Acute respiratory failure.
3.1 Anatomy and physiology of respiratory system.
One of the most important conditions of living is continuous gas exchange. Every day a human body consumes nearly 700 l of oxygen and produces 600 litersof carbon dioxide.
Oxygen is responsible for the mitochondrial and microsomal oxidation., peroxidation of unsaturated fatty acids and oxydase reactions. But the most significant role it plays when provides oxidative phosphorylation during energetic metabolism of the cell.
There are two types of breathing: external or lung respiration provides inflow of oxygen and carbon dioxide elimination; internal respiration is a complex process, which consists of haemoglobin transformation (connection and disconnection with oxygen), transportation of oxygenated haemoglobin trough circulatory system to the tissues and local cellular metabolism.
External breathing is being regulated by centres in medulla and pons. Increasing of carbon dioxide concentration, as well as acidosis of cerebrospinal fluid, stimulates inspiration. At the end of expiration inspiration centre is being stimulated automatically and thus respiratory act begins again. In addition receptors of aorta arch and carotid sinus are also involved into respiratory act regulation: they respond to the lowering of oxygen concentration in the arterial blood.
The act of ventilation itself is being done through contraction of chest muscles and diaphragm. Muscles, responsible for respiration, enlarge chest and thus create negative pressure inside of it, what makes air move through the airways to the alveoli. Expiration is usually passive: chest falls down to it previous position and “used” air gets back to the atmosphere.
Tidal volume (TV) is 450-800 ml for male and 400-700 for female. It can be measured by spirometer or volumeter. But not the whole air of one respiratory effort gets to the alveoli: part of it stays in oral cavity, nasal cavity, pharynx, trachea, bronchi and thus does not participate in the act of respiration itself. It is so called “dead space”- volume of airways which are ventilated, but are not involved in gas exchange. Dead space makes nearly 30% of the tidal volume (2,22 ml/kg of body weight).
Normal respiration rate (RR) is 14-20 per minute. Thus minute ventilation is calculated according to the formula:
Minute ventilation =Tidal volume* Respiratory rate (ml)
However the parameter, which helps to characterize the efficiency of breathing, is alveolar ventilation (AV): it shows the exact amount of the air which gets to the alveoli during the minute. The difference between minute ventilation and alveolar ventilation is the volume of dead space:
Alveolar ventilation= (Tidal volume-Dead space volume)* Respiratory rate (ml)
According to this formula breathing with lower frequency and higher tidal volume is more effective. In addition efficiency of breathing is increased through reduction of dead space volume. Thus endotracheal tube or tracheostomy make it two times less.
Oxygen gets to the arterial blood due to the difference of gas partial pressures. If the atmospheric pressure is 740-740 mm of Mercury and the amount of oxygen in the air is 20-21% partial pressure of Oxygen (pO2) will be 160-150 mm of Mercury. In the airways air is being mixed with “used gases” and water steam, so the partial pressure of oxygen inside the alveoli is 95-85 mm of Mercury. With such values pO2a , 3 ml of oxygen will be dissolved in one liter of blood (plasma).
The main amount of oxygen in blood is being bound to the haemoglobin. One gram of haemoglobin bounds 1,34-1,39 ml of oxygen. Iormal conditions haemoglobin of arterial blood (HbO2a)is saturated to the extent of 96%. So, with the concentration of haemoglobin 120-140 grams per liter, one liter of arterial blood contains 170-190 ml of oxygen (VO2a).
From every litre of blood only one third of oxygen amount (nearly 50 ml) is being used for the needs of the tissues. Thus venous blood contains nearly 120-140 ml of oxygen (VO2v) and it’s HbO2v is 70-75% and pO2v 45-55 mm of Mercury.
Partial pressure of carbon dioxide in the arterial blood (pCO2a) is an important index of ventilation adequacy. Normally it is 36-46 mm of Mercury. Worsening of lung ventilation causes increasing of pCO2a over 44 mm of Mercury – hypercapnia appears. Excessive ventilation, on the contrary, helps in elimination of carbon dioxide and appearance of hypocapnia: pCO2a is lower than 35 mm of Mercury.
Respiratory insufficiency is a condition in which metabolic needs of the body caot be sutisfied with adequate oxygen admission, blood transportation, cellular consumption and carbon dioxide elimination.
Classification of respiratory insufficiency according to L. Usenko (1993):
A. Primary (caused by disorders of external respiration). Reasons:
1. airway patency disorders (obstruction with tongue, vomit, mucus, gastric contents, foreign bodies; laryngeal spasm, etc.)
2. central nervous system disorders (intoxication, brain injuries, haemorrhages, inflammations, etc.)
3. disorders of respiratory muscles activity (myasthenia, botulism, tetanus, muscle relaxants, etc.)
4. defects of chest structure or functional chest disorders ( chest injuries, limited diaphragm mobility – for example due to enteroparesis)
5. disorders of pulmonary compliance (pneumonia, bronchiolitis, atelectasis, “shock lung” syndrome, etc.)
6. disorders of ventilation-perfusion system (irregularity of ventilation and perfusion during artificial ventilation, pulmonary oedema, etc.)
B. Secondary (caused by inability of blood to contain enough oxygen for metabolic needs of tissues or disorders of transportation and cellular consumption).
Respiratory insufficiency is characterized with hypoxia (“lowering of the oxygen”). Hypoxia occurs in case of:
1. Inability of external respiration to provide arterial blood with enough amount of oxygen (hypoxic hypoxia)
2. Lowering of oxygen amount due to anaemia – decreased level of haemoglobin, red blood cells or appearance of their atypical forms (haemic hypoxia).
3. Inability of cardiovascular system to provide systemic and pulmonary circulation enough for metabolic needs of the body (circulatory hypoxia).
4. Disorders of oxidative phosphorylation on cellular level of different organs and systems (tissue hypoxia).
Hypoxia itself can be accompanied with hypercapnia and hypocapnia. In case of tissue hypoxia there is also a possibility of hyperoxia (excessive oxygen amount) as its background.
In clinical conditions we usually deal with mixed gas exchange disorders.
Clinical symptoms of acute respiratory insufficiency
There are two types of respiratory insufficiency according to its duration: acute and chronic. Acute respiratory insufficiency develops in minutes or hours, can be life-threatening and thus needs urgent intensive treatment.
Symptoms of acute respiratory failure are really various.
Central nervous system. Conscious patients can complain of breathlessness (feeling of the air-lack), difficult inspiration or expiration. Due to development of hypoxia patients become restless, anxious, and sometimes euphoric; they caot evaluate critically their condition or environment. Terminal stages of insufficiency show total CNS inhibition – comatose state (hypoxic or hypercapnic). Quite often, especially in children, convulsions appear.
Skin and mucosa are mirror of respiratory insufficiency: their changes are quite illustrative.
In case of external respiration disorders the amount of oxygenated haemoglobin is decreased and thus quantity of reduced haemoglobin. Arterial blood becomes “venous” (dark): skin and mucosa become cyanotic (blue, purple). First of all their colour change lips, nail plates, earlobes, afterwards face and other body parts. In case of anaemic patients with haemoglobin level 60 grams per litre and lower skin stays pale even in terminal stages of respiratory insufficiency. In case of cyanic and carbon monoxide intoxication skin, nail plates and mucosa turn bright pink, although patients are greatly suffering from hypoxia. Hydrosis is quite significant feature of hypercapnia. Terminal respiratory insufficiency is characterized with dark-grey color cold skin covered with clammy sweat.
Disorders of external respiration are the most obvious symptoms of respiratory insufficiency. Clinically in case of those patients next symptoms might be observed:
complete breathing arrest (apnea);
low respiratory rate – less than 12 per minute (bradypnea);
high respiratory rate – more than 20 per minute (tachypnea);
shallow breathing (respiratory volume less than 5 ml per kilogram of body weight);
respiratory “anarchy” (irregular breathing with pauses and uneven amplitude of respiratory movements);
pathological types of respiration:
a. Cheyne-Stokes breathing (periods of apnea, which are followed with chaotic frequent breathing);
b. Biot’s breathing (periods of apnea which are followed with breathing of equal amplitude);
c. Difficult breathing (noticeable at a distance, correlation between inspiration and expiration is violated, with active participation of additional muscles):
1. inspiratory dyspnea (difficult inspiration) – inspiration is prolonged, intercostals spaces, jugular fossa and subclavian fossa are retracted; sometimes stridorous noise can be heard
2. expiratory dyspnea (difficult expiration) – patients should make a great physical effort in order to exhale; exhalation is prolonged, noisy, heard at a distance; chest is enlarged, becomes barrel shaped
Cardiovascular system at the beginning reacts trough compensative hyperdynamic reaction. Cardiac output, heart rate, systolic and diastolic pressure increase. Tissue perfusion improves, what makes cellular oxygen supply and carbon dioxide elimination more effective. But due to hypoxia development vessel tone decreases and heart action is depressed. Blood pressure critically lowers and in case of inadequate treatment cardiac arrest appears.
Indications for artificial ventilation:
– apnoea
– central nervous system disorders – coma
– gray-cyanotic colour of skin, covered with clammy sweat
– low breathing frequency (less than 6 per minute) or high breathing frequency (more than 40 per minute) in case of normal thermal conditions, which causes great lowering of alveolar ventilation
– excessive chest excursion, participation of additional muscles
– pathological types of breathing
– critical lowering of haemodynamic indexes (systolic blood pressure lower than 60 mm Hg), life-threatening arrhythmias
Decreasing of pO2a to 60 mm Hg and less or increasing of pCO2a mm Hg
Main types of external respiration disorders
Disorders of respiratory centre.
These disorders occur in case of narcotic intoxication, hypnotic and anaesthetic medicine usage. Injuries of the head, haemorrhages, brain strokes, inflammatory processes of the brain and meninges can violate breathing centre directly or through brain oedema. In these cases respiratory centre looses the ability of adequate reaction and thus acidosis, hypercapnia and hypoxia are not any more regulating ventilation.
In those patients we can see shallow, sometimes pathological breathing (Cheyne-Stokes, Biot’s), in the most severe cases respiratory arrest occurs. The concentration of oxygen decreases and the level of carbon dioxide increases and thus hypoxia and hypercapnia damage cells on central nervous system, myocardium, other organs and systems, causing cardiac arrest.
