CVS Physiology PDF

Cardiac Physiology Dr. M. Abdelmohsen Assistant Professor of Physiology MBBCh, MSc, DMSc, DHPE Faculty of Pharmacy 2021-2022  Objectives ❖ At the end of this lecture, the 2nd year st...

Cardiac Physiology Dr. M. Abdelmohsen Assistant Professor of Physiology MBBCh, MSc, DMSc, DHPE Faculty of Pharmacy 2021-2022  Objectives ❖ At the end of this lecture, the 2nd year student should be able to: Explain properties of cardiac muscle. Discuss cardiac output. Explain heart sounds. Structure of the heart The Heart is a muscular pump that drives the blood through the blood vessels. It is slightly bigger than a fist of your hand. structure of the heart The heart composed of 4 chambers. Two chambers on either side of the heart, one a receiving chamber (atrium) and the other a pumping chamber (ventricle) as follows: 1. Right atrium is a thin-walled chamber that receives the deoxygenated blood retuning from the body tissues via vena cava. 2.Right ventricle pumps the venous blood received from the right atrium to the lungs. 3. Left atrium receives oxygenated blood from the lungs. 4. Left ventricle, which has the thickest walls. It receives oxygenated blood from left atrium and pump it to all parts of the body through the arteries.  structure of the heart Heart walls are composed of three layers: 1. Outer epicardium 2. Myocardium 3. Inner endocardium The Heart myocardium consists of thick bundles of the cardiac muscle twisted into ringlike arrangements. This is the layer of the heart that contracts. Cardiac muscle Cardiac myocytes are short branched striated muscle cells connected with gap junctions. Gap junctions transmit electrical activity between cells so, cardiac myocytes act as a single functional unit (syncytium). Valves of the heart: 1-Mitral valve: lies between the left atrium Valves of the heart and left ventricle. Atrioventricular valves (A- V): Separate atria from the ventricles. 2-Tricuspid valve: lies between the right atrium and right ventricle. 1- Aortic valve: between left ventricle and aorta. Semilunar valves: Separate ventricles from the large arteries. 2-Pulmonary valve: between right ventricle and pulmonary artery. Cardiac Properties Cardiac properties Rhythmicity (Automaticity): the ability of the (SAN) to produce auto rhythm which can be conducted. Excitability: Ability of cardiac cells to initiate action potential, in response to inward depolarizing current. Conductivity: is the ability to propagate an impulse i.e from SA node to all cardiac muscle fibers Contractility: Intrinsic ability of cardiac muscle to develop force for contraction. Cardiac muscle contracts in response to the electrical impulse generated by the SA node. Auto-rhythmicity: The ability of the specialized muscle fibers in the heart mainly the sinoatrial node (SAN) to produce auto rhythm which can be conducted. Mechanism of pacemaker potential: No voltage gated Na+ channels activity in the normal pacemaker cells due to less negativity. The rapid depolarization phase of the AP in cardiac pacemaker cells is due to opening of rapid Ca2+ channels (L channels). Repolarization after the AP is due to opening of K+ channels. Spontaneous depolarization is produced by a progressive fall in the K+ permeability. Conductivity: As Syncytium: the whole atria and the whole ventricles each work as one syncytium because of the presence of gap junctions between cells (fibers). The Conduction System of the Heart: a) The sinoatrial node (SAN): located in the upper wall of the right atrium an initiate the heartbeat, so it is called the pacemaker of the heart. b) Atrioventricular node (AVN): located in the interatrial septum at the bottom of the right atrium. The relatively slow conduction through AV node allows time for the atria to contract and complete the filling of the ventricles. c) Atrioventricular bundle (bundle of His): located at the top of the interventricular septum then divides into right and left bundle branches. d) Purkinje fibers: are many branches of fibers (network) that extend from right and left bundle branches to all parts of the ventricular walls. The excitation wave travels rapidly through the bundle of His and then throughout the ventricular walls by means of the bundle branches and Purkinje fibers. Excitability: The cardiac muscle is an excitable tissue that produce an action potential when excited both ordinary muscle action potential and specialized muscle action potential. Ordinary cardiac muscle action potential (AP): its phases are: 1- Depolarization (phase 0) caused by Na+ influx. (2 m sec duration). 