia, certain infections, and also rheumatism in 10-30 per cent of cases. The purulent process in the pleura may be caused by pneumococci, streptococci, staphylococci, and other microbes. Haemorrhagic pleurisy arises in tuberculosis of the pleura,bronchogenic cancer of the lung with involvement of the pleura, and also in injuries to the chest.

Most diseases of the pleura (pleurisy included) are secondary to disease of the lung. Pleurisy usually develops as a reaction of the pleura to pathological changes in the adjacent organs, in the lungs in the first instance, and less frequently as a symptom of a systemic disease (polyserosites of various aetiology). Serous pleurisy often arises as an allergic reaction. Purulent pleurisy is often a complication of bronchopneumonia: inflammation may extend onto the pleura, or an inflammatory focus may turn into an abscess which opens into the pleural cavity. Inflammation of the pleura is always attended by markedly increased permeability of the wall of the affected capillaries of the pulmonary pleura.

Reactivity of the body is a very important factor in the pathogenesis of pleurisy. In fibrinous or dry pleurisy fibrin precipitates from the exudate (which is produced in a small amount) and gradually deposits on the pleura. Serous pleurisy may become infected to convert into purulent; exudate becomes turbid and contains many leucocytes. In the presence of purulent processes in the lungs or adjacent organs (pericarditis, perioesophagitis, etc.), purulent pleurisy often develops abruptly. The affection of the pleura in tumours, which in most cases are metastatic (less frequently primary), decreases its absorptive function to promote accumulation of pleural effusion (haemorrhagic effusion in most cases). Two basic forms of pleurisy are distinguished according to pathomorphological picture of tubercular inflammations of pleura: dry or fibrinous (pleuritis sicca, fibrinosa), and exudative (pleuritis exudativa).

During the initial stage of the disease the blood picture may show mild leucocytylosis (marked leucocytosis is characteristic of purulent pleurisy) and sometimes eosinophilia. The ESR is increased. Tuberculosis pleurisy is characterized by lymphocytosis, while rheumatic pleurisy by neutrophilosis.

Course. The course of pleurisy with effusion depends on the aetiology of the affection. Pleurisy in rheumatism would normally resolve in 2-3 weeks (with appropriate treatment). Pleurisy with effusion complicating pneumonia (metapneumonic pleurisy, usually serous) also has a com­paratively mild course. A protracted course is characteristic of pleurisy with effusion of tuberculous aetiology. Development of coarse adhesions interferes with resorption of the effusion (encapsulated pleurisy), while a prolonged purulent process may result in amyloidosis of the internal organs.

Resorption of effusion may be followed by some specific residual phenomena, such as sunken chest and the absence of diaphragmatic mobility on the affected side, displacement of the mediastinal organs toward the affected side, and sometimes permanent pleural friction.

Treatment depends on the cause. This, in the first instance, includes the therapy of the main disease, such as rheumatism (non-steroid antiinflammatory agents, corticosteroids), pneumonia (antibiotics), tuberculosis (PASA, phthivazide, streptomycin, canamycin, and others). Symptomatic therapy includes general strengthening (vitamins, etc.), desensitizing preparations and high-calorie diet.

If pleurisy is of viral origin can often resolve spontaneously, and if it is caused by bacteria need a specific antibiotic therapy. If the pleural cavity is present much pus antibiotic therapy may be accompanied by surgical drainage of pus. Purulent exudate should obligatory be removed.  In general, for the relief of symptoms may be useful anti-inflammatory drugs for persistent pain, antipyretics for fever and possibly counter remedies to combat cough

Thermal procedures (compresses, diathermy) are useful to accelerate the resolution process. If pleural fluid is not resorbed during 2—3 weeks, evacuation of the effusion is necessary. Withdrawal of the fluid should be slow to avoid collapse or faint. As a rule, 0.5-1 L of effusion is removed and antibioticsane injected instead into the pleural cavity. In order to accelerate resorption of the effusion, diuretics can be given. In the presence of cardiac failure, cordiamine, cardiac glycosides are indicated. To prevent pleural adhesion during resorption of the exudates, remedial exercises should be prescribed.

