CHF Flashcards
1
Q
what is the measurement of when is blood ejected from the ventricle
A
when the pressure in the ventricle exceeds the pressure in the aorta
2
Q
what is the measurement of when is blood ejected from the ventricle
A
when the pressure in the ventricle exceeds the pressure in the aorta
3
Q
isovolumetric contraction
A
phase 2
volume isn’t changing in diastolic volume and all four valves are closed
○ Initially: isovolumetric contraction (phase 2) = all 4 valves are closed, no blood is exiting the ventricles, ventricular pressure is building up
4
Q
isovolumetric relaxation
A
isovolumetric relaxation (phase 5) = valves are closed, LV pressure is decreasing, LV volume is staying constant
5
Q
phase 6) at end of heartbeat during ventricular diastole when atrium is also at rest
(ventricle is filling w/o contraction of either chamber)
A
Period of passive filling
6
Q
americans that have CHF
A
a. 5 million
7
Q
most common medicare pt discharge diagnoses
A
CHF
8
Q
PT with severe IV HF have has % chance of mortality in 1yr
A
g. Overall 5 yr survival is 50%
9
Q
HTN increases risk of HF by
A
x2
10
Q
5 yr survival for men with HF
A
25%
11
Q
5 yr survival for women with HF
A
38%
12
Q
how many men in their 50’s and 80’s have HF
A
8/1000
66/1000
13
Q
definition of HF
A
pathogenesis in myocardial contraction
there exists a mismatch between CO and need
14
Q
CO
A
HR x stroke volume
15
Q
a. Defect in myocardial contraction such that heart can’t keep up with metabolic demand. Why does it happen? (3 reasons)
A
i. Pressure overload (elevated SBP)
ii. Volume overload (increased diastolic volume)
- -> dilation of ventricle
iii. Injured myocardium (decrease in myocardial cells)
- -> MI is one of the leading causes of HF
16
Q
MCC of HF
A
DM
Coronary disease primarily
HTN and valve disease (rheumatic fever) improving with detection therapy
17
Q
AA RF for HF
A
greater portion of risk attributed to modifiable factors in AA
smoking
DM
HTN
lower SES more likely to get hF at younger age and overall
18
Q
your body reacts to a reduction in CO in what ways?
A
- myocardial hypertrophy
- increased sympathetic nervous system activity
- fluid retention
19
Q
compensated HF
A
when output meets demand through
physiological responses
20
Q
tachycardia is seen with HF as the result of
A
SNS
21
Q
myocardial hypetrophy will eventually lead to what physiological effects
A
delay filling time (increased to develop maximum tension in dilated myocardial cells)
longer contraction
decreased EF
22
Q
hypertrophy of myocardium leads to what oxygen demand consequences
A
iv. Increases myocardial oxygen consumption (greater O2 demand)
23
Q
SNS seen with HF
A
A. increased HR
leads to decreased diastolic filling time
(also seen slow time with hypertrophy)
b. Greater force of contraction of the heart muscle
24
Q
why do we see low GFR in HF
A
- A fall in cardiac output decreases blood flow to the kidney
a. Prompts release of renin, resulting in increase synthesis of angiotensin II and aldosterone
—–>Increased peripheral vasoconstriction and increased sodium and water retention
25
physiological changes of low CO
when you have low CO you get a back up of fluid, higher pressure, congestion of fluid in the lungs, and edema
26
BNP
vasodilator that responds to stretch receptors
27
BNP and ANP effects
a. One causes fluid loss and one causes fluid retention
b. Both are happening at the same time
i. If volume too high and there is strain on the heart, that is going to cause ANP and BNP to be released
28
IV. Underlying causes of CHF
a. Myocardial injury
i. MI, ischemia, cardiomyopathy, myocarditis
ii. Ischemic heart disease/CAD causes 75% of all CHF
b. Untreated HTN
c. Valvular heart disease
29
V. Precipitating Factors for CHF (you go from compensated to decompensated when there is an increase in demand - metabolic demand goes up or --)
a. Acute infections (eg pneumonia)
b. Arrhythmias will make HF worse
i. Tachyarrhythmia: atrial fibrillation supraventricular tachycardia
ii. Bradycardia or AV block
c. Excess exertion
d. Excess sodium intake b/c causes water retention and causes strain on heart
e. Pulmonary embolus
f. Anemia
i. If less red cell to oxygenate the tissue then lets circulate them faster
ii. If you go to altitude, your HR goes up
iii. You have to work harder to oxygenate
g. Thyrotoxicosis
h. Pregnancy í 50-100% increase in blood volume in a matter of weeks
i. Cardiac toxins (alcohol, chemotherapy agents)
i. ETOH is a vasodilator. How do we treat CHF? With Vasodilators
