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Cardiovascular Physiology. Dr. Abdulhalim Serafi, MB ChB,MSc,PhD,FESC Assistant Professor & Consultant Cardiologist Faculty of Medicine Umm Al-Qura University Makkah Al-Mukarramah Saudi Arabia. Part II CARDIOVASCULAR PHYSIOLOGY. LECTURE VIII: CORONARY CIRCULATION. Outline:

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Cardiovascular physiology

Cardiovascular Physiology

Dr. Abdulhalim Serafi, MB ChB,MSc,PhD,FESC

Assistant Professor & Consultant Cardiologist

Faculty of Medicine

Umm Al-Qura University

Makkah Al-Mukarramah

Saudi Arabia


Part II

CARDIOVASCULAR PHYSIOLOGY

LECTURE VIII:CORONARY CIRCULATION

  • Outline:

  • - Blood supply of the heart (arterial supply & venous

  • drainage)

  • - Characteristics of the coronary circulation

  • - Coronary blood flow (CBF)

  • - Factors affecting CBF (coronary circulation)

  • - Coronary Heart Disease (CHD)

  • - Angina pectoris and coronary thrombosis

  • Further Reading:

  • Guyton: Textbook of Medical Physiology

  • Ganong: Review of Medical Physiology


  • CORONARY CIRCULATION

  • BLOOD SUPPLY OF THE HEART:

  • a) Arterial supply:

  • - The cardiac muscle is supplied by the first two branches of the aorta i.e. right & left coronary arteries.

  • The coronary arteries branch freely to form a rich capillary network. There is about one capillary for each cardiac muscle fiber.

  • Coronary arteries are considered as functional end arteries. There are small anostomatic connections between the small branches of the two coronary arteries and between the coronary arterioles and extra cardiac arterioles.


  • These anatomizes are not sufficient to supply the cardiac muscle with blood if one of the coronary arteries is occluded.

  • Thus, occlusion of a large branch of the coronary artery e.g. by coronary thrombosis  necrosis (=death) of the muscle supplied by that branch.

  • Venous Drainage: Coronary venous drainage occurs through two systems:

  • 1) Superficial system: which drains the left ventricle. It is formed of coronary sinus and anterior cardiac veins that open into the right atrium.

  • 2) deep system: which drains the rest of the heart. It is formed of the basian veins and arterio-sinusoidal vessels that open directly into the heart chamber.


  • CHARACTERISTICS OF THE

  • CORONARY CIRCULATION

  • It is very short and very rapid (so it is essential to the heart).

  • The blood flow in this circulation occurs mainly during cardiac diastole

  • There is no efficient anastomoses between the coronary vessels.

  • It is a rich circulation (5% of the CO while the heart weight is 300gm).

  • Its regulation is mainly by metabolites and not neural

  • The capillary permeability is high (the cardiac lymph is rich in protein)


  • The coronary vessels are susceptible to degeneration and atherosclerosis.

  • There is evident regional distribution: The subendocardial myocardial layer in the left ventricle receives less blood, due to more myocardial compression (but this is normally compensated during diastoles by V.D). However, this renders this area more liable to ischemia and infarction.

  • CORONARY BLOOD FLOW

  • Under resting conditions coronary blood flow (CBF) in the human heart is about 250 ml/ minute (=5% of the cardiac output).

  • In severe muscular exercise, the work of the heart increased and the CBF may be increased up to 2 liters/ minute.


  • - atherosclerosis.Coronary Inflow (arterial) occurs mainly during diastole, because during systole the coronary arteries are mechanically compressed by the contracting myocardium, i.e.

  • Systole of the heart   coronary inflow

  • Diastole of the heart   coronary inflow

  • Coronary Outflow (venous) occurs mainly during systolic due to compression of the coronary veins by the contracting myocardium. During diastole coronary outflow  and veins are filled.

  • Normal diastolic blood pressure is important for coronary filling because filling of coronary arteries occurs mainly during ventricular diastolic.


  • FACTORS AFFECTING CBF atherosclerosis.

  • (coronary circulation)

  • The amount of blood passing through the coronary vessels (CBF) is directly proportional to the work done by the heart i.e.  cardiac work   CBF and  cardiac work   CBF. The following factors modify the CBF:

  • Nervous Factors:

  • The effect of the autonomic nerves to the heart on the coronary arteries is indirect through their effect on cardiac metabolism I.e

  • a) Stimulation of sympathetic   cardiac metabolism   coronary vasodilatation   CBF.

