Heart Physiology

Front 1

pause

Back 1

quiescent period of cardiac cycle

Front 2

tricuspid valve (lub)

Back 2

RT 5th intercostal, medial

Front 3

mitral valve (lub)

Back 3

LT 5th intercostal, lateral

Front 4

aortic semilunar valve (dub)

Back 4

RT 2nd intercostal

Front 5

aortic semilunar valve (dub)

Back 5

RT 2nd intercostal

Front 6

pulmonary semilunar valve (dub)

Back 6

LT 2nd intercostal

Front 7

Heart Murmurs

Back 7

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"; valve does not completely close, some regurgitation of blood, backflow
3. stenotic valve- high pitched swishing sound when blood should be flowing through valve; narrowing of outlet in the open state

Front 8

murmur

Back 8

sounds other than the typical "lub-dub"; typically caused by disruptions in flow

Front 9

incompetent valve

Back 9

swishing sound just after the normal "lub" or "dub"; valve does not completely close, some regurgitation of blood, backflow

Front 10

Cardiac Output- Blood pumping of the heart- General variables of cardiac output

Back 10

1. Cardiac output (CO)- blood amount pumped per minute
2. stroke volume (SV)- ventricle blood pumped per mm
3. heart rate (HR)- cardiac cycles per minute
4. CO (ml/mn)= HR (beats/mm) X SV (ml/beat)
5. normal CO = 75 beats/mm X 70ml/beat = 5.25 L/min

Front 11

cardiac output (CO)

Back 11

blood amount pumped per minute

Front 12

Stroke volume (SV)

Back 12

ventricle blood pumped per mm

Front 13

heart rate (HR)

Back 13

cardiac cycles per minute

Front 14

Length of absolute refractory period

Back 14

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

Front 15

Heart Pathologies (diseases of the heart)

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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 deposites on valves; particulary the mitral valve of LEFT side; leads to heart murmur
3. decline in cardiac reserve- heart effeciency decreases with age
4. fibrosis and conduction problems- nodes and conduction fibers become scarred over time; may lead to arrhythmias, could lead to AV block, conduction problems

Front 16

congenital heart defects

Back 16

heart problems that are present at the time of birth

Front 17

sclerosis of AV valves

Back 17

fatty deposits on valves; particulary the mitral valve of LEFT side; leads to heart murmur

Front 18

decline in cardiac reserve

Back 18

heart effeciency decreases with age

Front 19

fibrosis and conduction problems

Back 19

nodes and conduction fibers become scarred over time; may lead to arrhythmias, could lead to AV block, conduction problems

Front 20

congestive heart failure

Back 20

heart cannot pump suffeciently to meet the needs of the body, because of buildup in the lungs and tissues

Front 21

patent ductus arteriosus

Back 21

bypass hole between pulmonary trunk and aorta does not close

Front 22

Electrocardiography: Electrical activity of the heart. - Deflection Waves of ECG

Back 22

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 (0.16s)
4. PR(PQ) Interval- time period from begining of atrial contraction to begining of ventricular contraction (0.16s)
5. QT Interval- The time of ventricular contraction (about 0.36s); from begining of ventricular depolarization to end of repolarization

Front 23

The Normal Cardiac Cycle- General Concepts

Back 23

1. systole- period of chamber contraction
2. Diastole- period of chamber relaxation
3. Cardiac Cycle- all events of systole and diastole during one heart flow cycle

Front 24

Systole

Back 24

period of chamber contraction

Front 25

Diastole

Back 25

period of chamber relaxation

Front 26

Cardiac Cycle

Back 26

all events of systole and diastole during one heart flow cycle

Front 27

Events Of Cardiac Cycle- Mid-to-late diastole: ventricles filled

Back 27

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 to ventricles (30%). atrial diastole returns through end of cycle.