2- Repolarization: (Triphasic): Phase (1): It is a short rapid phase caused by K+ outflux. Phase (2): Plateau caused by Ca++ influx through L-type Ca++ channels. (200-300 m sec duration). Phase (3): It is a rapid repolarization caused by rapid outflow of K+ & closure of Ca++ channels. 3- RMP: return to resting potential. Contractility: The heart can adjust contraction strength to the amount of blood received. Frank-Starling law: It stated that "within limits the more the left ventricle filled with blood the more the wall stretched the stronger the contraction and the opposite". This occurs during exercise where the muscle contracts with greater strength so push the larger volume of blood out into the blood vessels to nourish the working muscles.  Cardiac Output (COP) Cardiac output (COP): It is the volume of blood pumped by each ventricles / minute. It is about 5 liter/minute. COP = SV× HR = 70X70= 4900ml/minute about 5litre/minute. Stroke volume (SV): Is the measurement of the volume of blood being forced from the left ventricle in one cardiac contraction. End diastolic volume (EDV): the volume of blood present within the left ventricle just prior to contraction (115 ml) End systolic volume (ESV): the volume of blood remain after the full contraction is complete (45 ml). Therefore, SV = EDV – ESV =115-45= 70 ml.  Factors determining the COP: 1-The pumping The heart has the ability to increase the COP from ability of the 5 liter/minute to 25 liter /minute during exercise by the effect of sympathetic stimulation. heart: 2-The venous The more the VR the more COP. return (VR):  Increase Excitement & anxiety (50-100%) Eating (30%). Exercise (up to 70%) High Environmental temperature. Factors affecting Epinephrine & Pregnancy. the COP Decrease Sitting or standing from lying position (20-30%) Rapid arrhythmia & heart diseases  Heart sounds 1st heart sound 2nd heart sound Cause 1- Contraction of mitral and 1-Contraction of tricuspid valves. semilunar valve. 2-Contraction of the ventricular muscle. Duration 0.14 seconds 0.11 seconds Pitch Low pitch due to low High pitched due to high frequency frequency Best area -Mitral area: 5th intercostal -Aortic area: 2nd right of space mid clavicular line. intercostal space. auscultati -Tricuspid area: at lower part -Pulmonary area: 2nd on of the sternum. left intercostal space Heart rate Heart rate is the number of contractions (beats) of the heart per minute (bpm). The normal resting adult human heart rate is 60–100 bpm. Tachycardia is a high heart rate, defined as above 100 bpm at rest. Bradycardia is a low heart rate, defined as below 60 bpm at rest. When the heart is not beating in a regular pattern, this is referred to as an arrhythmia.  1)The Autonomic Nervous System Parasympathetic: leads to a decrease in heart rate. Sympathetic: increases the heart rate as well as the force of contraction. 2)Hormonal Control: Hormones also can affect the heart rate. For example: Adrenaline and noradrenaline results in an increase in heart rate. Factor Thyroid hormones increase the heart rate 3) Age: infants have a faster heart rate. affecting 4) Gender: Adult females have a slightly higher heart rate than adult males. heart rate 5) Anger, stress, and painful stimuli: increase heart rate. 6) Caffeine and nicotine: both causing an increased heart rate 7) Fever, increase in body temperature: increase heart rate. 8) Hypoxia (decreased O2 level): increasing heart rate. 9) Exercise: increase heart rate. 10)Hypothermia: slows down the heart rate, by reducing metabolism.  Heart Failure Definition: Failure of the heart to pump enough blood to satisfy the needs of the body. Types: 1) Acute failure and sudden death. 2) Chronic congestive heart failure. Causes (Pathogenesis): 1) Coronary artery disease (also called coronary atherosclerosis or “hardening of the arteries”) affects the arteries that carry blood and oxygen to the heart (coronary arteries). 2) Heart attack. A heart attack happens when a coronary artery suddenly becomes blocked, and blood cannot flow to all areas of the heart muscle. The heart muscle becomes permanently damaged, and muscle cells may die. 3) Cardiomyopathy. 