Circulatory System Part 2- Heart PDF

Chapter 3 | Circulatory system Part 2- Heart  CHAPTER 3 CIRCULATORY SYSTEM 2- Heart Introduction Composition of circulatory system The circulatory system is composed of Heart (by which blood is pu...

Chapter 3 | Circulatory system Part 2- Heart  CHAPTER 3 CIRCULATORY SYSTEM 2- Heart Introduction Composition of circulatory system The circulatory system is composed of Heart (by which blood is pumped) and Blood vessels (Arteries, Capillaries, Veins in which blood circulates) (Fig. 3-1) The right heart receives venous blood from tissues through vena cava and pumps it into the pulmonary artery where it is changed into arterial blood and returned to left atrium via pulmonary veins (pulmonary circulation). The left heart receives arterial blood from lungs and pumps it into the aorta, to the tissues, where it is changed into venous blood and returned to right atrium via venae cava (systemic, greater or general circulation). Properties of cardiac muscle Fig. 3-1 Composition of circulatory system Types of cardiac muscle fibers: Rhythmic: initiate impulses e.g. sino-atrial node (S.A.N), atrio-ventricular node (A.V.N) & Purkinje fibers. Conductive: Conduct impulses rapidly through the heart (His-Purkinje system) Contractile (99%): Contract as 2 functional syncytia (separated by A.V. fibrous ring, the only m. connection is A.V. bundle). In summary there are 4 properties of cardiac muscle Auto-rhythmicity: It is the ability of the heart to beat regularly independent of any extrinsic stimuli. Conductivity: It is the ability of the heart to transmit excitation waves. Excitability: It is the ability of the heart to respond to a stimulus Contractility: It is the ability of the heart to change a part of the energy into mechanical work. 35  CHAPTER 3 CIRCULATORY SYSTEM 2- Heart Auto-rhythmicity Definition: It is the ability of the heart to beat regularly independent of any external stimuli. Origin: Its origin is myogenic, not neurogenic (Initiated in sino-atrial node (SAN), in the mammalian heart). The sympathetic and vagal innervations to SAN do not initiate heart beats, they only control heart rate (vagal innervation is predominant during rest). Normal frequency of discharge: SAN (Sinus rhythm): 100-110/minute. AVN (Nodal rhythm): 45-60/minute. Purkinje system (Idioventricular rhythm): 25-40/minute. Initiation of cardiac impulses in SAN (Electrical activity of auto-rhythmic type): a) Pacemaker potential (prepotential): pacemaker cells are characterized by a low unstable resting membrane potential of -55 to -60 mv. (It ↓steadily after each action potential) because of decreased membrane permeability to K+ → ↓K+ efflux (slow inward movement of Na+ exceeds K+ efflux) → membrane begins to depolarize producing the 1st early part of prepotential. This facilitates opening of T-type Ca2+ channels (transient) → Ca2+ influx → 2nd late part of prepotential b) Pacemaker action potential: The action potential in Pacemaker cells occurs when RMP reaches -40mv, due to opening of L-type Ca2+ channels (long, lasting) → Ca2+ influx. It is characterized by the following (Fig. 3-2): Low unstable RMP (-55 to -60 mv.) Slow upstroke with small magnitude (up to +10 mv.) due to slow Ca2+ influx through L-type Ca2+ channels. So, it is known as slow response action potential No plateau Gradual repolarization (by K+ efflux) Fig. 3-2 Electrical activity of auto-rhythmic type 36  CHAPTER 3 CIRCULATORY SYSTEM 2- Heart Electrical activity of the contractile type (Fig. 3-3): Resting membrane potential is stable at ~ -90 mv. Action potential: Stimulation of the cardiac muscle produces a propagated action potential consisting of 5 phases and responsible for initiating contraction. Phase 0: rapid depolarization due to opening