Toxic or hypoxic damage of the brain, in turn, causes or deepen the coma and thus brings obstructive respiratory disorders. The muscle tone is decreasing, so the tongue blocks upper airways. In this situation only immediate actions, providing normal air passage, can save the patient’s life.
It is quite often observed that in case of unconscious patient’s oral cavity and pharynx are overfilled with saline and trachea, bronchi filled with mucus, which normally should be swallowed or spitted out. Mucus gets infected quickly and thus inflammatory reactions begin, causing complications such as purulent bronchitis and tracheitis, pneumonia, which may lead coma patient to death.
Respiratory disorders of unconscious patients can be explained with passive outflow of gastric contents from stomach to the oral cavity and its father aspiration into airways (trachea and bronchi). According to A. Zilber (1989) aspiration of 10-15 ml of acid gastric contents in most cases end with the death of the patient.
Prevention and treatment of this disease belong to the most urgent.
Urgent help:
1. Evaluate central nervous system condition – deepness of coma (chapter 5)
2. To prevent aspiration turn patient into save position (side position with head turned aside and if possible lower upper part of the body – thus gastric contents will probably flow out rather than into trachea).
3. Open the mouth of the patient and clean the oral cavity, if necessary, using your finger or forceps with surgical drape).
4. Titled the head backwards (use roll or small cushion if possible). Thus airways should stay clear.
5. Thrust the jaw forward: place your thumbs over the chin and the rest of your fingers put on the jaw (little fingers on the angles of the jaw), push the jaw forward and up, in a position of malocclusion (lower teeth in front of upper). After this action is done further providing of airways patency is quite simple and can be achieved with one finger.
6. You can also use simple airway adjuncts such as oropharyngeal and nasopharyngeal airways. Guedel tube is inserted between teeth with its curved distal end turned up, than moved toward soft palate and turned 180º and placed over the tongue.
In case of inadequate breathing or complete lack of it artificial ventilation should be provided (mouth to mouth or with apparatus for ventilation).
Constantly check patient’s condition: control the heart and respiratory rate, blood pressure, body temperature, ECG. When there will be a possibility take biological material for the laboratory tests.
Immediate intensive treatment:
Perform direct laryngoscopy in order to check airways patency.
1. clean the oral cavity, if necessary, from foreign bodies and liquids such as vomit, sputum, blood cloths, gastric contents using electric vacuum suction
2. Provide oxygen supply of the patient: 8-10 liters per minute
3. In case of ineffective breathing begin artificial ventilation with Ambu bag or stationary respiratory apparatus.
4. Get the intravenous access, peripheral or central and start the infusion.
5. In case of further inadequacy of breathing give 0,5 ml of 0,1% of atropine intravenous and intubate the patient, because probably artificial ventilation will be prolonged.
6. Insert gastric sound and aspirate its contents.
7. Write down all the current data about patient’s condition and performed treatment actions.
8. Continue observation using laboratory and instrumental techniques.
9. Continue etiological and symptomatic treatment.
Alveolar hypoventilation caused by respiratory muscles violations.
This pathology appears when chest muscles are not able to perform a complete respiratory act. Hypoventilation is the most common reason of vital disorders in case of patients with polyneurophathies, myasthenia, botulism, tetanus, poliomyelitis, organophosphate poisoning. In case of patients after operations this type of hypoventilation may occur due to relaxants used for anaesthesia, hypokalemia or metabolic alkalosis.
Excursion of the chest is reduced and thus volumes of inspiration and expiration are lower. Conscious patients feel breathless and anxious; cyanosis, clammy sweat, tachycardia, hypertension, restlessness appear. If treatment is not provided, CNS is depressed and earlier or later cardiovascular system fails. Those patients should be ventilated with the help of respiratory apparatus immediately, as in their case oxygenation itself will not help (hypoxia will be corrected, but never the less elimination of carbon dioxide will not be improved and hypercapnia will cause cardiac arrest).
Residual relaxants effect is eliminated with anticholinergic drugs ( 1-2 ml of 0,05% proserin solution intravenous with previous administration of 0,1% atropine sulphate solution).
For hypokalemia correction special mix glucose, potassium and insulin is used (so called polarizing solution).
Low cholinesterase activity of plasma is compensated with fresh frozen plasma.
Organophosphate poisonings are treated with special antidotes (8.2); for elimination of convulsions specific medicines are used (5.3).
Brief lung ventilation (up to 30 minutes) can be provided with the mask. Ventilation up to 3 days needs intubation. If self-breathing is still inadequate after this time tracheostomy is recommended.
History of medicine knows cases, when patients were artificially ventilated for 18-20 years.
Team of medical professionals, responsible for treatment of patient with hypoventilation should follow all the asepsis and antiseptic rules and should be very careful and attentive to the patient’s condition and apparatus work.
Rules of care: patients on prolonged ventilation
1. Constantly check the condition of the patient (vital functions should be monitored), record in the papers parameters of ventilation, heart rate, blood pressure and central venous pressure, consciousness, physiologic and pathological liquid loss and medicines administered.
2. All the time control work of the respiratory apparatus (respiratory rate, volumes of respiration, minute ventilation, pressure in the airways during inspiration and expiration). If self-breathing is present, but inadequate it’s important to achieve synchronized patient-apparatus breathing (choose the correct mode or sometimes use pharmacological sleep to “turn off” the respiratory centre of the patient if respiratory efforts are exhausting for the organism).
3. Every 30 minutes change parameters of respiration, making tidal volume 40-50% more than the necessary every 5-10 minutes. This way you prevent the development of atelectasis.
4. Every hour carry our oral, tracheal and bronchial suction using plastic catheters with side foramina and blunt end. Catheters generally should not be reused, but if it’s necessary you can use them for one patient several times keeping them in antiseptic solution between suctions. Procedure: doctor or nurse puts on gloves and face mask, disconnects tube from the apparatus, carefully and at the same time quickly inserts the plastic catheter, previously connected to the vacuum suction, into the tube and turns it clockwise and counterclockwise. For cleaning of principal bronchi try to turn head of the patient and to push catheter deeper, but try not to make single suction try longer than 10-12 seconds. Iecessary – continue suction after a ventilation break (during this pause you can carefully clap over the chest of the patient to remove mucus from lower airways to their upper parts). After suction is done clean the catheter and place it into the antiseptic solution.
Cleaning of the trachea through tracheostomy tube has 2 main points:
– inserting the catheter keep the side foramen of it’s upper end open
– during the suction shut it with your finger to create negative pressure and aspirate mucus; taking it our don’t forget to scroll it.
The same technique should be used for oral and nasal cavities (right and left nostril), but not the same catheter. Every catheter container with antiseptic should be signed.
5. Every hour change the position of the patient: make it lateral, supine or prone, Fowler’s or Trendelenberg. Changing body position you change perfusion and ventilation correlations in the lungs and thus arterial blood becomes more oxygenated. This way appearance of bedsores is also prevented.
6. Every12-24 hours change the endotracheal or tracheostomy tube.
7. In case of excessive mucus accumulation (worsening of auscultatory picture, x-ray negative dynamics) or atelectasis suspicion perform therapeutic bronchoscopy.
8. To prevent development of inflammatory reactions pay special attention to humidifying and warming of the ventilation mix, use aerosol inhalations, adequate infusion level, enteral and parenteral nutrition, state of the immune system and choose antibiotics rationally.
Status asthmaticus
Status asthmaticus is an acute exacerbation of asthma that is caused by bronchial spasm and does not respond to standard treatments of bronchodilators and steroids. It occurs when parasympathetic-sympathetic balance is greatly violated. Pathological stimulation of vagus causes spasms of smooth bronchi muscles, what brings increasing of resistance worsening of their patency. In addition excessive secretion and oedema of bronchial walls make airways almost not conductive.
Such exacerbation can be caused by allergens, stress or endocrinological factors.
Main clinical asthma symptom is dyspnea attack, which begins with dry cough. Those attacks are sudden; patients feel more comfortably sitting in bed with their arms based on bed. This position is called orthopnea, it help to use additional muscles (abdominal, muscles of the shoulder girdle) in respiratory act. Extreme wheezing is heard at distance. Inspiration is extremely short and expiration much prolonged and forced. Lack of mucus is rather warning symptom. In case of complete obturation “silent lung” appears: breathing is asymmetric, there are silent parts of the lungs which do not contain any auscultative phenomena. Patients suffer from hypoxia and hypercapnia which earlier or later result in unconsciousness.
Treatment.
Most asthma attacks are successfully treated with inhalation of short acting β2-adrenoreceptor agonists (
In case of status asthmaticus spasm of bronchioles, inflammation and edema of bronchial wall and violation of mucus excretion and evacuation (due to abnormal cilia work) create pathogenetic base. Hyperventilation leads to greater water loss, what makes surface of bronchi dry and mucus more thick. This sick mucus caot be evacuated from airways during cough and thus it obstructs small bronchi and bronchioles, making ventilation impossible.
There are two types of status asthmaticus: anaphylactic and metabolic. Anaphylactic type is connected with allergic and immune reactions. It might appear after administration of some medicines (antibiotics, enzymes, aspirin, etc.) and develops very fast. Metabolic type of status asthmaticus is caused by metabolism disorders, which block β-adrenoreceptors. Long-term administration of sympatomimetics (asthmopent, ephedrine) can also cause metabolic type of status asthmaticus.
Status asthmaticus has certain stages:
1 stage: relative compensation. Patients are cyanotic, restless, sitting. Dyspnea has expiratory character with respiratory rate 26-40 per minute. Heart rate is 120 per minute, blood pressure in most patients is elevated. Auscultatory picture shows sibilant rales, prolonged expiration and “mosaic” breathing.
2 stage: decompensation. General condition of the patient is very serious. Patients are exhausted, sometimes excited and aggressive. Skin is cyanotic, wet. Respiratory rate might be 60 per minute, breathing is shallow, noisy at distance and extremely weak during auscultation, sometimes “silent lung” is observed. Heart rate is 120-140 per minute, blood pressure lowers to 80 mm of Mercury. Hypoxemia and hypercapnia cause mixed respiratory and metabolic acidosis.
