heart pump and cardiac cycle1-2007

7/28/2019 Heart Pump and Cardiac Cycle1-2007

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Heart Pump and Cardiac Cycle

Faisal I. Mohammed, MD, PhD


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Objectives

To understand the volume, mechanical, pressureand electrical changes during the cardiac cycle

To understand the inter-relationship between allthese changes

To describe the factors that regulate Cardiac

output and Stroke volume. Resources: Textbook of Medical Physiology By

Guyton and Hall 11th Edition.


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Intracellular Calcium Homeostasis1


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Intracellular Calcium Homeostasis2


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Cardiac Cycle

Cardiac cycle refers to all events

associated with blood flow throughthe heart

Systole contraction of heart

muscle

Diastole relaxation of heart

muscle


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Cardiac Cycle

Atrial systole 0.1 second

Atrial diastole 0.7 second

Ventricular systole 0.3 second Isovolumic contraction 0.01 secods

Rapid ejection period

Slow ejection period

Ventricular diastole 0.5 seconds

Isovoumic relaxation 0.02 secods

Rapid filling

Slow filling (Diastasis)

Atrial contraction


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Cardiac cycle cont

End diastolic volume (EDV)End systolic

volume (ESV) = Stroke volume (SV) SV X heart rate (HR) = cardiac output (CO)

Ejection fraction = SV/EDV

Inotropic vs. Chronotropic

Autonomic control of cardiac cycle (pump)


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Ventricular fillingmid-to-late

diastoleHeart blood pressure is low as blood

enters atria and flows into ventricles

AV valves are open, then atrial

systole occurs

Phases of the Cardiac Cycle


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Ventricular systole

Atria relax

Rising ventricular pressure results in

closing of AV valves

Isovolumetric contraction phase

Ventricular ejection phase opens

semilunar valves



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Isovolumetric relaxationearly diastole

Ventricles relax

Backflow of blood in aorta and pulmonary

trunk closes semilunar valves

Dicrotic notchbrief rise in aortic pressure

caused by backflow of blood rebounding off

semilunar valves


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Changes during Cardiac cycle

Volume changes: End-diastolic volume, End-systolic volume,Stroke volume and Cardiac output.

Aortic pressure: Diastolic pressure 80 mmHg, Systolic pressure 120 mmHg, most of systole ventricular pressure higher thanaortic

Ventricular pressure: Diastolic 0, systolic Lt. 120 Rt. 25mmHg.

Atrial pressure: A wave =atrial systole, C wave= ventricularcontraction (AV closure), V wave= ventricular diastole (Avopening)

Heart sounds: S1 = turbulence of blood around a closed AV

valves, S2 = turbulence of blood around a closed semilunarvalves.


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Cardiac Output (CO) and Reserve

CO is the amount of blood pumped by each

ventricle in one minute CO is the product of heart rate (HR) and stroke

volume (SV)

HR is the number of heart beats per minute

SV is the amount of blood pumped out by a

ventricle with each beat

Cardiac reserve is the difference between resting

and maximal CO


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Regulation of Stroke Volume

SV = end diastolic volume (EDV)

minus end systolic volume (ESV) EDV = amount of blood collected in a

ventricle during diastole

ESV = amount of blood remaining in a

ventricle after contraction


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Factors Affecting Stroke Volume

Preloadamount ventricles are

stretched by contained blood Contractilitycardiac cell contractile

force due to factors other than EDV

Afterloadback pressure exerted by

blood in the large arteries leaving the

heart


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Frank-Starling Law of the Heart

Preload, or degree of stretch, of cardiac

muscle cells before they contract is thecritical factor controlling stroke volume

Slow heartbeat and exercise increase venous

return to the heart, increasing SV Blood loss and extremely rapid heartbeat

decrease SV


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Preload and Afterload


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Extrinsic Factors Influencing

Stroke Volume

Contractility is the increase in contractile

strength, independent of stretch and EDV Increase in contractility comes from:

