Module 3 : Cardiac Hemodynamics Flashcards
(71 cards)
1
Q
Pressure - equation
A
Force/ unit area
2
Q
Potential energy (static pressure)
A
- ability to do work
- created by contraction of the ventricles AND vascular resistance from arteries
3
Q
Kinetic energy
A
- energy of motion
+ blood, walls
4
Q
Gravitational energy
A
- effect of gravity on static pressure
+ venous pressure in lower extremities
5
Q
Normal blood pressure (BP)
A
- 120/ 80 mmHg
+ top number = systolic = max pressure = 120 mmHg
+ bottom number = diastolic= min pressure = 80 mmHg
6
Q
High BP
A
- greater than 140/90 taken on 2 separate occasions
7
Q
Borderline BP
A
- 130/85 should be watch over time as it may increase
8
Q
Mean Pressure
A
- average pressure over the cardiac cycle
9
Q
Resting heart rate - systole time
A
- systole occupies 1/3 length of cardiac cycle time at resting heart rate
10
Q
Resting heart rate - diastole time
A
- diastole occupies 2/3 cardiac cycle time at resting heart rate
11
Q
How would the length change if heart rate (HR) increases
A
- systolic length would increase
12
Q
Mean Pressure Equation ( mean arteriole pressure MAP)
A
MAP = diastolic P+ 1/3 pulse pressure
- MAP= DBP + 1/3(systolic blood pressure - diastolic blood pressure)
- SBP = systolic blood pressure
- DBP = diastolic blood pressure
13
Q
Pulse pressure
A
- pulse pressure = SBP - DBP
Done with the cuff ( first sound - last sound)
14
Q
Pressure gradient
A
- difference in pressure between adjacent locations within the heart
15
Q
Natural flow direction
A
- higher to lower pressure until pressure equalize
16
Q
Relationship between pressure and volume
A
- as pressure gradient increases velocity increases
17
Q
Bernoulli’s equation (simplified)
A
- Pressure gradient = 4 x V^2
18
Q
The cardiac cycle - phases
A
1. IVCT = isovolumic contraction time
\+ heart about to contract
\+ END DIASTOLE
2. systole
3. IVRT - isovolumic relaxation time
\+ heart about to relax
\+ END SYSTOLE
4. Diastole ( 3 phases)
19
Q
IVCT - isovolumic contraction time
A
- iso= same ; volumic = volume
+ no change in volume of the heart ALL VALVES CLOSED - period time between MV closer and AV valve opening
- LV Pressure rising from 5 - 80 mmHg
- ventricle starting to squeeze
- 30 to 50ms
20
Q
Threshold pressure for systole
A
Ventricle needs to reach 80 mmHg before the aortic valves open
21
Q
Ventricular systole
A
- period of time it takes for the ventricles to eject their contents
- starts when LV/RV Pressure exceeds that of aorta and valves open
- finishes when LV/ RV Pressure falls below aorta and valves
22
Q
Valve movement
A
- valves are passive and only move in response to a pressure change
23
Q
Ventricular systole events
A
- MUSCLE CONTRACTION BEGINS AT THE APEX AND MOVES TOWARD THE BASE OF THE HEART
- rising pressure in the ventricles closes MV and TV and chordae prevent valve prolapse
- pap muscles contract to pull chordae back in valves
- 200-300ms
24
Q
IVRT- Isovolumic Relaxation Time
A
- period of time after the aortic valves closes that before the mitral valve open
- END SYSTOLE
- volume remains constant
- PRESSURE FALLING IN THE VENTRICLES
- 50 - 100ms
- pressure in atria rising in prep to fill ventricles
25
Atria falling
- ATRIA ALWAYS FILLING BECAUSE NO VALVES BETWEEN PULMONARY VEIN AND ATRIA
26
Diastole
- period of time when the MV/TV are open and blood moves from atria to ventricles
- STARTS WHEN LV PRESSURE FALLS BELOW ATRIA PRESSURE
- FINISHES WHEN LV PRESSURE ABOVE ATRIA
- 3 PHASES
27
3 phases of diastole
- early filling = rapid filling , suction, first bump
- diastasis = Pressure equalized, stopping
- late filling = atria contraction , double bump
28
Early filling
- pressure in LV falls below LA the MV opens
- LV chamber expands rapidly dropping pressure in LV which sucks blood from LA (negative pressure)
* 75% of filling done during this time
* lasts 150-220ms
- FIRST BUMB
29
Diastasis
- period of time after early filling has slowed down
- early filling stage pressure between LV and LA roughly equal causing the MV to “hang” in semi open position
- near end atria polarizes
30
Late filling
- slow filling or atrial kick
- atria depolarize and contract pressure in atria is higher than ventricle
- pushes MV open again and adds last 30% of blood to LV
31
Pressure changes within the heart - LV
100-140/ 3-12
32
Pressure changes within the heart - LA
Average 2-12
33
Pressure changes within the heart - RV
15-30/ 2-8
34
Pressure changes within the heart - RA
Mean 2-8
35
Volume changes in LV
```
IVCT = END DIASTOLE = VERY FULL
systole = emptying
IVRT = END SYSTOLE = SMALLEST
diastole = filling again
```
36
stroke volume
stroke volume is the volume of blood pushed in the heart
| * NORMAL = 50 - 100 ml/beat AT REST
37
stroke volume using chamber volume
we can use the LV chamber volume at end diastole and end systole to calculate the stroke volume
38
stroke volume equation - using chamber volume
SV = EDV - ESV
39
cardiac output
amount of blood ejected from the heart
40
cardiac output equation - using stroke volume
```
