Heart Failure Flashcards
1
Q
The the heart receives normal venous return but has an unexpected CO, what can be assumed?
A
Something is wrong with the heart itself
2
Q
What is used to measure venous return?
A
Right atrial pressure
CVP
3
Q
What is hypereffetive heart?
A
Higher CO than expected
4
Q
What is hypoeffective heart?
A
Lower CO than expected
5
Q
How can a heart become hypereffective?
A
SNS stimulation -increases contractility -increases HR Healthy hypertrophy -conditioning -healthy resting bradycardia Decreased after load with stable BP
6
Q
How can a heart become hypoeffective?
A
SNS inhibition PNS stimulation - vagal decreases HR Dysrhythmia Valve Dz Increased afterload Myocardial dysfunction
7
Q
What explains a low CO?
A
Hypoeffective heart
Decreased Venous return
8
Q
What explains decreased venous return?
A
Decreased blood volume
Obstructive
Distributive
9
Q
What decreases total blood volume?
A
Hemorrhage, hypovolemia
10
Q
What are some causes of obstruction to venous return?
A
Gravid uterus
Tumor
Cardiac tamponade
11
Q
What causes altered distribution of blood volume?
A
ACUTE vasodilation
Sudden increase in venous capacitance
Hypotension
12
Q
What causes high CO?
A
Hypereffective heart Chronic reduction in SVR -hyperthyroidism > incr metabolism > incr BF > peripheral vasodilation -certain Vit B deficiencies (Beriberi) -sepsis
13
Q
What is the relationship between CO and SVR?
A
Inversely related
14
Q
What does a sudden drop in SVR do to CO?
A
Decreases CO
-it allows blood to pool, so decreased venous return
15
Q
What initial effect does increased volume have on a euvolemic patient?
A
Initially it increases venous return and therefore SV
-this does not last long
16
Q
What happens after the initial increase in SV when volume is given to a euvolemic patient?
A
Venous reservoirs are filled
Autoregulated tissues vasoconstriction to reduce incoming volume
Volume returning to RA trigger reflexes
-increased RBF = increased UOP
-Decrease ADH release
-Bainbridge reflex > increased HR
-low pressure receptors >vasodilation to help reduce BP response to incr volume
Increased capillary pressure exudes fluid into interstitial space
17
Q
How is CO measured?
A
Healthy: right atrial pressure, CVP
Unhealthy: pulmonary artery catheter, PCWP, thermodilution
18
Q
When does diastolic step up occur on PA catheter insertion?
A
When catheter enters the pulmonary artery
19
Q
What is the gold standard for CO reading?
A
PCWP with PA catheter
20
Q
What preexisting heart condition must be considered before placing a PA catheter? Why?
A
LBBB
Conduction to the left ventricle is blocked, if conduction to the right ventricle is affected by catheter insertion you can cause complete heart block
21
Q
What West zone should a PA catheter be sitting in? Why?
A
West Zone 3
It has the most blood flow, so it is the most accurate
22
Q
How can you tell if the PA catheter tip is in Zone 3?
A
The PCWP should be the same or less than the pulmonary artery diastolic pressure
23
Q
What does a big wave mean on PA catheter reading about CO?
A
Big wave mean it takes longer for the temperature change, which means slower blood flow, which means a low CO
24
Q
If too much injectate is used for PA catheter thermodilution, how will this affect the result?
A
Too much injectate means it will take longer for the temperature change, which will give a false low CO reading
25
How will too small a volume of injectate affect the PA catheter reading for thermodilution test?
Too small a volume will have a rapid temperature change and give a false high CO result
26
How can preload be measured in a healthy heart? How is this different from an unhealthy heart?
Healthy heart: right atrial pressure, CVP
| In an unhealthy heart the venous return may no longer reflect preload, a PCWP would be more appropriate
27
What does Frank Starling mean SV?
That SV is dependent upon preload
28
What determines preload?
Venous return
29
What can be used to guide fluid administration?
