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58 Cards in this Set
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- Back
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Poiseulle's Law
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R = 8 * l * viscosity / pi (r^4)
l = length |
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LaPlace's Law
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T = P * r
T = wall tension P = intraluminal pressure r = radius |
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laminar flow
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all elements of the fluid move in streamlines parallel to the axis of the tube.
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turbulent flow
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the elements of the fluid move irregularly
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How is Flow (V) related to resistance (R) and pressure
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Flow = dP/R
dP = change in pressure |
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tension is the force generated by?
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vascular smooth muscle
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S1
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•Closure of AV valves
•Onset of systole •Loudest •Longest (0.14 sec) •Auscultate at the apex •Mitral v : 5th ICS mid-clavicular •Tricuspid v : 5th ICS left of sternum |
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S2
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•Closure of SL valves
•Onset of diastole •Higher frequency •Lower intensity •Auscultate at the base •Aortic v : 2nd ISC right of sternum •Pulmonary v : 2nd ISC left of sternum |
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S3
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•“Ventricular Gallop”
•Middle 1/3 of diastole •Rapid passive filling •Dull & low pitched •Normal in children •May indicate CHF or cardiomyopathy in adults |
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S4
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•“Atrial Gallop”
•Corresponds to atrial contraction •Rarely a normal finding •Associated with “stiff”, hypertrophied ventricle |
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resistance:
series parallel |
Series: Rtot = 1 + R2 + R3 + …
Parallel: 1/Rtot = 1/R1 + 1/R2 + 1/R3 + … |
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compliance =
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dV/dP
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normal hematocrit value is
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40
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chemical gradient drives K+ ____ electrical gradient drives K+ ____
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out
in |
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Resting membrane potential. rank the permeability of the following ions: K, Na, Ca
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K > Na = Ca
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[K+]: inside and outside
[Na+]: inside and outside [Ca++]: inside and outside |
[K+]: 140nM, 4mM
[Na+]: 10mM, 145mM [Ca++]: <10^-7mM, 1mM |
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2 tyoes if cardiomyocytes
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fast and slow response cells
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can AP occur during ERP?
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no
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can AP occur during RRP?
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yes, but not efficient
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depolarization of fast response cell is contributed what channel? the plateau?
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exflux of Na+
Influx of Ca++ |
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what effect does Ca++ blocker have on the fast response cell?
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reduces duration of AP
plateau phase changes reduction of force generated |
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Cardiac muscle relies on intra or extracellular Ca++
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extra
(both extra and intra contribute to Ca+ pool) |
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What cardiac cell cluster have slow response?
fast response? |
slow response cells: SA and AV nodes
fast response: atrium, purkinje and ventricle |
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In slow response cell what ions contribute to initial depolarization of membrane? the slight depolarization after repolarization is contributed by?
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Influx of Ca++
influx of Na+ |
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effect pf Ca++ blocker on slow response cells?
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reduction of depolarization
longer time btw AP - slower HR |
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Effect that sympathetic stimulation have on SA node firing? parasympathetic?
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sympathetic: accelerate slow depolarization phase. increases the rate of Na + channel opening.
parasympathetic: hyperpolarizes the cell (increasing K+ channel opening) takes longer to depolarize. |
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systole is divided into 2 phases.
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isovolumic and ejection phases
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cardiac Output =
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HR x Stroke Volume
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Cardiac output in mL/min
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5L/min
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during fight or flight situation: CO is ___ times that of normal CO
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5x
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preload
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heart receiving blood vol
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afterload
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heart pushing against blood pressure, depended upon vasoconstriction and vasodilation
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Stroke vol is equals to
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EDV - ESV
EDV: end diastolic vol ESV: end systolic vol |
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EDV
ESV |
EDV: amount of blood remaining in ventricle at the end of diastole
ESV: amount of blood remaining in ventricle at the end of systole |
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Frank-Starling effect
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increasing EDV (increasing preload) corresponds to increasing blood vol in the heart (returning more blood to the heart).
Heart responds by contracting with equal pressure but increased force. |
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EF (ejection fraction) =
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SV/EDV
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failed heart has higher or lower ejection fraction compared to a healthy heart?
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lower
b/c EF = SV/EDV SV stays the same as a normal heart, but EDV increases; hence lowering the EF. |
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staircase phenomenon of heart rate explains that. molecular concept.
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increase HR will increase the ability of the heart to generate force.
increased basal level of Ca++ in sarcoplasm allowing a increased Ca++ that binds to troponin C. |
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atropine blocks
propanolol blocks |
atropine blocks parasympathetic tone, fast HR
paropanolol blocks sympathetic tone, slow HR |
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positive inotropic effect of sympathetic system on the heart means that
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increased heart contractility
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w/o inputs from para and sympathetic inputs, the intrinsic HR is
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100 beats/min
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Both para and sym system are present at the same time but vagal tone are greater. (T/F)
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T
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If there's an increased venous return to the heart, what effect does bainbridge reflex on the HR?
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it increases HR
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If there's an increased venous return to the heart, what effect does baroreceptor reflex on the HR?
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decreases HR
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2 ways that atrial pressure change
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1. atrial pressure increases when ventricular contraction is low
2. right atrial pressure increases when there's increased venous return |
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Cardiac function modulation:
short term long term effects |
Short term: HR, SV, vascular resistance (syspathetics and parasympathetics), venous return.
Long term: hypertrophy, vascularization, hematocrit |
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what effect does slowed HR have on the transit time in the pulmonary circulation?
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increased transit time to allow more time for gas exchange in the lungs.
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Does SV change during blood infusion?
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No
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Define preload and afterload?
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preload: receiving blood vol.
afterload: pushing against blood pressure, depended upon vasoconstriction and vasodilation. |
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myocardial infarction (heart attack), it occurs where and how?
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it occurs when a cholesterol plaque in the wall of the coronary artery ruptures and causes a thrombus to form occluding the coronary artery and starving the myocardial cells of glucose and oxygen.
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the risk factors of myocardial infarction are (5)
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• Hypertension
• Hypercholesterolemia • Diabetes • Cigarette smoking • Family history of coronary artery disease |
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Coronary artery disease may manifest itself in 6 ways:
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• Asymptomatic
• Angina: Stable angina and Unstable angina • Myocardial infarction • Congestive heart failure • Cardiogenic shock • Sudden cardiac death |
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most common manifestation of stable angina is Stages of Hemostasis
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chest pain or chest pressure during excursion.
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treating stable angina - relax the heart
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decrease heart rate and contractility (beta blocker and Ca++ blocker) and prevent thrombus formation (nitrate and aspirin)
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cardiomyopathy caused by
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weakening of the heart muscle can be caused by
myocardial cell death (by not treating myocardial infarction and unstable angina fast enough) disease of the heart valves post-viral or idiopathic etiology |
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syncope
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heart fail to pump enough blood to the brain causing the body to lose consciousness
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Stages of Hemostasis
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•Vasoconstriction (Vascular phase)-Transient
•Primary Hemostasis (Platelet Activation phase) - non-covalent platelet clot •Secondary Hemostasis (Coagulation phase) - covalent platelet clot •Plug Formation and Dissolution |
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vasoconstriction result from
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nervous reflexes
local myogenic spasm local humoral factors |