Increased sympathetic stimuli

Certain hormones

Ca2+ and some drugs


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Extrinsic Factors Influencing

Stroke Volume

Agents/factors that decrease contractility

include: Acidosis

Increased extracellular K+

Calcium channel blockers

C t tilit d N i h i


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Contractility and Norepinephrine

Sympatheticstimulation

releases

norepinephrineand initiates a

cyclic AMP

second-

messen er Figure 18.22


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Regulation of Heart Rate

Positive chronotropic factors increase

heart rateNegative chronotropic factors decrease

heart rate


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Sympathetic nervous system (SNS) stimulation is

activated by stress, anxiety, excitement, or

exercise

Parasympathetic nervous system (PNS)

stimulation is mediated by acetylcholine and

opposes the SNS PNS dominates the autonomic stimulation,

slowing heart rate and causing vagal tone

Regulation of Heart Rate: Autonomic

Nervous System


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Atrial (Bainbridge) Reflex

Atrial (Bainbridge) reflexa

sympathetic reflex initiated byincreased blood in the atria

Causes stimulation of the SA node

Stimulates baroreceptors in the atria,

causing increased SNS stimulation


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Chemical Regulation of the Heart

The hormones epinephrine and thyroxine

increase heart rate Intra- and extracellular ion concentrations

must be maintained for normal heart

function


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Cardiac Output is the sum of all tissue flows and

is affected by their regulation (CO = 5L/min,

cardiac index = 3L/min/m2).

CO is proportional to tissue O2. use.

CO is proportional to 1/TPR when AP is constant. CO = (MAP - RAP) / TPR

Important Concepts About

Cardiac Output (CO) Control


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Electromagnetic flowmeter

Indicator dilution (dye such as cardiogreen) Thermal dilution

Oxygen F ick Method

CO = (O2consumption / (A-V O

2difference)

Measurement of Cardiac Output


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O2 Fick Problem

If pulmonary vein O2 content = 200 ml O2/Lblood

Pulmonary artery O2 content =160 ml O2 /L blood

Lungs add 400 ml O2 /min What is cardiac output?

Answer: 400/(200-160) =10 L/min


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NORMAL

HYPEREFFECTIVE

-4 0 +4 +8

25

20

15

10

5

0

CARDIACOU

TPUT(L/min)

RIGHT ATRIAL PRESSURE (mmHg)

HYPOEFFECTIVE

CARDIAC OUTPUT

CURVES


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Plateau of CO curve determined by

heart strength (contractility + HR)

Sympathetics plateau

Parasympathetics (HR) plateau) Plateau

Heart hypertrophy s plateau

Myocardial infarction plateau)

Plateau

The Cardiac Output Curve


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Valvular disease plateau(stenosis or regurgitation)

Myocarditis plateau Cardiac tamponade plateau)

Plateau

Metabolic damage plateau

The Cardiac Output Curve(contd)


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RIGHT ATRIAL PRESSURE (mmHg)

-4 0 4 8 12

V

ENOUSRETUR

N(L/MIN)

0

5

10

MSFP= 7

MSFP= 14

MSFP= 4.2

MSFP = Mean Systemic Filling Pressure

The Venous Return Curve

The Venous Return Curve


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Beriberi - thiamine deficiency arteriolar dilatation RVR

because VR = (MSFP - RAP) /RVR

(good for positive RAPs)

A-V fistula (? RVR)

RVR C. Hyperthyroidism (? RVR)

RVR

Venous Return (VR)


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Anemia RVR (why?)

Sympathetics MSFP

Blood volume MSFP + small in RVR

Venous compliance (muscle

contraction or venous constriction) SFP)

MSFP

Venous Return (VR) (contd)


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Blood volume MSFP

Sympathetics (? v. comp. and

MSFP) Venous compliance and MSFP

Obstruction of veins (? RVR)

RVR

Factors Causing Venous Return

heart pump and cardiac cycle1-2007

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