Cardiac physiology

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10/25/2012 Nabavian, O.; M.D. 1

description

lecture of Cardiac physiology by Dr. Omid Nabavian; anesthesiologist; assistant professor in TUMS

Transcript of Cardiac physiology

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CARDIAC PHYSIOLOGY

Miller’s AnesthesiaChapter 16

Nabavian, O.; M.D.Assistant Professor of Anesthesiology

TUMSVali-Asr Hospital

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There is difference between : “ Intact heart” & “ Isolated” heart muscle

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Ventricular structure

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Cardiac Vocabulary

Preload:  Preload is the muscle length prior to contractility, and it is dependent of ventricular filling (or end diastolic volume…EDV) 

The most important determining factor

for preload is venous return.

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PreloadPreload

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Cardiac Vocabulary

Afterload:  is the tension (or the arterial pressure) against which the ventricle must contract. 

If arterial pressure increases, afterload also increases.

Afterload for the left ventricle is determined by aortic pressure.

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Afterload

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Law of Laplace

σ= P*R/2h

h = wall thickness

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Heart Rate and Force-Frequency Relationshipan increase in the frequency of

stimulation induces an increase in the force of contraction.

This relationship is termed the “treppe” phenomenon or

the force-frequency the force-frequency relationshiprelationship

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EF=( LVEDV-LVESV)/LVEDV

Stroke (External) work=SV * P

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Cardiac Cardiac work

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External work is expended to eject blood under pressure, whereas

internal work is expended within the ventricle to change the shape of the heart and prepare it for ejection.

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Diastolic FunctionDiastolic Function

(1) Isovolumic relaxation (2) the rapid filling phase (80%) (3) slow filling, or diastasis;5%(4) final filling during atrial systole.

15% The isovolumic relaxation phase is

energy dependent

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Assessing diastolic function

(-dP/dt)

Aortic closing–mitral opening interval the isovolumic relaxation time peak rate of LV wall thinning as

determined by echocardiography

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CO= SV * HRCardiac output in a living organism

can be measured with the “Fick principle”

The Fick principle is based on the concept of

conservation of mass

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Fick’s Principleq1 = × CpaO2

q3 = × CpvO2

Because q1 + q2 = q3 ,

× (CpaO2 ) + q2 = ×(CpvO2 )

q2 = × (CpvO2 ) − × (CpaO2 )

q2 = ×(CpvO2 − CpaO2 )

= q2 /(CpvO2 − CpaO2 )

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Cellular Cardiac PhysiologyCellular Cardiac Physiology

Cellular anatomy:

Cardiac muscle tissue Conduction tissue Extracellular connective tissue

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Sarcoplasmic Reticulum (SR)

Figure 9.510/25/2012

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CARDIOMYOCYTE

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gap junctions>>electrical coupling

“spot” desmosomes>> mechanical linkage >> cytoskeleton

“sheet” desmosomes (or fasciae adherens)>> contractile apparatus

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Cardiomyocytes can be functionally separated into:

(1) the excitation system, (2) the ECC system, (3) the contractile system.

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Excitation System

Fast-response action potentials>> His-Purkinje system

atrial/ventricular cardiomyocytes

Slow-response action potentials, pacemaker cells in the

SA and AV nodes

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phase 0 : much less steep,

phase 1: absent, phase 2 : indistinct from phase 3 in the slow-response action potential

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ECC

Ca channel phosphorylation

Faster contraction

Phospholamban

Faster relaxation

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Ca++

Ca++

Ca++Ca++

Pictorial E-C CouplingPictorial E-C Coupling

Plb

Ca++

Ca++Ca++

Ca++Ca++

Ca

++

Ca++

Ca++

Ca ++Ca++

Ca++

Ca++

Ca++

Ca++

Ca++

Ca ++

Ca++

Ca ++ Ca ++

Ca

++

Ca++

Ca

++

Ca++

Ca++

Ca++

Ca++

Ca++

Ca++

Ca++

Ca++

Ca++Ca++

Ca++

Ca++

Ca++

Ca++Ca++

Ca ++

Ca

++

Ca++ Ca ++Ca

++

Ca++

Ca ++

Ca++

Ca++

Ca++

Ca++

Ca++

Ca++

Na+

Na+Na+

Ca++

SERCA

SR

L-Type Ca++

Channel

Na+/Ca++ Exchanger

Ca++

SarcolemmaCa++

RyR

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Contractile SystemContractile System

The basic working unit of contraction is the sarcomere.

A sarcomere is defined as the distance between Z lines

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Sarcomere

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Structure of Actin and MyosinStructure of Actin and Myosin

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Figure 9.4 (a)(b)10/25/2012

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Actin

Figure 9.4 (c)10/25/2012

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Troponin

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actin

actin

myosin

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processive movement of myosin V along F-actin

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actin

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actintroponin

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actintroponin

tropomyosin

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actintroponin

tropomyosin

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actintroponin

tropomyosinmyosin binding site

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Ca2+Ca2+ Ca2+ Ca2+

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Ca2+Ca2+ Ca2+ Ca2+

Calcium ions are released from the sarcolemma after stimulation from the T system

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Ca2+Ca2+

Ca2+

Ca2+

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Ca2+Ca2+

Ca2+

Ca2+

the calcium ions bind to the troponin and changes its shape

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Ca2+Ca2+

Ca2+

Ca2+

the calcium ions bind to the troponin and changes its shape

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Ca2+Ca2+

Ca2+

Ca2+

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Ca2+Ca2+

Ca2+

Ca2+

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Ca2+Ca2+

Ca2+

Ca2+

the troponin displaces the tropomyosin and exposes the myosin binding sites

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Ca2+Ca2+

Ca2+

Ca2+

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Ca2+Ca2+

Ca2+

Ca2+

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Ca2+Ca2+

Ca2+

Ca2+

the bulbous heads of the myosin attach to the binding sites on the actin filaments