Front 28

Events of Cardiac Cycle- Isovolumetric relaxation: early diastole

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ventricles relax, ventricular pressure becomes low. semilunar valves close, aorta and pulmonary trunk backflow. dicrotic notch- breif increase in aortic pressure

Front 29

Total Cardiac Cycle Time

Back 29

= 8 seconds (normal 70 beats/minute).
Atrial systole (contraction) = 0.1 second.
Ventricular systole (contraction) = 0.3 seconds
Quiescent period (relaxation) = 0.4 seconds

Front 30

Overview of Heart Sounds

Back 30

1. lub-dub, - , lub, dub, -
2. lub- closure of AV valves, onset of ventricular systole
3. dub- colsure of semilunar valves, onset of diastole
4. 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
8. pulmonary semilunar valve (dub)- LT 2nd intercostal

Front 31

lub

Back 31

closure of AV valves, onset of ventricular systole

Front 32

dub

Back 32

closure of semilunar valves, onset of diastole

Front 33

Purkinje fibers

Back 33

within the lateral walls of both the L and R ventricles; since left ventricle is much larger, Purkinjes more elaborate here; Purkinje fibers innervate "papillary muscles" before ventricle walls so AV valves can prevent backflow

Front 34

Arrhythmias

Back 34

uncoordinated heart contractions

Front 35

Fibrillation

Back 35

rapid and irregular contractions of the heart chambers; reduces effeciency of heart

Front 36

Ectopic focus

Back 36

autorhythmic cells other than SA node take over heart rhythm

Front 37

Nodal rhythm

Back 37

when AV node takes over pacemaker function (40-60 per minute)

Front 38

Extrasystole

Back 38

when outside influence (such as drugs) leads to premature contraction

Front 39

Heart block

Back 39

when AV node or bundle of his is not transmitting sinus rhythm to ventricles

Front 40

hyperkalemia

Back 40

increased K level; KCL used to stop heart on lethal injection

Front 41

hypokalemia

Back 41

lower K levels; leads to abnormal heart rate ryhthms

Front 42

hypocalcemia

Back 42

depresses heart function

Front 43

hypercalcemia

Back 43

increases contraction phase

Front 44

hypernatremia

Back 44

HIGH Na concentration; can block Na transport & muscle contraction

Front 45

Other facters affecting heart rate (HR)

Back 45

A. normal heart rate-
fetus= 140-160 beats/minute
female= 72-80 beats/minute
male= 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 fibrillation
F. bradycardia- LOWER than normal resting heart rate (below 60); parasympathetic drug side effects; physical conditioning; sign of pathology in non-healthy patient

Front 46

normal heart rate

Back 46

fetus- 140-160 beats/minute
female- 72-80 beats/minute
male 64-72 beats/minute

Front 47

exercise

Back 47

lowers resting heart rate (40-60)

Front 48

heat

Back 48

increases heart rate significantly

Front 49

cold

Back 49

decreases heart rate significantly

Front 50

All or none law

Back 50

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

Front 51

tachycardia

Back 51

HIGHER than normal resting heart rate (over 100); may lead to fibrillation

Front 52

bradycardia

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LOWER than normal resting heart rate (below 60); parasympathetic drug side effects; physical conditioning; sign of pathology in non-healthy patient

Front 53

Automicity (autorhythmicity)

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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.

Front 54

Theorotical mechanism of pacemaker potential

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A. K leak channels allow K out of the cell more slowly than in skeletal muscle
B. Na slowly leaks into the 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 expolsive entry of Ca from the cell, causing sharp rise in level of depolarization
D. When peak depolarization is acheived, voltage-gated K channels open, causing repolarization to the "unstable resting potential",
because it slowly drifts up
E. cycle begins again at step a.

Front 55

Anatomical sequence of excitation of the heart. - Autorhythmic cell location & order of impulses

Back 55

right atrium to sinoatrial node (SA) to right AV valve, atrioventricular node (AV) to atrioventricular bundle (bundle of his) to right & left bundle of his branches to purkinje fibers of ventricular walls (from SA through complete heart contraction = 220 ms = 0.22 s)

Front 56

sinoatrial node (SA) node "the pacemaker"

Back 56

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 the right atrial wall, just inferior to the superior vena cava

Front 57

atrioventricular node (AV) node

Back 57

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 the tricuspid valve (between right atrium & ventricle)

Front 58

Atrioventricular bundle (bundle of his)

Back 58

in the interATRIAL septum (connects L and R atria)

Front 59

L and R bundle of his branches

Back 59

within the interVENTRICULAR septum (between L and R ventricles)

Front 60

Internal conduction (Stimulation) system of heart

Back 60

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.

