Cardiovascular System PDF

 The heart is a myogenic organ; it does not need nerve stimulation to initiate its contraction. The heartbeat originates in the Sino-atrial node (SA node). It contains specialized cells, which discharge spontaneously and rapidly at a frequency of 60-100 per minute (automaticity or rhythmi...

 The heart is a myogenic organ; it does not need nerve stimulation to initiate its contraction. The heartbeat originates in the Sino-atrial node (SA node). It contains specialized cells, which discharge spontaneously and rapidly at a frequency of 60-100 per minute (automaticity or rhythmicity). Therefore, it is the normal cardiac pacemaker. Its rate of discharge determines the heart rate (HR).  Cardiac cycle Definition: Heart systole & diastole Duration: 60/ 75 = 0.8 second i- Atrial systole ( 0.1 sec) ii- Ventricular systole ( 0.3 sec) iii- Diastole of the whole heart ( 0.5 sec)  CARDIAC MUSCLE PROPERTIES Automaticity: Ability to spontaneously generate an electrical impulse. Excitability: Ability to respond to an electrical impulse. Conductivity: Transmission of electrical impulse to another cardiac cell. Contractility: Ability to contract after electrical impulse response 1- CARDIAC AUTOMATICITY (RHYTHMICITY) The ability of cardiac muscle to beat at regular intervals by the pace maker cardiac cells to spontaneously depolarize and generate an action potential. Simultaneous activation of the whole cardiac muscle cells is achieved primarily by the conduction of action potentials from one cell to the next via the gap junctions All cells of the heart into a functional syncytium (i.e., acting as one synchronous unit). Sino atrial node (SAN ) is the pace maker of the heart( highest rhythm, first to depolarize, all the heart follows its rhythm ) Different cardiac rhythms SAN 100/min. AVN 60/min. Atria 45/min Ventricles 25-40/min ( idioventricular rhythm )  2- CONDUCTIVITY It is the ability of cardiac muscle to transmit the cardiac impulses that originated in SAN to all parts of the heart. Cardiac cells are electrically coupled via gap junctions, excitation of one cell results in the spread of action potential throughout the heart.  The Specialized Excitatory and Conductive System of the Heart Sinoatrial (SA node) Internodal pathway Atrioventricular (AV node) Atrioventricular bundle (Bundle of His) Purkinje fibers  Control of Heart Rhythmicity and Conduction  The heart is supplied with both sympathetic and parasympathetic nerves  Parasympathetic nerves (vagi): mainly to the S-A and A-V nodes  Sympathetic nerves: all parts of the heart with strong supply to the ventricles  Sympathetic stimulation of the heart   rate of rhythm of the S-A node   transmission of impulses to the A-V node   force of contraction  Parasympathetic stimulation of the heart  rate of rhythm of the S-A node  transmission of impulses to the A-V node Strong stimulation of the vagi: Stop completely the rhythmical excitation by the S-A node Block completely transmission of cardiac impulses from the atria to the ventricle Some point in the Purkinje fibers develops a rhythm of its own “Ventricular Escape”  Heart rate regulation ▪ Normal heart rate 60-90 beat per minute ▪ Tachycardia…. Increase in HR ▪ Bradycardia…..Decrease HR  A. Nervous regulation 1. Afferent impulses from CVS a. Baroreceptors : - strech receptors in carotid sinus and aortic arch. - stimulated by ABP changes 60-180 mmHg b. Peripheral chemoreceptors : - In aortic and carotid bodies - Respond to hypoxia, increased arterial CO2 and H+ concentrations. - They stimulate VMC leading to Tachycardia ,systemic VC and hyperventillation C. Atrial strech receptors : ( Bainbridge reflex ) Significance : it prevents stasis of blood in the venous side. 2. Impulses from higher centers : a. Cerebral cortex : visual, auditory stimuli ( conditioned R) b. Hypothalamus Post. Hypoth. Control sympath. NS Ant. Hypoth. Control parasympath.  