Chapter 9 Cardiac Physiology

Credit: © L. Bassett/Visuals Unlimited 97935 Human heart.

Credit: © L. Bassett/Visuals Unlimited 97936 Human heart with coronary arteries exposed.

Outline Circulatory system overview Transplant surgery Anatomy Electrical activity Mechanical events Cardiac output Coronary circulation

Circulatory System Three basic components Heart Blood vessels Blood Serves as pump that establishes the pressure gradient needed for blood to flow to tissues Blood vessels Passageways through which blood is distributed from heart to all parts of body and back to heart Blood Transport medium within which materials being transported are dissolved or suspended Pulmonary circulation Closed loop of vessels carrying blood between heart and lungs Systemic circulation Circuit of vessels carrying blood between heart and other body systems

Transplant http://www.youtube.com/watch?v=cOBWMITf3co www.or-live.com

Circulatory System Anatomy Heart Hollow, muscular organ about the size of a clenched fist Positioned between two bony structures – sternum and vertebrate Dual pump Right and left sides of heart function as two separate pumps Divided into right and left halves and has four chambers Atria Upper chambers Receive blood returning to heart and transfer it to lower chambers Ventricles Lower chambers which pump blood from heart

Circulatory System Heart Arteries Veins Septum Carry blood away from ventricles to tissues Veins Vessels that return blood from tissues to the atria Septum Continuous muscular partition that prevents mixture of blood from the two sides of heart

Outline Anatomy Thoracic cavity, base, apex AV and semilunar valves endothelium, myocardium, epicardium cardiac cells, intercalated disks Comparison of cardiac cells to skeletal and smooth muscle cells pericardium

Blood Flow Through and Pump Action of the Heart What are the parts and what do they do? Know the flow of blood in order.

Heart Valves Atrioventricular (AV) valves Right and left AV valves are positioned between atrium and ventricle on right and left sides Prevent backflow of blood from ventricles into atria during ventricular emptying Right AV valve Also called tricuspid valve Left AV valve Also called bicuspid valve or mitral valve Chordae tendinae Fibrous cords which prevent valves from being everted Papillary muscles

Heart Valves Semilunar valves Aortic and pulmonary valves Lie at juncture where major arteries leave ventricles Prevented from everting by anatomic structure and positioning of cusps No valves between atria and veins Reasons Atrial pressures usually are not much higher than venous pressures Sites where venae cavae enter atria are partially compressed during atrial contraction

Heart Valves

Consists of three distinct layers Endothelium Thin inner tissue Epithelial tissue which lines entire circulatory system Myocardium Middle layer Composed of cardiac muscle Constitutes bulk of heart wall Epicardium Thin external layer which covers the heart Pericardium the fluid filled sac that surrounds the heart Endocardium Myocardium fig. 18-9; pg: 563 Epicardium

Heart is enclosed by pericardial sac Pericardial sac has two layers Tough, fibrous covering Secretory lining Secretes pericardial fluid Provides lubrication to prevent friction between pericardial layers Pericarditis Inflammation of pericardial sac

The next series of slides compares cardiac, skeletal, smooth muscle cells.

Cardiac Muscle Fibers Interconnected by intercalated discs and form functional syncytia Within intercalated discs – two kinds of membrane junctions Desmosomes Gap junctions

Credit: © Dr. Donald Fawcett/Visuals Unlimited 319540 Cardiac muscle in longitudinal section showing intercalated discs. TEM.

Skeletal Muscle Fiber Basal lamina Sacrolemma Myofibrils Longitudinal system Mitochondria Transverse tubule Nucleus Intercalated disc Myofibril Opening of Transverse tubule fig 16-8b, pg 487

Credit: © Dr. Richard Kessel/Visuals Unlimited 310127 Credit: © Dr. Richard Kessel/Visuals Unlimited Myofibrils within skeletal muscle fibers. All bands (A, I, Z, M) are evident as well as elements of the sarcoplasmic reticulum and small dots of glycogen. TEM X32,000.

Smooth Muscle Fiber Rough Endoplasmic reticulum Glycogen granules Nucleus Mitochondria Thin filament Thick filament Dense bodies Plasma membrane fig 16-9a, pg 479

Dense bodies Smooth muscle Cells Fig. 8-27b, p. 288 Figure 8.27: Microscopic view of smooth muscle cells. (b) Electron micrograph of smooth muscle cells at 14,000× magnification. Note the presence of dense bodies and lack of banding. Fig. 8-27b, p. 288

Outline Electrical activity of the heart Autorhymicity Pacemaker (function, ions) Conductive system (SA, AV, bundle of His, Purkinje fibers) Abnormal rhythms Spread of cardiac excitation Cardiac cell action potentials Characteristics vary by location

