CVS Flashcards
1
Q
CVS division
A
- vascular and cardiac
2
Q
vascular
A
- peripheral circulation
- flow
3
Q
cardiac muscle
A
- dealing with electrical activity (action potential of the heart)
- mechanics and dynamics (performance of the heart)
4
Q
action potential
A
- ventriclular action potential
- SA node action potential
5
Q
performance of the heart
A
- preload
- contractility
6
Q
ventricular action potential
A
- movement of ions
- Na,
- K,
- Ca++ skeletal action potential
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
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
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
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
11
Q
AV node
A
- slowest part of the pathway
- PR interval
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
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
14
Q
P wave
A
- atrial depolarization
- atria
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
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
17
Q
increasing preload
A
- increasing passive tension to the heart
- diastolic
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
cardiac output CO (HEMORRHAGE)
- preload and contractility
26
CONTRACTILITY RULES
- 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
Hemorrhage
- 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
over infusion/OVERLOAD of fluids effect on preload and contractility of the heart
- 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
venous return determines
- cardiac output
30
increase resistance does not affect
- venous return
| - cardiac output
31
heart rate has
- 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
decrease CARDIAC OUTPUT is due to
- decrease HEART RATE
| - increase HEART RATE filling problem massive tachycardia, arrhythmia not enough filling
33
dilation of arteries (ARTERIOLAR DILATOR) FLOW
- more forward flow
- into the veins
- INCREASE CO
34
constriction of the arteries (FLOW)
- decrease radius thereby decreasing flow
- less blood going to the venous system
- decrease venous return
- DECREASE CO
35
compensated failure parameters NORMAL VP and CO
- decreasing contractility
- maintaining the performance (preload)
- increase venous pressure
- CO is maintained in acceptable limits
36
decompensated failure parameters NORMAL VP and CO
- heart failure
- CO below >
- volume overload
37
SYSTOLIC DYSFUNCTION
- 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
DIASTOLIC DYSFUNCTION
- decrease in ventricular compliance during FILLING phase
- DECREASING venous return
- tissue stiffness
- impaired ventricular relaxation
- diminished Frank -Starling law mechanism
39
an INCREASE in afterload
- is due to PRESSURE/VOLUME OVERLOAD
40
CARDIOMYOPATHY
- failure of myocardium where the underlying cause originates within the MYOCYTES
41
BASIC TYPES OF CARDIOMYOPATHIES
- DILATED CARDIOMYOPATHY
- RESTRICTIVE CARDIOMYOPATHY
- HYPERTOPHIC CARDIOMYOPATHY
42
DILATED CARDIOMYOPATHY
- 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
RESTRICTIVE CARDIOMYOPATHY
- 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
HYPERTOPHIC CARDIOMYOPATHY
- 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
