13 - Heart Physiology

7/28/2019 13 - Heart Physiology

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Lecture: Heart Physiology

I. Cardiac Muscle (compare to Skeletal Muscle)

Cardiac Muscle Cells

fairly short

semi-spindle shape

branched, interconnectedconnected (intercalated discs)

electrical link (gap junction)

common contraction (syncytium)

1 or 2 central nucleidense "endomysium"

high vasculature

MANY mitochondria (25% space)

almost all AEROBIC (oxygen)myofibers fuse at ends

T tubules wider, fewer

Skeletal Muscle Cells

very long

cylindrical shape

side-by-sideno tight binding

no gap junctions

independent contract

multinucleatedlight "endomysium"

medium vasculature

less mitochondria (2%)

aerobic & anaerobicmyofibers 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 voltage-

gated 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 wavethroughout 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 (250ms vs. 2-3 ms), preventing wave

summation and tetanic contractions which would cause the heart to stop pumpingrhythmically.

III. Internal Conduction (Stimulation) System of the Heart

A. General Properties of Conduction

1. heart can beat rhythmically without nervous input

2. 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)3. gap junctions - electrically couple all cardiac muscle cells so that

depolarization sweeps across heart in sequential fashion from atria to

ventricles

B. "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 froma 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 thresholdto trigger Ca++ influx from outside (-40 mV)

c. when threshold for voltage-gated Ca++ channels is reached (-40 mV), fast calciumchannels 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, causingrepolarization 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) sinoatrial node (SA) ->

(right AV valve) 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 musclesbefore ventricle walls so AV can valves prevent backflow

D. Special Considerations of Wave of Excitation

1. initial SA node excitation causes contraction of both the R and L atria

2. contraction of R and L ventricles begins at APEX of heart (inferior point),

ejecting blood superiorly to aorta and pulmonary artery3. the bundle of His is the ONLY link between atrial contraction and ventricular

contraction; AV node and bundle must work for ventricular contractions

4. since cells in the SA node has the fastest autorhythmic rate (70-80 per minute), itdrives all other autorhythmic centers in a normal heart

5. arrhythmias - uncoordinated heart contractions

6. fibrillation - rapid and irregular contractions of the heart chambers; reduces

efficiency of heart7. defibrillation - application of electric shock to heart in attempt to retain normal

SA node rate

8. ectopic focus - autorhythmic cells other than SA node take over heart rhythm9. nodal rhythm - when AV node takes over pacemaker function (40-60 per minute)

10. extrasystole - when outside influence (such as drugs) leads to premature

contraction11. 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. heart can beat without external innervation2. external innervation is from AUTONOMIC SYSTEM

parasympathetic - (acetylcholine) DECREASES rate of contractionscardioinhibitory 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. 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 PWave

2. QRS complex - next series of deflections, demonstrates the depolarization

of AV node through both ventricles; the ventricles contract throughout theperiod 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 tobeginning 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

V. The Normal Cardiac Cycle

A. General Concepts

1. systole - period of chamber contraction2. diastole - period of chamber relaxation

3. 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 = 0.8 second(normal 70 beats/minute)

atrial systole (contraction) = 0.1 secondventricular systole (contraction) = 0.3 second

quiescent period (relaxation) = 0.4 second

VI. Heart Sounds: Stethoscope Listening

A. Overview of Heart Sounds

1. lub-dub, - , lub, dub, -

2. lub - closure of AV valves, onset of ventricular systole

3. dub - closure of semilunar valves, onset of diastole4. pause - quiescent period of cardiac cycle

5. tricuspid valve (lub) - RT 5th intercostal, medial

6. mitral valve (lub) - LT 5th intercostal, lateral

7. aortic semilunar valve (dub) - RT 2nd intercostal

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8. pulmonary semilunar valve (dub) - LT 2nd intercostal

B. Heart Murmurs

1. murmur - sounds other than the typical "lub-dub"; typically caused by disruptions

in flow

2. incompetent valve - swishing sound just AFTER the normal "lub" or "dub"; valvedoes not completely close, some regurgitation of blood

3. stenotic valve - high pitched swishing sound when blood should be flowing

through valve; narrowing of outlet in the open state

VII. Cardiac Output - Blood Pumping of the Heart

A. General Variables of Cardiac Output

1. Cardiac Output (CO) - blood amount pumped per minute

2. Stroke Volume (SV) - ventricle blood pumped per beat

3. Heart Rate (HR) - cardiac cycles per minute

CO (ml/min) = HR (beats/min) X SV (ml/beat)

normal CO = 75 beats/min X 70 ml/beat = 5.25 L/min

B. Regulation of Stroke Volume (SV)

1. end diastolic volume (EDV) - total blood collected in ventricle at end of

diastole; determined by length of diastole and venous pressure (~ 120 ml)2. 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)

SV (ml/beat) = EDV (ml/beat) - ESV (ml/beat)

normal SV = 120 m1/beat - 50 ml/beat = 70 ml/beat

3. 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. slow heart rate = more time to fill

ii. exercise = more venous blood return

C. Regulation of Heart Rate (Autonomic, Chemical, Other)

1. Autonomic Regulation of Heart Rate (HR)

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a. sympathetic - NOREPINEPHRINE (NE) increases heart rate

(maintains stroke volume which leads to increased Cardiac Output)

b. parasympathetic - ACETYLCHOLINE (ACh) decreases heart ratec. vagal tone - parasympathetic inhibition of inherent rate of SA node,

allowing normal HR

d. baroreceptors, pressoreceptors - monitor changes in blood pressureand allow reflex activity with the autonomic nervous system

2. Hormonal and Chemical Regulation of Heart Rate (HR)

a. epinephrine - hormone released by adrenal medulla during stress;

increases heart rate

b. thyroxine - hormone released by thyroid; increases heart rate inlarge quantities; amplifies effect of epinephrine

c. Ca++, K+, and Na+ levels very important;

* hyperkalemia - increased K

+

level; KCl used to stop heart on lethalinjection

* hypokalemia - lower K + levels; leads to abnormal heart raterhythms

* hypocalcemia - depresses heart function

* hypercalcemia - increases contraction phase* hypernatremia - HIGH Na+ concentration; can block Na+ transport

& muscle contraction

3. Other Factors Effecting Heart Rate (HR)

a. normal heart rate - fetus 140 - 160 beats/minute

female 72 - 80 beats/minutemale 64 - 72 beats/minute

b. exercise - lowers resting heart rate (40-60)c. heat - increases heart rate significantly

d. cold - decreases heart rate significantly

e. tachycardia - HIGHER than normal resting heart rate (over 100);

may lead to fibrillationf. bradycardia - LOWER than normal resting heart rate (below 60);

parasympathetic drug side effects; physical conditioning; sign of

pathology in non-healthy patient

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. coronary atherosclerosis - leads to gradual occlusion of heart

vessels, reducing oxygen nutrient supply to cardiac muscle cells;(fat & salt diet, smoking, stress)

b. high blood pressure - when aortic pressure gets too large, left

ventricle cannot pump properly, increasing ESV, and lowering SVc. myocardial infarct (MI) - "heart cell death" due to numerous

factors, including coronary artery occlusion

d. pulmonary congestion - failure of LEFT heart; leads to buildup ofblood in the lungs

e. peripheral congestion - failure of RIGHT heart; pools in body,

leading to edema (fluid buildup in areas such as feet, ankles,

fingers)

B. Heart Pathologies (Diseases of the Heart)

1. congenital heart defects - heart problems that are present at the time ofbirth

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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13 - Heart Physiology

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