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CARDIAC PHYSIOLOGY MODERATOR:DR.P. SRINIVASA RAO. PRESENTER:DR.M. MOUNIKA.

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Page 1: CARDIAC PHYSIOLOGY - rameshhospitals.com › ... › Cardiac-Physiology.pdf · CARDIAC ACTION POTENTIAL ⚫Normal ventricular Resting membrane potential is -80mv to -90mv. ⚫In contrast

CARDIAC PHYSIOLOGY

MODERATOR:DR.P. SRINIVASA RAO.PRESENTER:DR.M. MOUNIKA.

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INTRODUCTION⚫ Heart is the principle vital organ.⚫ It functionally divides into right and left

pumps, consisting of an atrium and ventricle.

⚫ Right ventricle receives deoxygenated blood and pumps it to pulmonary circulation.

⚫ Left ventricle receives oxygenated blood and pumps it to systemic circulation.

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⚫ Cardiac muscle - Involuntary striated muscle - Extensive branching - consists of INTERCALATED

DISCS and GAP JUNCTIONS.⚫ Heart is a MECHANICAL and FUNCTIONAL

SYNCITIUM.

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CARDIAC ACTION POTENTIAL⚫ Normal ventricular Resting membrane

potential is -80mv to -90mv.⚫ In contrast with action potentials in axons, the

spike in cardiac action potentials is followed by a plateau phase that lasts for 0.2 to 0.3 sec.

⚫ Action potential for skeletal muscle and nerves is due to abrupt opening of voltage gated sodium channels , in cardiac muscle it is initiated by voltage gated sodium channels but maintained by voltage gated calcium channels.

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CONDUCTING SYSTEM

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PACE MAKER POTENTIAL⚫ It usually originates in SA node , a group of specialised

pace maker cells in the sulcus terminalis,located posteriorly at the junction of right atrium and the superior vena cava.

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MECHANISM OF CONTRACTION

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CARDIAC CYCLE

⚫ Cardiac cycle can be defined by both mechanical and electrical events

⚫ Systole-contraction⚫ Diastole-relaxation⚫ Cardiac cycle begins with initiation of

heart beat .

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PHASES OF CARDIAC CYCLE:1.Atrial systole2.Isometric contraction3.Ejection4.Isometric relaxation5.filling

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VENTRICULAR STRUCTURE AND FUNCTION⚫ VENTRICULAR STRUCTURE:⚫ The specific architectural order of the cardiac

muscles provides the basis for the heart to function as a pump.

⚫ The ellipsoid shape of the left ventricle (LV) is a result of the laminar layering of spiraling bundles of cardiac muscles

⚫ The orientation of the muscle bundle is longitudinal in the subepicardial myocardium and circumferential in the middle segment and again becomes longitudinal in the subendocardial myocardium .

⚫ this type of orientation allows the LV to eject blood in a corkscrew type motion beginning from the base and ending at the apex.

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Cardiac Cycle

2 components:⚫ Diastole: Filling of the chamber⚫ Systole: Contraction of the chamber and

ejection of blood

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Cardiac Output⚫ The amount of blood ejected from the

ventricle in one minute CO = SV x HR⚫ Elements of cardiac output:⚫ Stroke volume⚫ Amount of blood ejected from the

ventricle in one contraction SV=EDV-ESV⚫ Heart rate⚫ The number of cardiac cycles in one

minute

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CARDIAC OUTPUT⚫ Ventricular function is often equated with

cardiac output(CO)⚫ To compensate with variations in body

size, it is often expressed in terms of cardiac index(CI)

CI=CO/BSABSA=Body surface area normal CI=2.5-4.2 lit/min/sq.mt

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HEART RATE⚫ Heart rate(HR) is an intrinsic function of

SA node.⚫ Normal intrinsic heart rate of young

adults is about 90-100beats/min.⚫ Usually decreases with age based on

formula: normal intrinsic HR=118

beats/min-(0.57*age)⚫ Decreased HR-M2 cholinergic receptors.⚫ Increased HR-Beta-1adrenergic

receptors.

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DETERMINATION OF STROKE VOLUME:

⚫ Preload: Amount of blood delivered to the chamber.

⚫ Depends upon venous return to the heart.⚫ Also dependent upon the amount of blood

delivered to the ventricle by the atrium.⚫ Heart rate and Rhythm also affects preload.⚫ Contractility : The efficiency and strength

of contraction⚫ Frank Starling’s Law⚫ Afterload : Resistance to forward blood

flow by the vessel walls

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FRANK-STARLING LAW

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⚫ Other factors determining stroke volume includes: Wall motion abnormalities

Valvular dysfunction

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PRESSURE-VOLUME RELATIONSHIP

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⚫ It is used to demonstrate how changes in preload and afterload affect stroke volume,ESV and EDV.

⚫ A drop in preload- decrease SV,ESV,EDV.⚫ Eg: clamping of IVC.⚫ An increase in afterload-increase in end

systolic pressure and volume, decrease in SV.

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Autonomic Nervous SystemSympathetic Nervous System⚫ Extensively innervates the SA node and

ventricular cells⚫ Increase in heart rate⚫ Increase in conduction and contractility in

the ventriclesParasympathetic Nervous System⚫ Innervates the SA and AV nodes⚫ Decreases heart rate⚫ Decreases conduction times through the AV

node

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The Vascular System⚫ The vascular system is composed of the

systemic and pulmonary circulation.⚫ Both systems consist of arteries,

capillaries and veins.⚫ Arterial system: away from the heart⚫ Venous system: capillary beds to heart⚫ Anatomical differences of arteries and

veins

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FACTORS CONTRIBUTING TO ARTERIAL BLOOD PRESSURE:

⚫ BP = CO x TPR⚫ Cardiac Pump⚫ Blood Volume⚫ Peripheral Resistance⚫ Elasticity of Arterial Walls⚫ Viscosity of Blood

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⚫ Mean arterial pressure(MAP):proortionate to the product of systemic vascular resistance and cardiac output.

⚫ MAP=diastolic pressure+1/3pulse pressure

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Control of arterial blood pressure⚫ Regulated by series of immediate

,intermediate and long term control.⚫ Immediate control includes: 1.Barorecetor reflexes. 2.Chemoreceptor reflexes. 3.Brain(CNS) Ischaemic responses.⚫ Intermediate control includes:Hormonal

control: 1.catecholamines 2.Renin–angiotensin–aldosterone system

3.vasopressin

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⚫ Long term control includes: - Renal body fluid control systems:

i.Kidneys alter total body water and sodium balance to restore blood pressure to normal.

ii. hypotension-sodium retention hypertension-sodium excretion

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Inhalational agents⚫ Nitrous oxide—used safely for cardiac pts.⚫ Halothane—B blocking action,BP

decreased,sensitises heart to adr,ventricular arrhythmias.so not to be used in cardiac pts.

⚫ Isoflurane—”controlled hypotension”,cardiac output best maintained. “Coronary steal “ phenomenon.

⚫ Desflurane—similar to isoflurane but no coronary steal phenomenon.

⚫ sevoflurane—cardiac output minimally depressed.

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Intravenous anaesthetics

⚫ Barbiturates—⚫ Thiopentone and methohexitone.—⚫ Hypotension,direct depression of the

vasomotor centre.,direct myocardial depressant.increase in heart rate (compensatory mechanism)

⚫ Nonbarbiturates⚫ Propofol—hypotension.⚫ Etomidate—most cardiovascular stable.⚫ Ketamine — tachycardia ,hypertension ,

DOC in shock.

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