ch 18 cardiovascular system- the heart 1/30 Flashcards
3 steps to cardiac muscle contractile
depolarize, plateau, repolarize.
depolarize phase of cardiac muscle cell
fast Na+ opens, ECF Na+ flows into making cell more positive, membrane potential reverses -90 mV to +30 mV. must happen for AP to take place
plateau phase of cardiac muscle cell
Ca+ channels open, Ca+ enters, K+ channels open, K+ leaves. This balances out the membrane potential in the cell. Plateau phase allows contractile cells to do friction, so heart contracts more eventually
repolarization phase of cardiac muscle cell
Ca+ channels close, K+ open, inside cell is more negative now, reaching resting membrane potential once again. tension decreases bc cardiac cells relax
electrocardiogram (ECG)
allows doctor to see heart activity, electrical impulses generated in and out heart, they produce P, QRS, T waves
P wave
depolarization of both atria sides from SA node to atria, first wave on ECG shown, after P wave is when it contracts, once depolarize is complete, depolarization moves to AV node
QRS complex
depolarization of ventricles, impulse goes down inter ventricular septum, hooks L/R apex, travels up via perkinje fibers. R is the peak, Q/S troughs occurs due to changing depolarization waves. current changes directions after.
T wave
relaxation of ventricles, repolarization of ventricles, T wave is wider than QRS complex bc repolarization takes longer than depolarization, heart relaxes at slower rate than contracts.
RR interval on an ECG
interval of actual ventricle contraction, the amount of time between individual heartbeats
junctional rhythms
due to dysfunctional SA node, P wave no longer there so HR slows to like 50 bpm, RR is farther spaced. intrinsic conduction issue here: AV node takes place of SA node to set the rhythm slow and bad
ventricular fibrillation
APs are occur rapid and irregularly chaotic, defibrillator must be used with EPI and heart is not a pump in this situation it is not an efficient blood mover
systole and diastole
systole- period of contraction
diastole- period of relaxation
each cycle occurs 75 x per min
cardiac cycle steps
ventricular filling, isovolumetric contraction phase, ventricular ejection, isovoulemtric relaxation
ventricular filling stop of cardiac cycle
mid to late diastole, low pressure in heart so heart is relaxed, atrial systole occurs atria contracts to push remaining blood into ventricle, AV valves open and end diastolic volume (EDV) occurs, where max blood volume is in ventricle before it contracts.
isovolumetric contraction phase, systole, of cardiac cycle
same value of blood in heart, blood won’t move, ventricle begin contract and pressure rises fast in ventricles, AV valves close and SL valves aren’t open yet, SL valves will open when pressure in ventricles > blood vessels. (blood flows high to low)
ventricular ejection, systole in cardiac cycle
blood flows from ventricles to aorta (left ventricle) and pulmonary trunk (right ventricle).
isovolumetric relaxation in cardiac muslce cycle, early diastole
ventricles relax and pressure drops fast in the ventricles, ESV (end diastolic volume) is reached (where remaining blood volume in ventricles after complete relax and contraction). SL valves closed and ventricles get closed off again. this prevents back flow and nearly empties ventricles
cardiac output
total blood pumped by ventricle in a single minute, cardiac output (CO) = stroke volume (SV) times HR
stroke volume
volume of blood pumped out by ventricle with each beat, EDV-ESV. SV is directly correlated to ventricular contraction. higher contraction = more SV
average adult SV and HR and CO
70 mL blood per beat, and avg 75 bpm making average CO 5,250 mL OR 5.25 L. around same amount of total blood volume.
what happens when to CO when stroke volume increases? HR?
if CO increase, SV and HR increase
how can cardiac output be physically altered
physical exercise, hormones, emotional states
maximal cardiac output
maximum Amt of blood that can be pumped in a single minute, depends on physical fitness. less fit- 20-25 L/min, more fit- 35 L/min, elite athletes can move more blood in a single minute than regular ppl
about 4-5 amt of resting level.