3 stage: hypoxic coma. General condition of the patient is extremely severe. Patients are unconscious, convulsions are possible. Skin is cyanotic, covered with clammy sweat. Pupils are wide, reflexes are depressed or pathologic reflexes appear. Respiratory rate is over 60 per minute (sometimes acute bradypnea); auscultation picture – “silent lung”. Heart rate is over 140 per minute, blood pressure lowers to critical values. Biochemical blood test results show mixed decompensated acidosis (pH <7,2) and serious homoeostatic disorders. Acute cardiopulmonary insufficiency may lead to death.
Intensive treatment of status asthmaticus.
1. Begin oxygenation as soon as possible; if there is such possibility you should add 20%-30% of helium to the gas mix.
2. Provide constant monitoring of vital functions (ventricular fibrillation is one of possible death reasons of these patients).
3. Get intravenous access and start infusion of warm saline (polarizing solution, etc.). In case of extreme dehydration total infusion volume might reach 5-7 litersper day. In case of metabolic acidosis use 4% solution of sodium bicarbonate (100-150 ml).
4. Use steroids: solution of hydrocortisone (intravenously 150-200 mg every 2-3 hours), solution of prednisolone (60 mg every 4-6 hours), solution of dexamethason (8-16 mg every 6 hours).
5. Add to the treatment spasmolytics, antihistaminic, sedative medicines (10 ml of 2,4% euphillin solution; 2 ml of 2% no-spa solution, 1 ml of 2% dimedrol solution, 2-4 ml of 0,5% solution of diazepam or 10-20 ml of 20% solution of sodium oxybate intravenously slowly). In the past for some cases halothane-nitrous oxide mix was used to fight with bronchi spasm.
7. In case of progressive cardiac insufficiency use heart stimulating medicines such as cardiac glycosides (0,5 ml of 0,05% solution of strophanthin with saline intravenously). 7. If patient’s condition is not getting worth and previously used treatment failed perform the intubation and begin artificial ventilation.
Indications for artificial ventilation in case of status asthmaticus:
– unconsciousness
– low blood pressure (<70 mm Hg)
– tachycardia (over 140 per minute)
– pCO2a>60 mm Hg, pO2a < 60 mm Hg, pH<7,25
In those cases patients might receive halothane-oxygearcosis. Therapeutic bronchoscopy should be performed with warm saline lavage (50-100 ml with its further suction, nearly 1,5 liters per one bronchoscopy). During lavage try to change patients position in order to remove more mucus cloths.
There are many important points in general asthma treatment. Among them: rational antibiotic treatment, elimination of allergens, treatment of comorbidities and adequate asthma attacks treatment, in order to avoid development of status asthmaticus.
Chest injuries
Multiple rib fractures, especially that causing flail chest, violate greatly biomechanics of breathing. Clinically one can see reduction of chest excursion, retraction of certain chest wall parts and asymmetric breathing movements. Patients show decreasing of tidal volume, cyanosis, violations of haemodynamics, microcirculation disorders and depression of central nervous system.
Rib fractures can also cause hemothorax and pneumothorax.One of the most dangerous complications of chest injury is a tension pneumothorax, which end with a severe hypoxia, mediastinum organs dislocation and thus death.
Chest trauma patients should be treated very carefully: use all your diagnostic possibilities, including inspection, palpation, percussion, auscultation and additional laboratory and instrumental tests. Especially important is such approach with unconscious victims.
The choice of treatment depends on specific type of injury and its complications: hemothorax and pneumothorax need to be drained; tension pneumothorax should be punctuated (transformed into open pneumothorax); ineffective spontaneous ventilation should be replaced with artificial; antibiotics and painkillers are generally recommended.
“Coronary Café-syndrome“
This name is used for a sudden asphyxia, which appears when foreign body gets between the vocal cords and obturates the airways.
It is caused by a violation of swallowing and breathing. Imagine a situation in which the victim speaks loudly during the meal and then suddenly stops talking and jumps to his feet. His efforts to inhale are ineffective, hands try to free the neck rending the clothes, face gets cyanotic and swollen, eyes get filled with fear. In 3-4 minutes patient losses the consciousness, convulsions begin and finally clinical death appears (respiratory efforts cease, pulse gets weaker, defecation and urination are possible).
Thus, during acute foreign body obturation of glottis we can see 3 subsequent stages:
1- patient conscious, on his feet
2- patient unconscious, convulsions develop
3- clinical death (lasts from 5-th to 10-th minute
On the first stage doctor or any health care system professional (even skilled witness who has no medical education) should try to perform Heimlich manoeuvre. Stand behind the patient and wrap your arms around the victim’s waist (hands on the epigastrium) and start making inwards and upwards thrusts. If the patient is still able to “collaborate” ask him to inhale during the manoeuvre.
Heimlich Manoeuvre
This manoeuvre allows to create a high pressure in the windpipe of the patient and thus exhaled air forces the foreign body to get out from the glottis. If the try will be unsuccessful only urgent conicotomy will save the life of the patient.
Procedure of conicotomy: put a roll (improvised one if necessary) under the neck of the patient, extending his neck as much as possible. In case of convulsions just ask someone to hold the patient. Then cover tightly with the first and third fingers of your left hand the thyroid cartilage and “slide” down with your index finger to the fossa, which divides thyroid and cricoid cartilages. At this place the thickness of the membrane is only few millimetres, so it can be easily pricked with a sharp object (for example kitchen knife). Limit the blade of the knife to 1cm long with the fingers of your right hand and sliding over the nail of your left hand index finger prick or cut the membrane. If it is possible insert a tube into the opening you made to prevent it’s closing (you can even use your ball pen for this purpose). The faster this manipulation will be done, the higher are chances of the patient to get fully recovered.
Conicotomy consists of 2 phases:
A. Cutting of the membrane with a scalpel with limiting its cutting length (with a plaster). It is done to save the posterior wall of trachea from injuring.
B. Restoring of airways patency with a needle (puncture of the membrane).
If the victim is in a state of clinical death (the third stage) perform the conicotomy immediately and start CPR. You can ventilate the patient through the conicotomy tube.
Advanced medical help includes direct laryngoscopy and extraction of a foreign body with a forceps. If necessary those patients can be treated with a bronchoscopy or tracheostomy.
Laryngospasm
Laryngospasm is a pathological muscular contraction of the laryngeal cords, which manifests itself with a difficult or impossible inspiration. It appears as a consequent of pathological reflex or excessive stimulation of vagal nerve.
Usual reasons for laryngospasm are traumatic operations on reflex zones (vocal cords, trachea bifurcation, epiglottis, eye bulbs, periosteums). Irritation of vocal cords by food, saline, gastric contents, chemical or thermal stimuli as long as allergic reaction are the most common reasons for laryngospasm.
There are two types of laryngospasm: total and partial. Both cases are sudden and characterized by an inspiration dyspnea. Patient tries to inhale, his respiratory muscles contract, retracting intercostals spaces, jugular and supraclavicular fossae. During partial laryngospasm a small amount of air gets through the vocal cords and the sound of this air movement reminds cry of a rooster. Total laryngospasm is silent (aphonic). Within few seconds patient becomes cyanotic, his blood pressure and heart rate rise, later victim becomes unconscious, reflexes are inhibited. In some cases after this muscles of larynx relaxes spontaneously and thus laryngospasm stops. But if deep hypoxia lasted for a while cardiac arrest still might appear.
Immediate aid
– begin oxygenation though the face mask as without proper oxygen supply partial laryngospasm becomes total
– whatever the reason of laryngospasm was eliminate it (remove the stimulator from the reflex zone if necessary, stop the operation for example)
– give intravenously atropine solution ( 0,01 mg per kilogram of body weight), euphillinum (5-10 ml of 2,4% solution, diluted in 10 ml of saline). If the initial damage was caused by thermal, chemical or allergic stimuli use antihistamine medicine (2 ml of 2,5% promethazine solution, 2 ml of 2% dimedrol solution) and steroids (60-90 mg of prednisolone).
Intensive treatment
– inhalation of bronchial spasmolytics (salbutamol);
– repeat the medicines mentioned above;
– in case of partial laryngospasm start artificial respiration through the mask with high oxygen speed and large ventilation volume;
– if your previous actions are not successful – use depolarising muscle relaxants (give 10 ml of 2% suxamethonium solution intravenously) and after total muscle relaxation perform direct laryngoscopy and trachea intubation. Of course if you have time and possibilities previously use hypnotics (for example 5-10 ml of propofol solution);
– if there are no conditions for intubation or your tries were unsuccessful, but situation is worsening into life-threatening (extreme bradycardia, unconsciousness, blood pressure less then 70 mm of Hg, general convulsions) perform conicotomy with the equipment you have and insert tube for oxygenation;
– in case of cardiac arrest start CPR according to general standards.
Bronchial spasm
Bronchial spasm is an acute disorder of external respiration caused by spasm of small bronchi smooth muscles. It can be total or partial. The reasons are the same as those for laryngospasm. Treatment for bronchial and laryngeal spasm are much alike, however muscle relaxants and conicotomy are not effective and thus death is almost unavoidable. What could be really useful is prophylactic premedication: before operations on reflex zones use atropine solution (0,01 mg per kg of body weight) in order to avoid pathological reflexes.
3.4 Medical operations and manipulations.
Usage of laryngeal mask.
Laryngeal mask is an elastic plastic tube with mask-shaped distant ending. It was invented in 1982 by British anaesthetist Archie Brain and now is popular worldwide among ambulance rescuers and anaesthesiology specialists.
Indications: providing of airways patency in case other methods failed; artificial ventilation during anaesthesia if intubation is not required.
Required equipment: laryngeal masks of different sizes, syringe (10 or 20 ml); equipment for oral cavity opening and cleaning if necessary (vacuum suction for example).
