The Cardiovascular System: The Heart 18 P A R T A The Cardiovascular System: The Heart

Approximately the size of your fist Location Heart Anatomy Approximately the size of your fist Location Superior surface of diaphragm Left of the midline Anterior to the vertebral column, posterior to the sternum

Heart Anatomy Figure 18.1

Coverings of the Heart: Physiology The pericardium: Protects and anchors the heart Prevents overfilling of the heart with blood Allows for the heart to work in a relatively friction-free environment

Pericardial Layers of the Heart Figure 18.2

Cardiac Muscle Bundles Figure 18.3

External Heart: Vessels that Supply/Drain the Heart (Posterior View) Arteries – right coronary artery (in atrioventricular groove) and the posterior interventricular artery (in interventricular groove) Veins – great cardiac vein, posterior vein to left ventricle, coronary sinus, and middle cardiac vein

Aorta Superior vena cava Left Right pulmonary artery pulmonary artery Left atrium Pulmonary trunk Left pulmonary veins Right atrium Right pulmonary veins Mitral (bicuspid) valve Fossa ovalis Aortic valve Pectinate muscles Pulmonary valve Tricuspid valve Left ventricle Papillary muscle Right ventricle Chordae tendineae Interventricular septum Myocardium Trabeculae carneae Visceral pericardium Inferior vena cava Endocardium (e) Figure 18.4e

Right and Left Ventricles Figure 18.6

Figure 18.5

Coronary Circulation Coronary circulation is the functional blood supply to the heart muscle itself Collateral routes ensure blood delivery to heart even if major vessels are occluded

Coronary Circulation: Arterial Supply Figure 18.7a

Coronary Circulation: Venous Supply Figure 18.7b

Heart Valves Figure 18.8a, b

Heart Valves Figure 18.8c, d

Atrioventricular Valve Function Figure 18.9

Semilunar Valve Function Figure 18.10

Microscopic Anatomy of Heart Muscle Cardiac muscle is striated, short, fat, branched, and interconnected The connective tissue endomysium acts as both tendon and insertion Intercalated discs anchor cardiac cells together and allow free passage of ions Heart muscle behaves as a functional syncytium InterActive Physiology ®: Anatomy Review: The Heart, pages 3–7

Microscopic Anatomy of Cardiac Muscle Figure 18.11

The Cardiovascular System: The Heart 18 P A R T B The Cardiovascular System: The Heart

Cardiac Muscle Contraction Heart muscle: Is stimulated by nerves and is self-excitable (automaticity) Contracts as a unit Has a long (250 ms) absolute refractory period Cardiac muscle contraction is similar to skeletal muscle contraction

Heart Physiology: Intrinsic Conduction System Autorhythmic cells: Initiate action potentials Have unstable resting potentials called pacemaker potentials Use calcium influx (rather than sodium) for rising phase of the action potential

Pacemaker and Action Potentials of the Heart Figure 18.13

Cardiac Membrane Potential Figure 18.12

Cardiac Intrinsic Conduction Figure 18.14a

Heart Physiology: Sequence of Excitation Sinoatrial (SA) node generates impulses about 75 times/minute Atrioventricular (AV) node delays the impulse approximately 0.1 second Impulse passes from atria to ventricles via the atrioventricular bundle (bundle of His)

Heart Physiology: Sequence of Excitation AV bundle splits into two pathways in the interventricular septum (bundle branches) Bundle branches carry the impulse toward the apex of the heart Purkinje fibers carry the impulse to the heart apex and ventricular walls

Cardiac Intrinsic Conduction Figure 18.14a

Cardiac Membrane Potential Figure 18.12

Heart Excitation Related to ECG SA node generates impulse; atrial excitation begins Impulse delayed at AV node Impulse passes to heart apex; ventricular excitation begins Ventricular excitation complete SA node AV node Bundle branches Purkinje fibers Figure 18.17

Heart Excitation Related to ECG SA node generates impulse; atrial excitation begins SA node Figure 18.17

Heart Excitation Related to ECG Impulse delayed at AV node AV node Figure 18.17

Heart Excitation Related to ECG Impulse passes to heart apex; ventricular excitation begins Bundle branches Figure 18.17

Heart Excitation Related to ECG Ventricular excitation complete Purkinje fibers Figure 18.17

Heart Excitation Related to ECG SA node generates impulse; atrial excitation begins Impulse delayed at AV node Impulse passes to heart apex; ventricular excitation begins Ventricular excitation complete SA node AV node Bundle branches Purkinje fibers Figure 18.17