Electrical Activity of Heart Heart beats rhythmically as result of action potentials it generates by itself (autorhythmicity) Two specialized types of cardiac muscle cells Contractile cells 99% of cardiac muscle cells Do mechanical work of pumping Normally do not initiate own action potentials Autorhythmic cells Do not contract but send electrical signals to the contractile cells Specialized for initiating and conducting action potentials responsible for contraction of working cells

Electrical Activity of Heart Locations of noncontractile cells capable of autorhymicity Sinoatrial node (SA node) Specialized region in right atrial wall near opening of superior vena cava Pacemaker of the heart Atrioventricular node (AV node) Small bundle of specialized cardiac cells located at base of right atrium near septum Bundle of His (atrioventricular bundle) Cells originate at AV node and enters interventricular septum Divides to form right and left bundle branches which travel down septum, curve around tip of ventricular chambers, travel back toward atria along outer walls Purkinje fibers Small, terminal fibers that extend from bundle of His and spread throughout ventricular myocardium

Specialized Conduction System of Heart

Electrical Activity of Heart Cardiac impulse originates at SA node Action potential spreads throughout right and left atria Impulse passes from atria into ventricles through AV node (only point of electrical contact between chambers) Action potential briefly delayed at AV node (ensures atrial contraction precedes ventricular contraction to allow complete ventricular filling) Impulse travels rapidly down interventricular septum by means of bundle of His Impulse rapidly disperses throughout myocardium by means of Purkinje fibers Rest of ventricular cells activated by cell-to-cell spread of impulse through gap junctions

Spread of Cardiac Excitation

Open K channels Closure of K channels Open Ca channels Figure 9.7: Pacemaker activity of cardiac autorhythmic cells. The first half of the pacemaker potential is due to closure of K+ channels, whereas the second half is due to opening of T-type Ca2+ channels. Once threshold is reached, the rising phase of the action potential is due to opening of L-type Ca2+ channels, whereas the falling phase is due to opening of K+ channels. Open Ca channels Closure of K channels Fig. 9-7, p. 305

Relationship of an Action Potential and the Refractory Period to the Duration of the Contractile Response in Cardiac Muscle

Figure 9.11: Action potential in contractile cardiac muscle cells. The action potential in cardiac contractile cells differs considerably from the action potential in cardiac autorhythmic cells (compare with Figure 9-7). Fig. 9-11, p. 310

fig. 18-10; pg: 564

Atrial muscle Atrioventricular Bundle branch Purkinje fibers SA node pacemaker Atrial muscle Atrioventricular Bundle branch Purkinje fibers Ventricular muscle Milliseconds fig. 18-13; pg: 568

Electrical Activity of Heart Atria contract as single unit followed after brief delay by a synchronized ventricular contraction Action potentials of cardiac contractile cells exhibit prolonged positive phase (plateau) accompanied by prolonged period of contraction Ensures adequate ejection time Plateau primarily due to activation of slow L-type Ca2+ channels

Electrical Activity of Heart Ca2+ entry through L-type channels in T tubules triggers larger release of Ca2+ from sarcoplasmic reticulum Ca2+ induced Ca2+ release leads to cross-bridge cycling and contraction

Excitation-Contraction Coupling in Cardiac Contractile Cells

Electrical Activity of Heart Because long refractory period occurs in conjunction with prolonged plateau phase, summation and tetanus of cardiac muscle is impossible Ensures alternate periods of contraction and relaxation which are essential for pumping blood

Relationship of an Action Potential and the Refractory Period to the Duration of the Contractile Response in Cardiac Muscle

Electrocardiogram (ECG) Record of overall spread of electrical activity through heart Represents Recording part of electrical activity induced in body fluids by cardiac impulse that reaches body surface Not direct recording of actual electrical activity of heart Recording of overall spread of activity throughout heart during depolarization and repolarization Not a recording of a single action potential in a single cell at a single point in time Comparisons in voltage detected by electrodes at two different points on body surface, not the actual potential Does not record potential at all when ventricular muscle is either completely depolarized or completely repolarized

Electrocardiogram (ECG) Different parts of ECG record can be correlated to specific cardiac events

Credit: © Mediscan/Visuals Unlimited 3202 Normal ECG.