4) Heart defects present at birth (congenital heart disease). 5) High blood pressure (hypertension).  1) Chest pain (angina) 2) Rapid or irregular heartbeat Symptoms 3) Fainting and dizziness due to inadequate blood and oxygen supply delivery to organs of heart 4) Fatigue due to inadequate blood and oxygen supply delivery to organs and muscles failure: 5) Shortness of breath resulting from fluid build-up in the lungs 6) Swollen feet, ankles and legs resulting from fluid build-up in the veins and body tissues 7) Sudden death  Vascular Physiology Dr. M. Abdelmohsen Assistant Professor of Physiology MBBCh, MSc, DMSc, DHPE Faculty of Pharmacy 2021-2022  Objectives ❖ At the end of this lecture, the 2nd year student should be able to: Explain blood flow regulation. Discuss blood pressure regulation. Explain hypertension. Discuss odema. Functional organization of the vascular system: 1. Aorta & arteries Little resistance to blood flow (Windkessel or More distensible than the peripheral arteries. elastic vessels): During systole distend to prevent marked elevation of Importance of blood pressure during blood ejection. windkessel effect During diastole recoil to render blood spread to the periphery. Functional organization of the vascular system: 2. Arterioles (high resistance vessels): Thick smooth muscular walls (myogenic tone) + it’s narrow diameter---- highest resistance in the vascular system. Function: As it is responsible for peripheral resistance so, it plays a major role in arterial blood pressure (ABP) regulation: By Contraction ----↑ABP Relaxation ----↓ABP Functional organization of the vascular system: 3. Capillaries Very delicate structure. Formed of single layer of endothelial cells with pores in between them. The smallest diameter of the body vessels. Total surface area is about 6,300 m2. Function: Exchange of gases, hormones, electrolytes, fluid and nutrient between blood and interstitial fluids. Functional organization of the vascular system: 4- Venules: Allow deoxygenated blood to return from the capillary beds to large veins. 5- Veins Carry deoxygenated blood to heart. Thin wall (reservoir- capacity- volume vessels) Carry 70% of blood More compliant vessels than arteries  Functional organization of the vascular system:  Blood flow Factors affecting blood flow: Definition: Quantity of blood that passes through the vessel per unit time (ml/sec).  Types of blood flow: 1) Laminar blood flow 2) Turbulent blood flow: blood (streamline flow): flowing in all directions in the When blood flows in layers each vessel. layer of blood remaining the same distance from the vessel wall. Also, the central most portion of the blood stays in the center of the vessel. Blood flow regulation 1. Extrinsic Regulation of Blood Flow: a) Sympathy-adrenal activation: causes increased cardiac output & resistance in periphery & viscera. Blood flow to skeletal muscles is increased as their arterioles dilate in response to acetyl choline released by sympathetic fibers. Thus, blood is shunted away from visceral & skin to muscles. b) Parasympathetic effects: parasympathetic only innervates digestive tract, genitalia, & salivary glands causing their arteriolar vasodilatation. c) Angiotensin II & ADH (vasopressin): cause general vasoconstriction of vascular smooth muscle which increases resistance & BP. 2. Paracrine Regulation of Blood Flow: Endothelium produces several paracrine regulators that promote relaxation or contraction: a) Vasodilators: Endothelium derived relaxing factor (EDRF): Nitric oxide (NO), bradykinin, prostacyclin. NO is involved in the resting “tone” of vessels and its levels are increased by parasympathetic activity. Vasodilator drugs such as nitroglycerin or Viagra act through NO release. b) Vasoconstrictors: Endothelin 1 is vasoconstrictor produced by endothelium specially during vascular injury. Blood flow regulation 3) Intrinsic Regulation of Blood Flow: (Autoregulation) Importance: Maintains constant blood flow despite Blood Pressure variation specially for cerebral circulation. a) Myogenic control mechanisms: occur in some tissues because vascular smooth muscle contracts when stretched & relaxes when not stretched e.g., decreased arterial pressure causes cerebral vessels to dilate & vice