CVP
30
Because a hypoeffective heart can’t keep up with venous return, what is a better measurement of CO?
LVEDP
LVEDV
PAC - PCWP
31
In hypoeffective heart, preload contains the venous return and what?
The volume remaining in the LV after systole (ESV) accumulates with each contraction since it is not able to eject a normal EF
32
What measurements can you get with an arterial/peripheral venous hemodynamic monitor?
CO
Preload
Contractility
33
What measurements can you get with an esophageal Doppler?
CO
| SV
34
What is cardiac index? Equation? Normal range?
CO adjusted for body size
CI = CO/BSA
Normal range: 2.5-4.2 L/min/m^2
Average CI is 3 L/min/m^2
35
What is the most common clinical measure or systolic function?
Ejection Fraction
36
List 2 equations for EF
((LVEDV-LVESV)) / LVEDV) x 100
(SV/LVEDV) x 100
37
If systolic function is a measure of ventricular ejection, what is diastolic function a measure of? How is it measured?
Ventricular filling
| TEE: transmittal flow measures
38
What besides EF is a measure of the strength of heart?
SVO2
39
What is SVO2
The saturation of oxygen in the venous blood
40
Where is an SVO2 sample obtained?
The pulmonary artery
41
What is SVO2 the best determination of?
Adequacy of CO
42
What influences SVO2?
Anemia
| Hypoxia
43
What is cardiac work?
How much work is done to move blood out of the heart
| Work = force x distance
44
How is cardiac work calculated?
Cardiac work = SV x aortic pressure
45
How can you visualize cardiac work?
The area in the ventricular volume loop
- bigger area means more work
- small area means less work
46
What is one of the strongest predictors for peri operative cardiac complications?
Active CHF
47
What is active CHF?
Symptomatic
48
What is the problem in heart failure
Forward pumping
| Decreased forward flow
49
Where does the volume go in HF?
It backs up
- LA
- Lungs
- Right heart
- Periphery
50
What is acute HF?
Decreased forward flow
51
What are the causes of acute HF?
Diminished contractility
Valvular disease
Disease of the muscle
External pressure
52
What are the symptoms of acute HF?
```
Hypotension
Cool, mottled skin
Nausea
SOB
Fatigue
```
Signs of poor perfusion
53
What causes initial compensation with a sudden event leading to HF?
Initial compensation is by SNS stimulation
- increased contractility (by increased preload)
- increased HR (reflexes)
- increased venous return (by decreasing venous capacitance)
Initially venous return stays the same by CO decreases
54
What happens if decreased CO decreases RBF?
Not enough RBF for the kidneys to make urine
| The kidneys retain fluid
55
How does the kidneys retaining fluid volume help?
Overtime the fluid increases venous return, which increases CO
When RBF is restored and UOP resumes, this is long term compensation
56
What determines if someone can maintain long term compensation?
If the fluid retained by the kidneys is enough to restore CO enough to restore RBF
57
HF compensation is determined by the relationship of what 2 things?
CO and renal function
58
What EF is found in patients with compensated HF?
30-50%
59
In order for a compensated HF patient to maintain CO and renal function, what measurement is elevated?
Right atrial pressure
60
Why is compensated HF patient’s RAP higher?
Increased venous return
61
What happens with HF if renal fluid retention can’t restore RBF?
Decompensated HF:
- excessive fluid accumulation
- pulmonary edema
- hypoxemia
- peripheral edema
62
Decompensated HF is seen typically with what EF?
<30%
63
Does a patient with decompensated HF have elevated RAP?
Yes, but CO is still not enough to restore RBF
64
What happens when Frank Starling mechanism has reached it’s limit?
Increasing preload no longer increases SV and decompensated HF ensues
65
How do patients with compensated chronic HF handle normal activity? What about stress or lots of activity?
```
Normal activity: pretty well
Stress or lots of activity: they become symptomatic because their CO is no longer enough
-hypotension
-fatigue
-cool, mottled skin
-SOB
-Nausea
```
66
Decompensation under stress is due to what?
