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95 Cards in this Set
- Front
- Back
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Pulmonary Circuit |
Carries deoxygenated blood to the lungs to become oxygenated |
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Systemic Circuit |
Carries oxygenated blood away from the heart to the rest of the body |
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Semilunar valves |
Between the ventricles and vessels Aorta and Pulmonary trunk |
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Atrioventricular valves |
Between the atria and ventricles Bicuspid (mitral) and Tricuspid |
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What is all around valves that keeps AP from going from atria to ventricles? |
Fibrous skeleton |
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What are the contractile cells called? |
Cardiocytes Cardiac myocytes |
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What is used to join cardiocytes together? |
Intercalated discs |
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What are the mechanical and electrical functions that are apart of intercalated discs? |
Mechanical: Desmosomes Electrical: Gap junctions |
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What are cardiac cells rich in? |
myoglobin and mitochondria |
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What are the non-contractile cells? |
Conducting cells, make up 1% of cell They initiate and coordinate heart beat Have automaticity (beat on own) |
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What are 99% of the rest of the cells? |
Contractile cells: shorten and generate force for contraction (forms cross bridges) |
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Hyper polarization? |
more negative than RMP |
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Depolarization |
more positive than RMP |
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Depolarization |
going back to RMP |
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SA Node |
Has unstable RMP = -60mV depolarizes due to slow influx of Na -called pacemaker potential Gets us from RMP to threshold (-40 mV) Faster Na/Ca channels open and trigger AP Peaks at 0 mV Once K channels close, pacemaker potential starts again Each depolarization of SA node sets off one heart beat |
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Sinus Rhythm |
normal heart beat triggered by SA node |
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SA Node bpm outside of body |
80-100 bpm |
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Heart rate inside of body due to vagus nerve |
60-80 bpm |
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Nodal Rhythm |
if SA node is damaged, HR set by AV node 40-60 bpm |
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Intrinsic ventricular rhythm |
if both SA and AV nodes are not functioning, rate set by purkinje fibers 20-40 bpm -would need a pacemaker |
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Contractile Myocyte |
RMP is stable at -90mV Peaks at +30 mV Fast depolarization (Na influx) Plateau during Ca influx Keeps cell depolarized by CICR (calcium induced, calcium release) ARP is long When Na channels recover, RRP starts K efflux causes repolarization |
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P wave |
SA node fires AP Atria depolarizing |
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PR segment |
Plateau, Ca influx Atria |
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QRS Complex |
Atria repolarizing Ventricles depolarizing |
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ST segment
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Plateau, Ca influx
Ventricles |
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T wave
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Ventricles repolarize |
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___ wave to ____ wave is equivalent to 1 beat of "single cardiac cycle" |
R wave to R wave |
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Rest between 2 heartbeats |
Quiescent period |
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Mechanical aspects |
Atria contract at peak of P wave Atria relax at the start of QRS complex Ventricles contract at peak of QRS complex Ventricles relax near end of T wave |
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Ectopic focus |
region of spontaneous firing in another part of heart |
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Causes of ectopic focus |
hypoxia electrolyte imbalance caffeine nicotine other drugs |
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Arrhythmia |
any abnormal cardiac rhythm |
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Cause of arrhythmia |
failure of conduction system to transmit signal (heart block) |
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Atrial fibrillation |
ectopic foci in atria |
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Ventricular fibrillation |
caused by electrical signals reaching different regions at widely different times kills quickly if not stopped |
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Defibrillation |
Strong electrical shock to depolarize entire myocardium, stop fibrillation, and reset SA nodes to sinus rhythm |
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Tachycardia |
Fast HR |
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Bradicardia |
Slow HR |
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Cardiac cycle |
one complete contraction and relaxation of all 4 chambers of heart |
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Systole |
contraction |
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Diastole |
relaxation |