1. When ETOH wears off, you get a rebound effect and get vasoconstriction so ETOH is a terrible thing for HF pt's
J. fluid overload (iatrogenic)
30
if you're anemic how does your body compensate
Tachy
move the RBC you have faster
31
systolic HF underlying causes
```
ischemia
MI
myocarditis
injury
1. Pressure overload
. Aortic stenosis
Uncontrolled HTN
2. Impaired contractility
MI/Ischemia
Volume overload
i. Mitral and aortic regurgitation
```
something is impairing the wall
32
systolic HF underlying causes
ischemia
MI
myocarditis
injury
something is impairing the wall
33
diastolic HF
not expanding to accommodate volume
| hypertrophy
eg from scar tissue, obstruction or concentric hypertrophy
34
Left ventricular systolic dysfunction
35
Left ventricular systolic dysfunction
36
isovolumetric contraction
phase 2
volume isn't changing in diastolic volume and all four valves are closed
○ Initially: isovolumetric contraction (phase 2) = all 4 valves are closed, no blood is exiting the ventricles, ventricular pressure is building up
37
isovolumetric relaxation
```
isovolumetric relaxation (phase 5) = valves are closed, LV pressure is decreasing, LV volume is staying
constant
```
38
phase 6) at end of heartbeat during ventricular diastole when atrium is also at rest
(ventricle is filling w/o contraction of either chamber)
Period of passive filling
39
americans that have CHF
a. 5 million
40
most common medicare pt discharge diagnoses
CHF
41
PT with severe IV HF have has % chance of mortality in 1yr
g. Overall 5 yr survival is 50%
42
HTN increases risk of HF by
x2
43
5 yr survival for men with HF
25%
44
5 yr survival for women with HF
38%
45
how many men in their 50's and 80's have HF
8/1000
66/1000
46
definition of HF
pathogenesis in myocardial contraction
there exists a mismatch between CO and need
47
CO
HR x stroke volume
48
a. Defect in myocardial contraction such that heart can't keep up with metabolic demand. Why does it happen? (3 reasons)
i. Pressure overload (elevated SBP)
ii. Volume overload (increased diastolic volume)
- -> dilation of ventricle
iii. Injured myocardium (decrease in myocardial cells)
- -> MI is one of the leading causes of HF
49
MCC of HF
DM
Coronary disease primarily
HTN and valve disease (rheumatic fever) improving with detection therapy
50
AA RF for HF
greater portion of risk attributed to modifiable factors in AA
smoking
DM
HTN
lower SES more likely to get hF at younger age and overall
51
your body reacts to a reduction in CO in what ways?
1. myocardial hypertrophy
2. increased sympathetic nervous system activity
3. fluid retention
52
compensated HF
when output meets demand through
| physiological responses
53
tachycardia is seen with HF as the result of
SNS
54
myocardial hypetrophy will eventually lead to what physiological effects
delay filling time (increased to develop maximum tension in dilated myocardial cells)
longer contraction
decreased EF
55
hypertrophy of myocardium leads to what oxygen demand consequences
iv. Increases myocardial oxygen consumption (greater O2 demand)
56
SNS seen with HF
A. increased HR
leads to decreased diastolic filling time
(also seen slow time with hypertrophy)
b. Greater force of contraction of the heart muscle
57
why do we see low GFR in HF
1. A fall in cardiac output decreases blood flow to the kidney
a. Prompts release of renin, resulting in increase synthesis of angiotensin II and aldosterone
----->Increased peripheral vasoconstriction and increased sodium and water retention
58
physiological changes of low CO
when you have low CO you get a back up of fluid, higher pressure, congestion of fluid in the lungs, and edema
59
BNP
vasodilator that responds to stretch receptors
60
BNP and ANP effects
a. One causes fluid loss and one causes fluid retention
b. Both are happening at the same time
i. If volume too high and there is strain on the heart, that is going to cause ANP and BNP to be released
61
IV. Underlying causes of CHF
a. Myocardial injury
i. MI, ischemia, cardiomyopathy, myocarditis
ii. Ischemic heart disease/CAD causes 75% of all CHF
b. Untreated HTN
c. Valvular heart disease
62
V. Precipitating Factors for CHF (you go from compensated to decompensated when there is an increase in demand - metabolic demand goes up or --)
a. Acute infections (eg pneumonia)
b. Arrhythmias will make HF worse
i. Tachyarrhythmia: atrial fibrillation supraventricular tachycardia
ii. Bradycardia or AV block
c. Excess exertion
d. Excess sodium intake b/c causes water retention and causes strain on heart
e. Pulmonary embolus
f. Anemia