Decreased cardiac reserve
67
What is cardiac reserve?
The ability to increase CO over normal
68
How is cardiac reserve assessed?
By activity tolerance
- Hx
- Stress test
69
What is another name for ventricular function curves
Frank Starling Curves
70
What relationship do ventricular function curves show?
Filling pressure to pumping ability
| -cardiac performance
71
What is on the horizontal axis of a ventricular function curve?
Filling pressure
- RAP
- CVP
- PCWP
- LVEDP
- PAD (pulmonary artery diastolic pressure)
72
What is on the vertical axis of a ventricular function curve?
Pumping ability
- CO
- SV
73
What is ultimate decompensated HF?
Cardiogenic shock
74
What volume is preload?
LVEDV
75
With poor ejection, what happens to LVEDV?
It accumulates with each contraction
76
What is optimal filling pressure?
The pressure at which the best preload is created for the best cardiac performance
77
How can you decrease preload?
Diuretics
| Venodilators
78
What is “unloading the heart”?
Decreasing afterload
79
Why is saying “increase contractility” just a clinical statement?
Because we can not technically alter contractility, it’s Inotropy we can manipulate
80
How can you increase contractility?
Inotropes
| Afterload reduction
81
Which does NTG dilate more, veins or arteries?
Veins
82
NTG decreases, preload or afterload?
Preload
83
Which does Nipride dilate more, veins or arteries?
Arteries
84
Nipride decreases, preload or afterload?
Afterload
85
Nipride AKA?
Sodium Nitroprusside
86
What on the ventricular function curves shows optimum filling pressure?
The point on the curve
87
To maintain optimum filling pressure what is manipulated? With?
Preload
Volume, diuretics, venodilation
88
What describes contractility on a ventricular function curve?
The position of the curve
89
To affect contractility what is manipulated? With?
Afterload
Arterial dilation
Inotropes
90
In left-sided HF, where does blood accumulate?
Lungs
| Progresses to right side, peripherally
91
An MI where will significantly affect LV muscle
Anterior wall
92
Where does blood accumulate in right-sided HF?
Veins and tissues
| -neck vein dissension, hepatomegaly, peripheral edema etc
93
What is right-sided HF as a consequence of lung disease called?
Cor pulmonale
94
Can HF occur without poor CO?
Yes. High output cardiac failure
95
What is HF without poor CO?
High output cardiac failure
- pumping isn’t the problem
- heart is overcome with excessive volume and can’t keep up
96
List 2 examples of condition that lead to high output cardiac failure
Hyperthyroidism
| Beriberi
97
What is usually the cause of increased CO?
Chronic decreased SVR
98
When tissues are suffering from poor perfusion and necrosis, this is called?
Cardiogenic shock
99
All forms of CHF have what?
Fluid retention
100
What is activated when RBF is decreased?
Activation of Renin-Angiotensin System and increased Aldosterone secretion
101
What is released by the heart to try and diurese this retained fluid?
Atrial Natriuretic Factor
| -ANF
102
What does atrial stretch do to increased venous return trigger?
```
Low pressure receptors (in atrial and pulmonary arteries)
-send impulse to vasomotor center
-to vasodilate
RA Stretch
-increases RBF, ANF and decreases ADH = increase UOP
RA Stretch
-incr HR via SA node stretch
-incr HR via Bainbridge reflex
```
103
Why is cardiogenic shock a vicious cycle?
Low CO > low coronary perfusion > heart gets weaker > infarct extends > progressive failure > progressive shock
104
What is the presentation of compensated HF?
Asymptomatic
- good perfusion (at rest)
- filling pressures elevated
- increased circulating volume
- decreased cardiac reserve
105
Presentation of decompensated HF?
```
Pulmonary edema
Dyspnea
Rales
Tachycardia
Peripheral edema
```
106
What is the number 1 CV risk factor for non cardiac surgery?
Active CHF
107
What makes CHF active?
