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Cardiovascular

QuestionAnswer
systole contraction in heart (allows blood to move from one place to another)
diastole relaxation
sinus rhythm normal heartbeat set by SA node (sinoatrial node=cluster of cells setting RATE for heart); @ rest, suppressed/ slowed by VAGAL TONE
vagal tone parasympathetic; slows down heart rhythm; if removed, heart would speed up
arrhythmias disturbances in the normal pacemaker or conduction system
pacemaker physiology NO RESTING POTENTIAL; sodium channels constantly open --> gradually depolarize until reach threshold --> action potential/ contraction that travels whole heart --> repolarization
pacemaker potential slow sodium inflow that gradually depolarizes SA node cells
sympathetic innervation speeding up heart: Norepinephrine binds to β-adrenergic receptors in the heart
speeding up heart: 2nd messenger system open CALCIUM channels --> increased Ca inflow SPEEDS UP DEPOLARIZATION of SA node --> more frequent, stronger contractions of muscle cells --> increase Ca uptake in SR
parasympathetic innervation heart slowing down heart: ACh binds muscarinic receptors --> allow POTASSIUM to counterbalance influx of sodium --> slows down rate of depolarization (takes longer to reach threshold)
impulse conduction to myocardium Action potential fired in SA node --> Spreading of potential --> AV node= antenna receiving info (action potential from SA), slows down signal to allow blood move through ventricle --> Signals go through AV Bundle (wall between right & left ventricles)
electrical behavior 1. SA node starts depolarization 2. depolarization stimulates heart muscles → opening of voltage gates → open SODIUM CHANNELS 3. quick RISE in membrane potential (very high; +30) 4. CALIUM channels SLOW to open; PROLONGS DEPOLARIZATION= PLATEAU
difference in heart physiology & neuron action potentials result of SLOW CALCIUM CHANNELS • calcium continue to flow in during REPOLARIZATION • slow to open, slow to close → long PLATEAU
calcium flowing into cells bind to... troponin complex (like in muscle cells) → myosin move out of way → binding site for myosin to actin → contraction o some of that same calcium Bind to sarcoplasmic reticulum o long contraction wave: no twitch, no summation, no tetanus
electrocardiograms measure... • Measures electrical activity, not contraction • Activities in heart during DEPOLARIZATION & REPOLARIZATION
P wave atrial DEpolarization
QRS complex 2 events @ same time; marked by sharp spike: •Atria: REpolarization (after depolarization) • Ventricles: DEpolarize
T wave ventricular REpolarization
flow occurs due to.... PRESSURE GRADIENT (greater pressure= faster flow)
heart valves role ensures one-way flow of blood; •atria contracts → blood moves downward • Continual contraction → build up pressure → blood go down in VENTRICLE; Contract ventricles → atriaventricular valves CLOSE (prevents backflow) → audible sound
S1 1st heart sound= louder & longer "lubb"; = closure of AV valves
S2 2nd heart sound= "da"; = closure of SEMILUNAR valves
blood movement; valves actions 1. atria contract, AV valves open, blood moves to ventricles; 2. atria relax, ventricles contract, AV valves close; 3. ventricles continue, semilunar valves OPEN, blood move out of ventricles; 4. ventricles relax, semilunar valves close
valvular insufficiency any failure of a valve to prevent reflux (regurgitation) = blood leaking backwards --> sound --> MURMUR
heart murmur abnormal heart sound produced by regurgitation of blood through incompetent valves
phases of cardiac cycle 1. ventricular filling 2. isovolumetric contraction 3. ventricular ejection 4. isovolumetric relaxation
ventricular filling rapid ventricular filling (blood enters very quickly), atria --> ventricles; DIASTASIS= filling slows down as pressure rises in ventricles --> P wave; atrial systole (contract)
isovolumetric contractions no volume change; atria repolarize, ventricles depolarize oVentricles contract → build up pressure → blood able to move into aorta/ pulmonary trunk •Ventricles go from LOW pressure → HIGH pressure oPressure in atria LOW, pressure builds in VENTRICLES
end diastolic volume amount of blood contained in each ventricle at the end of ventricular filling ; 130 mL
ventricular ejection blood moves out of ventricles --> volume in ventricles DECLINES; 120/80= peak & trough of pressure in ventricles; blood exits rapidly at first then slows
end systolic volume the remaining blood in ventricle (after ventricular ejection) 60mL
stroke volume amount of blood moved out; about 60-70 mL of blood ejected
ejection fraction proportion of blood moved out; about 50% of blood (of ventricular capacity) when at rest
isovolumetric relaxation semilunar valves closed; AV valves not yet open= NO MOVEMENT of blood; ventricles stop contraction (pressure greatly DECLINES)
congestive heart failure results from the failure of one ventricle to eject an equal volume of blood as the other; due to a weakened heart (myocardial infarction, chronic hypertension, valvular insufficiency, or congenital defects; leads to edema & heart failure
cardiac output= the volume of blood ejected by a ventricle in 1 minute = heart rate x stroke volume
cardiac reserve= difference between a person’s maximum CO (~25 L/min) and resting CO (5L/min); increases w/ fitness, decreases w/ disease
chronotropic effects= = affecting heart rate/ action potential rate; regulated by cardiac centers in medulla; drugs target muscarinic/ B-adrenergic RECEPTORS
chronotropic effects include... Sympathetic NS stimulations, Hormones (from adrenal medulla, thyroid gland: INCREASE heart rate), Parasympathetic NS (vagus nerves)
hyperkalemia SLOWS heart rate greatly o Increase in POTASSIUM levels → slow action potential
tachycardia resting adult heart rate above 100 bpm; too HIGH
bradycardia resting adult heart rate of less than 60 bpm; too LOW
inputs to cardiac center CHEMOreceptors (blood pH, CO2: high CO2 decreases pH, increase heart rate), BAROreceptors (blood pressure), PROPRIOceptors (body activity level), higher brain centers (sensory/ emotional stimuli)
contractility: preload amount of tension in ventricles •Further you stretch ventricles → stronger contractions •More blood into ventricles → more stretch → stronger contraction
Frank-Starling law more blood going into ventricles, the greater stroke volume (end diastolic volume); more volume in= more volume out
reduce contractility negative INOTROPIC agents; Calcium too low (HYPOCALCEMIA) → not enough contraction; VAGUS NERVES (affect atria but not ventricles)
increase contractility positive INOTROPIC agents; HYPERCALCEMIA can cause strong, prolonged contractions, CATECHOLAMINES increase intracellular calcium levels
afterload the blood pressure in the aorta and pulmonary trunk that resists the pumping of the ventricles; opposes opening of semilunar valves, limits stroke volume, increased by hypertension
when exercising.... proprioceptors signal cardiac center; SYMPATHETIC NS increases HR & SV; increased muscular activity increases VENOUS RETURN (increase preload, increase stroke volume), increase in HR & SV increase CO
after exercising..... exercise produces ventricular hypertrophy, enlarged cells increase resting SV, increased SV allows heart to beat more slowly/efficiently at rest
Created by: kpan
 

 



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