2024-newCardiac Physiology (1).pptx

CARDIOVASCULAR PHYSIOLOGY Functional Anatomy of the Heart Some Physics of Fluid Movement: Blood Flow Flow rate: (L/min) Flow velocity = rate/C-S area of vessel Resistance slows flow – Vessel diameter (radius) – Blood viscosity – Tube length Figure 14-4 c: Pressure differences of static and flowing f...

CARDIOVASCULAR PHYSIOLOGY Functional Anatomy of the Heart Some Physics of Fluid Movement: Blood Flow Flow rate: (L/min) Flow velocity = rate/C-S area of vessel Resistance slows flow – Vessel diameter (radius) – Blood viscosity – Tube length Figure 14-4 c: Pressure differences of static and flowing fluid Blood viscosity and tube length are basically constant. Vessel diameter has the most influence on blood flow. Therefore, 2 factors affect blood flow; a) Pressure gradient and b) Resistance (VESSEL DIAMETER, tube length, blood viscosity) Cardiac Muscle Cells: Myocardial Autorhythmic Cells – Membrane potential “never rests” pacemaker potential. Myocardial Contractile Cells – Have a different looking action potential due to calcium channels. General cardiac cell features: – Intercalated discs Allow branching of the myocardium – Gap Junctions (instead of synapses) Fast Cell to cell signals – Many mitochondria – Large T tubes Figure 14-10: Cardiac muscle Cardiac muscle Heart Physiology: Electrical Events Intrinsic cardiac conduction system – A network of noncontractile (autorhythmic) cells that initiate and distribute impulses to coordinate the depolarization and contraction of the heart Pacemakers-Autorhythmic Cells Have unstable resting potentials (pacemaker potentials or prepotentials) due to open slow Na+ channels At threshold, Ca2+ channels open Explosive Ca2+ influx produces the rising phase of the action potential Repolarization results from inactivation of Ca2+ channels and opening of voltage-gated K+ channels AUTOMATICITY Na + K+ Gradually increasing PNa Na+ K+ -70 mV THRESHOLD RESTING -0 Threshold Action potential 2 2 3 1 Pacemaker potential 1 1 Pacemaker potential 2 Depolarization The 3 Repolarization is due to This slow depolarization is due to both opening of Na+ channels and closing of K+ channels. Notice that the membrane potential is never a flat line. action potential begins when the pacemaker potential reaches threshold. Depolarization is due to Ca2+ influx through Ca2+ channels. Ca2+ channels inactivating and K+ channels opening. This allows K+ efflux, which brings the membrane potential back to its most negative voltage. Figure 18.13 Other myocytes- cardiac Muscle Contraction Depolarization of the heart is rhythmic and spontaneous About 1% of cardiac cells have automaticity— (are self-excitable) Gap junctions ensure the heart contracts as a unit Long absolute refractory period (250 ms) Other myocytes-Cardiac Muscle Contraction Depolarization opens voltage-gated fast Na+ channels in the sarcolemma Reversal of membrane potential from –90 mV to +30 mV Depolarization wave in T tubules causes the SR to release Ca2+ Depolarization wave also opens slow Ca2+ channels in the sarcolemma Ca2+ surge prolongs the depolarization phase (plateau) Cardiac Muscle Excitation, Contraction & Relaxation Figure 14-11: Excitation-contraction coupling and relaxation in cardiac muscle 1 Depolarization is 2 Tension development (contraction) 3 1 Absolute refractory period Time (ms) Tension (g) Membrane potential (mV) Action potential Plateau due to Na+ influx through fast voltage-gated Na+ channels. A positive feedback cycle rapidly opens many Na+ channels, reversing the membrane potential. Channel inactivation ends this phase. 