  • b) Stimulation of parasymp   cardiac metasbolism  coronary vasoconst.   CBF.


  • Chemical Factors atherosclerosis.:

  • a) Metabolic factors:  cardiac metabolism   O2 tension (local hypoxia),  CO2,  K+, lactic acid & adenosine in the cardiac muscle  coronary vasodilatation   CBF.  cardiac metabolites  active hyperemia during  cardiac activity = auto regulation of CEF O2 lack (hypoxia) is the most effective coronary vasodilator. It produces coronary vasodilatation through:

  • • Direct action on coronary blood vessels and

  • • Release of chemical substances such as adenosine (from ATP) which is a potent coronary vasodilator.

  • b) Drugs: Nitrites, angised, aminophylline, caffeine & Khellin are coronary vasodilator  coronary vasodilatation   CBF.

  • c) Hormones Thyroxin   cardiac metabolism   coronary vasodilator   CBF.


  • Vasopressin (antidiuretic hormone)  coronary vasoconst   CBF.

  • Mechanical factors (=effect of cardiac cycle):

  • - Ventricular systole   of the intra-myocardial pressure  compression of the coronary vessels   CBF mainly in the left coronary artery (due to stronger cont of the left vent.)

  • - CBF  during ventricular diastole (maximal at the end of isometric relaxation).

  • Other Factors:

  • a) Heart Rate: Excessive  in the heart rate e.g. paroxysmal tachycardia   diastolic period   coronary filling (as it occurs mainly during ventricular diastole)   CBF.


  • b)   CBF.Cardiac Output: CBF is directly proportional to COP i.e.  COP   CBF  COP   CBF increased cardiac output   BP in aorta + reflex inhibition of the vagal vasoconstrictor tone (a nrepis reflex)  coronary vasodilatation   CBF.

  • c) Arterial BP: CBF is directly proportional to aortic BP especially diastolic PO  diastolic pressure   CBF and  diastolic aortic pressure (as in aortic regurgitation)   CBF.


  • ANGINA PECTORIS & CORONARY THROMBOSIS   CBF.

  • The coronary arteries are liable to degenerative changes leading to their narrowing or occlusion by blood thrombosis. This is a common complication of the atherosclerosis and hypertension.

  • Angina Pectoris is to narrowing of the coronary arteries  ischemia of the cardiac muscle  pain which is retrosternal (behind the sternum). The anginal pain may radiate to left shoulder, left arm or forearm, or abdomen.

  • Coronary Thrombosis  occlusion of one of the coronary arteries or its branches  necrosis of the area supplied by the occluded artery  myocardial infarction.


  • CORONARY HEART DISEASE (CHD)   CBF.

    ANGINA PECTORIS

  • Angina Pectoris means severe chest pain (usually retrosternal i.e. behind the sternum) due to ischemia of the cardiac muscle.

    The anginal pain may radiate to the left shoulder, left arm or forearm (=referred pain).

  • Angina pectoris is usually due to narrowing of the coronary arteries  ischemia.

  • Anginal pain may be relieved by rest & coronary VD drugs.


MYOCARDIAL INFARCTION   CBF.

  • Myocardial Infarction means necrosis of a part of the myocardium due to

    a) Severe & prolonged ischemia due to narrowing of the coronary arteries.

    b) Occlusion of one of the coronary arteries or its branches by coronary thrombosis  severe ischemia.

  • Myocardial Infarction produces also chest pain which is more severe than that of angina and it cannot be relieved by rest or coronary VD drugs.

  • It is frequently complicated by ventricular fibrillation  death.


Part II   CBF.

CARDIOVASCULAR PHYSIOLOGY

LECTURE IXPULMONARY CIRCULATION & CEREBRAL CIRCULATION

  • Outline:

  • Pulmonary Circulation:

  • - Functions and Characteristics of pulmonary circulation

  • - Pulmonary blood pressure and factors affecting it.

  • - Pulmonary edema.

  • Cerebral Circulation:

  • - The CNS Ischaemic response and cushing’d reflex.

  • - Auto regulation and control of the cerebral blood flow (CBF).