Procedure: open the mouth and clean the oral cavity if necessary. Staying on the right side of the patient use fingers of your left hand to press the chin down and thus open the mouth. Insert the laryngeal mask to the oral cavity keeping it’s mask-shaped end with your index and long fingers. Glide it downwards and backwards along the tongue until you will feel a definitive resistance. After placement fill the inflatable cuff with air using the syringe: this way cuff will surround the laryngeal framework and air will be insuflated directly to the airways. The free end of the LMA can be connected to the AMBU bag or respiratory apparatus. Nowadays laryngeal masks have a variety of modifications: some of them even allow intubation, some are made with non-inflatible cuffs (i-gels), etc.
Tracheostomy
There are 3 types of tracheostomy according to anatomic placement of the incision: upper medial and low.
Indications: violations of airways patency in case of tumors, laryngeal stenosis; prolonged artificial ventilation of ITU patients.
Required equipment: tracheostomy tubes of different sizes, scalpel, clamps, tissue retraction blades, stitch material and dressing, antiseptics, electric suction, respiratory apparatus, anaesthetics.
Procedure: perfect conditions for tracheostomy are those in operating room, however it can be done in ITU with specific antiseptic and aseptic measures.
After antiseptic preparation of the operative field immobilize the trachea with fingers of your left hand and cut the skin strictly along the midline of the neck right under the thyroid cartilage (the length of the incision should be 4-
Pic.3.3 Pic.3.4
3.5 Control tests
1.Normally partial pressure of oxygen in alveoli is:
A. equal to atmospheric pressure
B. 80± mm of Mercury
C. 140±5 mm of Mercury
D. 100-110 mm of Mercury
E. during inspiration is equal to arterial partial oxygen pressure, during expiration – equal to partial oxygen venous pressure
2. Arterial blood is saturated with oxygen for:
A. 100%
B.96-97%
C. 90-95%
D.85-95%
E. percentage depends on the character of breathing
3. Partial pressure of carbon dioxide in arterial blood is:
A. depends on partial oxygen pressure
B. depends on intensity of tissue breathing
C. normally is 36-44 mm of Mercury
D. increases in case of hyperventilation
E. depends on haemoglobin dissociation curve
4. Which pathology does not need artificial respiration?
A. Kussmaul breathing
B. Biot’s breathing
C. Cheyne-Stokse breathing
D. lowering of pO2a to 60 mm of Mercury
E. respiratory rate over 40 per minute
5. What should be done for hypercapnia treatment?
A. sodium bicarbonate solution given
B. artificial ventilation started
C. cytochrome C given
D. oxygenation started
E. blood of the same group transfused
6. What is a method of laryngospasm treatment?
A. muscle relaxants and artificial ventilation
B. respiratory stimulators (cordiamin, lobelin)
C. sodium bicarbonate
D. diuretics
E. tracheostomy
7. What should be done to minimize the damage of prolonged (over one week) artificial ventilation?
A. intubation
B. tracheostomy
C. conicotomy
D. respiratory analeptics should be given
E. therapeutic lavage
8. What should be done in order to prevent laryngospasm?
A. peripheral M-cholinolitics should be given
B. oral cavity should be cleaned
C. spasmolytics should be given
D. artificial ventilation should be started
E. jaw should be thrusted forward
9. What should be done in case of foreign body in the airways?
A. tracheostomy
B. change of body position – upper part should be lowered
C. mouth-to-mouth ventilation
D. Heimlich manoeuvre
E. patient should be punched between blade bones
Task1.
Patience, the patient of 56 years, was transported by ambulance to the hospital reception with breathlessness and difficult breathing. He is restless, excited: his skin is cyanotic and dry. Respiration rate is 26, respiratory movements are deep, additional muscles participate respiration. Blood pressure is 180/110 mm of Mercury, heart rate – 106 per minute. Gasometry results are: pO2A 67 mm of Mercury, pCO2a – 49 mm of Mercury. Name the disorder and principles of its treatment.
Task 2.
Calculate normal spirography indexes of Andrew, medical student of 22 years (height 170 cm, weight 70 kg): respiratory rate, tidal volume, minute ventilation, dead space volume, alveolar ventilation.
Task 3.
Patience, the patient, during cleaning of his nasal cavity suddenly felt, that inspiration became difficult. His skin gets cyanotic, blood pressure increases. Name the type of complication and describe the urgent help, which is necessary in this situation.
Task 4.
Andrew, the medical student, during a casual meeting in a café was laughing and at the same time chewing his sandwich. Suddenly he became quiet, grabbed his neck and stopped breathing. His face turns blue.
what should be done immediately
What should be done if Bonnie, student of medicine, has convulsions. He is unconscious, his pulse is weak. Describe CPR.
What will be your decision if You find
Task 5.
Patience, the patient, was transported to the hospital in a severe condition: unconscious, skin cyanotic, respiratory rate 64 per minute, heart rate 124 per minute, blood pressure 90/60 mm of Mercury, body temperature – normal. Choose the type of help and algorithm of your actions.
Task 6.
Patience, the patient, suffers from bronchial asthma. After regular ambulance visit he doesn’t feel better, although medicines were given intravenously. His condition is critical: central nervous system depressed, skin is wet and cyanotic, expiration is prolonged greatly, sibilant rales are combined with “silent lung” parts. Blood pressure is 110/70 mm of Mercury. Heart rate is 116 per minute. Describe your immediate actions and algorithm of intensive care.
Student should repeat next questions
Violations of homoeostasis and their correction.
9.1 The importance of the water to the organism.
Life on earth was born in the water environment. Water is a universal solvent for all the biochemical processes of the organism. Only in case of stable quantitative and qualitative composition of both intracellular and extra cellular fluids homoeostasis is remained.
The body of an adult human contains 60% of water. Intracellular water makes 40% of the body weight, the water of intercellular space makes 15% of body weight and 5% of body weight are made by the water in the vessels. It is considered that due to unlimited diffusion of water between vessels and extra vascular space the volume of extracellular fluid is 20% of body weight (15%+5%).
Physiologically insignificant amounts of water are distributed beyond the tissues in the body cavities: gastrointestinal tract, cerebral ventricles, joint capsules (nearly 1% of the body weight). However during different pathologic conditions this “third space” can cumulate large amounts of fluid: for example in case of ascites caused by chronic cardiac insufficiency or cirrhosis abdominal cavity contains up to 10 liters of fluid. Peritonitis and intestinal obstructions remove the fluid part of blood from the vessels into the intestinal cavity.
Severe dehydration is extremely dangerous for the patient. Water gets to the body with food and drinks, being absorbed by the mucous membranes of gastro-intestinal tract in total amount of 2-3 litters per day. Additionally in different metabolic transformations of lipids, carbohydrates and proteins nearly 300 of endogenous water are created. Water is evacuated from the body with urine (1,5-
Water balance is regulated through complicated, but reliable mechanisms. Control over water and electrolytes excretion is realized by osmotic receptors of posterior hypothalamus, volume receptors of the aerial walls, bar receptors of carotid sinus, juxtaglomerular apparatus of the kidneys and adrenal cortical cells.
When there is a water deficiency or electrolytes excess (sodium, chlorine) thirst appears and this makes us drink water. At the same time posterior pituitary produces antidiuretic hormone, which decreases urine output. Adrenals reveal into the blood flow aldosterone, which stimulates reabsorption of sodium ions in the tubules and thus also decreases diuresis (due to osmosis laws water will move to the more concentrated solution). This way organism can keep precious water.
On the contrary, in case of water excess endocrine activity of glands is inhibited and water is actively removed from the body through the kidneys.
9.2 Importance of osmolarity for homoeostasis.
Water sections of the organism (intracellular and extracellular) are divided with semipermeable membrane – cell wall. Water easily penetrates through it according to the laws of osmosis. Osmosis is a movement of water through a partially permeable membrane from the solution with lower concentration to a solution with higher concentration.
Osmotic concentration (osmolarity) is the concentration of active parts in one liter of solution (water). It is defined as a number of miliosmoles per liter (mOsm/l). Normally osmotic concentration of plasma, intracellular and extracellular fluids is equal and varies between 285mOsm/l. This value is one of the most important constants of the organism, because if it changes in one sector the whole fluid of the body will be redistributed (water will move to the environment with higher concentration). Over hydration of one sector will bring dehydration of another. For example, when there is a tissue damage concentration of active osmotic parts increases and water diffuses to this compartment, causing oedema. On the contrary plasma osmolarity decreases, when there is a loss of electrolytes and osmotic concentration of the cellular fluid stays on the previous level. This brings cellular oedema, because water moves through the intracellular space to the cells due to their higher osmotic concentration.
Cerebral oedema appears when the plasma osmolarity is lower than 270 mOsm/l. Activity of central nervous system is violated and hypoosmolar coma occurs. Hyperosmolar coma appears when the plasma osmolarity is over 320 mOsm/l: water leaves the cells and fills the vascular bed and this leads to cellular dehydration. The sensitive to cellular dehydration are the cells of the brain.
Plasma osmolarity is measured with osmometer. The principle of measurement is based on difference in freezing temperature between distillated water and plasma. The higher is the osmolarity (quantity of molecules) the lower is freezing temperature.
Plasma osmotic concentration can be calculated according to the formula:
Osmotic concentration= 1,86*Na+glucose+urea+10,
Plasma osmolarity (osmotic concentration) – mOsm/l
Na- sodium concentration of plasma, mmol/l
Glucose- glucose concentration of the plasma, mmol/l
Urea- urea concentration of the plasma, mmol/l
According to this formula sodium concentration is the main factor influencing plasma osmolarity. Normally sodium concentration is 136-144 mmol/l. Water and electrolytes balance can be violated with external fluid and electrolytes loss, their excessive inflow or wrong distribution.
9.3 Fluid imbalance and principles of its intensive treatment.
Water imbalance is divided into dehydration and overhydration.
Dehydration is caused by:
– excessive perspiration in conditions of high temperature;
– rapid breathing (dyspnea, tachypnea) or artificial ventilation without humidification of the air;
– vomiting, diarrhoea, fistulas;
– blood loss, burns;
– diuretics overdose;
– excessive urine output;
– inadequate enteral and parenteral nutrition or infusion therapy (comatose patients, postoperative care);
– pathological water distribution (“third space” in case of inflammation or injury).