Decompensation
108
What is HF? What causes HF?
Reduced ability of the heart to pump enough blood to meet body’s need.
Usually caused by decreased contractility resulting from diminished BF of coronaries
-damaged valve
-external pressure
-Vit B deficiency
-primary cardiac muscle disease
109
What 2 main effects occur with acute severe myocardial damage?
Reduced CO
| Damming of blood in veins
110
What SNS reflexes compensate during acute cardiac failure?
```
Baroreceptor reflex
Chemoreceptors reflex
CNS ischemic reflex
Reflexes that originate in the damaged heart
-Bainbridge reflex
-
```
111
What does SNS stimulation do to vascular tone? What does this do?
```
Increases it (constriction)
Mobilizes venous blood to increase venous return > rise in systemic filling pressure
```
112
What 2 stages characterize the prolonged semi-chronic state of cardiac failure?
Retention of fluid by the kidneys
| Varying degrees of recovery of heart itself over weeks to months
113
How does fluid retention by the kidneys increase venous return and therefore CO?
Increases blood volume
- increases the mean systemic filling pressure
- distends veins which reduces the venous resistance
114
What happens when the heart’s pumping capacity is reduced?
CO drops and RBF becomes too low for kidneys to excrete enough salt and water, fluid retention ensues, if retained fluid is not enough to restore RBF to make urine retention continues, volume no longer has a beneficial effect and edema occurs
115
In severe cardiac failure, extreme excess fluid causes:
Increased workload on damaged heart
Overstretching heart, further weakening it
Filtration of fluid into lungs > pulmonary edema and hypoxemia
Edema in most parts of the body
116
What happens during the natural reparative process?
Collateral blood supply penetrates peripheral portions, can cause muscle to function again
Undamaged portions of muscle hypertrophy to offset damaged parts
117
After partial recovery, what happens to RBF and retention of fluid?
Once CO is restored so is RBF and fluid is no longer retained. Except for the fluid already retained continues to maintain a moderate excess of fluid
118
What happens in decompensated HF?
Compensation by SNS and fluid retention are unable to restore enough CO to perfuse kidneys, so they continue to retain fluid which continues to increase RAP. Eventually the overstretched and edematous heart function no longer increases by declines
119
Clinically, how can one detect decompensation?
Progressing edema, especially pulmonary edema
- dyspnea
- Rales
120
Treatment for decompensation
Strengthen heart
-cardiotonic drugs
Diuretics
-to increase kidney excretion of salt and water
121
MOA of cardiotonic glycosides like Digitalis
Strengthens heart contractions by increasing quantities of Ca+ in muscle fibers
122
What is more common, left or right sided HF?
Left
123
What does severe acute cardiac failure do to peripheral capillary pressure?
Initially capillary pressure falls (17 to 13mmHg)
| -this explains why it almost never causes immediate development of peripheral edema
124
Causes of reduced renal output of urine during cardiac failure?
Decreased GFR
Activation of Renin-Angiotenin system and increased reabsorption
Increased Aldosterone secretion
Activation of SNS
125
Why does a decrease in CO decrease glomerular pressure?
Reduced arterial pressure
| Intense SNS constriction of the afferent arterioles of the kidney
126
Reduced BF to the kidneys causes increase in secretion of what?
Renin > increased Angiotensin II > acts on arterioles of the kidney to decrease BF more which reduces peritubular capillary pressure promoting increased reabsorption
127
What 2 mechanism increase aldosterone secretion in chronic HF?
Mainly from Angiotensin II, but also from excess K+
128
What effects occur with secretion of Aldosterone in HF?
Aldosterone further increases reabsorption of Na from the renal tubules
-which secondarily increases water reabsorption, and ADH secretion is elicited
129
What effect does SNS stimulation play in retention of fluid by the kidneys?
Constriction of renal afferent arterioles > decreased GFR
Stimulation of renal tubule reabsorption by activating alpha adrenergic receptors on the tubular epithelial cells
Stimulation of RAAS
Stimulation of ADH release from posterior pituitary
130
What is atrial natriuretic factor? What is it’s effect?
| Peptide
A hormone released by the atrial walls in response to stretch.