of voltage gated (fast) Na+ channels. Phase 1: initial rapid repolarization, due to closure of Na+ channels with a gradually increasing K+ efflux Phase 2: prolonged plateau due to slow prolonged opening of voltage-gated Ca2+ channels accompanied by K+ efflux → membrane potential maintained at about 0 mv. Fig. 3-3 Electrical activity of contractile type Phase 3: rapid repolarization, due to closure of Ca2+ channels & increased K+ efflux. Phase 4: Restores the resting membrane potential by K+ efflux, then Na+/K+ pump, Ca2+ pump and Na+/ Ca2+ exchanger restore the normal ionic distribution around the cell membranes Factors affecting rhythmicity (Chronotropism) 1. Nervous factors: Parasympathetic stimulation ↓ rhythmicity by ↑ permeability to K+ and Inactivation of T-type Ca2+ channels. Sympathetic stimulation ↑ rhythmicity by opposite parasympathetic effects. 2. Physical factors: ↑temperature 1ᵒC→ ↑ heart rate 10-20 beat/min. due to ↑ metabolic activity. Temperature 45ᵒC stops the rhythmicity. 3. Mechanical factors: Distension of right atrium → ↑ heart rate. 4. Chemical factors: Hormones: e.g. catecholamines and thyroxin ↑ rhythmicity by a mechanism like sympathetic stimulation. Blood gases: Mild hypoxia ↑ rhythmicity by direct stimulation of the pacemaker cells and ↑sympathetic activity. While Severe hypoxia and hypercapnia ↓ rhythmicity and even cause cardiac arrest. 37  CHAPTER 3 CIRCULATORY SYSTEM 2- Heart pH of the blood: Alkalosis ↑ and acidosis ↓ rhythmicity. While, both alkalemia and acidemia ↓ rhythmicity and may cause cardiac arrest. Drugs: Digitalis depresses the nodal tissue. Conductivity: Definition: Ability of cardiac muscle to transmit excitation waves Heart beats are Initiated at SAN and spread through conducting system to reach the ventricular myocardium. Normal conducting pathway (Fig. 3-4): 3 Internodal bundles: 1 m./sec. Atrioventricular node (AVN): 0.05 m./sec.: A-V nodal delay: Protect the ventricles from Atrial flutter and fibrillation One-Way Conduction Post repolarization refractoriness: limit the conducted impulses to< 230/min. AV bundle (Bundle of His): 3 m./sec., reaches 5 m./sec. in the final branches (Purkinje fibers) to allow excitation of both ventricles nearly at same time (from the endocardium to epicardium). The conduction through ventricular muscle itself is slow (about 0.5 m/sec.) Fig. 3-4 Normal conducting pathway 38  CHAPTER 3 CIRCULATORY SYSTEM 2- Heart Excitability: Stages of excitability changes (Fig. 3-5): 1-Absolute refractory period (ARP): Excitability is zero. It coincides with the whole systole and early diastole. Long ARP prevents cardiac tetany, and fatigue. 2- Relative refractory period (RRP): Excitability is below normal. It coincides with 1st half of diastole. 3- Supernormal phase: excitability is above normal. It occupies 2nd half of diastole. Fig. 3-5 Stages of excitability changes Factors affecting excitability: 1. Nervous factors: Vagal stimulation: ↓ HR → ↑ refractory period Symp. stimulation: ↑ HR → ↓ refractory period 2. Mechanical factors: ↑ heart rate →↓ refractory period 3. Physical factors: ↑temperature →↑ HR →↓ refractory period. 4. Chemical factors: Cardiac ischemia or hypoxia, bacterial and chemical toxins: all slow repolarization → ↑refractory period. Drugs: calcium channel blockers ↑refractory period → used in treatment of atrial flutter and fibrillation. 