physio exam 2 lec 3

What initiates cardiac excitation-contraction coupling?

An action potential opens L-type voltage-gated Ca²⁺ channels allowing extracellular Ca²⁺ to enter the cardiac myocyte

What is calcium-induced calcium release (CICR)?

Incoming Ca²⁺ triggers clusters of SR calcium-release channels to open and release additional Ca²⁺

Where does calcium for cardiac contraction come from?

Approximately 20% enters from extracellular fluid and 80% comes from the SR with about 50% of SR stores released during activation

How does calcium cause contraction and how is it removed?

Ca²⁺ activates actin-myosin contraction and relaxation occurs as approximately 80% is pumped into the SR by Ca-ATPase and 20% is removed by membrane pumps and exchangers

What occurs during phases 0 and 1 of the ventricular action potential?

Phase 0 is rapid Na⁺ influx and depolarization while phase 1 is initial repolarization from K⁺ efflux

What occurs during phases 2 and 3 of the ventricular action potential?

Phase 2 is the plateau from Ca²⁺ influx and K⁺ efflux while phase 3 is repolarization mainly from K⁺ efflux

What occurs during phase 4 and the refractory periods?

Phase 4 is resting membrane potential near -90 mV and the absolute refractory period has unavailable fast Na⁺ channels followed by a relative refractory period

How do the ECG and ventricular action potential relate to contraction?

P wave represents atrial depolarization and QRS initiates ventricular depolarization and T wave reflects ventricular repolarization while ventricular pressure rises after electrical activation

What is the sequence of the cardiac cycle?

Atrial systole → isovolumic contraction → ventricular ejection → isovolumic relaxation → ventricular filling

What are ED and PEP and LVET and S1 and S2?

ED = electromechanical delay and PEP = pre-ejection period and LVET = LV ejection time and S1/S2 are first/second heart sounds

What are preload and afterload in the papillary muscle experiment?

Preload is initial muscle stretch before contraction while afterload is the load the muscle must move

How is muscle shortening velocity measured and affected by afterload?

Velocity is the slope dL/dt of length change over time and higher afterload reduces shortening velocity

How does sarcomere length affect contraction force at fixed calcium?

Greater initial length increases force with 2.0 µm producing more force than 1.9 µm or 1.8 µm in the lecture graph

How does increasing intracellular calcium affect contraction force at fixed sarcomere length?

Increased Ca²⁺ increases contraction force and reflects increased activation of the contractile machinery

How does increased preload affect shortening velocity at fixed afterload?

Increased preload increases shortening velocity through the Frank-Starling mechanism

How does increased afterload affect shortening velocity at fixed preload?

Increased afterload decreases shortening velocity because the muscle must overcome a larger load

What is Vmax and why does it indicate contractility?

Vmax is maximum shortening velocity as afterload approaches zero and is relatively independent of preload

How does increased contractility affect shortening velocity at fixed preload and afterload?

Increased contractility increases shortening velocity

How does earlier ectopic beat timing affect arterial pulse strength?

Earlier ectopic beats produce smaller pulses due to reduced filling with lecture pulse ratios of 78% and 60% for progressively earlier beats

What measurements indicate cardiac preload?

EDV and end-diastolic pressure (EDP) and CVP are preload indicators with the lecture relationship EDP = EDV/C_LV

What measurements indicate cardiac afterload?

Myocardial wall stress and TPR and aortic or ventricular pressure indicate afterload

How does ventricular wall mechanics produce ejection?

Myocytes overcome opposing wall tension and increase inward force causing chamber radius to decrease and ventricular pressure to rise until blood is ejected

What determines cardiac output and stroke volume?

CO = SV × HR with SV increased by preload and contractility but decreased by increased afterload

How do sympathetic and vagal stimulation affect cardiac output?

Sympathetic stimulation increases HR and contractility while vagal stimulation decreases HR

What effects result from sympathetic β1-receptor stimulation?

