hs375 unit 1

5 L/min

average cardiac output

0mmHg

pressure of venous circulation

20-30 mmHg

pressure in right ventricle

10 mmHg

pressure in lungs and pulmonary veins

100-140 mmHg

pressure in systemic circulation

GI tract → liver

organs that have circulation in series besides the heart

atrial natriuretic peptide and antidiuretic hormone

hormones synthesized/stimulated by heart

inotropy

forcefulness of contraction

Ach binds to M2 receptor or adenosine binds to A1 receptor→ inhibits adenylyl cyclase → decreases cAMP concentration → reduces inotropy

regulation of contraction via L-type channels

norepinephrine binds to alpha receptor → PL-C forms IP3 from PiP2 → stimulation of Ca release from SR → increased inotropy

regulation of contraction via SR calcium release

higher intracellular Ca or more stretch → increased inotropy, more acidic conditions → reduced inotropy

regulation of contraction via calcium binding to TN-C

increased cAMP → increased phosphorylation of myosin heads → increased inotropy

regulation of contraction via myosin ATPase

PK-A phosphorylates phospholamban → removes inhibitory effect on SERCA pump → more Ca pumped into SR → increased Ca release → increased inotropy

indirect regulation of contraction via calcium reuptake

inhibition of Na-Ca antiporter or active Ca pump → increased intracellular Ca → increased inotropy

regulation of contraction via calcium efflux

digoxin

intentionally reduces Calcium efflux to increase inotropy; inhibits Na-K pump → Na-Ca antiporter reverses → higher intracellular calcium

hypoxia

pathologic reduction of calcium efflux that decreases inotropy; lack of O2 → ATP deficiency → no Na-K pump activity → reversal of Na-Ca antiporter → increased intracellular calcium paired with ATP deficiency

lucitropy

relaxation; shares mechanisms with inotropy. rate of relaxation = how quickly intracellular calcium is reduced

calveolae

divots in vascular smooth muscle cells that enhance neurotransmitter response

vasoconstriction

decrease in lumen radius due to circumferential shortening of sarcomeres in smooth muscle

vasodilation

increase in lumen radius due to circumferential relaxation of sarcomeres in smooth muscle

intima

single endothelial cell-thick layer that facilitates blood flow through the lumen

media

middle layer of vessel containing smooth muscle and elastin

adventitia

outer layer of vessel containing collagen and nerves

vascular MLCK

phosphorylates myosin heads leading to vasoconstriction

vascular MLCP

dephosphorylates myosin heads leading to vasodilation

epinephrine, adenosine, and PGI2

agonists for Gs protein pathway (beta 2 receptor)

norepinephrine

agonist for Gi protein pathway (alpha 2)

norepinephrine, endothelin, angiotensin, vasopressin, acetylcholine (theory)

agonists for Gq protein pathways (alpha 1)

Gs protein increases cAMP → cAMP inhibits MLCK → myosin head not phosphorylated → vasodilation

Gs (beta 2) protein pathway

Gi inhibits cAMP → MLCK not inhibited → myosin heads phosphorylated → vasoconstriction

Gi (alpha 2) protein pathway

Gq activates IP3 → IP3 activates release of Ca from SR → Ca binds to calmodulin → Ca-calmodulin complex activates MLCK → myosin heads phosphorylated → vasoconstriction

Gq (alpha 1) IP3 protein pathway

Gq protein activates rho-kinase → rho-kinase inhibits MLCP → myosin heads not dephosphorylated → vasoconstriction

Gq (alpha 1) rho-kinase pathway

increased extracellular K+

results in depolarization and more opening of ion channels for contraction

NO

activates cGMP → activates MLCP → vasodilation; inhibits leukocyte activity

myogenic response

reflexive contraction following activation of ion channels from increased blood flow

-90 mV

resting membrane potential of a cardiac myocyte

depolarization phase of cardiac myocyte

m gates open, h gates close slowly

resting potential phase of cardiac myocyte

m gates is closed and h gate is open

repolarization phase of cardiac myocyte

m gates close and h gates open again

partial depolarization

results in activation of fast sodium channels due to closing of h gates; can be caused by hypoxia or hyperkalemic solution; heart does not beat

resting membrane potential is maintained by the Na-K pump in this phase

phase 4 of cardiac myocytes

depolarization due to influx of sodium

phase 0 of cardiac myocytes

initial repolarization due to potassium efflux and inactive sodium channels

phase 1 of cardiac myocytes

voltage gated calcium channels open, leading to calcium plateau and sustained contraction

phase 2 of cardiac myocytes

voltage gated calcium channels close and potassium efflux increases

phase 3 of cardiac myocytes

absolute refractory period

occurs when h gates are closed after phase 3 so no AP can be produced

relative refractory period

when myocytes are technically capable of AP given a suprathreshold stimuli, such as exercise

spontaneous depolarization due to slow T-type calcium and sodium leak channels

phase 4 of pacemaker cells

slow inward influx of calcium through L-type channels

phase 0 of pacemaker cells

repolarization due to increase in potassium efflux

phase 3 of pacemaker cells

calcium channel blockers

block L-type calcium channels to slow conduction rate and dilate vessels, leading to cardiac myocyte to look like pacemaker curve

vagal tone

when vagus nerve acts on heart rate to keep it below 100 bpm

chronotropy

adjustment in heart rate, negative or positive

norepinephrine increases heart rate, acetylcholine decreases heart rate

autonomic control of pacemaker activity

increase in thyroid hormone

positive chronotrope

increase in potassium or hypoxia

negative chronotropes

beta blockers

block beta-1 receptors to decrease heart rate and contractility

abnormal automaticity

spontaneous AP generation when fast sodium channels are blocked

early afterdepolarizations

AP generated during phase 3, current carried by calcium leak channel

delayed afterdepolarizations

AP generated during phase 3 or 4 as a result of ischemia, digoxin toxicity, or increased catecholamines

AV node

slowest point of electrical conduction

ectopic beat

beat originating outside of SA node

local re-entry

AP meets non-excitable tissues and keeps looping to stimulate cells off-cycle

global re-entry

AP bypasses AV pause before entering ventricles and keeps looping to cause inefficient beats

P wave

represents atrial depolarization

QRS complex

represents ventricular depolarization

T wave

represents ventricular repolarization

PR interval

time from onset of atrial depolarization to onset of ventricular depolarization

ST segment

period when ventricle is depolarized, corresponding to plateau of ventricular AP

QT interval

duration of ventricular APs

0.08-0.1 sec

duration of P wave

0.06-0.1 sec

duration of QRS complex

0.12-0.2 sec

duration of PR interval

0.2-0.4 sec

duration of QT interval

sinus rhythm

indicated when P:QRS is 1:1

2.0mm upwards or 0.5mm downwards

normal ST segment variation

atrial flutter

atrial fibrillation

1st degree AV block

2nd degree AV block

3rd degree AV block

premature ventricular complex

ventricular tachycardia

ventricular fibrillation

ST elevation

full-wall thickness infarction resulting in no repolarization of any cells

ST depression

semi-wall thickness infarction; some cells do not repolarize

T-wave inversion

result of previous MI; scar tissue results in altered depolarization and conduction, lack of activity in dead tissue