Dehydration signs: weight loss, decrease of skin turgor and eyeballs tone, dry skin and mucous membranes; low central venous pressure, cardiac output and blood pressure (collapse is possible); decreased urine output and peripheral veins tone; capillary refill over 2 seconds (microcirculation disorders) and low skin temperature; intracellular dehydration is characterized with thirst and consciousness disorders. Laboratory tests show blood concentration: hematocrit, hemoglobin concentration, protein level and red blood cells concentration increase.
Overhydration appears in case of:
– excessive water consumption, inadequate infusion therapy;
– acute and chronic renal failure, hepatic and cardiac insufficiency;
– disorders of fluid balance regulation;
– low protein edema.
Clinical findings in case of overhydration are: weight gain, peripheral oedema, transudation of the plasma into the body cavities (pleural, abdominal), high blood pressure and central venous pressure. In case of intracellular overhydration appear additional symptoms: nausea, vomiting, signs of cerebral edema (spoor, coma). Laboratory tests prove hemodilution.
According to the osmotic concentration of plasma dehydration and overhydration are divided into hypotonic, isotonic and hypertonic.
Isotonic dehydration is caused by equal loss of electrolytes and fluid from the extracellular space (without cellular disorders).Blood tests show hemoconcentration; sodium level and osmotic concentration are normal.
To treat this type of water imbalance use normal saline solution, Ringer solution, glucose-saline solutions, etc.. The volumes of infusions can be calculated according to the formula:
VH2O= 0,2*BW* (Htp-0,4)/0,4 ,
VH2O – volume of infusion, l
Htp – patient’s hematocrit, l/l,
BW – body weight, 0,2*BW – volume of extracellular fluid,
0,4- normal hematocrit, l/l,
Hypertonic dehydration is caused by mostly water loss: first it appears in the vascular bed, than in the cells. Laboratory tests show hemoconcentration: elevated levels of proteins, red blood cells, hematocrit. Plasma sodium is over 155 mmol/l and osmotic concentration increases over 310 mOsm/l.
Intensive treatment: if there is no vomiting allow patients to drink. Intravenously give 0,45% saline solution and 2,5 % glucose solution, mixed with insulin. The volume of infusions is calculated according to the formula:
VH2O=0,6*BW (Nap -140)/140,
VH2O – water deficiency, l
Nap – plasma sodium, mmol/l
BW – body weight, 0,6*BW volume of general body fluid
140 – physiological plasma sodium concentration
Hypotonic dehydration is characterized with clinical features of extracellular dehydration. Laboratory tests show decrease of sodium and chlorine ions. Those changes cause intracellular movement of the water (intracellular overhydration). Hemoglobin, hematocrit and protein levels are increased. Sodium is lower than 136 mmol/l, osmolarity is lower than 280 mOsm/l.
To treat this type of water imbalance use normal or hypertonic saline and sodium bicarbonate solution (depends on blood pH). Do not use glucose solutions!
The deficiency of electrolytes is calculated according to the formula:
Nad = (140-Nap)*0,2 BW,
Nad – sodium deficiency, mmol
Nap – plasma sodium, mmol/l
BW – body weight, 0,2 BW – volume of extracellular fluid
Isotonic overhydration is caused by excess of the water in the vascular bed and extracellular space; however intracellular homoeostasis is not violated. Hemoglobin is less than 120 g/l, protein level is less than 60 g/l, plasma sodium is 136-144 mmol/l, osmotic concentration is 285-310 mOsm/l.
Treat the reason of imbalance: cardiac failure, liver insufficiency, etc. Prescribe cardiac glycosides, limit salt and water consumption. Give osmotic diuretics (mannitol solution 1,5 g/kg), saluretics (furosemide solution 2 mg/kg), aldosterone antagonists (triamterene – 200 mg), steroids (prednisolone solution 1-2 mg/kg) albumin solution if necessary (0,2-0,3 g/kg).
Hypertonic overhydration is a state of extracellular electrolytes and water excess combined with intracellular dehydration. Blood tests show decrease of hemoglobin, hematocrit, protein level, however sodium concentration is increased over 144 mmol/l, osmotic concentration is over 310 mOsm/l.
To treat this condition use solutions without electrolytes: glucose with insulin, albumin solutions and prescribe saluretics (furosemide solution), aldosterone antagonists (spironolactone). If it is necessary perform dialysis and peritoneal dialysis. Do not use crystalloids!
Hypotonic overhydration is a state of extracellular and intracellular water excess. Blood tests show decrease of haemoglobin, hematocrit, proteins, sodium and osmotic concentration. Intensive therapy of this condition includes osmotic diuretics (200-400 ml of 20% mannitol solution), hypertonic solutions (50 ml of 10% saline intravenously), steroids. When it is required use ultrafiltration to remove water excess.
9.4 Electrolytes disorders and their treatment
Potassium is a main intracellular cation. Its normal plasma concentration is 3,8-5,1 mmol/l. Daily required amount of potassium is 1 mmol/kg of body weight.
Potassium level less than 3,8 mmol/l is known as kaliopenia. Potassium deficiency is calculated according to the formula:
Kd= (4,5-Kp)*0,6 BW
K- potassium deficiency, mmol;
Kp – potassium level of the patient mmol/l;
0,6*BW – total body water, l.
To treat this state use 7,5% solution of potassium chloride (1ml of this solution contains 1 mmol of potassium). Give it intravenously slowly with glucose and insulin (20-25 ml/hour). You can also prescribe magnesium preparations. Standard solution for kaliopenia treatment is:
10% glucose solution 400 ml
7,5% potassium chloride solution 20 ml
25% magnesium sulphate solution 3 ml
insulin 12 units
Give it intravenously slowly, during one hour. Forced bolus infusion of potassium solutions (10-15 ml) can bring cardiac arrest.
Potassium level over 5,2 mmol/l is a state called hyperkalemia. To treat this condition use calcium gluconate or calcium chloride solutions (10 ml of 10% solution intravenously), glucose and insulin solution, saluretics, steroids, sodium bicarbonate solution. Hyperkalemia over 7 mmol/l is an absolute indication for dialysis.
Sodium is the main extracellular cation. Its normal plasma concentration is 135-155 mmol/l. Daily required amount of potassium is 2 mmol/kg of body weight.
Sodium concentration which is lower than 135 mmol/l is known as hyponatraemia. This condition is caused by sodium deficiency or water excess. Sodium deficiency is calculated according to the formula:
Nad= (140-Nap)*0,2 BW,
Na- sodium deficiency, mmol;
Nap – sodium concentration of the patient mmol/l;
0,2*BW – extracellular fluid volume, l.
To treat it use normal saline (1000 ml contains 154 Na mmol) or 5,8% solution of sodium chloride – your choice will depend on osmotic concentration.
Sodium concentration over 155 mmol/l is a state called hypernatremia. This condition usually appears in case of hypertonic dehydration or hypertonic overhydration. Treatment was described in the text above.
Chlorine is the main extracellular anion. Its normal plasma concentration is 98-107 mmol/l. Daily requirement of chlorine is 215 mmol.
Hypochloremia is a condition of decreased plasma chlorine concentration (less than 98 mmol/l).
Chlorine deficiency is calculated according to the formula:
Cld = (100-Clp)*0,2 BW,
Cld- chlorine deficiency, mmol
Clp – plasma chlorine concentration of the patient, mmol/l
0,2*BW – extracellular fluid volume, l.
To treat hypochloremia use normal saline (1000 ml contains 154 mmol of chlorine) or 5,8% sodium chlorine solution (1 ml contains 1 mmol of chlorine). The choice of solution depends on the osmotic concentration of the plasma.
Hyperchloremia is a condition of increased chlorine concentration (over 107 mmol/l). Intensive therapy of this state includes treatment of the disease, which caused it (decompensated heart failure, hyperchloremic diabetes insipidus, glomerulonephritis). You can also use glucose, albumin solutions and dialysis.
Magnesium is mostly an intracellular cation. Its plasma concentration is 0,8-1,5 mmol/l. Daily requirement of magnesium is 0,3 mmol/kg.
Hypomagnesemia is a state of decreased magnesium concentration: less than 0,8 mmol/l. Magnesium deficiency is calculated according to the formula:
Mgd =(1,0 – Mgp)*0,6BW,
Mgd – magnesium deficiency, mmol
Mgp – plasma magnesium concentration of the patient, mmol/l
0,6*BW – extracellular fluid volume, l.
Use 25% magnesium sulphate solution to treat this state (1 ml of it contains 0,5 mmol of magnesium).
Hypermagnesemia is a state of increased magnesium concentration (more than 1,5 mmol/l). This condition appears usually in case of hyperkalemia and you should treat it as you treat hyperkalemia.
Calcium is one of the extracellular cations. Its normal concentration is 2,35-2,75 mmol/l. Daily requirement of calcium is 0,5 mmol/kg.
Calcium concentration less than 2,35 mmol/l is called hypocalcemia. Calcium deficiency is calculated according to the formula:
Cad = (2,5-Cap)*0,2 BW,
Cad – calcium deficiency, mmol
Clp – plasma calcium concentration of the patient, mmol/l
0,2*BW – extracellular fluid volume, l.
To treat this state use 10% calcium chloride (1 ml of the solution contains 1,1 mmol of calcium), ergocalciferol; in case of convulsions prescribe sedative medicines.
Hypercalcemia is a condition with increased calcium concentration (over 2,75 mmol/l). Treat the disease, which caused it: primary hyperparathyroidism, malignant bone tumors, etc. Additionally use infusion therapy (solutions of glucose with insulin), steroids, dialysis and hemosorbtion.
9.5 Acid-base imbalance and its treatment.
There are 2 main types of acid-base imbalance: acidosis and alkalosis.
pH is a decimal logarithm of the reciprocal of the hydrogen ion activity. It shows acid-base state of the blood.
Normal pH of arterial blood is 7,36-7,44. Acid based imbalance is divided according to the pH level into:
pH 7,35-7,21 – subcompensated acidosis
pH < 7,2 – decompensated acidosis
pH 7,45-7,55 – subcompansated alkalosis
pH > 7,56 – decompensated alkalosis
Respiratory part of the acid-base imbalance is characterized with pCO2. Normally pCO2 of arterial blood is 36-44 mm Hg. Hypercapnia (pCO2 increased over45 mm Hg) is a sign of respiratory acidosis. Hypocapnia (pCO2 less than 35 mm Hg) is a symptom of respiratory alkalosis.