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Quiescent period |
all 4 chambers in diastole (relaxed) at same time |
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Total duration of cardiac cycle |
0.8 second in a heart beating at 75 bpm |
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Equation |
60 sec x 1 beat = 75 beats = 75 bpm min 0.8 sec min |
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1. Atrial systole begins |
Atrial contraction forces a small amount of additional blood into relaxed ventricles |
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2. What happens in step 2 |
Atrial systole ends; atrial diastole begins |
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3. Ventricular systole |
First phase: ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valve Second phase: as ventricular pressure increases and exceeds pressure in the vessels, the semilunar valves open and blood is ejected (from ventricles to blood vessels) (blood vessels = pulmonary trunk and aorta) |
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Ventricular diastole |
Early: as ventricles relax, pressure in ventricles drops; blood flows back against cusps of semilunar valves and forces them closed. Blood flows into relaxed atria Late: All chambers are relaxed. Ventricles fill passively -passive filling is responsible for most of blood in ventricle |
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What effect does pressure have on fluid? |
Pressure causes a fluid to flow down a pressure gradient Blood flows from region of higher pressure to lower pressure Pressure in the contracting chamber exceeds pressure in a relaxed chamber |
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What do valves do? |
Help blood move in the right direction |
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What do blood vessels provide |
Blood vessels provide resistance to blood flow ( depends on diameter of bv) Ventricular pressure must rise above this resistance for blood to flow into great vessels |
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Atria systole |
atria contract, blood moves from atria into ventricles thru AV valves fills ventricles with 30% remaining volume blood (top off ventricles) |
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EDV |
When atrial systole is over and the ventricles are "full", this is the end diastolic volume -the END of ventricular diastole, beginning of ventricular systole -about 130 mL in normal resting adult |
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Atrial diastole |
relaxation of atria until the next cardiac cycle; fill with blood during "late" atrial diastole |
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Ventricular systole |
starts at the same time as atrial diastole; rising pressure in ventricles closes AV valves; forces blood from ventricles to pulmonary and systemic circuits; 3x longer than atrial systole |
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Equation for stroke volume |
SV= EDV - ESV |
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During ventricular systole |
pressure develops in ventricle; close AV valves |
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Isovolumetric contraction |
tension generated in ventricle but not enough to force open semilunar valve so ventricle remains full of blood; no change in volume
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Isotonic contraction |
enough pressure to force open the SL valves, so blood is ejected into aorta and pulmonary trunk; ventricular ejection |
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Stroke Volume |
Amt of blood ejected from a ventricle during a single cardiac cycle is the stroke volume about 70 mL |
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ESV |
Blood leftover in ventricle after isotonic contraction about 50-60 mL |
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Ventricular Diastole (early) |
When pressure in ventricle decreases, blood flows back from aorta and pulm trunk to close SL valves -dicrotic notch: recoil of aorta -this is how aortic sinus gets filled (how blood gets to coronary sinus) |
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Isovolumetric relaxation |
when all valves closed, ventricles are relaxing but pressure is still higher than in atria so AV valves remain closed and no blood fills atria yet |
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Ventricular Diastole (late) |
All chambers relaxed; blood begins to flow into atria once the pressure in the ventricles is lower than that in the atria (back to atrial systole-back to EDV) |
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Ejection Fraction |
portion ejected out of total ventricular volume 54% resting Can go as high as 90% during vigorous exercise |
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Auscultation |
Listening to sounds made by body -different stethoscope positions determine which heart sound is heard best |
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First heart sound |
louder and longer "lubb" occurs due to closure of AV valve and opening of SL valve |
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Second heart sound |
softer and sharper "dupp" occurs due to SL valves closing |
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Mitral valve prolapse (Murmur) |
Hear swoosh from some regurgitation when the AV valve doesn't close fully or if cusps are malformed or papillary muscle problem or chordae tendinae too short -backflow into atria |
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Cardiac Output |
Amount of blood ejected by ventricle in 1 minute CO = HR x SV About 4-6 L/min at rest |
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Cardiac reserve |
