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Cardiovascular
| Question | Answer |
|---|---|
| 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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