NURS 203 Lec 5 PDF - The Cardiovascular System

The Cardiovascular System The Heart Abdo Berro, PhD September 2024  Heart Location In the mediastinum between 2nd rib & 5th intercostal space On the superior surface of diaphragm Anterior to vertebral column, posterior to sternum Two-thirds to the left of the midsternal line...

The Cardiovascular System The Heart Abdo Berro, PhD September 2024  Heart Location In the mediastinum between 2nd rib & 5th intercostal space On the superior surface of diaphragm Anterior to vertebral column, posterior to sternum Two-thirds to the left of the midsternal line Heart Location Heart Anatomy Anterior View Posterior View Coverings and Layers of The Heart  Coverings of The Heart The Pericardium Double-walled sac Fibrous pericardium – Tough and dense CT – Protects – Anchors to surrounding structures – Prevent excess filling with blood Serous pericardium – Thin and slippery serous membrane made of two layers – Parietal layer ➔ Covers internal of fibrous pericardium – Visceral layer ➔ Covers external heart surface Epicardium  Layers of The Heart Wall (1) Epicardium (2) Myocardium Cardiac muscle – Muscle cells arranged in spiral or circular bundles CT fibers (fibrous skeleton) – Collagen and elastic – Reinforces myocardium and anchors muscle fibers – Supports great vessels and valves – Directs spread of action potentials to specific pathways (3) Endocardium – Endothelial layer – Lines heart chambers and covers fibrous skeleton of the valves – Continuous with blood vessels Chambers of The Heart Four chambers Two atria (superior) – Separated internally by the inter-atrial septum – Coronary sulcus (atrioventricular groove) encircles the junction of the atria and ventricles – Auricles increase atrial volume Two ventricles (inferior) – Separated by the inter-ventricular septum – Anterior and posterior inter-ventricular sulci mark the position of the septum externally Chambers of The Heart  Atria: The Receiving Chambers Thin walls are ridged by bundles of muscle tissue that look like comb teeth ➔ pectinate muscles Vessels entering right atrium – Superior vena cava – Inferior vena cava – Coronary sinus Vessels entering left atrium – Two right and two left pulmonary veins Ventricles: The Discharging Chambers Thick walls are ridged by irregular ridges ➔ trabeculae carneae Papillary muscles project into the ventricular cavities – Involved in valve function Vessel leaving the right ventricle – Pulmonary trunk – Into lungs for gas exchange Vessel leaving the left ventricle – Aorta Pathway of Blood Through The Heart The heart is two side-by-side pumps – Serve two separate blood circuits Right side is the pump for the pulmonary circuit – Vessels that carry blood to and from the lungs Left side is the pump for the systemic circuit – Vessels that carry the blood to and from all body tissues Pathway of Blood Through The Heart Superior & inferior vena cava → right atrium → tricuspid valve → right ventricle → pulmonary semilunar valve → pulmonary trunk → pulmonary arteries → lungs Pathway of Blood Through The Heart Lungs → pulmonary veins → left atrium → bicuspid valve → left ventricle → aortic semilunar valve → aorta → systemic circulation  Pathway of Blood Through The Heart Equal volumes of blood are pumped through the pulmonary and systemic circuits Pulmonary circuit is a short, low- pressure circulation Systemic circuit blood is longer and encounters five times as much resistance – Anatomy of the ventricles reflects these differences Coronary Circulation The functional blood supply to the heart muscle itself (A) Arteries Arterial supply varies considerably and contains many anastomoses (junctions) among branches – Collateral routes provide additional routes for blood delivery Right coronary – Marginal and posterior interventricular arteries Left coronary – Circumflex and anterior interventricular arteries (B)Veins Small cardiac, middle cardiac, and great cardiac veins → coronary sinus which empties in right atrium Anterior cardiac veins empty directly into RA Heart Valves Four heart valves enforce the one-way flow of blood through the heart Atrioventicular Heart Valves Atrioventricular (AV) Heart Valves Location: At the atrial-ventricular junctions Function: Prevent backflow into the atria when ventricles contract (I) Tricuspid valve (right) Three (3) flexible cusps (flaps of endocardium + CT) (II) Mitral valve (left) Bicuspid = 2 cusps Atrioventricular (AV) Heart Valves Chordae tendineae ➔ anchor AV valve cusps to papillary muscles – Protrude from the ventricular walls – Anchor the valves in their closed position How they work? When heart is relaxed ➔ AV flaps are relaxed so blood can flow into atria and then into valves When ventricles contract ➔ intraventricular blood pressure closes flaps Semilunar Heart Valves Semilunar (SL) Heart Valves Location: Three pocket-like cusps shaped like crescent moon Bases of the large arteries existing the ventricles Function: Prevent backflow into the ventricles when ventricles relax (I) Aortic semilunar valve Aorta (II) Pulmonary semilunar valve Pulmonary trunk Semilunar (SL) Heart Valves How they works? Open and close in response to differences in pressure When ventricles contract → intraventricular pressure rises and forces cusps to open and flatten against arterial wall When ventricles relax → blood backflow toward the heart fills the cusps → closes the valves Cardiac Muscle Fibers Cardiac muscle cells are striated, short, fat, branched, and interconnected Cells are connected via intercalated discs – Junctions between cells – Anchor cardiac cells – Desmosomes prevent cells from separating during contraction – Gap junctions allow ions to pass ➔ electrically couple adjacent cells ➔ Myocardium behaves as single coordinated functional unit Cardiac Muscle Fiber Cardiac Muscle Fibers Intercellular space ➔ Loose connective tissue matrix (endomysium) connects to the fibrous skeleton – Contains capillaries Numerous large mitochondria (25–35% of cell volume) – Enable muscle cells to resist fatigue T tubules are wide but less numerous and SR is simpler than in skeletal muscle Contraction of Cardiac Muscle Automaticity / autorhythmicity – Contraction initiated by autorhythmic cardiac muscle cells About 1% of all cardiac cells Induces Depolarization ➔ Own and rest of the heart Depolarization of the heart is rhythmic and spontaneous – Gap junctions ensure the heart contracts as a unit Allow for depolarization waves to travel from cell to cell Long absolute refractory period (250 ms) – Prevents tetanic contractions Contraction of Cardiac Muscle 1. Depolarization opens voltage-gated fast Na+ channels in the sarcolemma Reversal of membrane potential from –90 to +30 mV 2. Depolarization wave opens Ca2+ channels in the sarcolemma (slow Ca2+ channels) 3. Depolarization wave in T tubules and rise influx in Ca2+ induces the release Ca2+ from SR 4. Ca2+ surge prolongs the depolarization phase (plateau) 5. Na+ closes (early) and voltage-gated K+ opens, and inactivation of Ca2+ channels → repolarization Contraction of Cardiac Muscle Excitation-contraction coupling occurs as Ca2+ binds to troponin ➔ allows sliding of the actin filaments ➔ contraction Duration of the action potential and the contractile phase is much greater in cardiac muscle than in skeletal muscle – To provide sustained contraction needed to eject blood from heart Refractory period (unexcitable period) is longer in cardiac muscle than in skeletal muscle – Prevent tetanic contractions which would stop the heart’s pumping action Heart Physiology - Electrical Events The Intrinsic Conduction System Independent and coordinated function due to: – Presence of gap junctions – Activity of own conduction system Intrinsic cardiac conduction system consists of: – Non-contractile cardiac cells – Initiate and distribute impulses throughout heart ➔ Depolarization and contraction occur in orderly and sequential manner ➔ heart beats as a coordinated unit Autorhythmic Cells Initiate action potential Unstable resting membrane potential Continuously depolarize Spontaneous change of membrane potential – Pacemaker potentials or prepotentials – Initiate action potential ➔ triggers heart rhythmic contraction Autorhythmic Cells Hyperpolarization at end of action potential ➔ closing of K+ channels and opening of slow Na+ channels ➔ @ -40mV (threshold) Ca2+ channels open ➔ Ca2+ influx from extracellular space ➔ Ca2+ produces action potential – K+ channels open ➔ Falling phase of action potential and repolarization – Once repolarization is complete, K+ efflux declines ➔ slow depolarization to threshold begins again Autorhythmic Cells Pacemaker and Action Potentials Sequence of Excitation  Electrical Events Sequence of Excitation I. Sinoatrial (SA) node (pacemaker) – Depolarizes faster than any other part of the myocardium – Generates impulses about 80-100 times/minute – Sinus rhythm ➔ determines heart rate II. Atrioventricular (AV) node – Depolarization: SA node ➔ through atria ➔ AV node – Smaller diameter fibers and fewer gap junctions Delays impulses approximately 0.1 second Allows atria to contract before ventricles contract – Conducts impulses slower than other parts – Depolarizes 40-60 times/minute (50 average) in absence of SA node input Electrical Events Sequence of Excitation III. Atrioventricular (AV) bundle (bundle of His) – Only electrical connection between the atria and ventricles (no gap junctions between them) – Depolarize only 30 times per minute in absence of AV node input IV. Right and left bundle branches – Two pathways along the interventricular septum ➔ carry the impulses toward the apex of the heart – Excite septal cells Electrical Events Sequence of Excitation V. Purkinje fibers – Complete the pathway through the interventricular septum into the apex and then into ventricular walls – More elaborate in left ventricle – Depolarization of ventricular muscle cells (with help of gap junctions) – Depolarize only 30 times per minute in absence of AV node input Sequence of Excitation Extrinsic Innervation of the Heart Heartbeat is modified by the autonomic nervous system (ANS) Cardiac centers are located in the medulla oblongata – Cardioacceleratory center: Sympathetic neurons ➔ innervates SA and AV nodes, heart muscle, and coronary arteries ➔ increases heart’s rate and pumping force – Cardioinhibitory center: Parasympathetic fibers in the vagus nerves ➔ innervates SA and AV nodes ➔ slowing of heart rate Electrocardiography Electrocardiogram (ECG or EKG) – Graphic record of heart activity – A composite of all the action potentials generated by nodal and contractile cells at a given time Three waves: P wave: Results from movement of the depolarization wave from the SA node to atria – Followed by atrial contraction QRS complex: Results from ventricular depolarization – Followed by ventricular contraction T wave: Results from ventricular repolarization Electrocardiography Electrocardiography Atrial repolarization occurs during period of ventricular excitation ➔ obscured by QRS complex being recorded at same time P-Q (P-R) interval – Beginning of atrial excitation to beginning of ventricular excitation S-T segment – Ventricular myocardium in totally depolarized – Elevated/depressed ➔ cardiac ischemia Q-T interval – Beginning of ventricular depolarization through ventricular repolarization – Prolonged ➔ repolarization abnormality Normal and Abnormal ECG Tracings Normal and Abnormal ECG Tracings Heart Sounds Heartbeat ➔ two sounds (lub-dup) – Associated with closing of heart valves – Pause interval = relaxing heart 1) First = AV valves close – Ventricular pressure > atrial pressure – Louder and longer 2) Second = SL valves close – Beginning of ventricular relaxation – Short and sharp Heart Sounds Mechanical Events of The Cardiac Cycle Includes all events associated with the blood flow through the heart during complete heartbeat The heart alternates between contraction and relaxation – Contraction Period ➔ SYSTOLE – Relaxation Period ➔ DIASTOLE Mechanical Events of The Cardiac Cycle Atrial systole ➔ atrial diastole ➔ ventricular systole ➔ ventricular diastole These mechanical events ALWAYS follow the electrical events – As seen in EKG The Cardiac Cycle Cardiac Cycle (1) Ventricular Filling I. Pressure in heart is low, blood flowing passively through atria and AV valves, and SL valves are closed ➔ 80% of filling Blood filling causes the AV valve flaps to begin drifting toward the closed position II. Atrial depolarization (P wave) ➔ atria contract ➔ increase atrial pressure ➔ pushes blood into ventricles ➔ remaining 20% of filling Cardiac Cycle (1) Ventricular Filling In the meantime…. Ventricles are in last phase of their diastole EDV = end diastolic volume ➔Maximum blood volume ventricles can contain III. Atrial diastole (relaxation) ➔ Ventricular depolarization begins (QRS complex) Cardiac Cycle (2) Ventricular Systole I. As atria relax ➔ ventricles begin contracting II. Ventricular pressure rises ➔ AV valves closes (lub) Isovolumetric contraction phase ➔ very brief moment when ventricles are completely closed and blood volume remains constant as ventricles contract Cardiac Cycle (2) Ventricular Systole III. Ventricular pressure increases ➔ ventricular pressure > pressure in large arteries exiting ventricles ➔ SL valves forced open ➔ blood pushed through aorta and pulmonary trunk (ventricular ejection phase) Cardiac Cycle (3) Isovolumetric