B.Chemical regulation : a. Blood gas changes : Can affect CVC’s in two ways i. direct effect of hypoxia ,high Co2 ,high H+ in arterial blood on CVC’S ------ tachycardia ii. indirect effect via peripheral chemoreceptors b. Hormones : i. Adrenaline and noradrenaline -------> + beta adrenergic receptors ----→ tachycardia ii. Thyroid hormone : produces tachycardia by: - Direct SAN stimulation - Increased MR ( body temp. )  C. Physical regulation: Increased body temp. by 1c ----------> Increase HR 10-15 beats/min.via: - Effect on SAN directly - Hypothalamus + - CVC’s +  Cardiac out put It is the volume of blood pumped by each ventricle per unit time at rest, normally it equals 5-6L/min. Normally cardiac out put (COP ) = stroke volume X heart rate Stroke volume ,it is the volume of blood pumped by each ventricle per beat ,its resting value is 70 ml/beat  Factors affecting COP A. Venous return : That is the volume of venous blood returning to the right atrium via venae cavae/ min ,normally it equals 5-6 L/ minute at rest Factors affecting venous return 1. Rate of tissue metabolism 2. Thoracic pump 3. Muscle pump 4. Arteriolar diameter 5. Capillary tone 6. Gravity 7. Venous pressure gradient B. Heart rate : As we mentioned COP = HR X Stroke volume so, (a) With constant stroke volume Increased HR within limits ( not to exceed 200 beats/minute ) results in increased COP. (b) with variable venous return As the case during muscle exercise the more the VR the more will be the SV and COP  (c) Effects of severe HR changes on COP i- marked increase in HR more than 200 beats /minute as in paroxysmal ventricular tachycardia will shorten the cardiac cycle with short diastolic period leading to decreased diastolic filling resulting in decreased SV with decreased COP ii- marked decrease in HR as in complete heart block will prolong the cycle with longer diastole and more ventricular filling with overstrech of the ventricular muscle leading to low ventricular pumping power with decreased COP. C. Arterial blood pressure Increased ABP leads to transient decrease in COP. D. Condition of the myocardium The healthy heart can pump up to 30L/min, while the unhealthy one can’t pump even the normal COP  CORONARY CIRCULATION Normal value: During rest: it is about 225 ml/min. During severe muscular exercise: it is about 1000 ml/min. The maximal coronary blood flow occurs during diastole of the heart.  Factors controlling coronary blood flow: 1- O2 need: Hypoxia is the most powerful coronary vasodilator. 2-Metabolic factors: metabolic waste products(CO2, hydrogen ions, potassium ions and lactic acids dilate coronary vessels. 3- Cardiac output (COP): coronary blood flow is directly proportional to COP. 4- Arterial blood pressure (ABP): coronary blood flow is directly proportional to the diastolic BP 5- Nervous control: sympathetic dilatates coronaries,while parasympathetic constricts them. Ischemic heart disease  Atherosclerosis as a cause of ischemic heart disease: The most frequent cause of diminished coronary blood flow is atherosclerosis. A common site for development of atheromatous plaques is the first few centimeters of major coronary arteries.  Acute coronary occlusion : Acute occlusion can result from any one of several effects, two of which are the following 1. The atherosclerotic plaque can cause a local blood clot called a thrombus. 2. It is also believed that local muscular spasm of the coronary artery.  When a sudden occlusion occurs in one of the large coronary arteries , the small anastomoses ( collaterals ) begin to dilate within seconds. But later on there will be more enlargement of the collaterals , to reach almost normal coronary blood flow within about one month. By this way ,if the infarct is not massive, the patient may recover completely.  Myocardial infarction : Immediately after an acute coronary occlusion , the blood flow ceases in the coronary vessels beyond the occlusion. The area of muscle that has either zero flow or so little flow that is cannot sustain cardiac muscle function is said to be infracted.The overall process is called myocardial infarction.  