Sinoatrial (SA) node Electrical Conduction Sets the pace of the heartbeat at 70 bpm AV node (50 bpm) and Purkinje fibers (25 40 bpm) can act as pacemakers under some conditions Internodal pathway from SA to atrioventricular (AV) node Routes the direction of electrical signals so the heart contracts from apex to base AV node delay is accomplished by slower conductional signals through nodal cells
Electrical Conduction Purkinje fibers transmit electric signals down the atrioventricular bundle (bundle of His) to left and right bundle branches.
Figure 14.13 Electrical conduction in myocardial cells Cells of SA node Action potentials of autorhythmic cells Electrical current Action potentials of contractile cells Contractile cell Intercalated disk with gap junctions
Cardiac Action Potential Interactive Physiology Animation: Cardiovascular Physiology: Cardiac Action Potential
Figure 14.14 The conducting system of the heart Slide 1 SA node AV node Purple shading in steps 2 5 represents depolarization. SA node depolarizes. Electrical activity goes rapidly to AV node via internodal pathways. THE CONDUCTING SYSTEM OF THE HEART SA node Depolarization spreads more slowly across atria. Conduction slows through AV node. Depolarization moves rapidly through ventricular conducting system to the apex of the heart. Internodal pathways Depolarization wave spreads upward from the apex. AV node AV bundle Bundle branches Purkinje fibers FIGURE QUESTION What would happen to conduction if the AV node malfunctioned and could no longer depolarize?
Figure 14.14 The conducting system of the heart Slide 2 SA node SA node depolarizes. AV node THE CONDUCTING SYSTEM OF THE HEART SA node Internodal pathways AV node AV bundle Bundle branches Purkinje fibers
Figure 14.14 The conducting system of the heart Slide 3 SA node AV node Purple shading in steps 2 5 represents depolarization. SA node depolarizes. Electrical activity goes rapidly to AV node via internodal pathways. THE CONDUCTING SYSTEM OF THE HEART SA node Internodal pathways AV node AV bundle Bundle branches Purkinje fibers
Figure 14.14 The conducting system of the heart Slide 4 SA node AV node Purple shading in steps 2 5 represents depolarization. SA node depolarizes. Electrical activity goes rapidly to AV node via internodal pathways. THE CONDUCTING SYSTEM OF THE HEART Depolarization spreads more slowly across atria. Conduction slows through AV node. SA node Internodal pathways AV node AV bundle Bundle branches Purkinje fibers
Figure 14.14 The conducting system of the heart Slide 5 SA node AV node Purple shading in steps 2 5 represents depolarization. SA node depolarizes. Electrical activity goes rapidly to AV node via internodal pathways. THE CONDUCTING SYSTEM OF THE HEART SA node Depolarization spreads more slowly across atria. Conduction slows through AV node. Depolarization moves rapidly through ventricular conducting system to the apex of the heart. Internodal pathways AV node AV bundle Bundle branches Purkinje fibers
Figure 14.14 The conducting system of the heart Slide 6 SA node AV node Purple shading in steps 2 5 represents depolarization. SA node depolarizes. Electrical activity goes rapidly to AV node via internodal pathways. THE CONDUCTING SYSTEM OF THE HEART SA node Depolarization spreads more slowly across atria. Conduction slows through AV node. Depolarization moves rapidly through ventricular conducting system to the apex of the heart. Internodal pathways Depolarization wave spreads upward from the apex. AV node AV bundle Bundle branches Purkinje fibers FIGURE QUESTION What would happen to conduction if the AV node malfunctioned and could no longer depolarize?