Relaxation Early ventricular diastole I. Following the T wave = ventricles repolarizing ➔ ventricles relax II. Ventricular pressure drops ➔ blood in aorta and pulmonary trunk flows back toward heart ➔ closes SL valves (dup) Cardiac Cycle (3) Isovolumetric Relaxation ESV = end systolic volume ➔ Blood remaining in ventricles after contraction Dicrotic notch ➔ Brief rise in aortic pressure due to backflowing blood bouncing off closed valve cusps Mechanical Events of The Cardiac Cycle During ventricular systole, atria is in diastole ➔ atria filling with blood Atrial blood pressure > ventricular blood pressure ➔ AV valves forced open ➔ begin ventricular filling Mechanical Events of The Cardiac Cycle Assuming 75 bpm ➔ Cardiac cycle = 0.8 sec – Atrial systole = 0.1 sec – Ventricular systole = 0.3 sec – Quiescent (relaxation) period = 0.4 sec Blood flow through heart (1) is controlled by pressure changes, and (2) it flows down a pressure gradient Cardiac Output (CO) Amount of blood pumped out by each ventricle in one minute Determined by: Heart rate (HR) – Number of beats per minute Stroke volume (SV) – Volume of blood pumped out by one ventricle with each beat; Correlates with force of contraction Cardiac Output (CO) CO = heart rate (HR) x stroke volume (SV) Cardiac Output (CO) At rest CO (ml/min) = HR (75 beats/min) X SV (70 ml/beat) = 5.25 L/min Cardiac reserve: difference between resting and maximal CO – Cardiac reserve in nonathletic people is 4–5 times resting CO (20- 25 L/min) – Cardiac reserve in athletic people is 6–7 times resting CO (35 L/min) Cardiac Output Regulation of Stroke Volume SV = EDV – ESV Three main factors affect SV – Preload – Contractility – Afterload Cardiac Output Regulation of Stroke Volume Preload Frank-Starling law of the heart: The degree to which cardiac muscle cells are stretched just before they contract, PRELOAD, is the critical factor determining SV Cardiac cells normally shorter than optimal length Venous return is most important factor in stretching cardiac muscle – ↑ volume or speed ➔ ↑ EDV and ↑ SV – Slow heartbeat and exercise increase venous return Cardiac Output Regulation of Stroke Volume Contractility The contractile strength achieved at a given muscle length, independent of muscle stretch and EDV Enhanced contractility = greater SV and lower ESV Cardiac Output Regulation of Stroke Volume Contractility Cont’d Positive regulators of contractility = Positive ionotropic agents ➔ Increase contractility – Increased Ca2+ influx due to sympathetic stimulation – Hormones (thyroxine, glucagon, and epinephrine) Negative regulators of contractility = Negative ionotropic agents ➔ Decrease contractility – Acidosis (excess H+) – Increased extracellular K+ – Calcium channel blockers Cardiac Output Regulation of Stroke Volume Afterload Back pressure exerted by arterial blood – Must be overcome for ventricles to eject blood Not a major determinant in healthy people because it is relatively constant Hypertension increases afterload ➔ resulting in increased ESV and reduced SV Cardiac Output Regulation of Heart Rate Positive chronotropic factors ➔ increase heart rate Negative chronotropic factors ➔ decrease heart rate Autonomic Nervous System Regulation Sympathetic nervous system is activated by emotional or physical stressors – Norepinephrine is released at the cardiac synapses ➔ causes the pacemaker to fire more rapidly – And at the same time it increases contractility Cardiac Output Regulation of Heart Rate Autonomic Nervous System Regulation Atrial (Bainbridge) reflex ➔ A sympathetic reflex initiated by increased venous return and increased atrial filling Stretching of the atrial walls stimulates the SA node and the atrial stretch receptors ➔ activates sympathetic reflexes ➔ increased heart rate Cardiac Output Regulation of Heart Rate Autonomic Nervous System Regulation Parasympathetic nervous system opposes sympathetic effects – Acetylcholine hyperpolarizes pacemaker cells by opening K+ channels Sensory inputs from the cardiovascular system influence the action of ANS Regulation of Heart Rate Chemical Factors Hormones – Epinephrine from adrenal medulla enhances heart rate and contractility – Thyroxine increases heart rate and enhances the effects of norepinephrine and epinephrine Ions – Intra- and extracellular ion concentrations (e.g., Ca2+ and K+) must be maintained for normal heart function Other Factors Age, gender, exercise, and body temperature Regulation of Cardiac Output