Download Lecture: Heart Physiology

Lecture: Heart Physiology
I. Cardiac Muscle (compare to Skeletal Muscle)
Cardiac Muscle Cells
Skeletal Muscle Cells
fairly short
semi-spindle shape
branched, interconnected
connected (intercalated discs)
electrical link (gap junction)
common contraction (syncytium)
1 or 2 central nuclei
dense "endomysium"
high vasculature
MANY mitochondria (25% space)
almost all AEROBIC (oxygen)
myofibers fuse at ends
T tubules wider, fewer
very long
cylindrical shape
side-by-side
no tight binding
no gap junctions
independent contract
multinucleated
light "endomysium"
medium vasculature
less mitochondria (2%)
aerobic & anaerobic
myofibers not fused
T tubules at A/I spot
II. Mechanism of Contraction of Contractile Cardiac Muscle Fibers
1.
Na+ influx from extracellular space, causes positive feedback opening of voltagegated Na+ channels; membrane potential quickly depolarizes (-90 to +30 mV);
Na+ channels close within 3 ms of opening.
2.
Depolarization causes release of Ca++ from sarcoplasmic reticulum (as in skeletal
muscle), allowing sliding actin and myosin to proceed.
3.
Depolarization ALSO causes opening of slow Ca++ channels on the membrane
(special to cardiac muscle), further increasing Ca++ influx and activation of
filaments. This causes more prolonged depolarization than in skeletal muscle,
resulting in a plateau action potential, rather than a "spiked" action potential (as in
skeletal muscle cells).
Differences Between Skeletal & Cardiac MUSCLE Contraction
1.
All-or-None Law - Gap junctions allow all cardiac muscle cells to be linked
electrochemically, so that activation of a small group of cells spreads like a wave
throughout the entire heart. This is essential for "synchronistic" contraction of the heart as
opposed to skeletal muscle.
2.
Automicity (Autorhythmicity) - some cardiac muscle cells are "self-excitable" allowing
for rhythmic waves of contraction to adjacent cells throughout the heart. Skeletal muscle
cells must be stimulated by independent motor neurons as part of a motor unit.
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3.
Length of Absolute Refractory Period - The absolute refractory period of cardiac muscle
cells is much longer than skeletal muscle cells (250 ms vs. 2-3 ms), preventing wave
summation and tetanic contractions which would cause the heart to stop pumping
rhythmically.
III.
Internal Conduction (Stimulation) System of the Heart
A.
General Properties of Conduction
1.
2.
3.
B.
heart can beat rhythmically without nervous input
nodal system (cardiac conduction system) - special autorhythmic cells of
heart that initiate impulses for wave-like contraction of entire heart (no
nervous stimulation needed for these)
gap junctions - electrically couple all cardiac muscle cells so that
depolarization sweeps across heart in sequential fashion from atria to
ventricles
"Pacemaker" Features of Autorhythmic Cells
1.
pacemaker potentials - "autorhythmic cells" of heart muscle create action
potentials in rhythmic fashion; this is due to unstable resting potentials
which slowly drift back toward threshold voltage after repolarization from
a previous cycle.
Theoretical Mechanism of Pacemaker Potential:
a.
K+ leak channels allow K+ OUT of the cell more slowly than in skeletal muscle
b.
Na+ slowly leaks into cell, causing membrane potential to slowly drift up to the threshold
to trigger Ca++ influx from outside (-40 mV)
c.
when threshold for voltage-gated Ca++ channels is reached (-40 mV), fast calcium
channels open, permitting explosive entry of Ca++ from of the cell, causing sharp rise in
level of depolarization
d.
when peak depolarization is achieved, voltage-gated K+ channels open, causing
repolarization to the "unstable resting potential"
e.
cycle begins again at step a.
C.
Anatomical Sequence of Excitation of the Heart
1. Autorhythmic Cell Location & Order of Impulses
(right atrium)
(right AV valve)
sinoatrial node (SA) ->
atrioventricular node (AV) ->
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atrioventricular bundle (bundle of His) ->
right & left bundle of His branches ->
Purkinje fibers of ventricular walls
(from SA through complete heart contraction = 220 ms = 0.22 s)
a.
sinoatrial node (SA node) "the pacemaker" - has the fastest autorhythmic rate (70-80 per
minute), and sets the pace for the entire heart; this rhythm is called the sinus rhythm;
located in right atrial wall, just inferior to the superior vena cava
b.
atrioventricular node (AV node) - impulses pass from SA via gap junctions in about 40
ms.; impulses are delayed about 100 ms to allow completion of the contraction of both
atria; located just above tricuspid valve (between right atrium & ventricle)
c.
atrioventricular bundle (bundle of His) - in the interATRIAL septum (connects L and R
atria)
d.
