Cardiac physiology. b. myocardium -- cardiac muscle and fibrous skeleton of heart

Transcription

1 I. Heart anatomy -- general gross. A. Size/orientation - base/apex B. Coverings D. Chambers 1. parietal pericardium 2. visceral pericardium 3. Layers of heart wall a. epicardium Cardiac physiology b. myocardium -- cardiac muscle and fibrous skeleton of heart c. endocardium 1. atria/receiving 2. ventricles/pumping E. Path of blood 1. pulmonary circuit 2. systemic circuit II. Properties of cardiac muscle A. Microscopic anatomy 1. general - striated, branched cells, binucleate, many mitochondria, sarcomeres, T-tubules, SR 2. intercalated disks -- junctions between adjacent cells - structural and functional connections between cells

2 gap junctions desmosomes - functional syncytium --interconnected cells that function electrically and mechanically as a unit B. Metabolism atrial syncytium ventricular syncytium - anaerobic metabolism accounts for less than 1% of total energy liberated, thus relies on good O 2 supply - myoglobin abundance - fatty acids are preferred fuel source, can readily adapt to alterations in nutritional state C. Electrical properties 1. general - RMP = - 90 mv - cell types: a. cardiac muscle cells: excitation-contraction coupling b. autorhythmic cells: spontaneous depolarization 2. Cardiac cell action potential a. phase 0: opening voltage-gated Na + b. phase 1: closing voltage gated Na + ; opening/closing voltage-gated K + (transient outward rectifier, I TO ) c. phase 2: plateau: activation of slow voltage-gated Ca ++ ; as plateau progresses they gradually close decrease in K + permeability: at more positive membrane potentials resists K + efflux (inward rectifying) d. phase 3: repolarization: potassium efflux increases via voltage-gated K + channels, an there is inactivation of Ca ++ channels

3 inward rectifier (I Kr ): at lower membrane potentials permits K + efflux delayed outward rectifier(i Ks ): open at end of plateau, allow K + efflux. e. phase 4: return to RMP - note duration of AP and its ARP D. Mechanical properties 1. Contractile response - Ca ++ origin external - some Ca ++ induced - Ca ++ release from SR -- spiking prolongs cardiac action potential and contraction excitation-contraction coupling - ARP long -- by time it ends muscle almost relaxed -- prevents summation of contraction/tetanus - comparison with skeletal muscle: duration ARP duration of contraction tetanus means of stimulation all-or-none law 2. Correlation between muscle fiber length and tension - length of fibers --- diastolic filling -- diastolic pressure - intraventricular pressure -- tension development - Starling's law of the heart III. Origin of electrical activity of the heart A. Conduction system of the heart 1. Elements - noncontractile cells, some autorhythmic, others specialized for impulse conduction

4 - SA node, internodal pathways, AV node, common bundle (bundle of His), right bundle branch, left bundle branch, Purkinje fibers 2. Why this system if cardiac cells electrically coupled? - origin of autorhythmicity - coordination of atrial and ventricular contractile events - deliver impulses to specific areas of myocardium -- contraction needs to efficiently pump blood wringing effect right/left coordination B. Origin of excitation - AR cells in: SA node AV node bundle of His Purkinje fibers - prepotential: decay of RMP in AR cells 1. Membrane potential of pacemaker tissue i. ionic mechanism of autorhythmicity - repolarization: due to I K + - prepotential: decline in I K + (slow closure of K + channels), opening of voltage gated Ca ++ channels (T channels) - uplimb: opening of voltage-gated Ca ++ channels, long-lasting (L) channels ii. pacemaker potentials in different types of AR cells - various AR cells have different rates of slow depolarization to threshold - rates at which they can generate APs differ - SA nodes exhibits fastest rate of autorhythmicity -- drives rest of heart at 70v- 80 APs/min

5 - other AR cells unable to assume their own naturally slower rates because they are activated by action potentials originating in the SA node before they are able to reach threshold at their own slower rhythm 2. Autonomic influences on heart electrical activity a. parasympathetic influences: membrane hyperpolarized, duration prepotential increased - mechanism: increased K + (I K + Ach ) conductance of nodal tissue, slower opening of T Ca ++ channels b. sympathetic influences: membrane depolarized, duration of prepotential decreased - mechanism: opening of L Ca ++ channels facilitated c. note the sidedness of cardiac innervation by ANS C. Spread of cardiac excitation : impulse travels along conduction system, eventually delivered to specific locations of ventricular myocardium by Purkinje fibers D. Spread of depolarization of ventricular muscle 1. left interventricular septum 2. apex 3. up ventricular walls towards base; last part of the heart to depolarize is the left basal ventricular myocardium (also first part of heart to repolarize); thus ventricles relax in direction opposite to that in which they contract. IV. The electrocardiogram (ECG or EKG) A. General comments 1. ECG is a recording of electrical activity of the heart that reaches the body surface -- conducted through body fluids 2. ECG represents overall spread of activity throughout the heart during repolarization and depolarization it is not a recording of a single action potential in a single cell the record at a given time represents sum of all electrical activity in all cardiac muscle cells

6 3. Uses arrangements of surface electrodes to measure electrical activity of the heart; attempts to create a three dimensional electrical picture of the heart. B. ECG morphology P wave QRS complex T wave PR interval QT segment C. Recording of EKG - Eintoven's triangle 1. Bipolar leads lead I lead II lead III 2. Unipolar/augmented leads avr avl avf 3. Precordial/chest leads: v1 - v6 D. Example of recording of ECG: lead II E. EKG analysis Normal sinus rate rhythm Abnormalities in rate Abnormalities in rhythm Myopathies V. The cardiac cycle - cardiac cycle: all events associated with flow of blood through the heart during one complete heartbeat. - blood flow through the heart is controlled entirely by pressure gradients; blood flows from areas of high pressure to areas of low pressure through any available openings.

7 A. Period of ventricular filling. - atrial pressure is greater than ventricular pressure, therefore the AV valves open. - aortic pressure is greater than ventricular pressure, therefore SL valves closed. - atria provide conduit to blood entering ventricles; ventricular volume increases and atrial pressure constant. - P wave is followed by atrial systole, remaining 30% of blood is delivered to the ventricles. - produces increased ventricular volume along with a small increase in atrial pressure. - atria begin to repolarize while ventricles depolarize (QRS begins). B. Isovolumetric contraction/ejection. - ventricular systole begins. - ventricular pressure rises; when it is greater than atrial pressure, the AV valve closes. - ventricles become closed chambers (the SLV are still closed). - ventricles keep contracting; the ventricular pressure increases-- note that this is an isovolumetric contraction and there is no net change in ventricular volume. - when ventricular pressure is greater than aortic pressure, the SL valves open, and blood is ejected, period of ejection. - T wave; ventricular repolarization. C. Isovolumetric relaxation. - ventricular pressure decreases. - when ventricular pressure is less than aortic pressure the SLV closes causing a temporary increase in aortic pressure. - recall that the AV valves are still closed (ventricular pressure is still greater than atrial pressure), the ventricles are again closed chambers. - relaxation continues, ventricular pressure decreases, isovolumetric relaxation. D. Filling and diastasis.

8 - during ventricular systole, the atria have been in diastole slowly filling with blood, atrial pressure increases. - when atrial pressure is greater than ventricular pressure the AV valves open, rapid filling occurs. VI. Cardiac output (CO). - the amount of blood pumped by the heart per minute; highly variable; CO = HR X SV. - stroke volume (SV) is the amount of blood pumped by the ventricle in one beat.