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PHYSIOLOGY > CVS > Flashcards

CVS Flashcards

1
Q

CVS division

A
  • vascular and cardiac
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2
Q

vascular

A
  • peripheral circulation

- flow

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3
Q

cardiac muscle

A
  • dealing with electrical activity (action potential of the heart)
  • mechanics and dynamics (performance of the heart)
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4
Q

action potential

A
  • ventriclular action potential

- SA node action potential

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5
Q

performance of the heart

A
  • preload

- contractility

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6
Q

ventricular action potential

A
  • movement of ions
  • Na,
  • K,
  • Ca++ skeletal action potential
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7
Q

ventricular action potential

A

channels
voltage
- FAST- Na+ closed at rest
- depolarization is the signal for opening
- open quickly close quickly
- SLOW- K+ and Ca++ shares in cardiac muscle
- K+ is OPEN AT REST
- depolarization is the signal for closing
- Ca++
- depolarization is the signal for opening
UNGATED
- K+- ALWAYS OPEN

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8
Q

ventricular action phases

A 
phase 0
- due to net influx of sodium
- causing rapid depolarization
phase 1
- small efflux of K
phase 2
- small influx of Ca
- and balance by slow efflux of K
- causing a long plateau phase
- large ventricular action potential
- 200 msec duration
phase 3
- rapid efflux of K
- opened gated and ungated channels
phase 4
- small efflux of K
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9
Q

action potential

A

SA node

  • phase 4, phase 0, phase 3, phase 4
  • phase 0 net influx of calcium
  • phase 3 rapid efflux of K
  • phase 4 slow influx of Ca++
  • or slow influx of Na+
  • funny current
  • open at rest
  • closed at threshold
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10
Q

SA node

A
  • controlled by autonomic nervous system
  • sympathetic
  • parasympathetic
  • action potential fires electrical signal to atria then it depolarized causing the HEART RATE
  • pace maker of the heart
  • heart rate is determined from the SA node
  • P WAVE atrial depolarization
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11
Q

AV node

A
  • slowest part of the pathway

- PR interval

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12
Q

ventricles

A
  • generates its own action potential
  • travels in the septum
  • bundle of His
  • STROKE VOLUME (contracts and pumps blood out)
  • VENTRICULAR DEPOLARIZATION
  • QRS
  • T wave
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13
Q

performance of the heart

A
  • Cardiac output (CO)

- heart rate (SA NODE) x stroke volume (VENTRICLES) factor in EDV factor in venous return

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14
Q

P wave

A
  • atrial depolarization

- atria

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15
Q

performance of the heart (CHF)

A
  • preload (venous return, flow)
  • due to passive tension in the muscle
  • filling of the heart
  • during diastole
  • index of measurement of preload is END DIASTOLIC VOLUME proportional to preload (echocardio)
  • contractility
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16
Q

diastolic filling during diastole

A
  • heart muscle is being stretched to accommodate the filling of the incoming blood
  • passive tension increasing the length
  • directly proportional to the length
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17
Q

increasing preload

A
  • increasing passive tension to the heart

- diastolic

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18
Q

systole

A
  • active tension of the heart
  • heart muscle shortens
  • length shortens
19
Q

line that intersects with MEAN SYSTOLIC PRESSURE and MEAN DIASTOLIC PRESSURE

A
  • LO ultimate stretch of a muscle to have a maximum systolic performance of the heart
  • 120 mmHg optimally filled
20
Q

EDV>ESV

A
  • LESS stretch of the systolic
  • increasing the preload
  • affecting the performance of the heart
21
Q

to decrease PRELOAD

A
  • INCREASE VOLUME LOSS
    inc. urine output diuretics
  • DECREASE VENOUS RETURN
    venodilator DIGOXIN
22
Q

DIGOXIN (inotrophism benefits)

A
  • competes with K for the sodium K pump
  • it inhibit the sodium K pump
  • passive influx of Na is inhibited
  • decreasing secondary active transport of calcium from the heart cell is inhibited
  • causing build up of calcium in the cell
  • calcium binds to troponin
23
Q

before digoxin

A
  • heart beating lazy, slowly
24
Q

after digoxin

A
  • heart develops pressure at a faster rate
  • heart develops more pressure, power
  • rate of relaxation of the heart is faster
  • systolic interval is decrease (less time in systole, O2 demand decreases)
  • if the heart rate remain constant their will be more time for diastole ventricular filling increase coronary flow going back to normal
25
Q

cardiac output CO (HEMORRHAGE)