The Waves of Electrocardiogram (ECG) Waves and segments two major components of an ECG Three waves P depolarization of the atria QRS complex: wave of ventricular depolarization T repolarization of the ventricle Atrial repolarization is part of QRS
Millivolts Figure 14.15f The Electrocardiogram 5 mm 25 mm = 1 sec An electrocardiogram is divided into waves (P, Q, R, S, T), segments between the waves (the P-R and S-T segments, for example), and intervals consisting of a combination of waves and segments (such as the PR and QT intervals). This ECG tracing was recorded from lead I. P wave: atrial depolarization P-R segment: conduction through AV node and AV bundle QRS complex: ventricular depolarization +1 R R T wave: ventricular repolarization P-R segment S-T segment P wave Q S T wave FIGURE QUESTION 1. If the ECG records at a speed of 25 mm/sec, what is the heart rate of the person? (1 little square = 1 mm) 0 PR interval* QT interval QRS complex *Sometimes the Q wave is not seen in the ECG. For this reason, the segments and intervals are named using the R wave but begin with the first wave of the QRS complex.
The Electrical Events of the Cardiac Cycle Mechanical events lag behind electrical events: contraction follows action potential ECG begins with atrial depolarization, atrial contraction at the end of P wave P-R segment signal goes through AV node and AV bundle Q wave end: ventricular contraction begins and continues through T wave ECG analysis
The Electrical Events of the Cardiac Cycle Heart rate: time between two P waves or two Q waves Rhythm: regular pattern Waves analysis: presence and shape Segment length constant
Figure 14.16 Correlation between an ECG and electrical events in the heart START P P wave: atrial depolarization End R P T P-Q or P-R segment: conduction through AV node and AV bundle Q S P Atria contract T wave: ventricular repolarization R ELECTRICAL EVENTS OF THE P T Ventricular repolarization CARDIAC CYCLE Q S S-T segment Atrial repolarization P Q wave Q R P Q S R wave R Ventricles contract R P P S wave Q Q S
Figure 14.15h The Electrocardiogram Normal and abnormal ECGs. All tracings represent 10-sec recordings. R R P T P T 10 sec (1) Normal ECG P P R R R R P P P P P P P P P P P P (2) Third-degree block (3) Atrial fibrillation FIGURE QUESTIONS 2. Three abnormal ECGs are shown at right. Study them and see if you can relate the ECG changes to disruption of the normal electrical conduction pattern in the heart. 3. Identify the waves on the ECG in part (5). Look at the pattern of their occurrence and describe what has happened to electrical conduction in the heart. (4) Ventricular fibrillation (5) Analyze this abnormal ECG.
The Mechanical Events of the Cardiac Cycle Diastole: cardiac muscle relaxes Systole: cardiac muscle contracts Beginning of cycle: the heart at rest: atrial and ventricular diastole The atria are filling with blood from the vein AV valves open ventricles fill Atrial systole: atria contract Early ventricular contraction and AV valves close first heart sound
The Mechanical Events of the Cardiac Cycle Atrial diastole: all valves shut, isometric contraction of the heart, atria relax and blood flows in the atria Ventricular systole: ventricles finish contracting pushing semilunar valves open and blood is ejected in arteries: ventricular systole Ventricular diastole: ventricular relaxation and pressure drops, still higher than atrial pressure Arterial blood flows back pushing semilunar valves shut second heart sound
The Mechanical Events of the Cardiac Cycle Isovolumic ventricular relaxation, volume of blood in ventricles not changing AV valves open when ventricular pressure drops below atrial pressure
Figure 14.17a Mechanical events of the cardiac cycle Slide 1 The heart cycles between contraction (systole) and relaxation (diastole). Late diastole both sets of chambers are relaxed and ventricles fill passively. START Isovolumic ventricular relaxation as ventricles relax, pressure in ventricles falls. Blood flows back into cusps of semilunar valves and snaps them closed. Atrial systole atrial contraction forces a small amount of additional blood into ventricles. S 1 S 2 Ventricular ejection as ventricular pressure rises and exceeds pressure in the arteries, the semilunar valves open and blood is ejected. Isovolumic ventricular contraction first phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves.
Figure 14.17a Mechanical events of the cardiac cycle Slide 2 The heart cycles between contraction (systole) and relaxation (diastole). Late diastole both sets of chambers are relaxed and ventricles fill passively. START
Figure 14.17a Mechanical events of the cardiac cycle Slide 3 The heart cycles between contraction (systole) and relaxation (diastole). Late diastole both sets of chambers are relaxed and ventricles fill passively. START Atrial systole atrial contraction forces a small amount of additional blood into ventricles.
