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Page 1: Heart physiology

Heart Physiology

Department of Physiology

SKZMDC

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Cardiac Muscle

• Cardiac Muscle• Atrial muscle • Ventricular muscle • Specialized excitatory & conductive muscle fibers

• Cardiac Muscle as a Syncytium• Intercalated disc “communicating” junctions (gap junctions) -

totally free diffusion of ions• Atrial syncytium• Ventricular syncytium

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Cardiac Muscle - Histology

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Cardiac Muscle Action Potential

• Depolarization• Fast Na+ channels

• Plateau• Slow Ca++ channels

– Slow to open– Slow to close

• After depol. cardiac muscle membrane permeability to K+ decreases

• Ca++ thus pumped in – excitation-contraction coupling

• Repolarization• Slow K+ channels

• Refractory Periods• 0.25 - 0.3 sec (Absolute)

– Corresponds to plateau

• 0.05 sec (Relative)

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AP Comparison

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Cardiac Muscle Action Potential

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Cardiac Muscle Action Potential

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Problem

A drug is found to partially inactivate fast sodium channels.

Q: How would this drug alter the action potential in a ventricular myocyte?

Q: How would the drug alter conduction velocity within the ventricle?

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Cardiac Cycle• Cardiac events occurring from beginning of one

heartbeat to the beginning of the next beat• Each cycle – INITIATED by SA node

– Spontaneous generation of AP in SA node

– AP travels through both atria

– Through A-V bundle into the ventricles

» AV node delay (more than 0.1 second)

» Hence atria contract ahead of ventricles

• Diastole and Systole– Period of relaxation – Diastole

» Heart fills with blood

– Period of contraction – Systole

» Ejection of blood

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Cardiac Cycle - Components• ECG is the event marker1. Atrial Systole

– Follows P wave (electric activation of atria)– Contributes to ventricular filling– Forms the ‘a wave’ in the venous pulse curve– Ventricular filling by atrial systole – 4th heart sound (not

audible in normal adults)

2. Isovolumetric contraction of Ventricle– Occurs after QRS wave (electric activation of ventricles)– Ventricular P raised above atrial P:

» AV valves close (1st heart sound)» Split in 1st heart sound may occur (since mitral valve

closes b/f tricuspid)– Ventricular P rises – NO CHANGE IN VOLUME

» Aortic valve is closed

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Cardiac Cycle - Components3. Rapid Ventricular Ejection

– Ventricular P reaches its max.– When it b/c greater than aortic P – aortic valve opens

» Rapid ejection of blood takes place– Ventricular volume decreases rapidly– Atrial filling begins– Onset of “T wave” (ventricular repolarization) – marks

end of vent. contraction & ejection

4. Reduced Ventricular Ejection– Slower ejection of blood from ventricles

– Ventricle P decreases

– Aortic P decreases (runoff of blood from large arteries into smaller arteries)

– Atrial filling continues

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Cardiac Cycle - Components5. Isovolumetric Ventricular Relaxation

– Ventricle replorization is complete (end of “T wave”)– Aortic valve closes (followed by pulmonic valve)

» 2nd heart sound» Splitting occurs during inspiration

– AV valves remain closed mostly during this phase– Ventricle P drops rapidly– Ventricle volume remains CONSTANT – all valves are closed– Incisura – When ventricle P b/c < atrial P – mitral valve opens

6. Rapid Ventricular Filling– Post-mitral valve opening – rapid filling of ventricles occurs– Aortic P continues to decrease – more run-off of blood– 3rd heart sound (due to rapid flow from atria to ventricles

» Normally heard in children» Abnormal in adults

7. Reduced Ventricular Filling (Diastasis)– Longest phase of cardiac cycle– Ventricular filling slows down– Diastasis time period depends on heart rate!

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Cardiac Cycle

• End-diastolic volume (130 ml) • End-systolic volume (50 ml)• Stroke volume (70 to 90 ml - @ rest)• Ejection fraction

– % of end-diastolic ventricular volume that is ejected with each stroke

– Is about 65% – Valuable index of ventricular function

• Preload • Afterload

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Cardiac Chamber Pressures

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Length (L) –Tension (T) CurveIsolated Cardiac Muscle

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Pressure (‘T’) – Volume (‘L’) Curve – Whole Heart

• PV loops:– Depict cardiac

cycle– Show effects

of Preload, afterload & inotropic state on cardiac pumping ability (SV)

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Regulation of Heart Pumping

(1) INTRINSIC cardiac regulation of pumping in response to changes in volume of blood flowing into the heart (Frank-Starling Law)

(2) Control of heart rate and strength of heart pumping by ANS

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Frank-Starling Law

• “Volume of blood ejected by the ventricle depends on the volume present in the ventricle at the end of diastole”

• Underlying principle – Length-tension relationship in cardiac

muscle fibers• SV & CO correlate directly with

EDV• EDV correlates with VR• CO = VR (FS Law ensures this)• Cardiac muscle normally operates

only on the ascending limb of the systolic curve

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Explanation of FS Law

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Concept of Contractility

• Inherent cardiac M Ca++ based ability – INOTROPISM

• Modified by ANS, catecholamines

• Loading situations of the heart• Preload

– Stretch-induced enhancement in contraction» More overlapping of thick & thin filaments» More Ca++ sensitivity of troponin C» More Ca++ release from SR

• After load

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Heart Control by ANS

• Sympathetic • NE via action on Beta-1 receptors

– Positive CHRONOTROPIC» Increased HR (increase Phase-4 depolarization)

– Positive IONOTROPIC» Increased force of contraction (increased inward Ca+

+ current during plateau + increases the ability of SR Ca++ pump)

– Positive DROMOTROPIC» Increased conduction velocity through AV node

(increased inward Ca++ current)» Decreased PR interval

– Positive BATHMOTROPIC » Increased excitability of myocardium

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Heart Control by ANS

• Parasympathetic– SA node, atria & AV node have supply,

ventricles don’t!– Ach via muscarinic receptors

• Negative chronotropic» Decreasing phase-4 depolarizations

• Negative dromotropic• Negative ionotropic

• Vagal escape

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Determinants of Performance of Heart as a Pump

• 4 factors: ‘Loading’ conditions of the cardiac muscle

(1) Preload, or the initial length to which the muscle is stretched prior to contraction

(2) Afterload, or all the forces against which cardiac muscle must contract to generate pressure and shorten

‘Extrinsic’ factors

(3) Contractility, or inotropic state

(4) Inotropic effect of increased heart rate (beats/min)


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