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53 Cards in this Set

  • Front
  • Back

Cardiac myocytes:

have single nucleus, are striated (due to sarcomeres; sothey have myosin, troponin-tropomyosin, etc.)


- gap junctions allow cells to synchronize


- Heart muscles don’t sum. If they did, they would fatigue

Myocyte refractory period

the refractory period is 250 ms in a cardiac myocyte (25 times longer than in amuscle) Long refractory period means: contractile cell completelyrelaxes before refractory period ends, which prevents summation and tetanus.

Calcium in myocytes

Ca imbalance will lead to irregularity in the heart.

Autorhythmic (pacemaker) cells

- spontaneously depolarize


- unstable resting membrane potential


- depolarize via Ca++ & Na+ influx


- repolarize via K+ efflux


- gap junctions allow other cells to fire when these cells fire


- are in clusters like SA node, A-V node

depolarization of:


- SA node


- AV node


- purkinje fibers

SA Node: 90 x's per minute


AV node: 50x's per minute


Purkinje: 35 x's per minute

___ percent of the cells are contractile cells; ___ percent areautorhythmic/pacemaker cells

99, 1

T or F: two atria contract simultaneously, then two ventricles contractsimultaneously

True

Systole

contraction of a heart chamber; blood leaves the chamberduring systole.


- period of atrial systole and ventricular systole, whichfollows


- atria beat separately from the ventricles, so atrialsystole and ventricular systole happen separately


- atria contract and push blood into the ventricles

Diastole

relaxation of the heart chamber; blood fills the chamberduring diastole


- atrial are relaxing while ventricles are contracting


- there is a time (about .4 of a sec) when all fourchambers are in diastole

semilunar valvesseparate....

- ventricles and aorta


- open during ventricular systole when ventricles contract and push the blood up and out topulmonary/systemic circuit), close during ventricular diastole

Right A-V (tricuspid) & Left A-V (mitral/bicuspid)...

- Separate atria and ventricles


- close during ventricular systole, open duringventricular diastole.


- Atrial systole/diastole doesn’t have anything to dowith A-V valves


- Open when there’s no pressure to push up against them

Valve pathologies: stenosis & incompentence

Stenosis: failure of valve to open


Incompetence: failure to close

Trace Blood Flow

Ratrium → tricuspid valve→ R ventricle → pulmonary semilunar valve → pulmonarytrunk → lungs → L atrium → Bicuspid valve → L ventricle → Aortic semilunar valve → systemiccircuit

During atrial systole...

- A-V valves are open,pushing blood down through A/V valves


- blood is flowing from the atria to the ventricle- ventricles are in diastole (relaxed)

During ventricular systole....

- semilunar valves are open


- Blood is flowing to pulmonary/systemic circuit- atria are in diastole

When both atria and ventricles are relaxing (in diastole):

- this stage happens after ventricles finish systole.


- A-V valves are open


- Blood is flowing into the atria and the ventricles

T or F: atrial systole begins immediately once ventricularsystole is complete?

False (unless you’re working out) –there’s a period when all 4 chambers are in diastole

What electrical events are happening during:


- P wave


- QRS wave


- T wave

P wave: atrial depolarization


QRS: ventricles depolarizing, atria repolarizing


T wave: ventricles are repolarizing

End Systolic Volume

At end of ventricular systole.


The least amount of blood in theheart

End Diastolic Volume

At the end of atrial systole (right before the ventricles contract)


- when the most blood is in the heart


- happens at top of QRS

Formula for Stroke Volume

EDV-ESV = Stroke volume

functional reserve

Heart fills entirely but only pushes out about 50% of theblood (so average ESV is 50%). This is called functional reserve of the heart. It doesn't have to beat faster to pump more blood. It can justincrease its stroke volume by pumping more fully.

Ejection fraction

stroke volume made into a percent (about 50% is normal)

Lub

When ventricles contract, the A-V valves close and opens thesemi lunar valves. Happens atQRS.

Dup

Formula for cardiac output

heart rate x stroke volume


(L per min)

Parasympathetic Response (cardiac)

heart slows down

sympathetic (cardiac) response

heart beats faster and with more force

What determines heart rate?

- pacemakercells. inherent rate = 90 bpm.


- SANode is dually innervated by sympathetic & Parasympathetic nervous system


- parasympathetic slows it down and sympathetic speeds itup


- to increase the heartbeat, you can decrease PSstimulation or increase symp stimulation.

sympathetic NS increases HR through

norepinephrine binding to Beta 1’s


- affects heart rate and contractility

Parasympathetic decreases HR through

releasing acetylcholine onto muscarinic receptors (mACH-R)


- Has no effect on muscle/contractile cells

Stroke Volume is determined by

force of contraction.

force of contraction is determined by

preload, contractility, and afterload

Preload

- the degree of stress on the ventricle walls at the end of diastole (directly related to volume)


- More volume = more force. Less volume = less force


- duration of diastole and rate of venous return both affect EDV. longer duration = more volume, increased venous return = less volume

Contractility

- How forcefully is the heart beating? Strength ofcontraction at any preload.


- depends on how much calcium is inside it (intracellularcalcium)


- sympathetic activity innervates the muscle of the heart toincrease contractility

Afterload

- the degree of stress on ventricle walls at the start ofsystole; ventricular pressure needed to overcome peripheral resistance



peripheral resistance

- blood pressure in the rest of the body (systemiccircuit)


- if it’s low, the heart has an easier time pushing bloodout into the systemic circuit; if it’s high in the systemic circuit, it’sharder for the heart to get the blood out.

Inotropic Agent

a drug that affects contractility of the heart


- positive inotropic effect makes heart beat moreforcefully


- negative - less forcefully

How do increases in preload, contractility, and afterload affect stroke volume?

- if preload increases, stroke volume increases


- if contractility increases, stroke volume increases


- if afterload increases, stroke volume decreases



Systolic & Diastolic pressure

Systolic pressure: max pressure created byventricular systole in an artery


Diastolic Pressure: arterial pressure duringventricular diastole

Pulse pressure

Pulse pressure = systolic pressure – diastolicpressure

Mean arterial pressure

diastolic pressure + 1/3 (systolic – diastolic)

Vasoconstriction

Norepinephrine from sympathetic system binds to alpha receptors on vascular smooth muscle


- epinephrine binding to alpha receptors causes vasoconstriction

Vasodilation

epinephrine binds to beta-2 receptors and causes vasodilation


- decreased sympathetic stimulation also causes vasodilation

hyperemia

- matching blood flow to demand --> matches resistance --> increases flow

which receptors are dually innervated?

alpha and Beta-1

what will a non-specific beta blocker due toMAP/cardiac output?

- decrease heart rate, decrease stroke volume –bc of Beta1

Baroceptor reflex

- pressure sensors that are monitoring yourblood pressure. They initiate a reflexthat keeps the blood pressure homeostatic.


- Found in your carotid arteries and your aortic arch


- Tonic Mechanoreceptors -> stretch/pressure causes them to depolarizeMedullaoblongata is the integrating center, which monitors whether you’re above orbelow your set point.

Orthostatic hypotension

drop in blood pressure based on change in bodyposition (usually standing up)

hypo/hypervolemia

Hypovolemicshock: when your blood volume isdangerously low


Hypervolemia: when your blood volume is dangerously high

Alpha receptors

target cells: systemic arterioles


response NE → constrict

Beta-1 receptors

Target cells: SA Node & contractile


Response: Increased HR, increased stroke volume

Beta-2 receptors

Target cells: coronary artery, hepatic artery, skeletal muscle


Response: epinephrine --> dilates