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Flashcards in CVS Deck (44):
1

CVS division

- vascular and cardiac

2

vascular

- peripheral circulation
- flow

3

cardiac muscle

- dealing with electrical activity (action potential of the heart)
- mechanics and dynamics (performance of the heart)

4

action potential

- ventriclular action potential
- SA node action potential

5

performance of the heart

- preload
- contractility

6

ventricular action potential

- movement of ions
- Na,
- K,
- Ca++ skeletal action potential

7

ventricular action potential

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

ventricular action phases

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

action potential

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

SA node

- 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

AV node

- slowest part of the pathway
- PR interval

12

ventricles

- 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

performance of the heart

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

14

P wave

- atrial depolarization
- atria

15

performance of the heart (CHF)

- 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

diastolic filling during diastole

- heart muscle is being stretched to accommodate the filling of the incoming blood
- passive tension increasing the length
- directly proportional to the length

17

increasing preload

- increasing passive tension to the heart
- diastolic

18

systole

- active tension of the heart
- heart muscle shortens
- length shortens

19

line that intersects with MEAN SYSTOLIC PRESSURE and MEAN DIASTOLIC PRESSURE

- LO ultimate stretch of a muscle to have a maximum systolic performance of the heart
- 120 mmHg optimally filled

20

EDV>ESV

- LESS stretch of the systolic
- increasing the preload
- affecting the performance of the heart

21

to decrease PRELOAD

- INCREASE VOLUME LOSS
inc. urine output diuretics
- DECREASE VENOUS RETURN
venodilator DIGOXIN

22

DIGOXIN (inotrophism benefits)

- 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

before digoxin

- heart beating lazy, slowly

24

after digoxin

- 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