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Ca2+Ca2+

Ca2+

Ca2+

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Ca2+ Ca2+

Ca2+

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Ca2+ Ca2+

Ca2+

the myosin heads change position to achieve a lower energy state and slide the actin filaments past the stationary myosin

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Ca2+ Ca2+

Ca2+

APi PiPiAPi PiPiAPi PiPi

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Ca2+ Ca2+

Ca2+APi PiPi

APi PiPi

APi PiPi

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Ca2+ Ca2+

Ca2+APi PiPi

APi PiPi

APi PiPi

ATP binds to the bulbous heads and causes it to become detached

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Ca2+ Ca2+

Ca2+

APi PiPiAPi PiPi

APi PiPi

ATP binds to the bulbous heads and causes it to become detached

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Ca2+ Ca2+

Ca2+

APi Pi

Pi

APi Pi

Pi

APi Pi

Pi

hydrolysis of ATP provides the energy to “re-cock” the heads

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Ca2+ Ca2+

Ca2+

APi Pi

Pi

APi Pi

Pi

APi Pi

Pi

hydrolysis of ATP provides the energy to “re-cock” the heads

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Ca2+ Ca2+Ca2+

APi Pi

Pi

APi Pi

Pi

APi Pi

Pi

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Ca2+ Ca2+Ca2+

APi Pi

Pi

APi Pi

Pi

APi Pi

Pi

calcium ions are re-absorbed back into the T system

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APi Pi

Pi

APi Pi

Pi

APi Pi

Pi

calcium ions are re-absorbed back into the T system

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APi Pi

Pi

APi Pi

Pi

APi Pi

Pi

the troponin reverts to its normal shape and the tropomyosin move back to block the myosin binding sites

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APi Pi

Pi

APi Pi

Pi

APi Pi

Pi

the troponin reverts to its normal shape and the tropomyosin move back to block the myosin binding sites

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APi Pi

Pi

APi Pi

Pi

APi Pi

Pi

the troponin reverts to its normal shape and the tropomyosin move back to block the myosin binding sites

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APi Pi

Pi

APi Pi

Pi

APi Pi

Pi

phosphocreatine regenerates ATP

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APi Pi

Pi

APi PiPi

APi PiPi

phosphocreatine regenerates ATP

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APi PiPiAPi PiPi

APi PiPi

phosphocreatine regenerates ATP

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Mechanism of muscle contraction

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All Things Science - Heart excitation contraction coupling.flv - YouTube.FLV

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NEURAL REGULATION OF HEART

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At rest the heart has a tonic level of PNSAtria have more PNS innervation than

ventriclesM1-M5, M2 most oneM1,3,5, G proteineM2,4 pertussis toxin

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SNS more prominent in ventricles α receptors >> G protein>> phospholipase

C,D,A β receptors >> G protein>> cAMP β1,2,3 β1, both atria ventricle, 80% β2 atria 20%

ventricles β2>> β1 α1,2>>α1A,B,D α1 : cardiac hypertrophy

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Adrenoreceptors

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Hormones affecting cardiac function

Hormone source Cardiac action Increase with CHF

Adrenomedullin Cardiomyocyte + inotropy/ +chronotropy

+

Aldosterone Cardiomyocyte ? +

Angiotensin II Cardiomyocyte + inotropy/ +chronotropy +

Endothelin Cardiomyocyte ? +

Natriuritic peptide

ANP Atria+

BNP Ventricles+

Neuropeptide Y - Inotropy

Vasopressin Post pituitary + inotropy/ +chronotropy +

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Chemoreceptor ReflexChemoreceptor ReflexMediated by

– Chemosensitive cells in the carotid bodies and the aortic body.

– Sinus nerve of Hering and vagus nervesAt PaO2 <50 mm Hg or in acidosis

– respiratory centers stimulated and increasing ventilatory drive.

Activation of the parasympathetic system – reduction in heart rate and myocardial

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Bainbridge Reflex

Bainbridge (atrial) reflex – a sympathetic reflex initiated by

increased blood in the atria

Causes stimulation of the SA node

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Bezold-Jarisch reflexBezold-Jarisch reflex Elicited by

– chemoreceptors and mechanoreceptors within the LV wall

– ↑ parasympathetic tone Noxious ventricular stimuli induces the triad of

hypotension, bradycardia, and coronary artery dilatation.

Less pronounced in patients with

– Cardiac hypertrophy

– Atrial fibrillation

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Valsalva ManeuverValsalva ManeuverValsalva maneuver → ↓CO and BP. Sensed by baroreceptors → sympathetic

stimulation ↑heart rate and myocardial contractility.

When the glottis opens, venous return ↑ →↑BP.

Sensed by baroreceptors → stimulate parasympathetic efferent pathways to the heart.

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Cushing Reflex Cerebral ischemia at the medullary

vasomotor center ↓

Activation of the sympathetic nervous system

↓↑ HR, BP, and myocardial contractility

↓Improve cerebral perfusion

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Oculocardiac Reflex Oculocardiac Reflex Stretch receptors

↓ Short and long ciliary nerves

↓ Ophthalmic division of the trigeminal nerve

↓Gasserian ganglion

↓Increased parasympathetic tone

↓Bradycardia.

Incidence during ophthalmic surgery- 30% to 90%.

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