It has a direct effect on the kidneys to increase excretion of water and salt
131
What is cardiac reserve and what is the normal range in health hearts?
The maximum % that CO can increase above normal.
| 300-400%
132
What blood test can provide an estimate of the adequacy of CO?
SVO2
133
Norepinephrine enhances contractility primarily via activation of what receptor?
Beta 1
134
What depresses myocardial contractility?
```
Hypoxia
Acidosis
Depletion of catecholamines
Loss of functioning muscle mass
Large doses of most anesthetics and antiarrhythmics
```
135
How does stenosis of an AV valve reduce SV?
By decreasing ventricular preload
136
How does stenosis of an SL valve reduce SV?
By increasing ventricular afterload
137
How does valvular regurgitation reduce SV?
By allowing back flow
138
When is EF not an accurate measure of ventricular contractibility?
Mitral insufficiency
139
How does a health heart respond to increased venous return?
Increased SV
140
What could make a heart hypoeffective?
Loss of muscle mass
Valve disease
Dysthymia
141
What could make a heart hypereffective?
SNS stimulation
| Aerobic conditioning
142
How does increased afterload affect the heart?
This increases resistance to ejection and can decrease SV. A healthy heart can keep up if it’s not too excessive.
143
How does decreased afterload affect the heart?
This decreases resistance to ejection, but vascular tone matters. If afterload is decreased with vasodilation, then venous return is decreased and therefore so is SV
144
How can decreased resistance lead to increased SV?
By augmenting the circulating volume, “fill the tank”
145
Other than hypoeffective heart, what are other causes of decreased SV?
Decreased venous return: loss of volume, venodilation, obstruction
146
What can you give to decrease preload?
Diuretics
| Venodilators
147
What if CHF persists with optimal filling pressure?
You need to increase contractility
- inotropes
- decrease afterload: arterial vasodilators, IABP
148
Causes of systolic HF?
CAD
Dilated cardiomyopathy
Chronic pressure overload (aortic stenosis, chronic hypertension)
Chronic volume overload (regurgitative valve, high output heart failure)
149
A patient with LBBB and systolic HF is at high risk for?
Sudden death
150
Causes of Diastolic HF?
Ischemic heart disease
Long standing systemic hypertension
Progressive aortic stenosis
151
Most common causes of low output heart failure?
```
CAD
Cardiomyopathy
Hypertension
Valvular disease
Pericardial disease
```
152
Causes of high output HF?
```
Anemia
Pregnancy
AV fistula
Severe hyperthyroidism
Beriberi
Paget’s disease
```
153
What drugs are used in treatment of systolic HF?
```
Inhibitors of RAAS
-ACE inhibitors
-ARB
-Aldosterone antagonists
Beta blockers
Statins
Diuretics
Vasodilators
```
154
How are ACE inhibitors beneficial in HF?
Vasodilation
Reduce Na and water retention
Support K+ conservation
Decrease ventricular remodeling and potentially reverse
155
What affect do beta blocks have in HF treatment?
Reverse the harmful effects of SNS activation in HF
-with down regulation of B receptors, circulating catecholamines increase
-high plasma levels of NE are directly cardiotoxic and promote myocyte necrosis
Increase the EF
Decrease ventricular remodeling
156
What effect do statins have in HF treatment?
Anti inflammatory and decrease lipids
157
What role do diuretics play in HF treatment? Which are recommended?
```
Relieve circulatory congestion
-pulmonary edema
-peripheral edema
Diuretic induced decreases in ventricular diastolic pressure will decrease diastolic wall stress
Thiazides and Loops
```
158
What treatment is available for diastolic HF?
Low Na diet
Cautious use of diuretics to relieve congestion without excessive decrease in preload
Maintenance of NSR
Correct precipitating factors like ischemia or hypertension