Basis excess index is also a characteristic of metabolic processes. Normally H+ ions produced during metabolic reactions are neutralized with buffer system. BE of arterial blood is 0±1,5. Positive value of BE (with +) is a sign of base excess or plasma acid deficiency (metabolic alkalosis). Negative value of BE (with -) is a symptom of bases deficiency, which is caused by acid neutralization in case of metabolic acidosis.
Respiratory acidosis (hypercapnia) is a condition caused by insufficient elimination of CO2 from the body during hypoventilation. Laboratory tests show:
pH<7,35,
pCO2a > 46 mm Hg
BE – normal values
However when the respiratory acidosis progresses renal compensation fails to maintaiormal values and BE gradually increases. In order to improve this condition you should treat acute and chronic respiratory violations. When pCO2 is over 60 mm Hg begin artificial lung ventilation (through the mask or tube; when the necessity of ventilation lasts longer than 3 days – perform tracheostomy).
Respiratory alkalosis (hypocapnia) is usually an effect of hyperventilation, caused by excessive stimulation of respiratory centre (injuries, metabolic acidosis, hyperactive metabolism, etc.) or wrong parameters of mechanical ventilation. Gasometry shows:
pH>7,45,
pCO2a <33 mm Hg
BE < +1,5 mmol/l.
However prolong alkalosis brings decrease of BE due to compensatory retain of H+ ions. To improve this imbalance treat its reason: normalize ventilation parameters; if patients breathing has rate over 40 per minute – sedate the patient, perform the intubation and begin artificial ventilation with normal parameters.
Metabolic acidosis is characterized with absolute and relative increase of H+ ions concentration due to acid accumulation (metabolic disorders, block of acid elimination, excessive acid consumption in case of poisonings, etc.). Laboratory tests show:
pH<7,35,
pCO2a < 35 mm Hg
BE (-3) mmol/l.
Treat the main reason of acid-base disorder: diabetic ketoacidosis, renal insufficiency, poisoning, hyponatremia or hyperchloremia, etc. Normalize pH with 4% sodium bicarbonate solution. Its dose is calculated according to the formula:
V=0,3*BE*BW
V- volume of sodium bicarbonate solution, ml
BE – bases excess with “-”, mmol/l
BW – body weight, kg
Metabolic alkalosis is a condition of absolute and relative decrease of H+ ions concentration. Blood tests show:
pH>7,45,
pCO2a normal or insignificantly increased (compensatory reaction)
BE 3,0 mmol/l.
To treat this condition use “acid” solutions, which contain chlorides (saline, potassium chloride). In case of kaliopenia give potassium solutions.
Respiratory and metabolic imbalances can mix in case of severe decompensated diseases due to failure of compensatory mechanisms. Correct interpretation of these violations is possible only in case of regular and iterative gasometry blood tests.
Control tasks.
Task 1.
Calculate the total body water volume and its extracellular and intracellular volumes of the Patience, the patient of 48 years and body weight 88 kg.
Task 2.
Patience, the patient of 23 with body weight 70 kg has sodium level 152 mmol/l and hematocrit 0,49 l/l. Name the type of water balance disorder.
Task 3.
Patience, the patient of 54 with body weight 76 kg has sodium level 128 mmol/l. Calculate the volume of saline and 7,5% sodium chloride solutioecessary for the treatment of this condition.
Task 4.
Patience, the patient of 60 with body weight 60 kg has sodium level 140 mmol/l and hematocrit 0,55 l/l. Name the type of disorder and prescribe infusion therapy.
Task 5.
Patience, the patient of 42 with body weight 80 kg has potassium level 2,6 mmol/l. Calculate the volume of 4% potassium chloride solutioecessary for treatment of this condition.
Task 6.
Patience, the patient of 33 with body weight 67 kg and diagnosis “gastric ulcer, complicated with pylorostenosis” has potassium concentration 3 mmol/l, chlorine concentration 88 mmol/l. pH 7,49, pCO2a 42 mm Hg, BE + 10 mmol/l. Name the type of disorder.
Task 7.
Patience, the patient of 50 with body weight 75 kg, was transported to the admission unit of the hospital with: unconsciousness, cyanotic skin, low blood pressure, shallow breathing. Blood tests show: pH 7,18, pCO2a 78 mm Hg, pO2A – 57 mm Hg, BE -4,2 mmol/l. Name the type of acid-base disorder and prescribe treatment.
Task 8.
Patience, the patient with body weight 62 kg and renal insufficiency has: potassium concentration 5,2 mmol/l, sodium concentration 130 mmol/l, calcium concentration 1,5 mmol/l, pH 7,22, pCO2a 34 mm Hg, BE -9,2 mmol/l. Name the type of disorder.
Life is provided through a variety of mechanisms, however all of them depend on proper circulation. Circulation itself consists of 2 parts: work of heart (pump of the body) and vessels, through which blood is pumped to the most remote organs and tissues. During every systolic contraction heart pump 70-80 ml of blood 9so called stroke volume). Thus in case of heart rate 70 beats per minute heart pumps nearly 5 liters of blood, what makes more than 7 tones per day.
From the left ventricle blood gets to the arterial system of the systemic circuit. Arteries contain 15% of the whole circulating blood volume; they carry blood from the heart to their distal departments – arterioles (vessels of resistance). Arterioles themselves are defining blood distribution: in condition of constriction (spasm) they make blood supply of the capillaries impossible (ischemia appears). On the contrary, in condition of dilatation they provide maximal oxygenation. When arterioles are blocked due to the spasm blood is flowing through the arterio-venous anastomosis directly to the venous system.
Distribution of blood in the vascular bed (% of CBV).
a. heart cavity 3%
b. arteries 15%
c. capillaries 12%
d. venous system 70%
Among the natural vasoconstrictors (agents, which cause constriction of the blood vessel) are epinephrine, norepinephrine, serotonin, angiotensin II. Stress enhances the secretion of cathecholamines, their blood concentration increases and arterioles constrict. Spasm of the arterioles is the basis of blood flow centralization: peripheral flow is disregarded in order to provide brain with the oxygenated blood as long as possible. To the group of vasodilatators (agents, which provide dilatation of the vessels) belong “acid” metabolites (lactate, pyruvate, adenylic acid, inosinic acid), bradykinin, acetylcholine, different medicines (neuroleptics, α-adrenergic antagonists, peripheral vasodilatators, ganglionic blocking agents, etc.), some exogenous poisons. All of them cause blood flow decentralization: opening of arterioles and distribution of the blood from central vessels to the capillary bed.
Capillaries are the interweaving network of the smallest body vessels with the general length of 90-100 thousands of kilometers. However simultaneously work only 20-25% of them. They provide metabolic exchange bringing oxygen and nutrients to the tissues and take back wastes of metabolism. Periodically, every 30-40 seconds one of them get closed and others open (vasomotion effect). Capillaries contain 12% of the whole circulating blood volume, but different pathological conditions can increase this amount even 3 and more times.
“Used” blood from the capillaries flows to the venous system. Veins are the blood reservoir, which contains 70% of the total circulating blood volume. Unlike arteries they are capable of volume control and thus they influence the amount of blood, which returns to the heart.
The most important haemodynamic index of venous system is central venous pressure. CVP represents the pressure which blood causes to the walls of cava veins and right atrium. This parameter is an integral index of circulating blood volume, systemic vascular resistance and pump function of the heart. It can be measure with a special device called “phlebotonometer” (pic. 4.9) or with a usual infusion set and a ruler. Normally CVP measured from the sternum point is 0-14 cm H2O and from midaxillary line is 8-15 cm H2O.
Central venous pressure decreases (sometimes even to negative) in case of:
– blood loss
– excessive water loss (dehydration)
– distributive shock (decrease of peripheral resistance due to venous and arterial dilatation)
In those conditions decreases volume of blood returning to the heart and thus suffers cardiac output. In case of negative CVP cardiac arrest is highly probable.
Central venous pressure increases in case of:
– heart failure (insufficiency of left or right ventricle)
– hypervolemia (excessive blood infusion, improper infusion therapy)
– obstructions to blood flow (pulmonary embolism, cardiac tamponade, etc.)
When CVP over 15-16 cm H2O is combined with left ventricle insufficiency the risk of pulmonary edema is very high.
Blood pressure is an integral index of arterial part of systemic haemodynamics. Talking about blood pressure we may refer to systolic, diastolic, pulse and mean arterial pressure. Systolic (Psyst) and diastolic (P diast) pressures are measured with the manometer (method with the usage of phonendoscope was invented by M. Korotkoff). Pulse pressure (PP) is a difference between systolic and diastolic blood pressure.
Mean arterial pressure (MAP) is calculated according to the formula:
MAP= P dias + 1/3 PP mm Hg
MAP defines the level of pressure necessary for the metabolic exchange in the tissues. Its measurement allows the evaluation of tissue perfusion level.
Blood pressure depends on different factors, but the most important are cardiac output and vascular resistance (mostly arterioles). This dependence is direct, thus you can increase blood pressure using:
– infusion of vasoconstrictors – solutions of epinephrine, phenylephrine (mesaton), etc. (they will increase the vascular resistance);
– infusion of hydroxyethyl starch solutions or saline (they will increase circulating blood volume)
– infusion of cardiac glycosides or other medicine which stimulate myocardium
General volume of blood in the body of a healthy adult is nearly 7% from the body weight: 70 ml per kilogram for male and 65 mil per kilogram of body weight for female. Of course circulating blood volume is lower, because part of blood is out of metabolic processes as a reserve. CBV can be measured with the infusion of coloring substance to the blood flow (Evans blue, polyglucin) and later evaluation of its dissolution degree.
Therefore measurement of CVP, BP, cardiac output and circulating blood volume allow to evaluate condition of circulation system of the patients and to provide adequate correction.
4.2 Acute heart failure; shock and collapse.
Acute cardiovascular failure is a state of cardiac and vascular inability to provide adequate supply of tissue metabolic needs with oxygenated blood and nutrients. This, earlier or later, causes cellular death.