Electrocardiography Figure 18.16

Electrical activity is recorded by electrocardiogram (ECG) Electrocardiography Electrical activity is recorded by electrocardiogram (ECG) P wave corresponds to depolarization of SA node QRS complex corresponds to ventricular depolarization T wave corresponds to ventricular repolarization Atrial repolarization record is masked by the larger QRS complex PLAY InterActive Physiology ®: Intrinsic Conduction System, pages 3–6

Defective heart valves: Heart Murmurs Abnormal heart sounds produced by abnormal patterns of blood flow in the heart. Defective heart valves: Valves become damaged by antibodies made in response to an infection, or congenital defects. Mitral stenosis: Mitral valve becomes thickened and calcified. Impairs blood flow from left atrium to left ventricle. Accumulation of blood in left ventricle may cause pulmonary HTN. Incompetent valves: Damage to papillary muscles. Valves do not close properly. Murmurs produced as blood regurgitates through valve flaps.

Septal defects: Heart Murmurs Usually congenital. Holes in septum between the left and right sides of the heart. May occur either in interatrial or interventricular septum. Blood passes from left to right.

Electrocardiogram (ECG/EKG) The body is a good conductor of electricity. Tissue fluids have a high [ions] that move in response to potential differences. Electrocardiogram: Measure of the electrical activity of the heart per unit time. Potential differences generated by heart are conducted to body surface where they can be recorded on electrodes on the skin. Does NOT measure the flow of blood through the heart.

Ischemic Heart Disease Ischemia: Oxygen supply to tissue is deficient. Most common cause is atherosclerosis of coronary arteries. Increased [lactic acid] produced by anaerobic respiration. Angina pectoris: Substernal pain. Myocardial infarction (MI): Changes in T segment of ECG. Increased CPK and LDH.

Arrhythmias Detected on ECG Abnormal heart rhythms. Flutter: Extremely rapid rates of excitation and contraction of atria or ventricles. Atrial flutter degenerates into atrial fibrillation. Fibrillation: Contractions of different groups of myocardial cells at different times. Coordination of pumping impossible. Ventricular fibrillation is life-threatening.

Arrhythmias Detected on ECG (continued) Bradycardia: HR slower < 60 beats/min. Tachycardia: HR > 100 beats/min. First–degree AV nodal block: Rate of impulse conduction through AV node exceeds 0.2 sec. P-R interval. Second-degree AV nodal block: AV node is damaged so that only 1 out of 2-4 atrial APs can pass to the ventricles. P wave without QRS.

Arrhythmias Detected on ECG (continued) Third-degree (complete) AV nodal block: None of the atrial waves can pass through the AV node. Ventricles paced by ectopic pacemaker.

ECG Tracings Figure 18.18

Extrinsic Innervation of the Heart Heart is stimulated by the sympathetic cardioacceleratory center Heart is inhibited by the parasympathetic cardioinhibitory center Figure 18.15

Heart Sounds Figure 18.19

Heart sounds (lub-dup) are associated with closing of heart valves First sound occurs as AV valves close and signifies beginning of systole Second sound occurs when SL valves close at the beginning of ventricular diastole

Cardiac Cycle Cardiac cycle refers to all events associated with blood flow through the heart Systole – contraction of heart muscle Diastole – relaxation of heart muscle

Phases of the Cardiac Cycle Ventricular filling – mid-to-late diastole Heart blood pressure is low as blood enters atria and flows into ventricles AV valves are open, then atrial systole occurs

Phases of the Cardiac Cycle Ventricular systole Atria relax Rising ventricular pressure results in closing of AV valves Isovolumetric contraction phase Ventricular ejection phase opens semilunar valves

Phases of the Cardiac Cycle Isovolumetric relaxation – early diastole Ventricles relax Backflow of blood in aorta and pulmonary trunk closes semilunar valves Dicrotic notch – brief rise in aortic pressure caused by backflow of blood rebounding off semilunar valves PLAY InterActive Physiology ®: Cardiac Cycle, pages 3–18

Phase of contraction. Phase of relaxation. Cardiac Cycle Refers to the repeating pattern of contraction and relaxation of the heart. Systole: Phase of contraction. Diastole: Phase of relaxation. End-diastolic volume (EDV): Total volume of blood in the ventricles at the end of diastole. Stroke volume (SV): Amount of blood ejected from ventricles during systole. End-systolic volume (ESV): Amount of blood left in the ventricles at the end of systole.

Figure 18.20

Cardiac Cycle (continued) Step 1: Isovolumetric contraction: QRS just occurred. Contraction of the ventricle causes ventricular pressure to rise above atrial pressure. AV valves close. Ventricular pressure is less than aortic pressure. Semilunar valves are closed. Volume of blood in ventricle is EDV. Step 2: Ejection: Contraction of the ventricle causes ventricular pressure to rise above aortic pressure. Semilunar valves open. Ventricular pressure is greater than atrial pressure. AV valves are closed. Volume of blood ejected: SV.