Front 61

Gap junctions

Back 61

electrically couple all cardiac muscle cells so that depolarization sweeps across heart in sequential fashion from atria to ventricles

Front 62

Differences between skeletal & cardiac muscle contraction

Back 62

1. All or none law = Gap junctions allow all cardiac muscles 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-exciteable" 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.
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.

Front 63

Mechanism of contraction of contractile cardiac muscle fibers

Back 63

1. Na influx from intracellular space, causes positive feedback of voltage gated Na chanels; membrane potential quickly depolarizes (-90 to +30 mV); Na channels close within 3 seconds of opening causing refractory period.
2. Depolarization causes release of Ca from sarcoplasmic reticulum (as in skeletal muscle), allowing sliding actin and myosin to preceed.
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 ckeletal muscle cells).

Front 64

Cardiac muscle cells

Back 64

fairly short, semi spindle shape, branched, interconnected, connected intercalated disc, electrical link - gap junction, common contraction - syncytium, 1 or 2 central nuclei, dense "endomysium", high vasculature - high blood supply, many mitochondria - 25% space, almost all aerobic - oxygen, myofibers fuse at ends, T tubules wider, fewer

Front 65

Skeletal muscle cells

Back 65

very long, cylindrical shape, side-by-side, no tight binding, no gap junctions, independent contract, multinucleated, light "endomysium", medium vasculature, low blood supply, less mitochondria - 2%, aerobic & anaerobic, myofibers not fused, T tubules at interface between A/I spot

Front 66

Imbalance of cardiac output & heart pathologies- Imbalance of cardiac output

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1. congestive heart failure- heart cannot pump sufficiently to meet the needs of the body because of build-up in lungs and tissues
2. coronary atherosclerosis- leads to gradual occlusion of heart vessels, reducing oxygen nutrient supply to cardiac muscle cells; (fat & salt diet, smoking, stress)
3. high blood pressure- when aortic pressure gets to large, left ventricle cannot pump properly, increasing end systolic volume (ESV), & lowering SV because more left over
4. myocardial infarction (MI) "heart cell death" due to numerous factors, including coronary artery occlusion
5. pulmonary congestion- failure of LEFT heart; leads to buildup of blood in the lungs
6. peripheral congestion- failure of RIGHT heart; pools in body, leading to edema (fluid buildup in areas such as feet, ankles, fingers)

Front 67

coronary atherosclerosis

Back 67

leads to gradual occlusion of heart vessels, reducing oxygen nutrient supply to cardiac muscle cells; (fat & salt diet, smoking, stress)

Front 68

high blood pressure

Back 68

when aortic pressure gets to large, left ventricle cannot pump properly, increasing end systolic volume (ESV) and lowering SV because more left over

Front 69

myocardial infarction (MI)

Back 69

"heart cell death" due to numerous factors, including coronary artery occlusion

Front 70

pulmonary congestion

Back 70

failure of LEFT heart; leads to buildup of blood in the lungs, because left heart receives blood from the lungs

Front 71

peripheral congestion

Back 71

failure of RIGHT heart; pools in body, leading to edema (fluid buildup in areas such as feet, ankles, fingers)

Front 72

Defibrillation

Back 72

application of electrical shock to the heart in an attempt to retain normal SA node rate

Front 73

Special considerations of wave of excitation

Back 73

1. initial SA node excitation causes contraction of both the L and R atria.
2. Contraction of R and L ventricles begins at APEX of heart (inferior point), ejecting blood superiorly to aorta and pulmonary artery.
3. 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), it drives all other autorhythmic centers in a normal heart
5. Arrhythmias- uncoordinated heart conditions.
6. Fibrillation- Rapid and irregular contractions of the heart chambers; reduces efficiency of the heart
7. Defibrillation- application of electric shock to the heart in an attempt to retain normal SA node rate
8. Ectopic focus- autorhythmic cells other than SA node take over heart rhythm
9. Nodal ryhthm- when AV takes over pacemaker function (40-60 per minute)
10. extrasystole- when outside influence (such as drugs) leads to permature contraction
11. Heart block- When AV node or bundle of his is not transmitting sinus rhythm to ventricles