 

 

Pleurocentesis

When a patient has fluid around the lungs, sometimes we need to find out what caused it, other times we want to remove the fluid so the patient can breath easier. It takes place under sterile conditions by placing a needle into the chest wall from the back and connecting the needle with a catheter to a suction bottle which collects the fluid. Fluid is then sent for testing.

No matter the cause of pleural effusion, the objective of treatment is to relieve pressure on the patient’s lungs. This is most often done through a procedure called thoracentesis

, which involves the aspiration of fluid from the pleural space through a cannula, or long, hollow needle. The cannula is attached to a drainage bag or bottle into which fluid is collected.

In some patients with recurring pleural effusion (as with malignant mesothelioma), an outpatient procedure called a tube thoracotomy may be used. In this procedure, fluid is removed from the pleural space through a chest tube that is kept in place for several days.

Another pleural effusion procedure that can benefit mesothelioma patients is pleurodesis, which involves injecting a special substance into the pleural cavity. Then, reverse pressure through a catheter or cannula is used to seal the inner and outer pleural layers together to prevent further fluid buildup. With mesothelioma patients, pleurodesis is often done in conjunction with chemotherapy and/or radiation.

Prophylaxis. Prevention of serofibrinous pleuricy consists in early diagnosis and active treatment of tuberculosis, rheumatism and other diseases which may provoke pleuricy, and also in strengthening of the body (exercises, cool water etc.).

The syndrome of respiratory insufficiency in respiratory system pathology

 

Cyanosis in pleuricy with effusion due to respiratory insufficiency  is caused by lung collapse and limitation of its respiratory surface

Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination. In practice, it may be classified as either hypoxemic or hypercapnic. Respiratory failure is a condition in which not enough oxygen passes from your lungs into your blood. Your body’s organs, such as your heart and brain, need oxygen-rich blood to work well. Respiratory failure also can occur if your lungs can’t properly remove carbon dioxide (a waste gas) from your blood. Too much carbon dioxide in your blood can harm your body’s organs.

Both of these problems—a low oxygen level and a high carbon dioxide level in the blood—can occur at the same time.

•        When respiratory failure causes a low level of oxygen in the blood, it’s called hypoxemic (HI-pok-SE-mik) respiratory failure.

•        When respiratory failure causes a high level of carbon dioxide in the blood, it’s called hypercapnic (HI-per-KAP-nik) respiratory failure.

Diseases and conditions that affect your breathing can cause respiratory failure. Examples include COPD (chronic obstructive pulmonary disease) and spinal cord injuries. COPD prevents enough air from flowing in and out of the airways. Spinal cord injuries can damage the nerves that control breathing.

Acute respiratory failure

Acute respiratory failure develops over hours, and is characterised by an acute lack of oxygen delivery to the blood by the respiratory system or acute failure of the respiratory system to remove carbon dioxide (CO2) from the blood.

Chronic respiratory failure

Chronic respiratory failure develops over longer periods of time and is usually defined as long-term lack of oxygen delivery to the blood by the respiratory system. It causes progressively worsening respiratory acidosis (carbonic acid accumulation resulting from inefficient expulsion of CO2 from the respiratory system) in someone with chronically decreased arterial partial pressure of oxygen (PaO2) or chronically elevated arterial partial pressure of CO2 (PaCO2) levels.

Hypoxic respiratory failure

Also known as type 1 respiratory failure. This occurs when the PaO2 is <60 mmHg. The PaO2 of patients with chronic lung disease can be as low as 50 mmHg normally, and in these patients respiratory failure occurs when there are 10% decreases in baseline arterial oxygen measurements.