Angina pectoris In most people who develop progressive coronary arterial vasoconstriction ,cardiac pain called angina pectoris begin to appear. Usually pain is felt beneath the upper sternum over the heart ,it is often referred to the left arm and left shoulder but also frequently to the neck and even the side of the face. THANK YOU  CIRCULATORY HEMODYNAMICS Types of circulatory system  Systemic circulation Systemic circulation is made up of numerous different circuits arranged in parallel. Such arrangement permits wide variations in regional blood flow without changing total systemic flow  Hemodynamics of the circulation I- Pressure, Flow and Resistance Determinants of flow: Change in the pressure difference (perfusion pressure) across its vascular BLOOD FLOW bed THROUGH ANY ORGAN Change in the vascular resistance  I-Change in the pressure difference Blood always flow from areas of high pressure to areas of low pressure  II- Resistance (R): It is the resistance encountered by the blood cells and plasma when they contact the vessel walls Resistance results from : 1- Frictional forces between the blood & the wall of the vessel 2- Frictional forces between the blood molecules Resistance depends on: 1- Physical properties of the vessel (length, radius) 2- Physical properties the blood (viscosity) Vessel length (L) Viscosity of blood (V) Prof. Maha Hegazi 1-Vessel radius (r): Is the most important factor determining resistance. Increased resistance in narrow vessel decreases blood flow, increases upstream pressure, and decreases downstream pressure. Decreased resistance in wide vessel increases blood flow, decreases upstream pressure and increases downstream pressure.  The arterioles are the main site of the peripheral resistance. Arteriolar diameter The resistance. Doubling the diameter will decrease the resistance rate 16 fold  2-Blood viscosity (V ) : The viscosity The resistance The prime determinant of blood viscosity is the hematocrit. Viscosity is affected by the plasma proteins (fibrinogen and globulin) 3.Vessel length (L): Length Resistance. Vessel length is constant Changes in length are not a physiologic factor in regulation of resistance, pressure, or flow.  ARTERIAL BLOOD PRESSURE  ARTERIAL BLOOD PRESSURE Definition The force exerted by the blood against any unit area of the vessel wall Systolic Blood Pressure The force exerted by the blood against any unit area of the vessel wall while heart is contracting (Systole) Diastolic Blood Pressure The force exerted by the blood against the unit area of the vessel wall while heart is relaxing (Diastole) Average Normal Arterial Pressure 90-140 mmHg systolic 60-90 mmHg diastolic  Pulse pressure Pulse pressure is the difference between the systolic and diastolic pressures. It is the rise in pressure caused by the ejection of blood into the aorta by ventricular contraction. It is a measure of stroke volume and compliance of arteries. Systolic pressure – diastolic pressure Normally about 40 mmHg.  MEAN ARTERIAL BLOOD PRESSURE The average of the arterial pressures measured in millisecond over a period of time. It is responsible for driving blood into the tissues throughout the cardiac cycle. It is better indicator of perfusion to vital organs than systolic blood pressure. Because systole is shorter than diastole, the mean pressure is slightly less than the value halfway between systolic and diastolic pressure. Factors determining the arterial blood pressure  Factors determining the Cardiac output The cardiac output = heart rate X stroke volume a. Effect of changes in stroke volume: an increase the stroke volume raises mainly the systolic BP with no significant change in diastolic BP b. Effect of changes in heart rate: an increase in heart rate raises mainly the diastolic BP due to shortening of the diastolic period (which prevent fall of the diastolic pressure to the normal level).  The peripheral resistance It is the total resistance to blood flow through the systemic circulation. The peripheral resistance is essential for maintenance of arterial BP particularly the diastolic. It is produced mainly in the arterioles and is determined by the radius of the vessel, blood viscosity and length of vessel. Normally, adjusting the arteriolar diameter can modify it, because the other 2 factors are normally kept constant. THANK YOU