CV_system&Cardiac_Physio.csv

flow is equal to the change in pressure over the resistance

determines how much flow occurs for a given driving pressure

arterial compliance is low (stiff walls) and stays nearly constant; venous compliance is physiologically regulated to maintain a relatively constant pressure despite volume changes

transmural pressure = internal pressure - external pressure; compliance = _V/_Ptrans

ventricular pump; arterial distribution tree; microcirculation (arterioles & capillaries); venous return system

central control (heart & vasculature & kidneys); local control (tissues control own blood flow); renal control (vasculature & blood volume regulation)

used to calculate resistance in a cylindrical conduit; R is proportional to length and viscosity; R is inversely proportional to the radius raised to the 4th power

in arterial system - mean arterial pressure & tissue resistance = important; resistance (in arterioles) = most important; in venous system - volume & compliance = important; compliance = regulated

size variations in arteries & veins matter little in terms of blood flow because they are in series with high resistance arterioles; size variations in arterioles have major effects on flow

both must have the same flow because they are circuits in series; the pulmonary circuit has 1/5 the resistance and 1/5 the pressure of the systemic circuit

late diastole (atria & ventricles relaxed); atrial systole; isometric ventricular contraction; ventricular ejection; isometric ventricular relaxation

electrical impulses propagate rapidly from the SA node through atrial muscle to the AV node; delay in the AV node before transferrence of electrical impulses to the rapidly-conducting Purkinje fibers ensures that ventricular contraction is coordinated and occurs some time AFTER atrial contraction

contractile (aka quiescent) and conductive

atrial & ventricular cells; cannot contract in the absence of external stimulation (as from the CNS)

Purkinje cells & cells of the SA and AV nodes; can contract in the absence of external stimulation (as from the CNS)

skeletal muscle depolarization is primarily caused by opening of fast sodium channels; cardiac muscle depolarization is caused by opening of fast sodium channels AND slow calcium channels -> long plateau phase; permeability of cell membrane to potassium DECREASES after onset of action potential in cardiac cells but NOT skeletal muscle cells

SA node -> propagation through atria -> AV node (slow - delay) -> Purkinje fibers -> fast propagation through ventricles from septum -> apex -> base

consists of 5 segments: 0 upstroke (sodium channels open -> influx of sodium); 1 notch (potassium channels open -> potassium efflux); 2 plateau (calcium channels open -> influx of calcium against electrostatic gradient; potassium efflux slows); 3 repolarization (potassium efflux against electrostatic gradient); 4 rest (potassium influx balances efflux)

fast sodium; transient outward; L-type calcium; delayed rectifier; inward rectifier; funny

very fast; quickly inactivated; opens when cell is depolarized; plays role in phase 0; allows influx of sodium

fast; quickly inactivated; opens when cell is depolarized; plays role in phase 1; allows efflux of potassium

slow; slightly inactivated; opens when cell is depolarized; plays role in phase 2; allows influx of calcium (up charge gradient but down concentration gradient)

fast; not inactivated; opens when cell is hyperpolarized; plays role in late stage 3 and stage 4; allows efflux of potassium

very slow; not inactivated; opens when cell is depolarized; plays role in late stage 2 and stage 3; allows efflux of potassium

slow; permeable to sodium and potassium; opens when cell is hyperpolarized; present in AV node cells; play role in pacemaker function; increase in funny current decreases threshold for stimulation & thus increases heart rate

calcium enters cytoplasm during acition potential -> Ca2+ binding to ryanodine receptors on the sarcoplasmic reticulum -> SR releases Ca2+ -> Ca2+ from SR and cytoplasm bind to troponin-> contraction

calcium is released from troponin; phosphorylation of PLB up-regulates the activity of SERCA on the SR; calcium is taken up into the SR by SERCA; excess cytoplasmic calcium is exchanged with sodium at the cell membrane by the Na-Ca ATPase pump

calcium binds troponin C -> conformation change of troponin complex -> release of tropomyosin from active sites of actin -> binding of myosin head to actin -> power stroke using energy from ATP

sympathetic fibers innervate nodal regions & conduction system & atrial & ventricular myocytes; increase in inotropy (contractility) mediated by NE and beta-adrenergic receptors; beta-adrenergic receptor binding also phosphorylates phospholambin -> increased lusitropy (allows faster calcium release -> faster relaxation)

parasympathetic fibers innervate SAN (right vagus nerve) and AVN (left vagus nerve) and atria (sparse in ventricles); cholinergic fibers release ACh; muscarinic (G-protein coupled) receptors activated

alteration of size of calcium transient (through inotropic/lusotropic agents); Frank-Starling mechanism; myofilament sensitizers; frequency of stimulation

increased stretching of the sarcomere -> increased pressure -> increased cardiac output

in healthy hearts - strength of contraction increases as heart rate increases

force with which the heart ejects blood; increased contractility increases the stroke volume

cardiac output is approximately equivalent to mean arterial pressure divided by total peripheral resistance

equal to systolic pressure minus diastolic pressure

the pressure stretching the ventricles of the heart just prior to ejection; increased preload increases the stroke volume (according to the Frank-Starling mechanism)

equivalent to the pressure in the aorta leading from the ventricle; corresponds to the peak in systolic pressure in the left ventricle; corresponds to the arterial pressure against which the ventricle must contract; increasing the afterload decreases the stroke volume

equal to end diastolic volume - end systolic volume

approximately equal to the end diastolic pressure plus 1/3 of the pulse pressure

equivalent to the mean pressure in arteries AND veins

blood volume; venous compliance; cardiac performance

lead I = left arm (positive) - right arm (negative); lead II = left leg (positive) - right arm (negative); lead III = left leg (positive) - left arm (negative)

axis deviation (L ventricle -> L axis deviation; R ventricle -> R axis deviation)

axis deviation (L bundle branch block -> L axis deviation; R bundle branch block -> R axis deviation); inversion of T wave

refers to the overall direction of the heart's depolarizing wavefront; can be calculated from information from 2 leads

PVC occurs when ventricular contraction is initiated by ventricles instead of the SA node; produce large abnormal QRS waves on ECG followed by skipped beats

first-degree block results in prolonged P-R interval; second-degree block results in skipped ventricular beats; third-degree block results in spontaneous ventricular establishment of signal -> dissociation of P from QRS-T

delta P = hydrostatic pressure (tends to be outward & drive filtration); delta pi = colloid oncotic pressure (tends to be inward & drive absorption)

continuous; fenestrated; discontinuous

Kf; involved in the Starling equation to determine net filtration; describes the permeability of the capillary

increased venous pressure increases the net filtration rate

valves to prevent backflow & generate negative interstitial pressure; smooth muscle; body movements -> compression of lymphatics

excess interstitial fluid; results from excess filtration or inadequate reabsorption

have almost the same composition in most of the body b/c of capillary leakiness; exception = CNS (due to blood-brain barrier)