Lange CV Phys Flashcards
T/F: The interstitial fluid tends to take on the composition of the incoming blood/plasma
True- via diffusion
Formula for flow
Q = ΔP/R
Where Q = flow rate
ΔP = mmHg
R = resistance, in mmHg x time/volume
Poiseuille equation
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
Normal average pressure in arteries vs. pressure in veins
Arteries- 100 mmHg
Veins- 0 mmHg
Fick principle
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
Path of blood flow through the heart
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
Stroke volume
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
Adrenergic sympathetic fibers in the heart
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
Cholinergic parasympathetic fibers in the heart
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
For effective/efficient ventricular pumping action, the heart must be functioning in 5 basic respects:
- Synchronized contraction (no arrhythmia)
- Valves must fully open (not stenotic)
- Valves must not leak (no regurgitation)
- The muscle contractions must be forceful (not failing)
- The ventricles must FILL adequately during diastole
T/F: Ion CHANNELS are responsible for the resting membrane potential
True
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 ___
K: -90 mV
Na: +70 mV
Equilibrium potential for Ca++
+100 mV
Phase 0 (fast - response action potential of the cardiac myocyte)
Rapid inward current of Na+ - membrane potential moves positively to be more like the Na potential
Phase 1 (fast - response action potential of the cardiac myocyte)
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
Plateau phase (phase 2) (fast - response action potential of the cardiac myocyte)
1) sustained reduction in the K permeability
2) slowly developed and sustained increased in the membrane’s permeability to Ca++
Phase 3
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
Acetylcholine (parasympathetic) action on the heart muscle
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
Norepinephrine (sympathetic) action on the heart muscle
Acts on SA nodal cells to increase permeability to Na and Ca
Increases HR
How does digitalis work
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
How does Pimobendan work
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+.
How does norepinephrine increase fractional shortening (i.e. increase contractility)
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)
Explain norepinephrine’s positive lusitropic effect
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.
How does norepinephrine decrease the action potential duration
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
S1 heart sound
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
S2 heart sound
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.
S3 heart sound
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.
Gallop sound
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.
Isovolumetric contraction
The period of ventricular systole between when the mitral valve is closed and the aortic valve opens
Incisura/dichrotic notch
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
Isovolumetric relaxation
At the end of ventricular systole when the aortic valve is closed but the mitral valve hasn’t re-opened
Stroke volume
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
Pulse pressure
The difference between the peak systolic aortic pressure and the lowest aortic pressure at the end of diastole
Typical pulmonary artery diastolic and systolic pressures
Diastolic 8 mmHg
Systolic 24 mmHg