  • Further Reading:

  • Guyton: Textbook of Medical Physiology

  • Ganong: Review of Medical Physiology


  • PULMONARY CIRCULATION   CBF.

    Pulmonary Circulation is the circulation between right

    ventricle and left atrium. It has the following functions:

  • Carriage of blood from right to left side of the heart.

  • Exchange of gases between blood and alveolar air. The venous blood becomes oxygenated and some CO2 is removed.

  • Acts as a blood reservoir.

    The pulmonary circulation is shorter than systemic

    circulation, as the pulmonary circulation time is about 5 sec.

    only.


PULMONARY BLOOD PRESSURE (PBP)   CBF.

  • The blood pressure is 25 mm Hg systolic & 10 mm Hg diastolic in pulmonary arteries, 10 mm Hg in pulmonary capillaries & 6 mm Hg in pulmonary veins.

  • The mean pulmonary blood pressure is 16 of the aortic pressure as the pulmonary peripheral resistance is low because of:

    a) Little amount of smooth muscles in pulmonary arterioles.

    b) Short pulmonary capillaries and veins which are easily distensible


  • CHARACTERISTICS of the   CBF.

    PULMONARY CIRCULATION

    1. The pulmonary vascular The blood pressure is 25 mm Hg systolic & 10 mm Hg diastolic in pulmonary arteries, 10 mm Hg in pulmonary capillaries & 6 mm Hg in pulmonary veins.

  • The mean pulmonary blood pressure is 16 of the aortic pressure as the pulmonary peripheral resistance is low because of:

    a) Little amount of smooth muscles in pulmonary arterioles.

    b) Short pulmonary capillaries and veins which are easily distensible


  • The blood flow in the pulmonary capillaries is rapid 0.75 second at rest.

  • Both the capillary surface area and capillary permeability are great.

  • The regional pulmonary blood flow is controlled by gravity (it is greater in the bases of the lungs) and O2 tension (it is reduced in hypoxic areas).

  • The alveoli are normally kept dry. This prevents pulmonary edema, and is due to rich lymph drainage and –ve pressure in the lung interstitial spaces.

  • It has special reactions to gas changes. Hypoxia, hypercapnia and rise of H’ produce V.C. (and not V.D as they produce in other tissues).

    The large distensibility of the pulmonary vessels renders the pulmonary peripheral resistance to be considerably low (about 1/6 that of the systemic circulation). Accordingly, the pulmonary arterial B.P. is normally low (25/10 mm Hg).


  • FACTORS AFFECTING PULMONARY B.P. second at rest.

  • Respiratory Movements:

  • During Inspiration P.B.P is , because inspiration  expansion of the lung  dilatation of pulmonary vessels   P.B.P.

  • During expiration, P.B.P is , because expiration  recoil of the lungs  compression of pulmonary vessels   P.B.P.

  • Cardiac Output:

  • - The C.O.P. should increase 4 times normal before P.B.P. begins to rise. This is because the pulmonary vessels dilate and  the capacity of pulmonary vessels dilate and  the capacity of pulmonary circulation to accommodate the excess C.O.P.


  • The  in C.O.P. without much  in P.B.P. is useful because it  pulmonary gas exchange without over working the heart.

    3. Capacity of pulmonary circulation:

  • The ability of pulmonary circulation to change its capacity is very important in buffering excessive changes in P.B.P when excess blood is pumped to pulmonary vessels. These vessels dilate and their capacity  without excessive  without excessive  in P.B.P.

    4. Pulmonary peripheral vascular resistance = (PVR):

  • Any increase in pulmonary peripheral resistance  much  in P.B.P. as in left sided heart failure, mitral stenosis and emphysema. If the  in P.B.P. is prolonged, the right ventricles hypertrophies and it may finally fail.


5. because it  pulmonary gas exchange without over working the heart.Nerve Supply:

  • Sympathetic stimulation  constriction of pulmonary vessels   P.B.P.

  • Vagal stimulation  dilatation of pulmonary vessels   P.B.P.

  • Pulmonary Oedema:

  • It is the pathological presence of fluid inside the alveoli of the lungs.

  • This may due to:

  • 1. Increased pressure in pulmonary capillaries e.g. in left-sided heart failure or mitral stenosis  passage of fluid into the alveoli

  • 2. Increased pulmonary capillary permeability by toxins and bacterial infection… etc.  passage of fluid across the capillary wall into the alveoli.