Front 74

Nodal system (cardiac conduction system)

Back 74

special autorhythmic cells of the heart that initiate impulses for wave-like contraction of entire heart (no nervous stimulation needed for these)

Front 75

External Innervation Regulating Heart Function

Back 75

1. heart can beat without external innervation
2. external innervation is from AUTONOMIC SYSTEM
3. Parasympathetic- (acetylcholine) DECREASES rate of contractions. cardioinhibitory center (medulla) stimulates vagus nerve (cranial X) which leads to the heart
4. Sympathetic- (norepinephrine) INCREASES rate of contractions cardioacceleratory center (medulla) to lateral horn of spinal cord to preganglionics T1-T5 to postganglionics cervical/thoracic ganglia to the heart

Front 76

stenotic valve

Back 76

high pitched swishing sound when blood should be flowing through valve; narrowing of outlet in the open state

Front 77

Regulation of stroke volume (SV)

Back 77

1. End diastolic volume (EDV)- total blood collected in ventricle at the 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)

Front 78

regulation of stroke volume

Back 78

1. SV (ml/beat) = EDV (ml/beat) - ESV (ml/beat)
2. normal SV = 120 ml/beat - 50 ml/beat = 70 ml/beat

Front 79

end diastolic volume (EDV)

Back 79

total blood colected in ventricle at the end of diastole; determined by length of diastole and venous pressure (~120 ml)

Front 80

end systolic volume (ESV)

Back 80

blood left over in ventricle at the end of contraction (not pumped out); determined by force of ventricle contraction and arterial blood pressure (~50 ml)

Front 81

Frank-Starling law of the heart

Back 81

critical factor for stroke volume is "degree of stretch of cardiac muscle cells"; more stretch = more contraction force

Front 82

Frank-Starling law of the heart

Back 82

critical factor for stroke volume is "degree of stretch of cardiac muscle cells"; more stretch = more contraction force

Front 83

Frank-Starling law of the heart

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critical factor for stroke volume is "degree of stretch of cardiac muscle cells"; more stretch = more contraction force.
A. increased EDV = more contraction force
1. slow heart rate = more time to fill
2. exercise = more venous blood return

Front 84

Regulation of heart rate (autonomic, chemical, other

Back 84

autonomic regulation of heart rate (HR)
A. sympathetic - NOREPINEPHRINE (NE) increases heart rate (maintains stroke volume)
B. parasympathetic - ACETYLCHOLINE (ach) decreases heart rate
C. vagal tone- parasympathetic inhibition of inherent rate of SA node, allowing normal heart rate
D. baroreceptors, pressoreceptors- moniter changes in blood pressure and allow reflex activity with the autonomic nervous system

Front 85

sympathetic- norepinephrine (NE)

Back 85

increases heart rate (maintains stroke volume)

Front 86

parasympathetic- acetlycholine (ACH)

Back 86

decreases heart rate

Front 87

vagal tone

Back 87

parasympathetic inhibition of inherent rate of SA node, allowing normal HR

Front 88

Hormonal and chemical regulation of heart rate (HR)

Back 88

A. epinephrine - hormone released by the adrenal medulla during stress; increases heart rate
B. thyroxine- hormone released by throid; increases heart rate in large quantities; amplifies effect of epinephrine
C. Ca, K, and Na levels very important
D. hyperkalemia- increased K level; KCL used to stop heart on lethal injection
E. hypokalemia- lower K levels; leads to abnormal heart rhythms
F. hypocalcemia- depresses heart function
G. hypercalcemia- increases contraction phase
H. hypernatremia- HIGH Na concentration; can block Na transport & muscle contraction

Front 89

epinephrine

Back 89

hormone released by adrenal medulla during stress; increases heart rate

Front 90

thyrxine

Back 90

hormone released by throid; increases heart rate in large quantities; amplifies effect of epinephrine

Front 91

Events Of Cardiac Cycle- Ventricular systole: blood ejected from heart

Back 91

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 because semilunar valves open, blood goes to aorta and pulmonary trunk