Cardiovascular System PDF

Cardiovascular System Learning Objectives: Cardiovascular System Physiology of cardiac muscle contraction List the parts of the electrical conduction system of the heart in sequence, beginning at the sinoatrial (SA) node, and explain how the electrical conduction system functions. List the...

Cardiovascular System Learning Objectives: Cardiovascular System Physiology of cardiac muscle contraction List the parts of the electrical conduction system of the heart in sequence, beginning at the sinoatrial (SA) node, and explain how the electrical conduction system functions. List the waveforms and segments of a typical electrocardiogram (ECG or EKG), and explain the electrical events represented by each waveform or segment. Define cardiac cycle, systole, and diastole. Diagram or describe the atrial and ventricular events of the cardiac cycle, beginning with atrial and ventricular diastole. Describe atrioventricular (AV) and semilunar (SL) valve position (open/closed) and the direction of blood flow during ventricular filling, isovolumetric ventricular contraction, ventricular ejection, and isovolumetric ventricular relaxation. Diagram or describe the relationships among the left atrial and ventricular pressure and volume curves, heart sounds, and the electrocardiogram during one cardiac cycle (the Wiggers diagram).  Setting the Basic Rhythm: The Intrinsic Conduction System Sequence of excitation – Cardiac pacemaker cells pass impulses, in following order, across heart in ∼0.22 seconds 1. Sinoatrial node → 2. Atrioventricular node → 3. Atrioventricular bundle → 4. Right and left bundle branches → 5. Subendocardial conducting network (Purkinje fibers) © 2016 Pearson Education, Ltd. Figure 18.13 Intrinsic cardiac conduction system and action potential succession during one heartbeat. Slide 6 Superior vena cava Right atrium Pacemaker potential 1 The sinoatrial (SA) node (pacemaker) SA node generates impulses. Internodal pathway 2 The impulses Left atrium pause (0.1 s) at the atrioventricular Atrial muscle (AV) node. 3 The Subendocardial atrioventricular conducting (AV) bundle network AV node connects the atria (Purkinje fibers) to the ventricles. Ventricular 4 The bundle branches Pacemaker muscle conduct the impulses Inter- Plateau through the ventricular potential interventricular septum. septum 5 The subendocardial conducting network depolarizes the contractile 0 200 400 600 cells of both ventricles. Milliseconds Anatomy of the intrinsic conduction system showing the sequence Comparison of action potential shape of electrical excitation at various locations © 2016 Pearson Education, Ltd.  Clinical – Homeostatic Imbalance 18.4 Defects in intrinsic conduction system may cause: – Arrhythmias: irregular heart rhythms – Uncoordinated atrial and ventricular contractions – Fibrillation: rapid, irregular contractions Heart becomes useless for pumping blood, causing circulation to cease; may result in brain death Treatment: defibrillation interrupts chaotic twitching, giving heart “clean slate” to start regular, normal depolarizations © 2016 Pearson Education, Ltd.  Clinical – Homeostatic Imbalance 18.4 To reach ventricles, impulse must pass through AV node If AV node is defective, may cause a heart block – Few impulses (partial block) or no impulses (total block) reach ventricles – Ventricles beat at their own intrinsic rate Too slow to maintain adequate circulation – Treatment: artificial pacemaker, which recouples atria and ventricles © 2016 Pearson Education, Ltd.  Modifying the Basic Rhthym: Extrinsic Innervation of the Heart Heartbeat modified by ANS via cardiac centers in medulla oblongata – Cardioacceleratory center: sends signals through sympathetic trunk to increase both rate and force Stimulates SA and AV nodes, heart muscle, and coronary arteries – Cardioinhibitory center: parasympathetic signals via vagus nerve to decrease rate Inhibits SA and AV nodes via vagus nerves © 2016 Pearson Education, Ltd. Figure 18.14 Autonomic innervation of the heart. The vagus nerve Dorsal motor nucleus (parasympathetic) of vagus decreases heart rate. Cardioinhibitory center Cardioacceleratory center Medulla oblongata Sympathetic trunk ganglion Thoracic spinal cord Sympathetic trunk Sympathetic cardiac nerves increase heart rate and force of contraction. AV node SA node Parasympathetic neurons Sympathetic neurons Interneurons © 2016 Pearson Education, Ltd.  Action Potentials of Contractile Cardiac Muscle Cells Contractile muscle fibers make up bulk of heart and are responsible for pumping action – Different from skeletal muscle contraction; cardiac muscle action potentials have plateau Steps involved in AP: 1. Depolarization opens fast voltage-gated Na+ channels; Na+ enters cell Positive feedback influx of Na+ causes rising phase of AP (from −90 mV to +30 mV) 2. Depolarization by Na+ also opens slow Ca2+ channels At +30 mV, Na+ channels close, but slow Ca2+ channels remain open, prolonging depolarization – Seen as a plateau 3. After about 200 ms, slow Ca2+ channels are closed, and voltage-gated K+ channels are open Rapid efflux of K+ repolarizes cell to RMP Ca2+ is pumped both back into SR and out of cell into extracellular space © 2016 Pearson Education, Ltd. Figure 18.15 The action potential of contractile cardiac muscle cells. Slide 4 Action 1 Depolarization is due to Na+ influx potential through fast voltage-gated Na+ channels. A positive feedback cycle rapidly opens 20 Plateau many Na+ channels, reversing the membrane potential. Channel inactivation Membrane potential (mV) 2 ends this phase. 