Cardiac Cycle (continued) Step 3: T wave occurs: Ventricular pressure drops below aortic pressure. Step 4: Isovolumetric relaxation: Back pressure causes semilunar valves to close. AV valves are still closed. Volume of blood in the ventricle: ESV. Step 5: Rapid filling of ventricles: Ventricular pressure decreases below atrial pressure. AV valves open. Rapid ventricular filling occurs.

Cardiac Cycle (continued) Step 6: Atrial systole: P wave occurs. Atrial contraction. Push 10-30% more blood into the ventricle.

Cardiac Cycle (continued)

Correlation of ECG with Heart Sounds First heart sound: Produced immediately after QRS wave. Rise of intraventricular pressure causes AV valves to close. Second heart sound: Produced after T wave begins. Fall in intraventricular pressure causes semilunar valves to close.

Figure 18.20

Cardiac Output (CO) and Reserve CO is the amount of blood pumped by each ventricle in one minute CO is the product of heart rate (HR) and stroke volume (SV) HR is the number of heart beats per minute SV is the amount of blood pumped out by a ventricle with each beat Cardiac reserve is the difference between resting and maximal CO

Cardiac Output: Example CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat) CO = 5250 ml/min (5.25 L/min)

Regulation of Stroke Volume SV = end diastolic volume (EDV) minus end systolic volume (ESV) EDV = amount of blood collected in a ventricle during diastole ESV = amount of blood remaining in a ventricle after contraction

Factors Affecting Stroke Volume Preload – amount ventricles are stretched by contained blood Contractility – cardiac cell contractile force due to factors other than EDV Afterload – back pressure exerted by blood in the large arteries leaving the heart

Cardiac Output (CO) Volume of blood pumped/min. by each ventricle. Pumping ability of the heart is a function of the beats/ min. and the volume of blood ejected per beat. CO = SV x HR Total blood volume averages about 5.5 liters. Each ventricle pumps the equivalent of the total blood volume each min. (resting conditions).

Frank-Starling Law of the Heart Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume Slow heartbeat and exercise increase venous return to the heart, increasing SV Blood loss and extremely rapid heartbeat decrease SV

Preload and Afterload Figure 18.21

Extrinsic Factors Influencing Stroke Volume Contractility is the increase in contractile strength, independent of stretch and EDV Increase in contractility comes from: Increased sympathetic stimuli Certain hormones Ca2+ and some drugs

Extrinsic Factors Influencing Stroke Volume Agents/factors that decrease contractility include: Acidosis Increased extracellular K+ Calcium channel blockers

Heart Contractility and Norepinephrine Extracellular fluid Norepinephrine b1-Adrenergic receptor Adenylate cyclase Ca2+ Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP second-messenger system Ca2+ channel Cytoplasm GTP 1 GTP GDP ATP cAMP Active protein kinase A Inactive protein kinase A Ca2+ 3 Ca2+ uptake pump 2 Enhanced actin-myosin interaction binds Troponin to Ca2+ SR Ca2+ channel Cardiac muscle force and velocity Sarcoplasmic reticulum (SR) Figure 18.22

Regulation of Heart Rate Positive chronotropic factors increase heart rate Negative chronotropic factors decrease heart rate

Circulatory Changes During Exercise (continued)

Regulation of Heart Rate: Autonomic Nervous System Sympathetic nervous system (SNS) stimulation is activated by stress, anxiety, excitement, or exercise Parasympathetic nervous system (PNS) stimulation is mediated by acetylcholine and opposes the SNS PNS dominates the autonomic stimulation, slowing heart rate and causing vagal tone

Atrial (Bainbridge) Reflex Atrial (Bainbridge) reflex – a sympathetic reflex initiated by increased blood in the atria Causes stimulation of the SA node Stimulates baroreceptors in the atria, causing increased SNS stimulation

Chemical Regulation of the Heart The hormones epinephrine and thyroxine increase heart rate Intra- and extracellular ion concentrations must be maintained for normal heart function InterActive Physiology ®: Cardiac Output, pages 3–9

Figure 18.23

Congestive Heart Failure (CHF) Congestive heart failure (CHF) is caused by: Coronary atherosclerosis Persistent high blood pressure Multiple myocardial infarcts Dilated cardiomyopathy (DCM)

Baroreceptor Reflex (continued)

Renin-Angiotension-Aldosterone System (continued)

Dehydration or excess salt intake: Regulation by ADH Released by posterior pituitary when osmoreceptors detect an increase in plasma osmolality. Dehydration or excess salt intake: Produces sensation of thirst. Stimulates H20 reabsorption from urine.