39  CHAPTER 3 CIRCULATORY SYSTEM 2- Heart Contractility: Contractile response of cardiac m. begins 0.02 sec. after depolarization start; when depolarization wave reaches T-tubules, it induces: Ca2+ releases from SR. (activator Ca2+) Ca+2 influx from ECF through L-Ca2+ channels (depolarizing Ca2+) → release of more activator Ca2+. Activator Ca2+ binds to troponin C → cross bridges formation between actin and myosin → muscle contraction. Relaxation occurs by pumping Ca2+ to sarcoplasmic reticulum and ECF (via Na+/ Ca2+ exchanger) (Fig. 3-6). Fig. 3-6 Mechanism of contraction and relaxation in cardiac muscles The cardiac m. is considered as a single muscle fiber, it either contracts maximally or does not contract at all, provided that other factors affecting contractility remain constant (All or Non rule). Types of contraction in cardiac muscle: Isometric contraction: increase in m. tone without change in its length. Isotonic contraction: shortening of the m. without change in its tone. 40  CHAPTER 3 CIRCULATORY SYSTEM 2- Heart Factors affecting contractility (inotropism). 1. Nervous factors: Vagal stimulation: ↓ contractility of atrial muscles only. Sympathetic stimulation: ↑ cytosolic Ca2+ ↑contractility (even the initial length has not increased). 2. Mechanical factors: Frank- Starling’s law (Heterometric–autoregulation): The power of myocardial contraction is directly proportional to the end diastolic volume (initial length) within limits (Overstretch weaken the contraction). Staircase phenomenon (treppe): ↑HR → ↑contractility of the ventricle over the first few beats (due to excitability, thermal and chemical changes that improves physiological state of the cardiac m). 3. Chemical factors: Digitalis: inhibit Na+/K+ pump → activate Na+/Ca+2 exchanger → Na+ outflux and Ca+2 influx →↑cytosolic Ca+2. O2 lack, bacterial & chemical toxins. All ↓cardiac contractility. Changes in pH. Alkalosis  while acidosis  contractility due to / affinity of troponin C to Ca2+. Severe acidosis stops heart in diastole, while severe alkalosis stops heart in systole 4. Physical factors: Moderate warming:  cardiac contractility Moderate cooling:  cardiac contractility Excessive warming or cooling: Stops cardiac contractility 41  CHAPTER 3 CIRCULATORY SYSTEM 2- Heart Cardiac Innervation Cardiac centers: The nervous system can regulate cardiac activities through 2 main centers (Fig. 3-7): Cardio-inhibitory center (CIC): It is a part of the dorsal motor nucleus of vagus. Its axons leave the medulla as preganglionic fibers that relay in terminal ganglia. There is a tonic vagal inhibitory discharge during rest (vagal tone) in humans and animals. Cardio-acceleratory center (CAC): It lies in the medulla oblongata, near the CIC, its axons descend in the spinal cord, and end at: upper 5 thoracic LHCs → pregang. fibers relay in the 3 cervical symp. ganglia → postgang. fibers pass to the heart. remaining thoracic & lumber LHCs → to bl. Fig. 3-7 Cardiac centers and vessels (generalized VC) & adrenal medulla Innervation (↑ catecholamines) Functions of Cardiac Nerves In mammalian heart, the vagi supply auricles, SA node, AV node and the main A.V. bundle only. They do not supply ventricular m. and Purkinje fibers. On the other hand, the sympathetic supplies the mammalian ventricles as well as the auricles. The vagi inhibit all cardiac properties and produces Coronary V.C. by decreasing the oxygen consumption of the heart. The sympathetic excites all cardiac properties and produces Coronary V.D. by increasing the oxygen consumption of the heart. 42  CHAPTER 3 CIRCULATORY SYSTEM 2- Heart Regulation of the heart rate Normal heart rate under basal condition is 60:90 beat/ min., due to continuous vagal tone. Mechanism of vagal tone (Fig. 3-8): ABP > 60 mmHg (normal ABP) constantly stimulates baroreceptors in aortic arch and carotid sinus → Aortic n. (vagus) and Carotid sinus n. (glossopharyngeal) → stimulate CIC → discharges along vagi → depress the inherent high auto-rhythmicity of SA node. Vaso-Sensory Areas These are regions in CVS, contain receptors that send impulses to the respiratory & CVS centers → reflexes controlling respiration