Difference between a persons max and resting CO; can usually increase 5x HR and SV can increase 2x Increase w fitness, decreases with disease HR increases as SV decreases |
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Factors Affecting Heart Rate |
Autonomic innervation Hormones |
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Factors Affecting Heart Rate: Autonomic Innervation |
ANS Sympathetic, increase HR, SA node Parasympathetic, decrease HR, Vagus nerve |
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Parasympathetic Stimulation |
More - RMP (hyper polarized) Take longer to repolarize Decrease HR Have more Na leaking in slowly |
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Sympathetic Stimulation |
Less - RMP (depolarized) More rapid depolarization Increase HR Little bit of Na leaking in Quicker to repolarize |
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Cardioinhibitory Center |
Parasympathetic Nerves Fibers of vagus nerve from medulla oblongata lead to SA node and AV node Little to no effect on ventricles contraction Reduces HR Hormone: Ach- Acetylcholine binds to muscarinic receptors -opens k gates in nodal cells -as k leaves, cells become hyper polarized and fire less frequently Vagal tone slows down heart beat from SA node which is 80-100 to 60-80 bpm |
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Cardioacceleratory Center |
Cardiac nerves to heart terminate in SA and AV nodes, in atrial and ventricular myocardium, aorta, pulm trunk, and coronary arteries Hormone: NE binds to Beta-adrenergic receptors which activate cAMP second mess system Lead to opening of Ca channels in plasma membrane Causes: - increased HR - increased contraction strength - vasodilate coronary arteries to increase myocardial blood flow |
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ANS |
Does not initiate heart beat, it modulates rhythm and force |
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Positive Chronotropic agents |
Factors that raise HR -sympathetic stimulation -hormones -drugs -Nicotine stim catecholamines (NE E) - Thyroid hormone increases number of adrenergic receptors on heart so more responsive to symp stim -caffeine inhibits cAMP breakdown |
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Tachycardia |
resting adult HR > 100 bpm occurs due to: -stress -anxiety -drugs -heart disease -fever -blood loss -damage to myocardium |
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Negative Chronotropic Agents |
Factors that low HR Parasym stim or Ach |
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Bradycardia |
Resting adult HR < 60 bpm Occurs in: -sleep -low body temp -endurance trained athletes |
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Baroreceptors |
Pressure sensors in aorta and internal carotid arteries (sinuses) signal cardiac center -problems detected, send signals to rectify problem BP low, signal rate drops, cardiac center increases HR BP high, signal rate increases, cardiac center decreases HR |
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Factors Affecting SV |
Preload Contractility After load |
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Preload |
AFFECTS BOTH EDV AND ESV how much tension you get in ventricle from blood (stretch in ventricle) |
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Venous return |
AFFECTS PRELOAD How much blood is coming from superior and inferior vena cava -determined by skeletal muscle activity, blood volume, and changes in peripheral circulation |
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Filling time |
AFFECTS PRELOAD low HR, longer filling time high HR, shorter filling time |
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Contractility |
WILL AFFECT ESV how forcefully can cells contract -determined by autonomic innervation and hormones Sympathetic = high contractility = E and NE Parasymp = no effect = Ach |
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After load |
WILL AFFECT ESV resistance due to aorta -vasodilation: bigger diameter, decrease after load, decrease resistance -vasoconstriction: smaller diameter, increase after load, increase resistance |
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Preload stuff |
high blood in ventricle (high EDV), high preload exercise increases venous return and stretches myocardium -high preload causes high force of contraction -high CO matches high venous return -HIGH preload, HIGH EDV, HIGH SV, LOW ESV -LOW preload, LOW EDV, LOW SV, HIGH ESV |
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Frank Starling law of heart |
SV proportional to EDV "more in = more out" the more myocytes stretched (by venous return increase) the stronger they will contract -stretching will optimize position of sarcomeres, so allow max cross bridge formation |
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Positive inotropic agents to increase contractility |
-Sympathetic stimulation (NE) -Hypercalcemia -Catecholamines |
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Negative inotropic agents to decrease contractility |
Hypocalcemia |
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After load stuff |
Limits SV (how much you can pump out) -related to the amt of pressure required to open the semilunar valves and eject blood - high BP (in aorta), high amt of force needed to open semilunar valve; decrease in force available to eject blood -INCREASE after load, DECREASE SV -DECREASE after load, INCREASE SV |
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Exercise and CO |
Exercise increase CO, HR, and SV Proprioreceptors signal cardiac center -increase muscular activity, increase venous return, increase preload, increase CO Exercise produces hypertrophy -athletes with high cardiac reserve can tolerate more exertion than a sedentary person |