0 Tension development (contraction) 2 Plateau phase is due to Ca2+ influx Tension (g) −20 through slow Ca2+ channels. This keeps 1 3 the cell depolarized because most K+ −40 channels are closed. −60 Absolute 3 Repolarization is due to Ca2+ refractory channels inactivating and K+ channels −80 period opening. This allows K+ efflux, which brings the membrane potential back to its resting voltage. 0 150 300 Time (ms) © 2016 Pearson Education, Ltd.  Electrocardiography Electrocardiograph can detect electrical currents generated by heart Electrocardiogram (ECG or EKG) is a graphic recording of electrical activity – Composite of all action potentials at given time; not a tracing of a single AP – Electrodes are placed at various points on body to measure voltage differences 12 lead ECG is most typical Main features: – P wave: depolarization of SA node and atria – QRS complex: ventricular depolarization and atrial repolarization – T wave: ventricular repolarization – P-R interval: beginning of atrial excitation to beginning of ventricular excitation – S-T segment: entire ventricular myocardium depolarized – Q-T interval: beginning of ventricular depolarization through ventricular repolarization © 2016 Pearson Education, Ltd. Figure 18.16 An electrocardiogram (ECG) tracing. QRS complex R Ventricular depolarization Atrial Ventricular depolarization repolarization Sinoatrial P T node Atrioventricular node Q P-R S-T Interval Segment S Q-T Interval 0 0.2 0.4 0.6 0.8 Time (s) © 2016 Pearson Education, Ltd. Figure 18.17 The sequence of depolarization and repolarization of the heart related to the deflection waves of an ECG tracing. Slide 7 SA node R P T Q S 1 Atrial depolarization, initiated by the SA node, causes the P wave. AV node R P T Q S 2 With atrial depolarization complete, the impulse is delayed at the AV node. R P T Q S 3 Ventricular depolarization begins at apex, causing the QRS complex. Atrial repolarization occurs. R P T Q S 4 Ventricular depolarization is complete. R P T Q S 5 Ventricular repolarization begins at apex, causing the T wave. R P T Q S Depolarization 6 Ventricular repolarization is complete. Repolarization © 2016 Pearson Education, Ltd.  Clinical – Homeostatic Imbalance 18.5 Changes in patterns or timing of ECG may reveal diseased or damaged heart, or problems with heart’s conduction system Problems that can be detected: – Enlarged R waves may indicate enlarged ventricles – Elevated or depressed S-T segment indicates cardiac ischemia Problems that can be detected: (cont.) – Prolonged Q-T interval reveals a repolarization abnormality that increases risk of ventricular arrhythmias – Junctional blocks, blocks, flutters, and fibrillations are also detected on ECG © 2016 Pearson Education, Ltd. Figure 18.19 Normal and abnormal ECG tracings. Normal sinus rhythm. Junctional rhythm. The SA node is nonfunctional, P waves are absent, and the AV node paces the heart at 40–60 beats/min. Second-degree heart block. Some P waves are not conducted through the AV node; hence more P than QRS waves are seen. In this tracing, the ratio of P waves to QRS waves is mostly 2:1. © 2013 Pearson Ventricular fibrillation. These chaotic, grossly irregular ECG Education, Inc. deflections are seen in acute heart attack and electrical shock. Figure 20–13 Cardiac Arrhythmias. Premature Atrial Contractions (PACs) Premature atrial contractions (PACs) increase the incidence of PACs, presumably often occur in healthy individuals. In a PAC, by increasing the permeabilities of the SA the normal atrial rhythm is momentarily pacemakers. The impulse spreads along the P P P interrupted by a “surprise” atrial contraction. conduction pathway, and a normal ventricu- Stress, caffeine, and various drugs may lar contraction follows the atrial beat. Paroxysmal Atrial Tachycardia (PAT) In paroxysmal (par-ok-SIZ-mal) atrial tachycardia, or PAT, a premature atrial contraction triggers a flurry of atrial activity. P P P P P P The ventricles are still able to keep pace, and the heart rate jumps to about 180 beats per minute. Atrial Fibrillation (AF) During atrial fibrillation (fib-ri-LĀ-shun), are now nonfunctional, their contribution the impulses move over the atrial surface at to ventricular end-diastolic volume (the rates of perhaps 500 beats per minute. The maximum amount of blood the ventricles atrial wall quivers instead of producing an can hold at the end of atrial contraction) is organized contraction. The ventricular rate so small that the condition may go cannot follow the atrial rate and may remain unnoticed in older individuals. within normal limits. Even though the atria Premature Ventricular Contractions (PVCs) Premature ventricular contractions called an ectopic pacemaker. The (PVCs) occur when a Purkinje cell or frequency of PVCs can be increased by ventricular myocardial cell depolarizes to exposure to epinephrine, to other P T P T P T threshold and triggers a premature stimulatory drugs, or to ionic changes contraction. Single PVCs are common and that depolarize cardiac muscle plasma not dangerous. The cell responsible is membranes. Ventricular Tachycardia (VT) Ventricular tachycardia is defined as four or more PVCs without intervening normal beats. It is also known as VT or P V-tach. Multiple PVCs and VT may indicate that serious cardiac problems exist. Ventricular Fibrillation (VF) Ventricular fibrillation (VF) is respon- sible for the condition known as cardiac arrest. VF is rapidly fatal, because the ventricles quiver and stop pumping blood. 