and circulation. Fig. 3-8 Mechanism of vagal tone The most important areas are: Arterial baroreceptors: in Carotid sinus (dilatation at beginning of int. carotid a.) and Aortic arch (curve between ascending & descending parts of thoracic aorta). Arterial chemoreceptors: in Carotid body (at origin of external carotid a.), and Aortic body (near the arch of the aorta). Impulses from Carotid sinus/body are carried by Sinus n. (branch of glossopharyngeal n.), while impulses from Aortic arch/body are carried by Aortic n. (branch of vagus n.) Factors regulating HR: 1) Nervous factors: affecting cardiac centers I. Reflexes (Intrinsic or Extrinsic) II. Impulses from other centers 2) Chemical factors (Blood gases & Hormones). 3) Physical factors (temperature). 1) Nervous factors: I. Reflexes: Intrinsic reflexes: (from C.V.S): initiated from left or right sides. From the left side of the heart: Arterial baroreceptors (carotid sinus and aortic arch; Fig. 3-9A): Stimulus:  ABP, their activity disappears at ~ 40 mmHg. 43 CHAPTER 3 CIRCULATORY SYSTEM 2- Heart Receptors: Baroreceptors in Carotid sinus & Aortic arch Afferents: Sinus n. and Aortic n. Center & effects (Function): They send inhibitory impulses to respiratory & cardiovascular centers (+CIC & -CAC)→ ↓ heart rate, ABP, catecholamines secretion & Resp. rate Fig. 3-9 Reflexes from the left side of the heart; A: Arterial baroreceptors; B: Marey’s Law; C: Arterial chemoreceptors Marey’s Law: heart rate is inversely proportional to ABP provided the other factors affect HR remain constant. So, ↑ ABP→↓HR while, ↓ABP→↑HR. Mechanism: ↑ ABP → stimulate baroreceptors in aortic arch & carotid sinuses → impulses discharged via aortic & carotid sinus n. → stimulation of CIC & inhibition of CAC →↓HR (Fig. 3-9B). Arterial chemoreceptors (carotid & aortic bodies). Stimulus: ↓O2, ↑CO2 & ↑H+. Receptors: Chemoreceptors in Carotid & Aortic bodies Afferents: Sinus n. & Aortic n. Center & effects (Function): They send excitatory impulses to respiratory & cardiovascular centers → heart rate & ABP & Resp. rate (Fig. 3-9C) 44 CHAPTER 3 CIRCULATORY SYSTEM 2- Heart From the right side of the heart: Rt atrial baroreceptors: Sudden ↑ in venous return → ↑rt. atrial pressure → stimulates mechanoreceptors in its wall → afferent vagal fibers → stimulate CAC & inhibit CIC resulting in: heart rate (Bainbridge reflex; Fig. 3-10), respiratory rate (Harrison reflex), coronary V.D. (Anrep’s reflex). Bainbridge effect: ↑heart rate caused by local stretch of SA node due to ↑VR, it can be produced in isolated heart–lung. Fig. 3-10 Bainbridge reflex Extrinsic reflexes (out of C.V.S): initiated from extracardiac areas e.g.: Skeletal muscles (Alam Smirk reflex). Afferent fibers from contracted sk. m. → stimulate CAC & inhibit CIC →↑ heart rate. Pain. Mild pain → tachycardia Severe pain e.g. severe trauma → bradycardia. Lung inflation Stimulates baroreceptors in bronchial walls →afferent vagus →stimulate CAC & inhibit CIC→↑ heart rate 1) Nervous factors: II. Impulses from other centers: Cerebral cortex & hypothalamus: Descending tracts from cerebral cortex & hypothalamus produces: Tachycardia in certain emotions as anger, Or Bradycardia in others as fear. Respiratory center: heart rate ↑during inspiration & ↓during expiration. “Respiratory sinus arrhythmia” due to the following mechanisms. Distention of the lung → Stimulates baroreceptors →stimulate CAC & inhibit CIC→↑ heart rate Bainbridge reflex, due to ↑ VR with inspiration. Irradiation of inspiratory center → stimulate CAC 45 CHAPTER 3 CIRCULATORY SYSTEM 2- Heart 2) Chemical factors: Blood gases: Mild hypoxia: HR Mild hypercapnia & acidosis produce initial  HR, followed by HR Severe hypoxia, hypercapnia & acidemia, all  HR even cause cardiac arrest