Pulmonary Blood Pressure (P.B.P) because it  pulmonary gas exchange without over working the heart.

  • Factors that  pulmonary arterial BP:

  • Expiration (VC)

  • Sympathetic stimulation (VC)

  • Catecholamine and angiotensin II (VC)

  • Histamine and serotonin (VC)

  • Hypoxia (VC)

  • Lung disease e.g. emphysema

  • Left-sided heart failure.

  • Factors that  pulmonary arterial BP:

  • Inspiration (VD)

  • Parasympathetic stimulation (VD)


  • Pulmonary circulation because it  pulmonary gas exchange without over working the heart.

    VC = Vasoconstriction of pulmonary arterioles   PVR

    VD = Vasodilatation of pulmonary arterioles   PVR

    CEREBRAL CIRCULATION

  • The brain is richly supplied with blood. In a normal adult, the brain weight about 1.5 kg (=2% of body weight) and it receives about 750 ml blood/minute (15% of the cardiac output). The O2 consumption of the brain is about 50 ml/min (=20% of total O2 consumption by the body).


  • The brain is highly sensitive to because it  pulmonary gas exchange without over working the heart.hypoxia or ischaemia because of 3 factors:

  • The high metabolic rate of the brain compared with that of the whole body.

  • All metabolic reactions of the brain are aerobic.

  • The lack of significant energy stores in the brain; glucose is the main metabolic substrate of the brain.

  • The glycogen content of the brain meets its metabolic needs only for 2 minutes.

  • Interruption of blood flow to the brain (severe brain ischaemia) leads to loss of consciousness in about 5 seconds.


  • The CNS Ischaemic response because it  pulmonary gas exchange without over working the heart.:

    Ischaemia of the CNS (brain) produces generalized

    vasoconstriction and elevation of ABP. This response is

    important in cases of severe hypotension ( ABP) at arterial

    pressure below 40 mm Hg.

    Hypotension   blood flow to the brain (ischaemia). In

    the medulla oblongata, ischaemia  local hypoxia,

    hypercapnia ( CO2) and acidosis ( H+) which are strong

    stimulants of the vasoconstrictor centre (VMC)   ABP

    toward normal to improve blood flow to the brain.


  • Cushing’s reflex (reaction) because it  pulmonary gas exchange without over working the heart.:

  • This is a special type of the CNS Ischaemic response

  • where the CNS ischaemia is due to increase of the

  • intracranial pressure above 33 mm Hg. e.g. by a tumour. The

  • high intracranial pressure  compression of the intracranial

  • arteries   blood flow to the brain  ischaemia of the

  • medullary centers  generalized vasoconstriction   of

  • ABP to maintain the blood flow to the brain (despite the

  • increased intracranial pressure).

  • The elevated ABP stimulates the arterial baroreceptors of

  • the aortic arch and carotid sinus  reflex slowing of the

  • heart.

+


  • Cerebral Blood Flow (CBF) because it  pulmonary gas exchange without over working the heart.:

  • Total cerebral blood flow increases in hypoxia (O2 lack),

  • hypercapnia ( CO2) and acidosis ( H+). It decreases

  • during deep quiet sleep.

  • Regional blood flow in the brain varies during different

  • physiological or pathological conditions e.g.

  • Thinking increases blood flow in the prefrontal association area.

  • Voluntary clinching of the right hand, increases blood flow in the right hand, increases the blood flow in the hand area of the left motor cortex.

  • During an epileptic attack, the blood flow increases in the epileptic focus but  in other parts of the brain.


  • Autoregulation of the Cerebral Blood Flow (CBF) because it  pulmonary gas exchange without over working the heart.

  • A sudden  in the ABP  transient increase in the

  • cerebral BF. If the rise (mean pressure 70-140 mm Hg) in

  • pressure is maintained, auto-regulation mechanisms operate

  • to restore the cerebral BF to its normal level within 1-2

  • minutes.

  • A  in the ABP  opposite mechanisms which cause

  • vasodilatation to maintain a constant blood flow rate.

  • Control of the Cerebral Blood Flow (CBF):


  • Control of the Cerebral Blood Flow (CBF) because it  pulmonary gas exchange without over working the heart.:

  • Nervous Control: Sympathetic stimulation  weak vasoconstriction of the cerebral blood vessels but it  the CBF because it simultaneously  the ABP.

