Heart Physiology

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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
pulmonary semilunar valve (dub): LT 2nd intercostal
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"; 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
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, backflow
Cardiac Output- Blood pumping of the heart- General variables of cardiac output: 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
cardiac output (CO): blood amount pumped per minute
Stroke volume (SV): ventricle blood pumped per mm
heart rate (HR): cardiac cycles per minute
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
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 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
congenital heart defects: heart problems that are present at the time of birth
sclerosis of AV valves: fatty deposits on valves; particulary the mitral valve of LEFT side; leads to heart murmur
decline in cardiac reserve: heart effeciency decreases with age
fibrosis and conduction problems: nodes and conduction fibers become scarred over time; may lead to arrhythmias, could lead to AV block, conduction problems
congestive heart failure: heart cannot pump suffeciently to meet the needs of the body, because of buildup in the lungs and tissues
patent ductus arteriosus: bypass hole between pulmonary trunk and aorta does not close
Electrocardiography: Electrical activity of the heart. - 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 (0.16s)
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
The Normal Cardiac Cycle- General Concepts: 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
Systole: period of chamber contraction
Diastole: period of chamber relaxation
Cardiac Cycle: all events of systole and diastole during one heart flow cycle
Events Of Cardiac Cycle- Mid-to-late diastole: ventricles filled: 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.
Events of Cardiac Cycle- Isovolumetric relaxation: early diastole: ventricles relax, ventricular pressure becomes low. semilunar valves close, aorta and pulmonary trunk backflow. dicrotic notch- breif increase in aortic pressure
Total Cardiac Cycle Time: = 8 seconds (normal 70 beats/minute).
Atrial systole (contraction) = 0.1 second.
Ventricular systole (contraction) = 0.3 seconds
Quiescent period (relaxation) = 0.4 seconds
Overview of Heart Sounds: 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
lub: closure of AV valves, onset of ventricular systole
dub: closure of semilunar valves, onset of diastole
Purkinje fibers: 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
Arrhythmias: uncoordinated heart contractions
Fibrillation: rapid and irregular contractions of the heart chambers; reduces effeciency of heart
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
hyperkalemia: increased K level; KCL used to stop heart on lethal injection
hypokalemia: lower K levels; leads to abnormal heart rate ryhthms
hypocalcemia: depresses heart function
hypercalcemia: increases contraction phase
hypernatremia: HIGH Na concentration; can block Na transport & muscle contraction
Other facters affecting heart rate (HR): 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
normal heart rate: fetus- 140-160 beats/minute
female- 72-80 beats/minute
male 64-72 beats/minute
exercise: lowers resting heart rate (40-60)
heat: increases heart rate significantly
cold: decreases heart rate significantly
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
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
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.
Theorotical 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 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.
Anatomical sequence of excitation of the heart. - Autorhythmic cell location & order of impulses: 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)
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 the right atrial wall, just inferior to the superior vena cava
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 the tricuspid valve (between right atrium & ventricle)
Atrioventricular bundle (bundle of his): in the interATRIAL septum (connects L and R atria)
L and R bundle of his branches: within the interVENTRICULAR septum (between L and R ventricles)
Internal conduction (Stimulation) system of 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.
Gap junctions: electrically couple all cardiac muscle cells so that depolarization sweeps across heart in sequential fashion from atria to ventricles
Differences between skeletal & cardiac muscle contraction: 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.
Mechanism of contraction of contractile cardiac muscle fibers: 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).
Cardiac muscle cells: 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
Skeletal muscle cells: 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
Imbalance of cardiac output & heart pathologies- Imbalance of cardiac output: 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)
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 to large, left ventricle cannot pump properly, increasing end systolic volume (ESV) and lowering SV because more left over
myocardial infarction (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, because left heart receives blood from the lungs
peripheral congestion: failure of RIGHT heart; pools in body, leading to edema (fluid buildup in areas such as feet, ankles, fingers)
Defibrillation: application of electrical shock to the heart in an attempt to retain normal SA node rate
Special considerations of wave of excitation: 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
Nodal system (cardiac conduction system): special autorhythmic cells of the heart that initiate impulses for wave-like contraction of entire heart (no nervous stimulation needed for these)
External Innervation Regulating Heart Function: 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
stenotic valve: high pitched swishing sound when blood should be flowing through valve; narrowing of outlet in the open state
Regulation of stroke volume (SV): 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)
regulation of stroke volume: 1. SV (ml/beat) = EDV (ml/beat) - ESV (ml/beat)
2. normal SV = 120 ml/beat - 50 ml/beat = 70 ml/beat
end diastolic volume (EDV): total blood colected in ventricle at the end of diastole; determined by length of diastole and venous pressure (~120 ml)
end systolic volume (ESV): 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)
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
1. slow heart rate = more time to fill
2. exercise = more venous blood return
Regulation of heart rate (autonomic, chemical, other: 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
sympathetic- norepinephrine (NE): increases heart rate (maintains stroke volume)
parasympathetic- acetlycholine (ACH): decreases heart rate
vagal tone: parasympathetic inhibition of inherent rate of SA node, allowing normal HR
Hormonal and chemical regulation of heart rate (HR): 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
epinephrine: hormone released by adrenal medulla during stress; increases heart rate
thyrxine: hormone released by throid; increases heart rate in large quantities; amplifies effect of epinephrine
Events Of Cardiac Cycle- 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 because semilunar valves open, blood goes to aorta and pulmonary trunk

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