The reasons of the failure vary greatly: mechanic injuries, blood loss, burns, dehydration, exogenous and endogenous intoxications, immediate hypersensitivity reaction, ischemic heart disease, neural and humoral regulation disorders of vascular tone.
Acute cardiac failure is a disorder of heart pumping action. It develops due to primary heart problems or secondary, under the influence of extracardiac factors such as infection or intoxication. There are two types of heart failure: left-sided and right-sided.
Left-sided heart failure is an inability of left ventricle to pump blood from the pulmonary circuit to the systemic circuit. The most common reasons of it are myocardial infarction, mitral insufficiency, left AV valve stenosis, aortic valve stenosis, aortal insufficiency, hypertonic disease, coronary sclerosis, acute pneumonia.
Coronary circulation is possible only during the diastole and in those conditions every violation of coronary passability decreases cardiac output. This way during the systole part of the blood is not injected into aorta, but stays in the left ventricle. Diastolic pressure in the left ventricle increases and blood is literally forced to stagnate in the left atrium. At the same time right ventricle functions normally and continues to pump usual amounts of blood to the pulmonary circuit. Thus hydrostatic pressure in the vessels of pulmonary circulation increases, fluid part of the blood moves first to the lung tissue and then, through alveolar-capillary membrane, to the alveolar lumen.
Clinically pulmonary edema begins with dyspnea (during physical activity or rest). Later attacks of dyspnea are connected with persistent cough with white or pink blood-tinged phlegm. During the attack patient tries to sit as in this position breathing is easier. This condition is called “heart asthma”. When hydrostatic pressure is over 150-200 mm Hg, fluid part of blood moves to the alveolar lumen causing development of pulmonary edema.
Pulmonary edema is divided into interstitial and alveolar edema.
Interstitial edema is a condition during which serous part of stagnated in the pulmonary circuit blood infiltrates the lung tissue, including peribronchial and perivascular spaces.
During alveolar edema not only the plasma, but also blood components (red and white blood cells, platelets) get out from the vessels. During the respiratory act blood mixes with the air creating large amount of “foam”, which violates gas exchange. This way, in addition to circulatory hypoxia, hypoxic hypoxia appears.
Condition of the patient gets worth quickly. Sitting position is optimal, but not as helping as previously. Respiratory rate is nearly 30-35 breathes per minute, but attacks of breathlessness are constant. Skin is pale with acrocyanosis. Hypoxia of central nervous system usually causes psychomotor agitation. Respiratory acts are noisy; during cough pink blood-tinged phlegm is released. Auscultation allows you to hear different wet rales, sometimes it’s even possible to hear them standing aside the patient without phonendoscope.
Pulmonary edema can be also divided according to the blood pressure level: the one with elevated pressure is caused by a hypertonic disease, aorta valve insufficiency or disorders of cerebral perfusion; another one is caused by total myocardial infarction, acute inflammation of myocardial muscle, terminal valve defects, severe pneumonia and is characterized with normal or low blood pressure.
Immediate aid
– make sure patient is sitting with his legs down (orthopnea)
– provide oxygenation through nasal catheter (before placing oil it with glycerin, insert it to the depth of 10-12 cm – distance from the wing of the nose to auricle) or face mask. Do not use Vaseline, because it can burn in atmosphere with high concentration of oxygen.
However if catheter is not deep enough patient will suffer from an unpleasant “burning” feeling, because oxygen flow will dry mucosa layer of the nasal cavity; also in this situation concentration of oxygen will be lower than expected.
– put venous tourniquets on the limbs in order to reduce amount of blood returning to heart: venous bed of limbs can reserve up to 1,7 liters of blood;
– constantly control heart and kidney activity (ECG, SaO2 , and blood pressure are checked automatically trough the monitor; to control diuresis you should insert Foley catheter;
– catheterize central vein, because amount of infusions should be based on central venous pressure;
– use medical “defoamers” if they are available (ethyl alcohol or antiphomsylan solution) combined with oxygen inhalation
Scheme of oxygenation set connected to “defoamer” container
a. oxygen source (cylinder with oxygen)
b. tube with numerous holes sunk into container with defoamer
c. tube for humidified oxygen (its opening should be over the level of fluid);
d. patient
– medical treatment: 1% morphine solution (decreases intravascular pressure of pulmonary circuit, inhibits respiration center in medulla oblongata preventive dyspnea progress, sedates patient);
– solutions of diuretics are used to decrease the circulating blood volume ( 6-12 ml of 1% furosemid solution, solution of ethacrynic acid), however be careful with them in case of low blood pressure; diuretic effect will last up to 3 hours after i/v infusion, the expected diuresis is 2-
– if blood pressure allows you can try to use nitroglycerin to reduce intravascular pressure of pulmonary circuit (1 or 2 tablets with 10 minutes interval)
– cardiac glycosides for improvement of heart action (0,025% digoxin solution, 0,05% strophanthin solution, 0,06% corglicon solution);
– in case of high pressure (over 150 mm Hg) use ganglionic blocking agents (1 ml of 5% pentamin solution diluted in 150 ml of saline, give i/v slowly; diluted with saline 250 mg of trimethaphan solution), because they reduce pressure in pulmonary circuit and lower the amount of blood getting to right half of the heart, however be careful with the dosage and monitor blood pressure level carefully;
– never use osmotic diuretics in case of pulmonary edema – they will increase blood volume and thus heart load!!!
– when everything listed above failed and patient is worsening with every second you should intubate him and start artificial ventilation with positive end expiratory pressure (begin with 4-6 cm H2O)
Right-sided heart failure is an inability of right ventricular to pump blood from systemic circuit to the pulmonary circuit due to its weakness or an obstruction to the blood flow.
It occurs in case of pulmonary embolism, right ventricular infarction, excessive infusion therapy (especially including citrated blood) for patients with heart insufficiency, lung diseases (bronchial asthma, emphysema, pneumosclerosis) which cause increase of right ventricular load.
Patients have acrocyanosis, tachycardia, dyspnea, pronounced neck veins, ankle swelling, enlarged liver, ascytis. Central venous pressure is highly increased (up to 20-25 cm H2O), however pulmonary edema does not appear.
Intensive treatment is mostly pathogenetic:
– limit the infusions (give only life-necessary solutions, check the water balance of the patient and reduce drinking water if necessary);
– in case of citrated blood transfusions use 5-10 ml of 10% calcium gluconate solution per every 500 ml of blood to prevent hypocalcaemia;
– in case of bronchial spasm use bronchial spasmolytics;
– to remove excessive fluid from the body use diuretics (furosemide solution for example);
– metabolic acidosis is corrected with 4% solution of sodium bicarbonate (i/v slowly with acid-base state control);
– in case of pulmonary embolism anticoagulants are used – fraxiparine 0,6 mg subcutaneously; heparin solution – 5000 IU every 4 hours; fibrinolytic drugs (streptokinase, fibrinolysin, urokinase, etc.)
Shock is a pathological state which can be described as a tissue hypoxia caused by hypoperfusion. Pathogenetic basis of shock depends on its reason (trauma, toxins, thermal injury) and at the same time on reactivity of the organism (level of defense mechanisms mobilization).
Stimulation of sympathetic nervous system – production of catecholamines and other vasoactive substances by hypothalamus and adrenal glands are the universal response of the body to the stress. Those mediators interact with the receptors of peripheral vessels causing their constriction and at the same time they dilatate the vascular bed of life-important organs. This is so called “centralization of the flow”: rational decrease of blood flow in less important tissues (skin, organs of abdominal cavity, kidneys) in case of aggressive external influence for protecting life itself (brain, heart, lungs).
However influence of shock agents (pain, hypovolemia, destroyed cells, toxic metabolites), extended microcirculation violations (vascular spasm, microthrombosis and sludge) and caused by them tissue ischemia lead to hypoxic affection and cellular death of the internal organs. Further it can bring multiple organ dysfunction syndrome.
Collapse is a vascular failure. It occurs when body is not able to provide blood flow according to the new level of its needs (either because reaction is not fast enough or because sympathetic activation fails).Vascular bed volume and circulating blood volume are disproportional: too much blood gets to the microcirculation vascular reserve and the amount, which returns to the heart is not enough for the systemic needs (so called “decentralization” of the blood flow). Cardiac output and blood pressure decrease, that causes hypoperfusion of the central nervous system and thus unconsciousness and life-threatening complications.
Collapse definition is a bit nominal, because if such reaction extends in time the state of shock develops. Shock itself can equally run as a vascular failure or as a sudden clinical death.
Pathogenetic classification of shock (according to P. Marino, 1998):
– hypovolemic
– cardiogenic
– distributive
– mixed (two and more factors).
Clinical classification of shock:
– traumatic shock;
– haemorrhagic shock;
– dehydration shock;
– burn shock;
– septic shock;
– anaphylactic shock;
– cardiogenic shock;
– exotoxic shock.
4 Shock caused by dehydration
It is a type of hypovolemic shock, which occurs during excessive body fluid loss (not blood, because hemorrhagic shock is another shock type).
Its reasons vary greatly:
– gastrointestinal diseases (profuse vomiting, diarrhea, loss of intestinal fluid through fistula);
– polyuria (uncontrolled diuretic treatment, diabetes mellitus and insipidus, diuretic phase of acute renal failure);
– fluid loss through skin and wound surface (burns, high fever);
– inadequate infusion treatment of postoperative or comatose patients;
– hyperventilation (rapid breathing, Kussmaul breathing, inadequate artificial ventilation parameters in case of apparatus without air humidification).
However not only the complete fluid loss can be the reason of shock, but also it’s pathological distribution into the extracellular space (intestinal cavity in case of intestinal paralysis, abdominal cavity in case of ascites, pleural cavity in case of pleurisy). This way will can also act prolonged heavy tissue inflammations (peritonitis) or massive injuries (crush-syndrome).
In cases described above electrolytes are also lost (cations of sodium, potassium, calcium, magnesium; anions of chlorine, hydrocarbonate). It causes complex osmolar, acid-base and electrolytic disorders.
Stage of dehydration shock is evaluated according to the actual fluid loss:
less than 5% of body weight – mild dehydration
5-10% of body weight – moderate dehydration
over 10% of body weight – severe dehydration
Water deficiency brings lowering of cardiac output, blood pressure and central venous pressure (through decrease of blood volume returning to the heart, which leads to compensatory adrenergic vasoconstriction).