  • Chemical or metabolic control: Blood flow to the brain is regulated mainly by its own metabolism. Hypoxia, hypercapnia and acidosis  VD   cerebral BF.

  • These chemical factors produce regional variation in CBF.

  • The blood flow  in active areas due to VD produced by 

  • PCO2,  PO2 &  H+(mainly  PCO2) and vice versa (VV).

  • The effect of CO2 on the cerebral vessels is indirect

  • through formation of H2CO3   H+ions which dilate the

  • cerebral vessels.


  • Physical Factors that control the cerebral blood flow (CBF) because it  pulmonary gas exchange without over working the heart.

  • Effective perfusion pressure i.e. difference between the arterial and venous pressures at the brain level. The CBF varies directly with this pressure.

  • Blood Viscosity: CBF varies inversely with the blood viscosity.

  • Intracranial pressure: This is normally about 10 mm Hg. The CBF varies inversely with the intracranial pressure.


Part II because it  pulmonary gas exchange without over working the heart.

CARDIOVASCULAR PHYSIOLOGY

LECTURE X:HAEMORRHAGE, SHOCK &

HEART FAILURE

  • Outline:

  • - Haemorrhage:

  • : Effects of haemorrhage.

  • : Compensatory reactions (immediate and delayed).

  • - Shock (types and causes)

  • - Heart Failure:

  • : Left-sided heart failure (causes & manifestations)

  • : Right-sided heart failure (causes & manifestations)

  • Further Reading:

  • Guyton: Textbook of Medical Physiology

  • Ganong: Review of Medical Physiology


HAEMORRHAGE because it  pulmonary gas exchange without over working the heart.

  • Haemorrage means loss of blood (bleeding) from the

  • cardiovascular system.

  • It may be:

  • External haemorrhage: in which the blood is shed outside the body or

  • Internal haemorrhage: in which the blood passes from vascular system to tissue spaces or to the body cavities (e.g. chest and abdomen)

    Also, haemorrhage may be:

  • Small repeated haemorrhage (as in piles) or

  • Big sudden haemorrhage.


EFFECTS OF HAEMORRHAGE because it  pulmonary gas exchange without over working the heart.

  • These depend upon two factors:

  • 1. Volume of blood lost.

  • 2. The rate at which this loss occurs.

  • So, loss of small amounts of blood every day over many months, does not disturb the circulation though it may produce anaemia. The body can compensate for it.

  • But when more than 30% of the blood volume is lost, the body can not compensate for it and unless blood transfusion is done death results.

  • If the lost blood volume exceeds 30%: the replacement of the lost blood volume by I.V. administration of fluid becomes life saving: fluids which can be given are: blood, saline, plasma or plasma substitutes.


EFFECTS OF HAEMORRHAGE because it  pulmonary gas exchange without over working the heart.

  • The following effects are produced by haemorrhage:

  • Hypotension: because the loss of blood   blood volume   C.O.P.   A.B.P.

  • Rapid and weak pulse: and in severe haemorrhage, the pulse is hardly felt.

  •  Respiration in rate and depth.

  • Pale and cold skin: the skin is pale due constriction of skin capillaries and it is cold due to constriction of skin arterioles   blood volume passing through the skin.

  •  Urine Formation: due to  renal blood flow and  secretion of antidiuretic hormone.

  • Fainting (=loss of consciousness) and death may occur in severe haemorrhage due to brain ischaemia.


EFFECTS OF HAEMORRHAGE because it  pulmonary gas exchange without over working the heart.

  • Hypotension ( ABP)  inadequate perfusion

  • Cerebral hypoxia (ischaemia)  depression of brain (cortex and centers)  coma.

    BODY REACTION TO HAEMORRHAGE

    Compensatory reactions in acute haemorrhage

    Immediate compensatory reactions

  • Immediate reactionsaim at rapid elevation of the arterial B.P.

    1. Reactions that correct the hypovolaemia: (a) Capillary fluid shift from the tissue spaces to the bloodstream (b) Mobilization of the labile tissue protein into the bloodstream (c) Splenic contraction (which adds the stored blood in the spleen to the circulating blood).