Figure 14.17a Mechanical events of the cardiac cycle Slide 4 The heart cycles between contraction (systole) and relaxation (diastole). Late diastole both sets of chambers are relaxed and ventricles fill passively. START Atrial systole atrial contraction forces a small amount of additional blood into ventricles. S 1 Isovolumic ventricular contraction first phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves.
Figure 14.17a Mechanical events of the cardiac cycle Slide 5 The heart cycles between contraction (systole) and relaxation (diastole). Late diastole both sets of chambers are relaxed and ventricles fill passively. START Atrial systole atrial contraction forces a small amount of additional blood into ventricles. S 1 Ventricular ejection as ventricular pressure rises and exceeds pressure in the arteries, the semilunar valves open and blood is ejected. Isovolumic ventricular contraction first phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves.
Figure 14.17a Mechanical events of the cardiac cycle Slide 6 The heart cycles between contraction (systole) and relaxation (diastole). Late diastole both sets of chambers are relaxed and ventricles fill passively. START Isovolumic ventricular relaxation as ventricles relax, pressure in ventricles falls. Blood flows back into cusps of semilunar valves and snaps them closed. Atrial systole atrial contraction forces a small amount of additional blood into ventricles. S 1 S 2 Ventricular ejection as ventricular pressure rises and exceeds pressure in the arteries, the semilunar valves open and blood is ejected. Isovolumic ventricular contraction first phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves.
First heart sound Heart Sounds Vibrations following closure of the AV valves Lub Second heart sound Vibrations created by closing of semilunar valve Dup Auscultation is listening to the heart through the chest wall through a stethoscope.
Cardiac Cycle Interactive Physiology Animation: Cardiovascular Physiology: Cardiac Cycle
Stroke Volume and Cardiac Output End diastolic volume (EDV) End systolic volume (ESV) Stroke volume Amount of blood pumped by one ventricle during a contraction Volume of blood before contraction-volume of blood after contraction = stroke volume EDV ESV = stroke volume Average = 70 ml
Stroke Volume and Cardiac Output Cardiac output (CO) Volume of blood pumped by one ventricle in a given period of time Cardiac output = heart rate stroke volume Average = 5 L/min
Stroke Volume Force of contraction is affected by Length of muscle fiber Determined by volume of blood at beginning of contraction Contractility of heart As stretch of the ventricular wall increases, so does stroke volume Preload is the degree of myocardial stretch before contraction
Stroke Volume Sympathetic activity speeds heart rate β 1 -adrenergic receptors on the autorhythmic cells Parasympathetic activity slows heart rate
Figure 14.19a-b Autonomic control of heart rate
Figure 14.19c Autonomic control of heart rate
Figure 14.19d Autonomic control of heart rate
Figure 14.19e Autonomic control of heart rate
Stroke Volume Frank-Starling law states Stroke volume increases as EDV increases EDV is determined by venous return Venous return is affected by Skeletal muscle pump Respiratory pump Sympathetic innervation of veins
Figure 14.20a Length-tension relationships
Figure 14.20b Length-tension relationships
Contractility Any chemical that affects contractility is an inotropic agent Epinephrine, norepinephrine, and digitalis have positive inotropic effects Chemicals with negative inotropic effects decrease contractility
Figure 14.20c Length-tension relationships
Cardiac Output Interactive Physiology Animation: Cardiovascular Physiology: Cardiac Output
Figure 14.21 Catecholamines increase cardiac contraction
Afterload and Ejection Fraction Afterload is the combined load of EDV and arterial resistance during ventricular contraction Ejection fraction is the percentage of EDV ejected with one contraction Stroke volume/edv Average = 52%
Figure 14.22 Stroke volume and heart rate determine cardiac output
Summary Overview of the cardiovascular system Pressure, volume, flow, and resistance Cardiac muscle and the heart The heart as a pump