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.
b) 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

1) It is very short and very rapid (so it is essential to the

heart).

2) The blood flow in this circulation occurs mainly during

cardiac diastole vessels.

3) There is no efficient anastomoses between the coronary 4) It is a rich circulation (5% of the CO while the heart

weight is 300gm).

5) Its regulation is mainly by metabolites and not neural 6) The capillary permeability is high (the cardiac lymph is

rich in protein)

7) The coronary vessels are susceptible to degeneration and

atherosclerosis.

8) 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.

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

(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: 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.

1) Nervous Factors: -

2) Chemical Factors:

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.

3) Mechanical factors (=effect of cardiac cycle):

- Ventricular systole of the intra-myocardial pressure compression of the coronary vessels mainly in the left coronary artery (due to stronger of the left vent.)

CBF cont

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

4) 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) 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

- 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) 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
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 rest or coronary VD drugs.
It is frequently complicated by ventricular fibrillation

by

death.

Part II

CARDIOVASCULAR PHYSIOLOGY LECTURE IX PULMONARY 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 cushingd 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
Pulmonary Circulation is the circulation between right ventricle and left atrium. It has the following
1. 2.

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.

3.

The pulmonary circulation is shorter than systemic circulation, as the pulmonary circulation time is about 5 sec. sec only.

PULMONARY BLOOD PRESSURE (PBP)

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 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

6. 7. 8.

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. 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).

9.

10. It has special reactions to gas changes. Hypoxia,

FACTORS AFFECTING PULMONARY B.P.

1. Respiratory Movements: 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.

2. Cardiac Output: 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: 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): (PVR)

-

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

5. Nerve Supply: 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)

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
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).

1. 2. 3.

The brain is highly sensitive to 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. 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:

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. 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.

Cushings reflex (reaction):

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):

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)

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):

1.

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.

2.

3. -

Physical Factors that control the cerebral blood flow (CBF) 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

CARDIOVASCULAR PHYSIOLOGY
LECTURE X:
Outline:

HAEMORRHAGE, SHOCK & HEART FAILURE

- 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
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
-

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
1. 2. 1. 1.

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.

1. 1.

EFFECTS OF HAEMORRHAGE

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

(A) Immediate reactions
aim 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. 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

(B) Delayed reactions
aim 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- 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

BODY REACTION TO HAEMORRHAGE

Immediate Compensatory Reactions

Delayed Compensatory Reactions Secretion of ADH & aldosterone retention of water plasma volume. Mobilization of labile and reserve proteins from the tissues to the plasma proteins.

heart rate COP Vasoconstriction of arterioles (PR)

Venoconstriction VR Contraction of spleen. secretion of adrenaline & Noradrenaline

Activation of renin-agiotensin sys secretion of vaso-pressin (ADH). Capillary fluid shift urine formation.

formation of erythropoietin production of RBCs

These reactions restore blood pressure and blood volume in mild or moderate haemorrhage.

SHOCK
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

CARDIOGENIC SHOCK It occurs as a result of decreased pumping action of the left ventricle e.g. due to: Myocardial infarction. Severe ventricular tachycardia

It occurs a result of excessive loss of blood or plasma, e.g. Haemorrhagic shock Traumatic shock Surgical shock Burn shock It is also called cold shock.

LOW-RESISTANCE SHOCK
-

OBSTRUCTIVE SHOCK This occurs as a result of obstruction of blood flow in the lungs or Heart e.g. due to a large pneumotorax. Cardiac tamponade or massive pulmonary embolism.

It occurs as a result of massive vasodilatation circulatory capacity and venous return COP ABP e.g. neurogenic shock, septic shock anaphylactic shock (histamine shock).

It is also called warm shock.

HEART FAILURE
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).

Left-sided heart failure

:Causes Systemic hypertension (.chronic or untreated ) Coronary heart disease myocardial infarction in the .LV Aortic stenosis or incompetence (valvular (.disease

Right-sided heart failure

:Causes Pulmonary hypertension Mitral stenosis pulmonary .hypertension Left sided heart failure

Left sided heart failure

Forward failure i.e. failure to maintain an adequate cardiac output from the left .ventricle Backward failure i.e. failure of the left ventricle to pump the blood it receives from the .pulmonary veins

Right sided heart failure

Forward failure i.e. failure to maintain an adequate cardiac .output from the right ventricle Backward failure i.e. failure of the right ventricle to pump the venous blood it receives from .the systemic veins

Forward failure
Easy fatigability and .weakness Skin pallor and cold .extremities Pulmonary congestion dyspnea, orthopnea and .pulmonary edema Pulmonary hypertension and .right-sided HF

Forward failure
Same manifestations as those produced by left-sided HF

Backward failure

Backward failure
Systemic venous congestion edema in dependent parts of the body + congested neck veins + enlargement of the limbs + transudation of fluid in .the pleural sac