Hypercapnic respiratory failure

Also known as type 2 respiratory failure. This occurs when there is hypoxia associated with a PaCO2 that is >50 mmHg.

Overview

To understand respiratory failure, it helps to understand how the lungs work. When you breathe, air passes through your nose and mouth into your windpipe. The air then travels to your lungs’ air sacs. These sacs are called alveoli.

Small blood vessels called capillaries run through the walls of the air sacs. When air reaches the air sacs, the oxygen in the air passes through the air sac walls into the blood in the capillaries. At the same time, carbon dioxide moves from the capillaries into the air sacs. This process is called gas exchange.

In respiratory failure, gas exchange is impaired.

Respiratory failure can be acute (short term) or chronic (ongoing). Acute respiratory failure can develop quickly and may require emergency treatment. Chronic respiratory failure develops more slowly and lasts longer.

Signs and Symptoms of Respiratory Failure

The signs and symptoms of respiratory failure depend on its underlying cause and the levels of oxygen and carbon dioxide in the blood.

A low oxygen level in the blood can cause shortness of breath and air hunger (feeling like you can’t breathe in enough air). If the level of oxygen is very low, it also can cause a bluish color on the skin, lips, and fingernails. A high carbon dioxide level can cause rapid breathing and confusion.

In severe cases, signs and symptoms may include a bluish color on your skin, lips, and fingernails; confusion; and sleepiness. Some people who have respiratory failure may become lose consciousness. They also may develop arrhythmias  or irregular heartbeats. These symptoms can occur if the brain and heart are not getting enough oxygen.

•        Respiratory failure is not a disease itself, but the end result of many disorders.

•        Some of the symptoms and signs relate to the underlying disorder.

•        Shortness of breath/dyspnea

•        Flaring of nostrils

•        Pursed-lips breathing

•        Use of accessory muscles of respiration

•        Supine abdominal paradox (diaphragmatic paralysis)

•        Peripheral muscle weakness

•        Central and/or peripheral cyanosis

•        Increased or decreased respiratory rate

•        Altered level of consciousness

•        Confusion

•        Disorientation

•        Coma

•        Stridor

•        Suggests the presence of large airway or laryngeal obstruction

•        Wheezing

•        Rhonchi

•        Evidence of consolidation on auscultation

•        Tubular breath sounds

•        Dullness to percussion

•        Egophony

•        Evidence of right-heart dysfunction

•        Elevated jugular venous pressures

•        Pronounced or delayed pulmonic component of the second heart sound

•        Right-sided heave

•        Right-sided third heart sound

           Murmur of tricuspid regurgitation

One of the main goals of treating respiratory failure is to get oxygen to your lungs and other organs and remove carbon dioxide from your body. Another goal is to treat the underlying cause of the condition.

Acute respiratory failure usually is treated in an intensive care unit. Chronic respiratory failure can be treated at home or at a long-term care center.

Laboratory Tests

•        Arterial blood gases

•        Toxicology screen

•        Complete blood count

•        Sequential Multiple Analyzer 12

•        Additional laboratory testing based on clinical suspicion of underlying disease process

Causes of Respiratory Failure

Diseases and conditions that impair breathing can cause respiratory failure. These disorders may affect the muscles, nerves, bones, or tissues that support breathing, or they may affect the lungs directly.

When breathing is impaired, your lungs can’t easily move oxygen into your blood and remove carbon dioxide from your blood (gas exchange). This can cause a low oxygen level or high carbon dioxide level, or both, in your blood.

Respiratory failure can occur as a result of:

•        Conditions that affect the nerves and muscles that control breathing. Examples include muscular dystrophy, amyotrophic lateral sclerosis (ALS), spinal cord injuries, and stroke.

•        Damage to the tissues and ribs around the lungs. An injury to the chest can cause this damage.

•        Problems with the spine, such as scoliosis (a curve in the spine). This condition can affect the bones and muscles used for breathing.