2 Plateau phase is due to Ca2+ influx through slow Ca2+ channels. This keeps the cell depolarized because few K+ channels are open. 3 Repolarization is due to Ca2+ channels inactivating and K+ channels opening. This allows K+ efflux, which brings the membrane potential back to its resting voltage. Figure 18.12 Regulation of myocyte action through adrenergic system Cardiac Muscle Contraction Ca2+ influx triggers opening of Ca2+-sensitive channels in the SR, which liberates bursts of Ca2+ E-C coupling occurs as Ca2+ binds to troponin and sliding of the filaments begins Duration of the AP and the contractile phase is much greater in cardiac muscle than in skeletal muscle Repolarization results from inactivation of Ca2+ channels and opening of voltage-gated K+ channels Modulation of Contraction Graded Contraction: proportional to crossbridges formed More [Ca++]: crossbridges, more force & speed Under catecholemine control: – Norepinephrine – Epinephrine Coordinating the Pump: Electrical Signal Flow Figure 14-18: Electrical conduction in myocardial cells Cardiac Cycle Coordinating the activity Cardiac cycle is the sequence of events as blood enters the atria, leaves the ventricles and then starts over Synchronizing this is the Intrinsic Electrical Conduction System Influencing the rate (chronotropy & dromotropy) is done by the sympathetic and parasympathetic divisions of the ANS THE CARDIAC CYCLE LATE DIASTOLE DIASTOLE ISOMETRIC VENTRICULAR RELAXATION VENTRICULAR EJECTION ATRIAL SYSTOLE ISOMETRIC VENTRICULAR CONTRACTION Electrical conduction in the heart Cardiac Cycle Coordinating the activity Electrical Conduction Pathway – Initiated by the Sino-Atrial node (SA node) which is myogenic at 70-80 action potentials/minute – Depolarization is spread through the atria via gap junctions and internodal pathways to the AtrioVentricular node (AV node) The fibrous connective tissue matrix of the heart prevents further spread of APs to the ventricles A slight delay at the AV node occurs – Due to slower formation of action potentials – Allows further emptying of the atria – Action potentials travel down the Atrioventricular bundle (Bundle of His) which splits into left and right atrioventricular bundles (bundle branches) and then into the conduction myofibers (Purkinje cells) Purkinje cells are larger in diameter & conduct impulse very rapidly – Causes the cells at the apex to contract nearly simultaneously Cardiac Cycle Phases Systole = period of contraction Diastole = period of relaxation Cardiac Cycle is alternating periods of systole and diastole Phases of the cardiac cycle 1. Rest Both atria and ventricles in diastole Blood is filling both atria and ventricles due to low pressure conditions 2. Atrial Systole Completes ventricular filling 3. Isovolumetric Ventricular Contraction Increased pressure in the ventricles causes the AV valves to close… why? – Creates the first heart sound (lub) Atria go back to diastole No blood flow as semilunar valves are closed as well Cardiac Cycle Phases Phases of the cardiac cycle 4. Ventricular Ejection Intraventricular pressure overcomes aortic pressure – Semilunar valves open – Blood is ejected 5. Isovolumetric Ventricular Relaxation Intraventricular pressure drops below aortic pressure – Semilunar valves close = second heart sound (dup) Pressure still hasn’t dropped enough to open AV valves so volume remains same (isovolumetric) Back to Atrial & Ventricular Diastole Autonomic Nervous System Regulation Sympathetic nervous system is activated by emotional or physical stressors – Norepinephrine causes the pacemaker to fire more rapidly (and at the same time increases contractility) Parasympathetic system opposes sympathetic effects – Acetylcholine hyperpolarizes pacemaker cells by opening K+ channels The heart at rest exhibits vagal tone (parasympathetic) Atrial (Bainbridge) reflex: a sympathetic reflex initiated by increased venous return – Stretch of the atrial walls stimulates the SA node – Also stimulates atrial stretch receptors activating sympathetic reflexes Chemical Regulation of Heart Rate 1. Hormones – Epinephrine from adrenal medulla enhances heart rate and contractility – Thyroxine increases heart rate and enhances the effects of norepinephrine and epinephrine 2. Intra- and extracellular ion concentrations (e.g., Ca2+ and K+) must be maintained for normal heart function Other Factors that Influence Heart Rate Age Gender Exercise Body temperature Age-Related Changes Affecting the Heart Sclerosis and thickening of valve flaps Decline in cardiac reserve Fibrosis of cardiac muscle Atherosclerosis