2. because it  pulmonary gas exchange without over working the heart.Reactions that increase the cardiac output (CO) and peripheral resistance (PR): These are produced due to stimulation of the VCC by (a) signals from the ischaemic peripheral chemoreceptors (b) its release from the inhibitory effect of the arterial and atrial baroreceptors (c) the CNS ischaemic response. The VCC leads to generalized sympathetic stimulation and secretion of catecholamine, and both produce the following effects:

a) Tachycardia and increase of the stroke volume (both increase the CO)

b) Generalized V.C. (which increases the PR)

c) Generalized venoconstriction (which increases the VR, CVP and CO)

Respiration is also accelerated (which helps increasing the VR and consequently the CO) and ACTH is secreted (this hormone stimulates release of glucocorticoids which increase the vascular reactivity to catecholamine)


Delayed compensatory reactions because it  pulmonary gas exchange without over working the heart.

  • Delayed reactionsaim at keeping the arterial B.P. close to its normal level

    1. Reactions that maintain a high PR: These include mainly (a) Secretion of ADH (= vasopressin, which causes V.C) (b) Formation of angiotensin II (which is also V.C) as a result of rennin secretion by the ischaemic kidneys.

    2. Reactions that maintain a normal blood volume: These include:

    a- Restoration of the plasma volume by (a) ADH (helps water retension in the body) (b) Secretion of aldosterone (by effect of angiotensin II) which increases Na+ and water retension in the body (c) Drinking water (as a result of the increased thirst sensation) (d) Inhibition of secretion of the atrial natriuretic peptide (ANP).


b- because it  pulmonary gas exchange without over working the heart.Restoration of the plasma proteins (by increased synthesis from the tissue reserve proteins as well as the diet proteins)

c- Restoration of the red blood cells (by increased formation in the bone marrow under effect of the erythropoietin hormone, which is released by the kidneys as a result of O2 lack).


Summary because it  pulmonary gas exchange without over working the heart.

BODY REACTION TO HAEMORRHAGE

Immediate CompensatoryDelayed Compensatory

ReactionsReactions

  •  heart rate   COP  Secretion of ADH &

  • Vasoconstriction of aldosterone  retention

    arterioles (PR)of water   plasma

    volume.

  • Venoconstriction   VR  Mobilization of labile

  • Contraction of spleen. and reserve proteins

  •  secretion of adrenaline & from the tissues to the

    Noradrenaline   plasma proteins.


  • Activation of because it  pulmonary gas exchange without over working the heart.  formation of renin-agiotensin sys erythropoietin  

  •  secretion of vaso-pressin production of RBCs

    (ADH).

  • Capillary fluid shift

  •  urine formation.

    These reactions restore blood pressure and blood volume in

    mild or moderate haemorrhage.


SHOCK because it  pulmonary gas exchange without over working the heart.

  • - Shock is a clinical syndrome characterized by inadequate

  • tissue perfusion due to decreased cardiac output and

  • decreased ABP (hypotension).

  • It is generally classified into 4 types:

  • 1. Hypovolaemic shock

  • 2. Low-resistance shock

  • 3. Cardiogenic shock

  • 4. Obstructive shock


  • HYPOVOLAEMIC SHOCK because it  pulmonary gas exchange without over working the heart.CARDIOGENIC SHOCK

  • -It occurs a result of - It occurs as a result of

  • excessive loss of blood decreased pumping

  • or plasma, e.g. action of the left ventricle

  • Haemorrhagic shock e.g. due to:

  • Traumatic shock  Myocardial infarction.

  • Surgical shock  Severe ventricular

  • Burn shock tachycardia

    - It is also called cold shock.


  • LOW-RESISTANCE SHOCK because it  pulmonary gas exchange without over working the heart.OBSTRUCTIVE SHOCK

  • It occurs as a result of - This occurs as a result

  • massive vasodilatation of obstruction of blood

  •   circulatory capacity flow in the lungs or

  • and  venous return Heart e.g. due to a large

  •   COP   ABP e.g. pneumotorax. Cardiac

  • neurogenic shock, tamponade or massive

  • septic shock anaphylactic pulmonary embolism.

  • shock (histamine shock).

  • - It is also called warm shock.


HEART FAILURE because it  pulmonary gas exchange without over working the heart.

Heart failure (HF) means decreased ability of the

heart to perform its proper pumping action (due to

decreased force of contraction of the ventricles).

HF may be left-sided HF or right sided HF or both

(congestive HF).


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