Lange CV Phys

Question 1

T/F: The interstitial fluid tends to take on the composition of the incoming blood/plasma

Answer 1

True- via diffusion

Question 2

Formula for flow

Answer 2

Q = ΔP/R

Where Q = flow rate
ΔP = mmHg
R = resistance, in mmHg x time/volume

Question 3

Poiseuille equation

Answer 3

Q = ΔP (π r^4/8Lη)

assumes laminar flow

ΔP has to be greater than 0 for there to be any flow - flow directly proportional
r = inside radius of the tube - flow directly proportional
L = length of tube - flow indirectly proportional
η = fluid viscosity - flow indirectly proportional

Question 4

Normal average pressure in arteries vs. pressure in veins

Answer 4

Arteries- 100 mmHg
Veins- 0 mmHg

Question 5

Fick principle

Answer 5

Xtc = Q x (Xa- Xv)

Xtc = transcapillary efflux rate of substance X
Xa = arterial concentration of X
Xv = venous concentration of X
Q = flow rate

If something goes in one side and doesn’t come out the other, must have been absorbed in the organ

Question 6

Path of blood flow through the heart

Answer 6

Systemic venous circulation –> vena cavae –> R atrium –> tricuspid valve –> R ventricle –> pulmonic valve –> pulmonary arteries –> lungs –> pulmonary veins –> L atrium –> mitral valve –> L ventricle –> aortic valve –> aorta –> systemic circulation

Question 7

Stroke volume

Answer 7

SV = the blood volume inside the the ventricle at the end of diastole minus the ventricular volume at the end of systole

SV = EDV - ESV

Question 8

Adrenergic sympathetic fibers in the heart

Answer 8

All portions of the heart
Sympathetic nerves release norepinephrine
Interacts with B1 adrenergic receptors on cardiac muscle cels to increase HR, increase action potential conduction velocity, and increase the force of contraction

Question 9

Cholinergic parasympathetic fibers in the heart

Answer 9

Travel to the heart via the vagus nerve
Innervate the SA node, AV node, and atrial muscle
Release acetylcholine - interacts with muscarinic receptors on cardiac cells to decrease the HR (SA node) and decrease action potential conduction velocity (AV node)
Decrease the force of contraction of atrial (not ventricular) muscle cells

Question 10

For effective/efficient ventricular pumping action, the heart must be functioning in 5 basic respects:

Answer 10

1. Synchronized contraction (no arrhythmia)
2. Valves must fully open (not stenotic)
3. Valves must not leak (no regurgitation)
4. The muscle contractions must be forceful (not failing)
5. The ventricles must FILL adequately during diastole

Question 11

T/F: Ion CHANNELS are responsible for the resting membrane potential

Answer 11

True

Question 12

The more permeable a membrane is to K+ means the membrane potential will be closer to ____ vs. the more permeable a membrane is to Na+ the membrane potential will be closer to ___

Answer 12

K: -90 mV
Na: +70 mV

Question 13

Equilibrium potential for Ca++

Answer 13

+100 mV

Question 14

Phase 0 (fast - response action potential of the cardiac myocyte)

Answer 14

Rapid inward current of Na+ - membrane potential moves positively to be more like the Na potential

Question 15

Phase 1 (fast - response action potential of the cardiac myocyte)

Answer 15

Very brief increase in potassium permeability - i.e. losing + charges - responsible for brief outward potassium current and membrane potential becoming more negative –> small non-sustained repolarization after the peak of the action potential

Question 16

Plateau phase (phase 2) (fast - response action potential of the cardiac myocyte)

Answer 16

1) sustained reduction in the K permeability
2) slowly developed and sustained increased in the membrane’s permeability to Ca++

Question 17

Phase 3

Answer 17

In both types of cells, phase 3 is when the membrane is depolarized and highly permeable to K+, and lowly permeable to Na/Ca thus making the membrane potential more negative

Question 18

Acetylcholine (parasympathetic) action on the heart muscle

Answer 18

Acetylcholine interacts with the M2 muscarinic receptors on the SA nodal cell membrane that in turn are linked to inhibitory G proteins, Gi. The activation of Gi has two effects:

1) Ach increases the permeability of the resting membrane to potassium –> increase in potassium conductance
2) suppression of adenylate cyclase leading to a fall in intracellular cAMP which reduces the inward-going pacemaker current

This causes initial hyperpolarization of the resting membrane potential by bringing it more negative (i.e. closer to the pure potassium potential) and slows the rate of spontaneous depolarization of the resting membrane

Question 19

Norepinephrine (sympathetic) action on the heart muscle

Answer 19

Acts on SA nodal cells to increase permeability to Na and Ca
Increases HR

Question 20

How does digitalis work

Answer 20

Digitalis slows down the cardiac Na/KATPase pump –> reduces gradient of sodium across the cell membrane which in turn results in decreased activity of the Na/Ca exchanger (normally would exchange 3 Na INTO the cell for every 1 Ca OUT) –> increased intracellular Ca levels and better contractility

Question 21

How does Pimobendan work

Answer 21

Pimobendan (0.25 mg/kg PO q12h), a benzimidazole-pyridazinone drug, is classified as an inodilator because of its nonsympathomimetic, nonglycoside positive inotropic (through myocardial calcium sensitization) and vasodilator properties.

