Cardiac physiology
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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
Flash player Active-X Macro’s enabled
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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
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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
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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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