Cardiac Physiology • Two types of heart cells • 1. conducting cells – control & coordinate heartbeat
• 2. contractile cells – generate pressure to propel blood
Bundle branches
Purkinje fibers
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Cardiac Conduction system • specialized cells that – Initiate/distribute impulses
• components: – SA node – internodal pathways • To atrial muscle cells
– AV node – AV bundle – bundle branches – Purkinje fibers • To ventricular muscle cells
conducting cells • exhibit prepotentials …cation leak… • SA node (natural pacemaker) – located in wall of R atrium – spontaneously depolarizes
• AV node • Purkinje fibers
80-100X/minute
40-60X/minute 20-40X/minute
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AV node • Conducts impulses from ___________ to ___________
• maximal conductance rate of AV node – 230 impulses per minute – determines maximal heart rate – 230 beats per min
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ECG/EKG • P wave • QRS complex
• T wave • Useful for – assessing heart – detection of arrhythmias
• Where is the wave for atrial repolarization?
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Cardiac Arrhythmias • Abnormal patterns of electrical activity • Reduce pumping efficiency • Indicate damage to – myocardium – pacemakers or conduction system
• Some causes – exposure to drugs – electrolyte imbalances in ECF
Contractile cells • bulk of heart: myocardium • action potentials are due to – increased [Ca++] sarcoplasm
• calcium-troponin interactions result in contraction- just like skeletal muscle • gap junctions – allow cytoplasm to be confluent in adjacent cells – ions flow through – depolarize neighboring cell
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action potential in contractile cells • voltage-gated fast Na+ channels – open at threshold due to cation flow from adjacent cell – rapidly depolarize the membrane • plateau, voltage-gated slow Ca++ channels open – allow depolarization to persist • voltage gated slow K+ channels – allow repolarization
long refractory period • lack of membrane response • absolute refractory period – Na channels closed and inactivated – contraction cannot reoccur
• relative refractory period – channels can open – requires stronger than usual stimulus
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Calcium ions & Cardiac Contraction • sources of calcium: ECF and SR • roles of ECF Ca+2 ions – bind to troponin for contraction: accounts for 20% of calcium used during contraction – stimulate release of Ca+2 from SR (this is the other 80% of Ca+2 ions binding to troponin for contraction)
• FYI – heart is highly sensitive to [Ca+2]pla – hypercalcemia – cardiac arrhythmias – hypocalcemia – weak heartbeat, arrhythmias
Action Potentials and contraction • Skeletal muscle – Refractory period brief, precedes contraction…so multiple rapid stimuli cause tetany.
• Cardiac muscle – Refractory period extends into relaxation phase…so no tetany is possible
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Cardiac cycle • Pattern of activity of the heart – Contraction – Relaxation – Contraction – Relaxation – etc.
Phases of the cycle: systole and diastole • Used to refer to chamber activity… • Systole -- contraction – Blood ejected
• Diastole -- relaxation – Chamber fills with blood
• Blood flows due to differences in pressure
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Fig. 20-16, p. 682
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Atrial systole • Atria contract – blood forced into ventricles
• Atrial contribution to ventricular volume – Only 30% of ventricular volume
• End-diastolic volume (EDV) – At this point each ventricle holds the maximal amount of blood for this cycle…
Ventricular systole 2 phases • First phase: isovolumetric contraction – Pressure rises – AV Valves are pushed closed – no blood moves
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Ventricular systole 2 phases • Second phase: ventricular ejection • Ventricular pressure is enough to open aortic and pulmonary valves – L ventricular pressure exceeds aortic pressure of ~ 80 mmHg – FYI: R ventricular pressure exceeds pulmonary trunk pressure of ~ 10 mm Hg
Ventricular systole • Blood is ejected – 70-80 ml blood – stroke volume
• Stroke volume at rest: ~60% of end diastolic volume (EDV) – (called ejection fraction) • End-systolic volume at rest: – Amount of blood remaining 50 ml
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ventricular diastole • isovolumetric relaxation • All valves are closed until……. ventricular pressure drops below atrial pressure • then AV valves open, blood flows in….
cardiodynamics • Movements and forces generated by the heart • Cardiac output (CO) – CO = HR X SV – Given: HR is 80 beats/min and SV is 70 ml/beat – CO = 80 beats/min X 70 ml/beat – = 5600 ml/min – = 5.6 L/min
Factors affecting Heart Rate • Autonomic innervation – vagus nerves – sympathetic cardiac nerves – Control emanates from cardiac centers in the medulla oblongata – cardioacceleratory center – cardioinhibitory center
Autonomic innervation • Both ANS divisions innervate – SA node – AV node – Atria
• Sympathetic division – ventricles
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Autonomic reflexes • cardiac reflexes: baro- and chemoreceptor monitoring – Monitor BP and blood gases – Aorta and carotid arteries
• Autonomic tone determines heart rate – Finely adjusted up or down depending on stimuli – Parasympathetic effects dominate
Autorhythmic cells & HR
• How can we change heart rate?
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Autonomic Innervation • Effects on SA node ANS alters permeability of SA node • parasympathetic division Ach opens K+ channels…
• sympathetic division NE opens Na-Ca channels
Factors affecting HR: the atrial reflex • Atrial reflex – Responds to increased venous return – Stretch of right atrial walls causes an increase in HR – Receptors • stretch receptors in the right atrium
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Factors affecting Heart Rate • Hormones that increase the HR – EPI – NE – Thyroid hormone
• Venous Return – Increased venous return initiates atrial reflex – Also stretched SA nodal cells depolarize more rapidly
Factors affecting Cardiac Output
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Factors affecting Stroke Volume • Recall SV = EDV - ESV • SV is effected by changes in – EDV or – ESV
EDV depends on • 1. Filling time • 2. Venous return – Affected by many factors – Changes in CO, BP, circulation patterns – Skeletal muscle activity
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Preload determines ESV • Preload: Degree of stretch of heart prior to contraction • If EDV is large, so is preload...implications: – Striated muscle when slightly stretched can form more cross bridges, and contract more forcefully • “More blood in = more blood out” • Frank-Starling principle or Starling’s law of the heart • As EDV increases, so does SV
ESV determined by • 1 preload: determines ESV • 2 contractility: forcefulness of contraction – determined by • Humoral agents (+ or - inotropic agents) – Hormones, ECF [ion]’s
• ANS
• 3 afterload: pressure that must be exceeded for blood to be ejected from heart – Increased afterload = increased ESV = decreased CO
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Factors affecting Stroke Volume
Summary: Factors affecting Cardiac Output
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Congestive Heart Failure • Heart fails as a pump • various causes: – myocardial infarcts, chronic high blood pressure, congenital defects, coronary artery disease, etc.
• Left heart failure = pulmonary edema Pulmonary congestion
• Right heart failure = peripheral edema especially noticeable in feet & ankles