15 © 2018 Pearson Education, Ltd.  Heart Sounds Two sounds (lub-dup) associated with closing of heart valves – First sound is closing of AV valves at beginning of ventricular systole – Second sound is closing of SL valves at beginning of ventricular diastole – Pause between lub-dups indicates heart relaxation Mitral valve closes slightly before tricuspid, and aortic closes slightly before pulmonary valve – Differences allow auscultation of each valve when stethoscope is placed in four different regions © 2016 Pearson Education, Ltd. Figure 18.20 Areas of the thoracic surface where the sounds of individual valves are heard most clearly. Aortic valve sounds heard in 2nd intercostal space at right sternal margin Pulmonary valve sounds heard in 2nd intercostal space at left sternal margin Mitral valve sounds heard over heart apex (in 5th intercostal space) in line with middle of clavicle Tricuspid valve sounds typically heard in right sternal margin of 5th intercostal space © 2016 Pearson Education, Ltd. Figure 20–18b Heart Sounds. 120 Semilunar Semilunar valves open valves close 90 Pressure (mm Hg) 60 Left ventricle Left AV valves AV valves 30 atrium close open 0 S1 S2 S4 S3 S4 Heart sounds “Lubb” “Dupp” b The relationship between heart sounds and key events in the cardiac cycle 18 © 2018 Pearson Education, Ltd.  Clinical – Homeostatic Imbalance 18.6 Heart murmurs: abnormal heart sounds heard when blood hits obstructions Usually indicate valve problems – Incompetent (or insufficient) valve: fails to close completely, allowing backflow of blood Causes swishing sound as blood regurgitates backward from ventricle into atria – Stenotic valve: fails to open completely, restricting blood flow through valve Causes high-pitched sound or clicking as blood is forced through narrow valve © 2016 Pearson Education, Ltd.  18.6 Mechanical Events of Heart Systole: period of heart contraction Diastole: period of heart relaxation Cardiac cycle: blood flow through heart during one complete heartbeat – Atrial systole and diastole are followed by ventricular systole and diastole – Cycle represents series of pressure and blood volume changes – Mechanical events follow electrical events seen on ECG Three phases of the cardiac cycle (following left side, starting with total relaxation) © 2016 Pearson Education, Ltd.  18.6 Mechanical Events of Heart 1. Ventricular filling: mid-to-late diastole Pressure is low; 80% of blood passively flows from atria through open AV valves into ventricles from atria (SL valves closed) Atrial depolarization triggers atrial systole (P wave), atria contract, pushing remaining 20% of blood into ventricle – End diastolic volume (EDV): volume of blood in each ventricle at end of ventricular diastole Depolarization spreads to ventricles (QRS wave) Atria finish contracting and return to diastole while ventricles begin systole © 2016 Pearson Education, Ltd.  18.6 Mechanical Events of Heart 2. Ventricular systole Atria relax; ventricles begin to contract Rising ventricular pressure causes closing of AV valves Two phases 2a: Isovolumetric contraction phase: all valves are closed 2b: Ejection phase: ventricular pressure exceeds pressure in large arteries, forcing SL valves open » Pressure in aorta around 120 mm Hg End systolic volume (ESV): volume of blood remaining in each ventricle after systole © 2016 Pearson Education, Ltd.  18.6 Mechanical Events of Heart 3. Isovolumetric relaxation: early diastole Following ventricular repolarization (T wave), ventricles are relaxed; atria are relaxed and filling Backflow of blood in aorta and pulmonary trunk closes SL valves – Causes dicrotic notch (brief rise in aortic pressure as blood rebounds off closed valve) – Ventricles are totally closed chambers (isovolumetric) When atrial pressure exceeds ventricular pressure, AV valves open; cycle begins again © 2016 Pearson Education, Ltd. Figure 18.19 Summary of events during the cardiac cycle. Left heart QRS P T P Electrocardiogram 1st 2nd Heart sounds Dicrotic notch 120 Pressure (mm Hg) 80 Aorta Left ventricle 40 Atrial systole Left atrium 0 120 volume (ml) Ventricular EDV SV 50 ESV Atrioventricular valves Open Closed Open Aortic and pulmonary valves Closed Open Closed Phase 1 2a 2b 3 1 Left atrium Right atrium Left ventricle Right ventricle Ventricular Atrial Isovolumetric Ventricular Isovolumetric Ventricular filling contraction contraction phase ejection phase relaxation filling 1 2a 2b 3 Ventricular filling Ventricular systole Early diastole (mid-to-late diastole) (atria in diastole) © 2016 Pearson Education, Ltd.