Positive chronotropic and inotropic and dromotropic effects with increased HR and contractility and conduction plus faster relaxation

What is peak isovolumic pressure (PIP) and how is it measured?

Maximum ventricular pressure during contraction without ejection measured experimentally with aortic outflow clamped

How does sympathetic stimulation affect peak isovolumic pressure?

It increases contractility and contraction rate which increases the maximum pressure generated during isovolumic contraction

What is the Frank-Starling law of the heart?

Increased preload or EDV stretches cardiac muscle and increases contraction force and stroke volume and achievable peak isovolumic pressure

How does increased contractility change the PIP line?

It increases PIP line slope allowing greater SV at the same preload or the same SV with less preload

What is the difference between moving on versus between cardiac function curves?

Movement along a curve reflects Frank-Starling preload changes while movement between curves reflects contractility changes

What is the ventricular wall stress equation?

Wall stress σ = P × r/w where P is transmural pressure and r is chamber radius and w is wall thickness

How does wall stress change between isovolumic contraction and ejection?

Wall stress is high during isovolumic contraction due to high pressure and large radius and generally decreases as radius becomes smaller during ejection

How does ventricular wall stress affect myocardial oxygen demand?

Energy demand increases with wall stress and time and is elevated with high pressure or prolonged contraction such as in hypertension or aortic stenosis

What is the tension-time integral (TTI)?

TTI is the integral of wall stress over time expressed as ∫[P(t) × r(t)/w(t)]dt

What is the double product used to estimate ventricular energy demand?

MAP × HR is the lecture's clinically measurable indicator of cardiac energy demand

What is (dP/dt)max and how does it relate to contractility?

Maximum rate of ventricular pressure rise is an indicator of contractility with the lecture curves showing B > A > C

How does intrathoracic pressure change during normal breathing?

Intrathoracic pressure becomes more negative during inspiration and increases during expiration

How does intrathoracic pressure affect effective LV afterload?

LV wall stress = (PLV − PTH) × r/w so decreasing intrathoracic pressure increases LV transmural pressure and effective afterload

What happens during deep inspiration against a closed glottis?

Intrathoracic pressure decreases substantially and increases LV transmural pressure and afterload which may reduce SV

How does inspiration affect lung blood volume and ventricular filling?

Inspiration increases pulmonary blood volume and can shift the interventricular septum reducing LV filling and SV

How does inspiration affect systemic venous return?

More negative intrathoracic pressure decreases central venous pressure and increases the venous pressure gradient and right-heart venous return

How does inspiration normally affect systolic BP and what is pulsus paradoxus?

Inspiration normally decreases systolic BP by less than 12 mmHg while a decrease greater than 12 mmHg is pulsus paradoxus and may trigger baroreflex HR changes

How does myocardial wall stress differ between endocardium and epicardium?

Radial and tangential myocardial stresses during contraction are greater toward the endocardium than the epicardium

Why is the subendocardium especially vulnerable to ischemia?

Systolic contraction compresses subendocardial vessels more strongly so much of their blood flow occurs during diastole and reduced perfusion increases ischemic risk

What happens to arterial pulse pressure when arterial compliance decreases?

Pulse pressure increases because a given stroke volume produces a greater pressure change in stiffer arteries

At constant perfusion pressure which vessel change increases flow the most?

Doubling radius increases flow 16-fold while halving vessel length or viscosity only doubles flow

How do shear rate and shear stress relate to blood flow?

Average shear rate is proportional to U/D while shear stress = viscosity × shear rate and wall shear stress is proportional to ηQ/D³

What determines organ flow distribution and how does venous resistance affect capillary pressure?

Relative vascular resistance determines an organ's fraction of CO while venous vasoconstriction or increased CVP can decrease flow and increase capillary pressure

How does turbulent flow affect vascular resistance?

Turbulence occurs when the critical Reynolds number is exceeded and increases energy loss and resistance compared with laminar flow