regulating stroke volume
more blood means more force, can change EDV by increasing preload.
what is preload when regulating SV
the stretch of muscle cells prior to contraction, can do this by loading heart with blood stretching sarcomere diastolic filling with blood
frank starling relationship
increasing total blood volume of blood at end of diastole (EDV) will increase strength of contraction during systole. increase preload, increase SV so CO can increase. muscle cells respond with a stronger contraction!
how change ESV
contractility and decreasing after load
contractility and changing ESV
contractility is the natural strength of ventricle on its own, more contraction means more blood ejected. ESV will decrease when contractility increases, SV increase and CO too.
*Ca+ increase means more contractility
decreasing after load and changing ESV
after load refers to forces that oppose blood ejection from ventricles. how much blood is left in heart after it contracts! depends on resistance created by blood vessels leading out of ventricles. if after load is low, ESV is decreased too, so more blood moves out of ventricles. SV and CO increase
how resistance affects ability to pump blood
less resistance, less friction, more blood moved
more resistance, more friction, less blood moved.
regulating heart rate HOW
ANS input and chemical regulation
how does ANS regulate HR
ANS
sympathetic- fight or flight, NORepinepherin released making threshold reached faster and SA nodes fire faster so heart beats faster, contracts more, affecting SV
parasympathetic- rest and digest, acH released, opposes sympathetic and vagal tone (which optimizes HR) makes HR slower than it would be. if no vagus nerve, HR would be 100 BPM
chemical regulation of HR (hormones)
hormones- EPInepherin and NORepinepherin increase HR and contractility.
thyroxine thyroid hormone increases metabolic rate of cells, so HR increases over longer amt of time. also can increase effects of EPI and NEPI- its longer lasting bc released over time
chemical regulation of HR (ions)
imbalance in ION concentration can increase or decrease HR, it affects the APs
calcium- hypocalcemia (Ca+ too low) makes HR decrease bc APs and pacemakers depolarize slower w no Ca+, hypercalcemia (Ca+ too high) makes HR increase.
potassium- wayyy more serious than Ca+ imbalance, hypokalemia is too low K+ with weak HR, hyperkalemia is way too high K+ causes cardiac arrest bc electrical pulses are too fast. the pacemakers will reach threshold voltage so much faster, so HR increases way too much
other factors affecting HR
Age (HR declines naturally with age bc metabolic rate slows), Biological sex (females higher HR than males bc they r smaller), exercise (more fit better HR), body temp (higher temp increases HR)
congestive heart failure
inefficiency of blood pump by heart to body tissues, cardiac output and venous return are not balanced, a progressive condition, weakens myocardium overtime.
common causes of congestive heart failure
coronary atherosclerosis- fatty buildup blocks coronary arteries, blockages stop good nutrients from coming in
hypertension- persistent high blood pressure, high artery pressure (especially aorta) forces heart too work harder and overcome high pressure despite same blood amt. myocardium weakens with time and become thicker, making heart move less blood and after load increased.
myocardial infarctions, multiple- repeating heart attacks kill muslce cells and use scar tissue buildup, small tissue amt is killed off each time and scar tissue builds up. scar tissue has no function!
dilated cardiomyopathy- ventricles stretch out and myocardium deteriorates, so contractility is compromised/ thinner walls occur, since ventricles and atria are so big, fills only half. ventricles work overtime to move blood over the stretched heart.
pulmonary congestion
left side of heart fails, right side is still normal.
pulmonary edema
lungs fill with fluid, L side affected bc not enough pumped systematically to keep up with pulmonary circuit. so, blood goes to lungs and drowns…
peripheral congestion
right side fails, left side normal. edema occurs in systemic body tissues, body cells cannot get what they need, extra fluid is in tissues, and makes more work to do for nutrients.
what happens if there’s prolonged inefficiency on one side of the heart
heart eventually fails due to too much stress on other side,
treatments- remove excess fluid, decrease BP, increase contractility of defective side