The positive inotropic effects of pimobendan are mediated through a combination of 1) increased cyclic adenosine monophosphate mediated by phosphodiesterase III (PDEIII) inhibition, and 2) sensitization of the cardiac contractile apparatus to intracellular calcium. Calcium sensitization results in a positive inotropic effect without increasing myocardial oxygen demand.

Racemic pimobendan increased the contractile force of guinea pig papillary muscle preparations and this positive inotropic action was associated with potentiation of the Ca2+-dependent slow action potentials (APs). Experiments with chemically skinned heart muscle fibers showed that pimobendan, in a dose-dependent manner, increased active tension developed at submaximally activating concentrations of Ca2+.

Question 22

How does norepinephrine increase fractional shortening (i.e. increase contractility)

Answer 22

Interaction with B1 receptors - activation of the Gs protein cAMP-protein kinase A, which phosphorylates the Ca++ channel and increases inward calcium current during the plateau of the action potential —> loads internal calcium stores which means more can be released during subsequent depolarizations –> increase in free Ca ++ during activation allows more cross-bridges to be formed and greater tension to be developed (isometrically with any given preload) and more fractional shortening to occur (isotonically with any given preload and after load)

Question 23

Explain norepinephrine’s positive lusitropic effect

Answer 23

Norepinephrine-induced increase in the rate of muscle relaxation because norepinephrine causes phosphorylation of the regulatory protein phospholamban on the sarcoplasmic reticular Ca-ATPase pump and the rate of calcium re-trapping into the SR is enhanced.

Question 24

How does norepinephrine decrease the action potential duration

Answer 24

By alteration of the potassium channel, in response to increases in intracellular Ca, that results in increased potassium permeability and terminates the plateau phase of the AP, contributing to early repolarization –> very useful to decrease systolic interval but also allow filling during diastole

Question 25

S1 heart sound

Answer 25

The first heart sound (S1) represents closure of the atrioventricular (mitral and tricuspid) valves as the ventricular pressures exceed atrial pressures at the beginning of systole

Question 26

S2 heart sound

Answer 26

The second heart sound (S2) is a short burst of auditory vibrations of varying intensity, frequency, quality, and duration. It has two audible components, the aortic closure sound (A2) and the pulmonic closure sound (P2), which are normally split on inspiration and virtually single on expiration.

Question 27

S3 heart sound

Answer 27

The third heart sound (S3) is a low-frequency, brief vibration occurring in early diastole at the end of the rapid diastolic filling period of the right or left ventricle

Any cause of ventricular dysfunction, including ischemic heart disease, dilated or hypertrophic cardiomyopathy, myocarditis, cor pulmonale, or acute valvular regurgitation, may qualify. Myocardial ischemia without ventricular dysfunction or volume overload is not a cause of an S3. The presence of an S3 is the most sensitive indicator of ventricular dysfunction.

Any cause of a significant increase in the volume load on the ventricle(s) can cause an S3. Examples include valvular regurgitation, high-output states (anemia, pregnancy, arteriovenous fistula, or thyrotoxicosis), left-to-right intracardiac shunts, complete A-V block, renal failure, and volume overload from excessive fluids or blood transfusion.

Although the third heart sound is a very important clue to heart failure or volume overload, it does not appear until the problem is relatively far advanced. In some patients, for reasons that are not clear or because of chest size, obesity, or lung disease, an S3 may never be heard despite severe hemodynamic impairment. Therefore, the absence of a third heart sound cannot be used to exclude ventricular dysfunction or volume overload. In addition, the intensity of the third heart sound is influenced by several factors and correlates only roughly with the clinical status of the patient.

Question 28

Gallop sound

Answer 28

Rapid ventricular filling generates the S3 (also known as S3, protodiastolic, or ventricular gallop). A presystolic gallop (also called S4 or atrial gallop) is heard just before S1 and occurs just after the P wave on the ECG. An audible S4 (dog or cat) is usually associated with increased ventricular concentric hypertrophy and stiffness. Rapid ventricular filling and atrial systole transpire very close together at rapid heart rates (common in cats), making differentiation between S3 and S4 impossible. The resulting single accentuated sound is referred to as a summation gallop.

Question 29

Isovolumetric contraction

Answer 29

The period of ventricular systole between when the mitral valve is closed and the aortic valve opens

Question 30

Incisura/dichrotic notch

Answer 30

The momentary decrease in aortic pressure at the end of systole- a small amount of aortic blood is required to flow backwards to close the aortic valve

Question 31

Isovolumetric relaxation

Answer 31

At the end of ventricular systole when the aortic valve is closed but the mitral valve hasn’t re-opened

Question 32

Stroke volume

Answer 32

Equal to the amount of blood in the ventricle at the end of diastole, minus the amount left over in the ventricle at the end of systole
Under normal conditions, the heart ejects about 60% of its end diastolic volume

SV = EDV - ESV

Question 33

Pulse pressure

Answer 33

The difference between the peak systolic aortic pressure and the lowest aortic pressure at the end of diastole

Question 34

Typical pulmonary artery diastolic and systolic pressures

Answer 34

Diastolic 8 mmHg
Systolic 24 mmHg