CO = stroke volume x heart rate
CO = SV x HR
```
41
cardiac index
amount of blood being ejected from the heart compared to body surface area
42
cardiac index equation - using cardiac output
```
CI = cardiac output / body surface area
CI = CO / BSA
```
43
stroke volume using doppler
individual flow velocities must be integrated over the time period of the ejection
44
stroke volume equation - using VTI and CSA
```
SV = cross sectional area x velocity time integral
SV = CSA x VTI
```
45
velocity time integral VTI
the amount of individual flow velocities calculated over the time period of ejections
46
cross sectional area CSA
calculated at the LVOT diameter
| CSA = pi x r^2
47
stroke volume calculation
stroke volume through any valve in the heart can calculated by using the CSA of the valve annulus and the PW VTI
48
oxygen saturation - pulmonary artery
75% = deoxygenated
49
oxygen saturation - aorta
98% = oxygenated
50
oxygen saturation - coronary sinus
50% saturated
51
oxygen demand - Left Ventricle
comprises most of the hearts mass
uses aprox 50% of the oxygen supplied in the coronary arteries at rest
* hypertrophied LV the amount of oxygen needed by the LV would increase
52
ischemia
feels line angina pectoris
| not felt until affected coronary artery blocked about 75%
53
angina pectoris
caused by not enough oxygen and nutrients getting to the heart muscle
or too much heart muscle
or high after load
54
factors affecting stroke volume
preload, after load, inotropic force, chronotropic force
55
preload
AMOUNT OF VOLUME OF BLOOD IN THE VENTRICLE AT END DIASTOLE
+ volume load delivered to the ventricle
in diseased heart increased preload or afterload the ventricle fails and they go into CHF
56
End diastolic volume + Stroke volume
Frank - Starling law
57
Frank - Starling law
- the heart adapts to different preloads by pumping the volume of blood delivered to it
+ more blood enters the heart = greater force of contraction = due to greater stretch of the myocardial muscle fibers
58
Frank - Starling principle (length-tension relationship)
- degree of stretch of the cell in the ventricle wall
+ determined by the volume of blood within the chamber
- the FORCE OF CONTRACTION is greater when the LV muscle is stretched prior to contraction by increased preload
+ more blood to the heart (preload) , greater tension, greater force generated during systole , greater stoke volume
59
heart rate + preload + frank - starling
slow HR - more time for ventricular filling = more ventricular stretch
high HR - less time for filling, less time for ventricle to expand and stretch = less stretch
60
factors affecting cardiac output
preload - degree of stretch on heart before contraction
after load - resistance heart must pump against
inotropic force - contractility of the heart
chronotropic heart - HR of rate of contraction
61
inotropic force ( force - velocity relationship)
- contractility of the heart muscle or force of contraction
62
preload + inotropy
- further you stretch a rubber band the faster it comes back together the stronger the force
- increasing preload = increase inotropy
63
after load
- resistance to ventricular emptying (arterial hypertension or valvular stenosis)
64
factors affecting after load
- viscosity of blood ( little effect)
- arterial resistance ( thickness of tunica intima)
- vascular geometry (plaque, curves, bifurcation)
- valvular stenosis
65
factors effecting inotropic force
- structural organisation = hypoxic, ischemic, infarcted, fibrosed, infiltrated muscle tissue
* LEADS TO NEGATIVE INOTROPIC RESPONSE LV CANNOT CONTRACT ENOUGH
- medication = digitalis / sympathetic nervous system
* POSITIVE INOTROPIC RESPONSE MAKE IT EASIER FOR LV TO CONTRACT
66
chronotropic force
- heart rate / rate of contraction
| - how fast and how much the walls move inward during systole
67
chronotropic force - sympathetic nervous system
- increases chronotropic force
+ times of stress
+ physical
+ emotional
68
chronotropic force - parasympathetic nervous system
```
- decreases chronotropic force
+ rest
+ beta blockers / calcium
+ being fit
+ meditation and relaxation
```
69
force - velocity relationship
- AN INCREASE IN AFTERLOAD DECREASES THE VELOCITY OF FIBER SHORTENING
- small amount of time for ejection so a decrease in fibre shortening velocity reduces rate of volume ejection so more blood left in ventricle after systole
* INCREASE AFTERLOAD = DECREASED STROKE VOLUME AND CARDIAC OUTPUT
70
relationship summary
length - tension relaionship
+ frank - starling principle / preload
force - velocity relationship
+ inotropic force / contractility / afterload
interval - strength relationship
+ chronotropic force / time for ventricles to fill / starlings P
71
provocative maneuvers
- inspiration increases venous return ( VR) to the right heart
- expiration decreases VR to the right heart
- valsalva reduces VR reducing preload and afterload
- standing decreases VR = gravity pulls blood down into legs
- squatting increases VR = squeezes blood in veins toward the heart