Dehydration causes body weight loss, skin and mucosa dryness, decrease of subcutaneous turgor and eyeballs tone, hypothermia, tachycardia, oliguria, thirst. While dehydration progresses compensatory mechanisms weaken and central nervous system suffers: patients become sluggish, confused; hallucinations, cramps and unconsciousness are also possible. Laboratory tests show blood concentration.
One of the most important things in treatment of dehydrated patients is daily balance of fluid: check it carefully trough measuring of daily received and lost fluids (food, infusions, stool and urine output). In case of fever or tachypnea make necessary corrections. Balance should be calculated every 12-24 hours (special paper forms make this easier).
Daily fluid balance is calculated by adding all the received fluids (both enteral and parenteral ways) and deducting urine output, stool, perspiration and breathing water loss.
You should remember, that perspiration depends on body temperature: in case of normal temperature (36,6ºC) patient looses 0,5 ml/kg of water during every hour; 1 degree of temperature elevation adds 0,25 ml/kg to normal value of 0,5 ml/kg.
According to the fluid balance infusion therapy is divided into positive (for dehydrated patients), negative (for overhydrated patients) and “zero” (for patients without balance disorders).
Water deficiency is calculated according to the formula:
W def = (Htp-Htn)* 0,2 BW/ Htn,
W def – water deficiency, l;
Htp – hematocrit of the patient, l/l;
Htn – normal hematocrit, l/l;
BW – body weight, kg.
Use crystalloids to treat water deficiency: saline solution, Ringer’s solution, Ringer-lactate solution, electrolytic solutions, 5%, 10, 20% glucose solution. To control potassium concentration (during dehydration this cation is widely lost) prescribe polarizing GIK mixture (pic.9.4), but don’t you ever infuse concentrated potassium solutions quickly – it can cause cardiac arrest (not more than 400 of GIK solution ml per hour).
The essential components of the human cardiovascular system are the heart, blood, and blood vessels. It includes: the pulmonary circulation, a “loop” through the lungs where blood is oxygenated; and the systemic circulation, a “loop” through the rest of the body to provide oxygenated blood. An average adult contains five to six quarts (roughly 4.7 to 5.7 liters) of blood, accounting for approximately 7% of their total body weight.
While it is convenient to describe the flow of the blood through the right side of the heart and then through the left side, it is important to realize that both atria contract at the same time and that both ventricles contract at the same time. The heart works as two pumps, one on the right and one on the left that works simultaneously. The right pump pumps the blood to the lungs or the pulmonary circulation at the same time that the left pump pumps blood to the rest of the body or the systemic circulation. Venous blood from systemic circulation (deoxygenated) enters the right atrium through the superior and inferior vena cava. The right atrium contracts and forces the blood through the tricuspid valve (right atrioventricular valve) and into the right ventricles. The right ventricles contract and force the blood through the pulmonary semilunar valve into the pulmonary trunk and out the pulmonary artery. This takes the blood to the lungs where the blood releases carbon dioxide and receives a new supply of oxygen. The new blood is carried in the pulmonary veins that take it to the left atrium. The left atrium then contracts and forces blood through the left atrioventricular, bicuspid, or mitral, valve into the left ventricle. The left ventricle contracts forcing blood through the aortic semilunar valve into the ascending aorta. It then branches to arteries carrying oxygen rich blood to all parts of the body.
Blood Flow Through Capillaries
From the arterioles, the blood then enters one or more capillaries. The walls of capillaries are so thin and fragile that blood cells can only pass in single file. Inside the capillaries, exchange of oxygen and carbon dioxide takes place. Red blood cells inside the capillary releases their oxygen which passes through the wall and into the surrounding tissue. The tissue then releases waste, such as carbon dioxide, which then passes through the wall and into the red blood cells.
The Circulatory System
The circulatory system is extremely important in sustaining life. It’s proper functioning is responsible for the delivery of oxygen and nutrients to all cells, as well as the removal of carbon dioxide, waste products, maintenance of optimum pH, and the mobility of the elements, proteins and cells, of the immune system. In developed countries, the two leading causes of death, myocardial infarction and stroke are each direct results of an arterial system that has been slowly and progressively compromised by years of deterioration.
Arteries
Arteries are muscular blood vessels that carry blood away from the heart, oxygenated and deoxygenated blood . The pulmonary arteries will carry deoxygenated blood to the lungs and the sytemic arteries will carry oxygenated blood to the rest of the body. Arteries have a thick wall that consists of three layers. The inside layer is called the endothelium, the middle layer is mostly smooth muscle and the outside layer is connective tissue. The artery walls are thick so that when blood enters under pressure the walls can expand.
Arterioles
An arteriole is a small artery that extends and leads to capillaries. Arterioles have thick smooth muscular walls. These smooth muscles are able to contract (causing vessel constriction) and relax (causing vessel dilation). This contracting and relaxing affects blood pressure; the higher number of vessels dilated, the lower blood pressure will be. Arterioles are just visible to the naked eye.
Capillaries
Capillaries are the smallest of a body’s vessels; they connect arteries and veins, and most closely interact with tissues. They are very prevalent in the body; total surface area is about 6,300 square meters. Because of this, no cell is very far from a capillary, no more than 50 micrometers away. The walls of capillaries are composed of a single layer of cells, the endothelium, which is the inner lining of all the vessels. This layer is so thin that molecules such as oxygen, water and lipids can pass through them by diffusion and enter the tissues. Waste products such as carbon dioxide and urea can diffuse back into the blood to be carried away for removal from the body.
The “capillary bed” is the network of capillaries present throughout the body. These beds are able to be “opened” and “closed” at any given time, according to need. This process is called autoregulation and capillary beds usually carry no more than 25% of the amount of blood it could hold at any time. The more metabolically active the cells, the more capillaries it will require to supply nutrients.
Veins
Veins carry blood to the heart. The pulmonary veins will carry oxygenated blood to the heart awhile the systemic veins will carry deoxygenated to the heart. Most of the blood volume is found in the venous system; about 70% at any given time. The veins outer walls have the same three layers as the arteries, differing only because there is a lack of smooth muscle in the inner layer and less connective tissue on the outer layer. Veins have low blood pressure compared to arteries and need the help of skeletal muscles to bring blood back to the heart. Most veins have one-way valves called venous valves to prevent backflow caused by gravity. They also have a thick collagen outer layer, which helps maintain blood pressure and stop blood pooling. If a person is standing still for long periods or is bedridden, blood can accumulates in veins and can cause varicose veins. The hollow internal cavity in which the blood flows is called the lumen. A muscular layer allows veins to contract, which puts more blood into circulation. Veins are used medically as points of access to the blood stream, permitting the withdrawal of blood specimens (venipuncture) for testing purposes, and enabling the infusion of fluid, electrolytes, nutrition, and medications (intravenous delivery).
Venules
A venule is a small vein that allows deoxygenated blood to return from the capillary beds to the larger blood veins, except in the pulmonary circuit were the blood is oxygenated. Venules have three layers; they have the same makeup as arteries with less smooth muscle, making them thinner.
The double circulatory system of blood flow refers to the separate systems of pulmonary circulation and the systemic circulation in amphibians, birds and mammals (including humans.) In contrast, fishes have a single circulation system. For instance, the adult human heart consists of two separated pumps, the right side with the right atrium and ventricle (which pumps deoxygenated blood into the pulmonary circulation), and the left side with the left atrium and ventricle (which pumps oxygenated blood into the systemic circulation). Blood in one circuit has to go through the heart to enter the other circuit. Blood circulates through the body two to three times every minute. In one day, the blood travels a total of 19,000 km (
The Pulmonary Circuit
In the pulmonary circuit, blood is pumped to the lungs from the right ventricle of the heart. It is carried to the lungs via pulmonary arteries. At lungs, oxygen in the alveolae diffuses to the capillaries surrounding the alveolae and carbon dioxide inside the blood diffuses to the alveolae. As a result, blood is oxygenated which is then carried to the heart’s left half -to the left atrium via pulmonary veins. Oxygen rich blood is prepared for the whole organs and tissues of the body. This is important because mitochondria inside the cells should use oxygen to produce energy from the organic compounds.
The Systemic Circuit
The systemic circuit supplies oxygenated blood to the organ system. Oxygenated blood from the lungs is returned to the left atrium, then the ventricle contracts and pumps blood into the aorta. Systemic arteries split from the aorta and direct blood into the capillaries. Cells consume the oxygen and nutrients and add carbon dioxide, wastes, enzymes and hormones. The veins drain the deoxygenated blood from the capillaries and return the blood to the right atrium.
Pic. 4.1 Distribution of blood in the body:
a. hear cavity itself 0 3% (% of blood volume)
b.arteries -15%
c. capillares -12%
d. venous system – 70%
Cardiac cycle is the term used to describe the relaxation and contraction that occur, as a heart works to pump blood through the body. Heart rate is a term used to describe the frequency of the cardiac cycle. It is considered one of the four vital signs. Usually it is calculated as the number of contractions (heart beats) of the heart in one minute and expressed as “beats per minute” (bpm). When resting, the adult human heart beats at about 70 bpm (males) and 75 bpm (females), but this rate varies between people. However, the reference range is nominally between 60 bpm (if less termed bradycardia) and 100 bpm (if greater, termed tachycardia). Resting heart rates can be significantly lower in athletes, and significantly higher in the obese. The body can increase the heart rate in response to a wide variety of conditions in order to increase the cardiac output (the amount of blood ejected by the heart per unit time). Exercise, environmental stressors or psychological stress can cause the heart rate to increase above the resting rate. The pulse is the most straightforward way of measuring the heart rate, but it can be deceptive when some strokes do not lead to much cardiac output. In these cases (as happens in some arrhythmias), the heart rate may be considerably higher than the pulse. Every single ‘beat’ of the heart involves three major stages: atrial systole, ventricular systole and complete cardiac diastole. Throughout the cardiac cycle, the blood pressure increases and decreases. As ventricles contract the pressure rise, causing the AV valves to slam shut.