L and R bundle of His branches - within the interVENTRICULAR septum (between L
and R ventricles)
e.
Purkinje fibers - within the lateral walls of both the L and R ventricles; since left ventricle
much larger, Purkinjes more elaborate here; Purkinje fibers innervate “papillary muscles”
before ventricle walls so AV can valves prevent backflow
D. Special Considerations of Wave of Excitation
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
initial SA node excitation causes contraction of both the R and L atria
contraction of R and L ventricles begins at APEX of heart (inferior point),
ejecting blood superiorly to aorta and pulmonary artery
the bundle of His is the ONLY link between atrial contraction and ventricular
contraction; AV node and bundle must work for ventricular contractions
since cells in the SA node has the fastest autorhythmic rate (70-80 per minute), it
drives all other autorhythmic centers in a normal heart
arrhythmias - uncoordinated heart contractions
fibrillation - rapid and irregular contractions of the heart chambers; reduces
efficiency of heart
defibrillation - application of electric shock to heart in attempt to retain normal
SA node rate
ectopic focus - autorhythmic cells other than SA node take over heart rhythm
nodal rhythm - when AV node takes over pacemaker function (40-60 per minute)
extrasystole - when outside influence (such as drugs) leads to premature
contraction
heart block - when AV node or bundle of His is not transmitting sinus rhythm to
ventricles
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E.
External Innervation Regulating Heart Function
1.
2.
heart can beat without external innervation
external innervation is from AUTONOMIC SYSTEM
parasympathetic - (acetylcholine) DECREASES rate of contractions
cardioinhibitory center (medulla) ->
vagus nerve (cranial X) ->
heart
sympathetic - (norepinephrine) INCREASES rate of contractions
cardioacceleratory center (medulla) ->
lateral horn of spinal cord to preganglionics Tl-T5 ->
postganlionics cervical/thoracic ganglia ->
heart
IV.
Electrocardiography: Electrical Activity of the Heart
A.
V.
Deflection Waves of ECG
1.
P wave - initial wave, demonstrates the depolarization from SA Node
through both ATRIA; the ATRIA contract about 0.1 s after start of P
Wave
2.
QRS complex - next series of deflections, demonstrates the depolarization
of AV node through both ventricles; the ventricles contract throughout the
period of the QRS complex, with a short delay after the end of atrial
contraction; repolarization of atria also obscured
3.
T Wave - repolarization of the ventricles (0.16 s)
4.
PR (PQ) Interval - time period from beginning of atrial contraction to
beginning of ventricular contraction (0.16 s)
5.
QT Interval the time of ventricular contraction (about 0.36 s); from
beginning of ventricular depolarization to end of repolarization
The Normal Cardiac Cycle
A.
General Concepts
1.
2.
3.
systole - period of chamber contraction
diastole - period of chamber relaxation
cardiac cycle - all events of systole and diastole during one heart flow
cycle
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B.
Events of Cardiac Cycle
1.
mid-to-late ventricular diastole: ventricles filled
*
*
*
*
*
*
*
the AV valves are open
pressure: LOW in chambers; HIGH in aorta/pulmonary trunk
aortic/pulmonary semilunar valves CLOSED
blood flows from vena cavas/pulmonary vein INTO atria
blood flows through AV valves INTO ventricles (70%)
atrial systole propels more blood > ventricles (30%)
atrial diastole returns through end of cycle
2.
ventricular systole: blood ejected from heart
*
*
*
*
*
filled ventricles begin to contract, AV valves CLOSE
isovolumetric contraction phase - ventricles CLOSED
contraction of closed ventricles increases pressure
ventricular ejection phase - blood forced out
semilunar valves open, blood -> aorta & pulmonary trunk
3.
isovolumetric relaxation: early ventricular diastole
*
*
*
ventricles relax, ventricular pressure becomes LOW
semilunar valves close, aorta & pulmonary trunk backflow
dicrotic notch - brief increase in aortic pressure
TOTAL CARDIAC CYCLE TIME
(normal 70 beats/minute)
=
0.8 second
atrial systole (contraction)
ventricular systole (contraction)
quiescent period (relaxation)
=
=
=
0.1 second
0.3 second
0.4 second
VI.
Heart Sounds: Stethoscope Listening
A.
Overview of Heart Sounds
1.
2.
3.
4.
5.
6.
7.
lub-dub, - , lub, dub, lub - closure of AV valves, onset of ventricular systole
dub - closure of semilunar valves, onset of diastole
pause - quiescent period of cardiac cycle
tricuspid valve (lub) - RT 5th intercostal, medial
mitral valve (lub) - LT 5th intercostal, lateral
aortic semilunar valve (dub) - RT 2nd intercostal
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B.
8.
pulmonary semilunar valve (dub) - LT 2nd intercostal
Heart Murmurs
1.
2.
3.