•        Drug or alcohol overdose. An overdose affects the area of the brain that controls breathing. During an overdose, breathing becomes slow and shallow.

•        Lung diseases and conditions, such as COPD (chronic obstructive pulmonary disease),pneumonia, ARDS (acute respiratory distress syndrome), pulmonary embolism, and cystic fibrosis. These diseases and conditions can affect the flow of air and blood into and out of your lungs. ARDS and pneumonia affect gas exchange in the air sacs.

•        Acute lung injuries. For example, inhaling harmful fumes or smoke can injure your lungs.

Normal Lungs and Conditions Causing Respiratory Failure

Figure shows the location of the lungs, airways, diaphragm, rib cage, pulmonary arteries, brain, and spinal cord in the body. Figure B shows the major conditions that cause respiratory failure.

How Is Respiratory Failure Diagnosed?

To check the oxygen and carbon dioxide levels in your blood, you may have: 

•        Pulse oximetry. For this test, a small sensor is attached to your finger or ear. The sensor uses light to estimate how much oxygen is in your blood.

•        Arterial blood gas test. This test measures the oxygen and carbon dioxide levels in your blood. A blood sample is taken from an artery, usually in your wrist. The sample is then sent to a laboratory, where its oxygen and carbon dioxide levels are measured.

Treatment for respiratory failure depends on whether the condition is acute (short-term) or chronic (ongoing) and its severity. Treatment also depends on the condition’s underlying cause.

Acute respiratory failure can be a medical emergency. It often is treated in an intensive care unit at a hospital. Chronic respiratory failure often can be treated at home. If chronic respiratory failure is severe, your doctor may recommend treatment in a long-term care center.

One of the main goals of treating respiratory failure is to get oxygen to your lungs and other organs and remove carbon dioxide from your body. Another goal is to treat the underlying cause of the condition.

Oxygen Therapy and Ventilator Support

If you have respiratory failure, you may receive oxygen therapy. Extra oxygen is given through a nasal cannula (two small plastic tubes, or prongs, that are placed in both nostrils) or through a mask that fits over your nose and mouth.

The image shows how a nasal cannula and portable oxygen container are attached to a patient.

Oxygen also can be given through a tracheostomy. This is a surgically made hole that goes through the front of your neck and into your windpipe. A breathing tube, also called a tracheostomy or trach tube, is placed in the hole to help you breathe.

Figure shows a side view of the neck and the correct placement of a tracheostomy tube in the trachea, or windpipe. Figure B shows an external view of a patient who has a tracheostomy.

If the oxygen level in your blood doesn’t increase, or if you’re still having trouble breathing, your doctor may recommend a ventilator. A ventilator is a machine that supports breathing. It blows air—or air with increased amounts of oxygen—into your airways and then your lungs. The illustration shows a standard setup for a ventilator in a hospital room. The ventilator pushes warm, moist air (or air with increased oxygen) to the patient. Exhaled air flows away from the patient.

Your doctor will adjust the ventilator as needed. This will help your lungs get the right amount of oxygen. It also can prevent the machine’s pressure from injuring your lungs. You’ll use the ventilator until you can breathe on your own.

Noninvasive positive pressure ventilation (NPPV) and a rocking bed are two methods that can help you breathe better while you sleep. These methods are very useful for people who have chronic respiratory failure.

NPPV is a treatment that uses mild air pressure to keep your airways open while you sleep. You wear a mask or other device that fits over your nose or your nose and mouth. A tube connects the mask to a machine, which blows air into the tube.

CPAP (continuous positive airway pressure) is one type of NPPV.

A rocking bed consists of a mattress on a motorized platform. The mattress gently rocks back and forth. When your head rocks down, the organs in your abdomen and your diaphragm (the main muscle used for breathing) slide up, helping you exhale. When your head rocks up, the organs in your abdomen and your diaphragm slide down, helping you inhale.