Effects of asphyxia; a state of hypercapnia (CO2), acidosis ( H+) & hypoxia (O2): it affects the HR in the following stages: Initial slowing: (Initial effect of hypercapnia) Acceleration: (effect of hypercapnia & mild hypoxia) Premortal slowing, (persistent hypercapnia & hypoxia): During recovery, the same stages occurred in reverse order. Hormones: Adrenaline: ↑HR by direct action on the heart (β1 receptors in SAN). Noradrenaline: Potent VC →↑ABP →↓HR by Marey's law Thyroxin: ↑HR due to: Direct stimulation of SA node ↑sensitivity of SA node to catecholamines. ↑metabolic rate →VD →↑ VR →↑ HR by Bainbridge reflex & effect. 3) Physical factors (temperature). 1Coin body temp. →~10-20 beats/ minute and vice versa, due to: Direct effect on the SA node. Effect of temperature on the hypothalamus and the cardiac centers 46  CHAPTER 3 CIRCULATORY SYSTEM 2- Heart Cardiac output Definitions Stroke volume (SV): Volume of blood pumped by each ventricle per beat (about 80 ml/beat during rest) Cardiac output (minute volume, CO): Volume of blood pumped by each ventricle per minute (about 5 L/minute during rest), CO = SV x HR. End Diastolic volume (EDV): Volume of blood in the ventricle at the end of diastole (about 130 ml) End systolic volume (ESV): Volume of blood in the ventricle at the end of systole (about 50 ml) Factors affecting: Cardiac output = stroke volume x heart rate 1. Stroke volume which is affected by: Venous return (and factors affecting): ↑ VR → ↑CO (starling's low) Myocardial contractility (and factors affecting): ↑ contractility → ↑CO ABP: Transient changes (corrected by starling's law) 2. Heart rate: depending on the degree of changes in the HR Moderate change with constant VR: no change in CO Excessive change with constant VR: ↓CO moderate↑ with ↑VR: ↑CO Factors affecting VR Factors affecting contractility 1. Pressure gradient 1. Nervous factors: Vagal ↓ while Symp. ↑ 2. Gravity contractility 3. respiratory movement 2. Mechanical factors: Frank-Starling’s law 4. Skeletal m. contraction 3. Chemical factors: Digitalis ↑ contractility 5. arterial pulsation while O2 lack, bacterial, chemical toxins 6. diameter of arterioles and sever changes in PH ↓ contractility 7. capillary dilatation 4. Physical factors: Moderate warming ↑ 8. venous tone while moderate cooling ↓ cardiac 9. Contraction of spleen contractility 47  CHAPTER 3 CIRCULATORY SYSTEM 2- Heart Cardiac Reserve The difference between work performed by heart under basal conditions & that performed during severe m. exercise. Or, Maximal %  in COP above normal, it is about; 600% in athletes. 400% in young adults. 200% in asthenic or elderly persons. Zero in heart failure. Mechanisms of cardiac reserve: 1. Acceleration of the heart rate 2. Increased stroke volume 3. Hypertrophy of the cardiac m. Arterial blood pressure Definition and Normal values: Arterial blood pressure: It is the lateral pressure exerted by blood on the arterial walls, normally it oscillates during cardiac cycle between max. value (systolic blood pressure, about 100-140 mmHg) & min. value (diastolic blood pressure, about 60-90 mmHg) & reported as systolic over diastolic e.g. 120/80. Pulse pressure: It is the difference between systolic & diastolic BP (~ 40 mmHg) Mean arterial blood pressure: It is the average ABP throughout the cardiac cycle. It equals 2/3 diastolic + 1/3 systolic (=diastolic + 1/3 pulse), about 100 mmHg. Factors maintaining (ABP= COP  PR): Cardiac output (CO): affects mainly SBP Peripheral resistance (R α L.η/r4): affects mainly DBP Blood volume in relation to circulatory capacity (V/A) as in severe hemorrhage and histamine injection. Elasticity of aorta and big arteries (↑capacity during systole &↓it during diastole, thus prevent excess ↑ in SBP & excess ↓ in DBP) 48