Abnormalities in Rate Tachycardia Rapid heart rate of more than 100 beats per minute Bradycardia Slow heart rate of fewer than 60 beats per minute

Abnormalities in Rhythm Regularity or spacing of ECG waves Arrhythmia Variation from normal rhythm and sequence of excitation of the heart Examples Atrial flutter (200-300 BPM) Atrial fibrillation Ventricular fibrillation Heart block

Cardiac Myopathies Damage of the heart muscle Myocardial ischemia Inadequate delivery of oxygenated blood to heart tissue Necrosis Death of heart muscle cells Acute myocardial infarction (heart attack) Occurs when blood vessel supplying area of heart becomes blocked or ruptured

Representative Heart Conditions Detectable Through ECG

Outline Mechanical events Systole, diastole animation (volumes, pressures, sounds and EKG)

Specialized Conduction System of Heart

http://library.med.utah.edu/kw/pharm/hyper_heart1.html Figure 9.17: Cardiac cycle. This graph depicts various events that occur concurrently during the cardiac cycle. Follow each horizontal strip across to see the changes that take place in the electro-cardiogram; aortic, ventricular, and atrial pressures; ventricular volume; and heart sounds throughout the cycle. The last half of diastole, one full systole and diastole (one full cardiac cycle), and another systole are shown for the left side of the heart. Follow each vertical strip downward to see what happens simultaneously with each of these factors during each phase of the cardiac cycle. See the text (pp. 317–318) for a detailed explanation of the circled numbers. The sketches of the heart illustrate the flow of O2-poor (dark blue) and O2-rich (bright red) blood in and out of the ventricles during the cardiac cycle. Fig. 9-17, p. 316

Cardiac Output Volume of blood ejected by each ventricle each minute Determined by heart rate times stroke volume

Cardiac Output Heart rate is varied by altering balance of parasympathetic and sympathetic influence on SA node Parasympathetic stimulation slows heart rate Sympathetic stimulation speeds it up

= Inherent SA node pacemaker activity Threshold potential = Inherent SA node pacemaker activity = SA node pacemaker activity on parasympathetic stimulation = SA node pacemaker activity on sympathetic stimulation Fig. 9-20, p. 322

Heart rate Sympathetic activity (and epinephrine) Parasympathetic Fig. 9-20b, p. 322

Cardiac Output Stroke volume Determined by extent of venous return and by sympathetic activity Influenced by two types of controls Intrinsic control Extrinsic control Both factors increase stroke volume by increasing strength of heart contraction

Frank-Starling Law of the Heart States that heart normally pumps out during systole the volume of blood returned to it during diastole

Figure 9.22: Intrinsic control of stroke volume (Frank–Starling curve). The cardiac muscle fiber’s length, which is determined by the extent of venous filling, is normally less than the optimal length for developing maximal tension. Therefore, an increase in end-diastolic volume (that is, an increase in venous return), by moving the cardiac muscle fiber length closer to optimal length, increases the contractile tension of the fibers on the next systole. A stronger contraction squeezes out more blood. Thus, as more blood is returned to the heart and the end-diastolic volume increases, the heart automatically pumps out a correspondingly larger stroke volume. Fig. 9-22, p. 323

Figure 9.23: Effect of sympathetic stimulation on stroke volume. (a) Normal stroke volume. (b) Stroke volume during sympathetic stimulation. (c) Stroke volume with combination of sympathetic stimulation and increased end-diastolic volume. Fig. 9-23, p. 324

Figure 9.24: Shift of the Frank–Starling curve to the left by sympathetic stimulation. For the same end-diastolic volume (point A), there is a larger stroke volume (from point B to point C) on sympathetic stimulation as a result of increased contractility of the heart. The Frank–Starling curve is shifted to the left by variable degrees, depending on the extent of sympathetic stimulation. Fig. 9-24, p. 324

Outline Coronary circulation

Nourishing the Heart Muscle Muscle is supplied with oxygen and nutrients by blood delivered to it by coronary circulation, not from blood within heart chambers Heart receives most of its own blood supply that occurs during diastole During systole, coronary vessels are compressed by contracting heart muscle Coronary blood flow normally varies to keep pace with cardiac oxygen needs

Coronary Artery Disease (CAD) Pathological changes within coronary artery walls that diminish blood flow through the vessels Leading cause of death in United States Can cause myocardial ischemia and possibly lead to acute myocardial infarction Three mechanisms Profound vascular spasm of coronary arteries Formation of atherosclerotic plaques Thromboembolism

Collagen-rich smooth muscle cap of plaque Plaque Normal blood vessel wall Lipid-rich core of plaque Endothelium Fig. 9-29, p. 328

Fig. 9-30, p. 330 Figure 9.30: Consequences of thromboembolism. (a) A thrombus may enlarge gradually until it completely occludes the vessel at that site. (b) A thrombus may break loose from its attachment, forming an embolus that may completely occlude a smaller vessel downstream. (c) Scanning electron micrograph of a vessel completely occluded by a thromboembolic lesion. Fig. 9-30, p. 330

Area of cardiac muscle deprived of blood supply if coronary vessel is blocked at point Area of cardiac muscle deprived of blood supply if coronary vessel is blocked at point Left coronary artery Right coronary artery Left ventricle Right ventricle Fig. 9-31, p. 331

Possible Outcomes of Acute Myocardial Infarction (Heart Attack)