The Heart (Chapter 9) Heart is the main pump of the circulatory system. Blood flows from the left side of the heart into the larger arteries arterioles capillaries venules veins and into right side of the heart. Right heart pumps unoxygenated blood to pulmonary system. Oxygenated blood flows back into the receiving chamber on the left side. Slide 8-1 Location of the Heart Slide 8-2 1
Surface Anatomy of the Heart Slide 8-3 Internal Anatomy of the Heart Distinct right and left sides. Each side contains 2 chambers (atrium, ventricle). Large veins (inferior and superior vena cavae) enter the right side. Large artery (aorta) leaves the left side. Slide 8-4 2
The Heart Valves Slide 8-5 The Heart Wall Slide 8-6 3
The Coronary Circulation Slide 8-7 Cardiac Muscle Cells Two types of muscle cells present in the heart: Contractility Capable of generating contraction independent of neural or hormonal stimulation. Most of the muscle cells of the heart. First step in triggering cardiac contraction is appearance of an action potential in the sarcolemma. Rate and duration of depolarization and repolarization is much longer for cardiac contractile cells than for skeletal muscle cells. Contractile cells unable to achieve tetany. Conduction (consist of nodal cells and conducting cells) Nodal cells are responsible for initiating and maintaining contractile rate. Conducting cells are responsible for transmitting electrical impulses to rest of the heart. Slide 8-8 4
Cardiac Conduction Pathway Contraction is initiated at the sinoatrial (SA) node in the posterior right atrium. Impulse moves through atrial walls via specialized conduction pathways. Impulse is then focused at the atrioventricular (AV) node, located within the ventricular septum. Specialized conduction pathways (Bundle of His) carry impulse toward the ventricular apex. Other specialized fibers (Purkinje fibers) carry the impulse to ventricular walls. Impulse spreads throughout ventricular myocardium. Slide 8-9 Cardiac Contraction Slide 8-10 5
The Electrocardiogram (EKG) Slide 8-11 The Electrocardiogram (EKG) P wave: Atrial depolarization signals beginning of atrial contraction. QRS complex: Signals beginning of ventricular depolarization, and therefore ventricular systole. T-wave: Repolarization of the ventricle, corresponds to ventricular diastole. Slide 8-12 6
Events in the Cardiac Cycle Slide 8-13 Control of Cardiac Function Cardiac output = Stroke volume X Heart rate. Typical values: SV = 80 cc/beat; HR = 70 bpm CO = 5.6 L/min. CO can increase X 5 during periods of physical stress. This occurs through combination of increases in heart rate and stroke volume. Main components of CO control: Blood volume reflexes. Autonomic innervation. Hormones. Slide 8-14 7
Blood Volume Reflexes Increase in heart rate triggered by the atrial reflex. Stretch receptors are present in the walls of the right atrium. Increase in venous filling causes expansion of right atrial walls. Stretch receptors are activated causes a local increase in pacemaker cell firing rate, as well as increased sympathetic stimulation. Increase in SV is a function of the Frank-Starling law. Preload (LA pressure) increases transiently causes increase in diastolic left ventricular filling volume causes cardiac muscles to move further up on the stress-strain curve (increased stretch) causes increased force of contraction to expel the extra blood. Afterload (peripheral resistance) increases temporarily LV contraction does not push out normal amount of blood more blood remains in LV after systole usual amount of blood enters LV during diastole causes increase in end diastolic volume stretches cardiac muscles further increases force of next ventricular contraction extra blood is expelled. Slide 8-15 Autonomic Innervation Basic heart rate is established by pacemaker cells and propagation of action potential through the cardiac conduction system. Heart rate can be changed transiently through the autonomic nervous system. Heart responds to sympathetic and parasympathetic stimulation. Sympathetic produces excitatory effects. Increase in HR, contractile force (SV). Parasympathetic causes inhibitory effects. Decreases HR, decreases SV. Slide 8-16 8
Autonomic Innervation Heart rate: ANS stimulation affects SA node firing frequency. Acetylcholine released by parasympathetic motor neurons causes decrease in SA rate (negative chronotropic effect). Norepinephrine released by sympathetic neurons increases SA activity (positive chronotropic effect). Also have increase in HR due to release of epinephrine and norepinephrine by adrenal medulla. Stroke Volume: Sympathetic release of epinephrine and norepinephrine at myocardial synapses and adrenal medulla increases cardiac muscle cell contraction (positive inotropic effect). Parasympathetic release of Ach inhibits muscle contraction and decreases SV (negative inotropic effect). Slide 8-17 9