ABNORMALITIES IN HEART MUSCLE Congenital Heart Defects Narrowed aorta Occurs in about 1 in every 500 births (a) Ventricular septal defect. The superior part of the interventricular septum fails to form; thus, blood mixes between the two ventricles. More blood is shunted from left to right because the left ventricle is stronger. Occurs in about 1 in every 1500 births (b) Coarctation of the aorta. A part of the aorta is narrowed, increasing the workload of the left ventricle. Occurs in about 1 in every 2000 births (c) Tetralogy of Fallot. Multiple defects (tetra = four): (1) Pulmonary trunk too narrow and pulmonary valve stenosed, resulting in (2) hypertrophied right ventricle; (3) ventricular septal defect; (4) aorta opens from both ventricles. Figure 18.24 Arrhythmias The most common disorders are atrial fibrillation and flutter. The incidence is highly related to age and the presence of underlying heart disease What are the clinical symptoms? Patients may describe an arrhythmia as a palpitation or fluttering sensation in the chest. A "racing" heart is another description. Proper diagnosis of arrhythmias requires an ECG. Depending on the severity of the arrhythmia, patients may experience dyspnea (shortness of breath), syncope (fainting), fatigue, heart failure symptoms, chest pain or cardiac arrest. Causes A frequent cause of arrhythmia is coronary artery disease because this condition results in myocardial ischemia or infarction. When cardiac cells lack oxygen, they become depolarized, which leads to altered impulse formation and conduction. The former concerns changes in rhythm that are caused by changes in the automaticity (spontaneous activity) of pacemaker cells or by abnormal generation of action potentials at sites other than the SA node (termed ectopic foci). Altered impulse conduction is usually associated with complete or partial block of electrical conduction within the heart. Altered impulse conduction commonly results in reentry, which can lead to Abnormal conduction within heart Ectopic foci are abnormal pacemaker sites outside of the SA node that show automaticity. They can occur within the atria or ventricles. Ectopic foci can cause additional beats (observed as premature beats) or take over the normal pacemaker activity of the SA node. These ectopic pacemakers can lead to either tachycardia or bradycardia depending upon their location and surrounding electrical conditions. They can also be generated after reentry. Wolfe Parkinson White Syndrome rkinson-White Syndrome (WPW) is a relatively common cause of suprav dia in children. A small percentage of people, about 3 in 1000, have extra g tissue from the top to the bottom chambers. This extra conducting tissue is n “accessory pathway.” The majority of the time the accessory pathway does no lectricity. However, if circumstances are just right, it is possible for electricity to wn the normal pathway through the AV node and then immediately travel back cessory pathway. Subsequently, an electrical circuit can be established between and the accessory pathway. Supraventricular Arrhythmias Sinus Tachycardia: high sinus rate of 100-180 beats/min, occurs during exercise or other conditions that lead to increased SA nodal firing rate Atrial Tachycardia: a series of 3 or more consecutive atrial premature beats occurring at a frequency >100/min Paroxysmal Atrial Tachycardia (PAT): tachycardia which begins and ends in acute manner Atrial Flutter: sinus rate of 250-350 beats/min. Atrial Fibrillation: uncoordinated atrial depolarizations. AV blocks A conduction block within the AV node , occasionally in the bundle of His, that impairs impulse conduction from the atria to the ventricles. ventricular Arrhythmias Ventricular Premature Beats (VPBs): caused by ectopic ventricular foci Ventricular Tachycardia (VT): high ventricular rate caused by abnormal ventricular automaticity or by intraventricular reentry;; rates of 100 to 200 beats/min; life-threatening. Ventricular Flutter - ventricular depolarizations >200/min. Ventricular Fibrillation - uncoordinated ventricular depolarizations