A
  • preload and contractility
26
Q

CONTRACTILITY RULES

A
  • all points on the same line/plane have the SAME contractility
  • as it moves from the center of the LINE to the LEFT it will increase contractility
  • as it move to the RIGHT it will decrease contractility DECREASE CO leading to compensated and decompensated failure
27
Q

Hemorrhage

A
  • loose PRELOAD decreasing the performance of the heart decreasing CO
  • preload is determined by venous return
  • it doesn’t affect the contractility/muscles of the heart
  • but thought compensation heart increase contractility to make up the loss of performance
28
Q

over infusion/OVERLOAD of fluids effect on preload and contractility of the heart

A
  • overload increase preload by Frank Starling law performance increase
  • to compensate heart decrease contractility towards normal but it will not go back to normal
  • INCREASE VENOUS PRESSURE
  • INCREASE CARDIAC OUTPUT
29
Q

venous return determines

A
  • cardiac output
30
Q

increase resistance does not affect

A
  • venous return

- cardiac output

31
Q

heart rate has

A
  • no effect on cardiac output in normal settings (stroke volume (VENTRICLES) factor in EDV factor in venous return HAS)
  • but very low/very high heart rate impedes VR and CO
32
Q

decrease CARDIAC OUTPUT is due to

A
  • decrease HEART RATE

- increase HEART RATE filling problem massive tachycardia, arrhythmia not enough filling

33
Q

dilation of arteries (ARTERIOLAR DILATOR) FLOW

A
  • more forward flow
  • into the veins
  • INCREASE CO
34
Q

constriction of the arteries (FLOW)

A
  • decrease radius thereby decreasing flow
  • less blood going to the venous system
  • decrease venous return
  • DECREASE CO
35
Q

compensated failure parameters NORMAL VP and CO

A
  • decreasing contractility
  • maintaining the performance (preload)
  • increase venous pressure
  • CO is maintained in acceptable limits
36
Q

decompensated failure parameters NORMAL VP and CO

A
  • heart failure
  • CO below >
  • volume overload
37
Q

SYSTOLIC DYSFUNCTION

A
  • abnormal reduction in ventricular emptying due to impaired contractility or excessive afterload
  • PRESSURE OVERLOAD–increase TPR (hypertension), increase afterload (HTN), obstruction (aortic stenosis)
  • heart develops CONCENTRIC HYPERTROPHY
  • VOLUME OVERLOAD– increase EDV (aortic insufficiency, mitral insufficiency/regurgitation) increase back flow of blood to left ventricle
  • heart develops ECCENTRIC HYPERTROPHY
38
Q

DIASTOLIC DYSFUNCTION

A
  • decrease in ventricular compliance during FILLING phase
  • DECREASING venous return
  • tissue stiffness
  • impaired ventricular relaxation
  • diminished Frank -Starling law mechanism
39
Q

an INCREASE in afterload

A
  • is due to PRESSURE/VOLUME OVERLOAD
40
Q

CARDIOMYOPATHY

A
  • failure of myocardium where the underlying cause originates within the MYOCYTES
41
Q

BASIC TYPES OF CARDIOMYOPATHIES

A
  • DILATED CARDIOMYOPATHY
  • RESTRICTIVE CARDIOMYOPATHY
  • HYPERTOPHIC CARDIOMYOPATHY
42
Q

DILATED CARDIOMYOPATHY

A
  • LEFT ventricular dilatation
  • modest hypertrophy
  • chamber size is INCREASED
  • affected LEFT and RIGHT heart
  • intact diastolic function
  • compensation increased sympathetic stimulation to the myocardium can lead to
  • systolic dysfunction despite increase contractility
  • mitral and tricuspid failure can lead to complete failure
43
Q

RESTRICTIVE CARDIOMYOPATHY

A
  • decrease ventricular compliance
  • DIASTOLIC filling/dysfunction
  • decrease ventricular cavity size
  • increase filling pressure
  • left and right sided congestion
  • ventricular hypertrophy (+/-)
  • maintain systolic function
  • NARROWED chamber size
44
Q

HYPERTOPHIC CARDIOMYOPATHY

A
  • septal or ventricular hypertrophy is unrelated to a pressure
  • diastolic dysfunction is due to INCREASE muscle STIFFNESS and impaired relaxation
  • ASYMMETRIC HYPERTROPHY of the septum
    due to restriction of ventricular outflow
  • IDIOPATHIC HYPERTROPHIC SUBAORTIC STENOSIS
  • PULMONARY CONGESTION
  • SEPTAL FIBER DISARRAY

PHYSIOLOGY (40 decks)

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