versa. b) Metabolites: Low O2 or pH or high CO2, adenosine, or K+ from high metabolism cause vasodilation which increases blood flow (active hyperemia). c) Ions: Cations: ↑ Ca++ concentration → vasoconstriction. ↑ K+ concentration → vasodilation. ↑ Mg++ concentration → vasodilation. ↑ H+ (PH) → vasodilation. Anions: acetate and citrate cause mild degrees of vasodilatation. Arterial blood pressure (ABP) - ABP: The force exerted by blood against the vessel wall that depends on volume of blood forced into the vessel and compliance of the vessel wall. -Systolic blood pressure: Maximum pressure reached in the systemic arteries during systole due to ejection of blood into the systemic arteries. It's range 90-140mmHg average 120mmHg. -Diastolic blood pressure: Minimum pressure reached in the systemic arteries during the diastole due to elastic recoil of the vessels. It's range 60-90 mmHg average 80mmHg. -Pulse pressure: Systolic blood pressure – diastolic blood pressure  1. Sex: male is more than female due to hormonal difference (testosterone). 2. Age: old, aged persons have more blood pressure due to atherosclerosis. 3. Emotions: they increase ABP due to increased secretion of adrenaline & noradrenaline. Physiological 4. Exercise: increases SBP due to increased venous return and cardiac output but decrease the DBP due to vasodilatation and so decreased peripheral resistance. factors 5. Hormones: Adrenaline, noradrenaline, and thyroxin increase ABP. affecting ABP 6. Gravity: ABP in lower limbs is more than upper limbs. 7. Race: Orientals have mor ABP than westerns due to dietary factors or weather. 8. Sleep: decreases ABP due to decreased venous return. 9. Pregnancy: It increases ABP due to increased metabolism. Hypertension (HTN) Definition: Blood pressure more than normal range for age and gender (more than 140/90 mm Hg). Primary or essential hypertension: unknown cause but may be genetic inherited disease. Majority of the population have this type of hypertension. Increase in total peripheral resistance (TPR) is a universal characteristic. Also, CO and HR are elevated in many patients. But secretion of renin, angiotensin II, and aldosterone is variable. Sustained high stress (via sympathetic nervous system) and high Na+ intake act synergistically in development of this type of hypertension. Thickening of arterial wall is a famous adaptive response, resulting in atherosclerosis. Kidneys may not be able to properly excrete Na+ and water that is shared characteristic of all cases. Secondary hypertension: It is a result of a known disease process either renal artery stenosis and kidney disease or atherosclerosis which both are considered as cause and result of hypertension.  Complication of Hypertension Damage to the heart and coronary arteries, including heart attack, congestive heart failure, aortic dissection, and atherosclerosis. Stroke. Kidney damage. Vision loss. Memory loss. Fluid in the lungs. Angina. Treatment of Hypertension: a) Modification of lifestyle: 1. Cessation of smoking. 2. Moderation in alcohol intake. 3. Weight reduction. 4. Programmed exercise. 5. Reduction in Na+ intake. 6. Diet high in K+. b) Medications: 1. Diuretics: which increase urine volume. 2. Beta-blockers: decrease HR. 3. Calcium antagonists: block Ca2+ channels. 4. ACE inhibitors: inhibit conversion to angiotensin II. 5. Angiotensin II-receptor antagonists: block receptors.  Edema Definition: Causes and mechanisms of edema: swelling of the tissues due to Increase of capillary blood pressure abnormal accumulation of excess (increase of filtration force) tissue fluid in the interstitial Decrease of the colloidal osmotic spaces. pressure of the plasma proteins (decrease of reabsorption force) Increase of capillary permeability (increase of filtration) Obstruction of lymph vessels (decrease of lymph drainage) due to e.g., elephantiasis caused by filarial worms. Salt and water retention (increase of plasma volume)  Edema Types of oedemas: b) According to its location or a) According to its nature: distribution: 2. Generalized 1. Soft “pitting” 2. Hard “non- 1. Local edema edema e.g., edema e.g., pitting” edema e.g., cardiac, cardiac edema, e.g., in inflammatory nutritional, renal, nutritional hypothyroidism edema. or hepatic edema… etc. (myxedema). edemas.  Thank You Faculty of Pharmacy 2021-2022