VII.
murmur - sounds other than the typical "lub-dub"; typically caused by disruptions
in flow
incompetent valve - swishing sound just AFTER the normal "lub" or "dub"; valve
does not completely close, some regurgitation of blood
stenotic valve - high pitched swishing sound when blood should be flowing
through valve; narrowing of outlet in the open state
Cardiac Output - Blood Pumping of the Heart
A.
General Variables of Cardiac Output
1.
2.
3.
Cardiac Output (CO) - blood amount pumped per minute
Stroke Volume (SV) - ventricle blood pumped per beat
Heart Rate (HR) - cardiac cycles per minute
CO (ml/min) =
HR (beats/min) X
normal CO =
75 beats/min X 70 ml/beat =
B.
5.25 L/min
Regulation of Stroke Volume (SV)
1.
2.
SV (ml/beat) =
normal SV
=
3.
end diastolic volume (EDV) - total blood collected in ventricle at end of
diastole; determined by length of diastole and venous pressure (~ 120 ml)
end systolic volume (ESV) - blood left over in ventricle at end of
contraction (not pumped out); determined by force of ventricle contraction
and arterial blood pressure (~50 ml)
EDV (ml/beat) 120 m1/beat -
ESV (ml/beat)
50 ml/beat
=
70 ml/beat
Frank-Starling Law of the Heart - critical factor for stroke volume is
"degree of stretch of cardiac muscle cells"; more stretch = more
contraction force
a.
increased EDV = more contraction force
i.
ii.
C.
SV (ml/beat)
slow heart rate = more time to fill
exercise = more venous blood return
Regulation of Heart Rate (Autonomic, Chemical, Other)
1.
Autonomic Regulation of Heart Rate (HR)
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a.
b.
c.
d.
2.
Hormonal and Chemical Regulation of Heart Rate (HR)
a.
b.
c.
*
*
*
*
*
3.
sympathetic - NOREPINEPHRINE (NE) increases heart rate
(maintains stroke volume which leads to increased Cardiac Output)
parasympathetic - ACETYLCHOLINE (ACh) decreases heart rate
vagal tone - parasympathetic inhibition of inherent rate of SA node,
allowing normal HR
baroreceptors, pressoreceptors - monitor changes in blood pressure
and allow reflex activity with the autonomic nervous system
epinephrine - hormone released by adrenal medulla during stress;
increases heart rate
thyroxine - hormone released by thyroid; increases heart rate in
large quantities; amplifies effect of epinephrine
Ca++, K+, and Na+ levels very important;
hyperkalemia - increased K+ level; KCl used to stop heart on lethal
injection
hypokalemia - lower K+ levels; leads to abnormal heart rate
rhythms
hypocalcemia - depresses heart function
hypercalcemia - increases contraction phase
hypernatremia - HIGH Na+ concentration; can block Na+ transport
& muscle contraction
Other Factors Effecting Heart Rate (HR)
a.
normal heart rate -
b.
c.
d.
e.
exercise - lowers resting heart rate (40-60)
heat - increases heart rate significantly
cold - decreases heart rate significantly
tachycardia - HIGHER than normal resting heart rate (over 100);
may lead to fibrillation
bradycardia - LOWER than normal resting heart rate (below 60);
parasympathetic drug side effects; physical conditioning; sign of
pathology in non-healthy patient
f.
fetus 140 - 160 beats/minute
female 72 - 80 beats/minute
male 64 - 72 beats/minute
VIII. Imbalance of Cardiac Output & Heart Pathologies
A.
Imbalance of Cardiac Output
1.
congestive heart failure - heart cannot pump sufficiently to meet needs of
the body
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a.
b.
c.
d.
e.
B.
coronary atherosclerosis - leads to gradual occlusion of heart
vessels, reducing oxygen nutrient supply to cardiac muscle cells;
(fat & salt diet, smoking, stress)
high blood pressure - when aortic pressure gets too large, left
ventricle cannot pump properly, increasing ESV, and lowering SV
myocardial infarct (MI) - "heart cell death" due to numerous
factors, including coronary artery occlusion
pulmonary congestion - failure of LEFT heart; leads to buildup of
blood in the lungs
peripheral congestion - failure of RIGHT heart; pools in body,
leading to edema (fluid buildup in areas such as feet, ankles,
fingers)
Heart Pathologies (Diseases of the Heart)
1.
congenital heart defects - heart problems that are present at the time of
birth
a.
patent ductus arteriosus - bypass hole between pulmonary trunk
and aorta does not close
2.
sclerosis of AV valves - fatty deposits on valves; particularly the mitral
valve of LEFT side; leads to heart murmur
3.
decline in cardiac reserve - heart efficiency decreases with age
4.
fibrosis and conduction problems - nodes and conduction fibers become
scarred over time; may lead to arrhythmias
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