i. If less red cell to oxygenate the tissue then lets circulate them faster
ii. If you go to altitude, your HR goes up
iii. You have to work harder to oxygenate
g. Thyrotoxicosis
h. Pregnancy í 50-100% increase in blood volume in a matter of weeks
i. Cardiac toxins (alcohol, chemotherapy agents)
i. ETOH is a vasodilator. How do we treat CHF? With Vasodilators
1. When ETOH wears off, you get a rebound effect and get vasoconstriction so ETOH is a terrible thing for HF pt's
J. fluid overload (iatrogenic)
63
if you're anemic how does your body compensate
Tachy
move the RBC you have faster
64
impaired ejection of blood as a result of poor contractility
systolic HF
65
systolic HF underlying causes
ischemia
MI
myocarditis
injury
something is impairing the wall
66
diastolic HF
not expanding to accommodate volume
| hypertrophy
eg from scar tissue, obstruction or concentric hypertrophy
67
how do you measure EF
echo
68
Left ventricular systolic dysfunction
69
underlying causes of diastolic HF
1. Ventricular hypertrophy
2. Hypertrophic cardiomyopathy
3. Restrictive cardiomyopathy
Fibrosis, infiltration
4. Transient ischemia
5. Obstruction of ventricular filling
Mitral stensos
Pericardial constriction (scarring,
effusion, tamponade)
70
abrupt onset of left sided HF could be
MI
71
signs and sxs of left sided HF
i. Pulmonary congestion or edema, orthopnea, exercise intolerance, paroxysmal nocturnal dyspnea, dyspnea on exertion
1. Reflects accumulation of fluid upstream to affected ventricle
72
c. Increased venous pressures can develop more easily on the____ side because
left side Venous capacity of the pulmonary system is smaller than that of the systemic venous system
73
right sided HF signs and sxs
i. Peripheral edema, ascites, congestion liver
74
pulmonary causes of right sided HF
Cor pulmonale (restrictive dz of the lung where you can't feel the lung and have afterload of the heart which fails), pulmonary embolus with shunt, COPD, valvular disease
75
GI complaints and cyanosis are seen with
right sided HF
76
why do we see limited urine output in HF
Low output failure
hypoperfusion problem; there is low CO, don't make much urine b/c not perfusing kidneys
77
pulse pressure
difference between systolic and diastolic
78
caused by a hyperactive circulatory condition like anemia leads to this type of HF
X. High output failure
79
High output failure can be due to
your body is trying, you are trying to circulate blood more frequently but your CO still does not match demand and so that's technically HF
i. Examples: anemia, thyrotoxicosis, pregnancy, Paget's dz of bone, AV fistula (pt shunting blood directly from the arterial system to the venous system and is not oxygenating tissues)
80
signs and sxs of high-output failure
i. Warm, flushed skin, bounding pulse, arterial-venous oxygen difference is normal in ABG
81
a. Backward failure
i. Transmission of increased pressure backward (upstream) to the venous system draining into a ventricle
82
example of backward failure (backing up pressure into pulmonary circuit)
ii. Example: pulmonary HTN
| 1. Increased LV diastolic pressure and LA pressure lead to pulmonary venous pressure, transmitting pressure backward
83
if forward failure from left ventricle
not great profusion, can lead to altered mental status
84
1. Altered mental status from decreased cerebral perfusion
2. Fatigue, weakness from decreased skeletal muscle perfusion
3. Edema from decreased renal perfusion
Sodium and water retention
Venous congestion
are all seen with forward or backward HF
forward
Inadequate cardiac output (systolic failure)
85
definition Jugular venous distention
(over 4cm above sternal angle with patient lying at 45 degrees)
86
lung exam findings in pt with HF
v. Crackles at bases of lungs or throughout lung fields from the excess volume
87
cardiac PE on pt with HF
iii. Tachycardia (heart is working harder to move that volume), S3 gallop. S4 may be present if decreased ventricular compliance particularly if the heart failure is only on one side b/c the valves on one side don't match valves on the other side
88
Class I HF
- Heart disease present, but without limitation of physical activity
i. Nobody is a Class I HF b/c they don't have sx
By the time they come in and have sx
they are automatically class II or higher
89
Class II
slight limitation of physical activity, symptoms on significant exertion
i. Only notice it when they really try to exert themselves
90
Class III
Marked limitation of physical activity; less than ordinary activity leads to symptoms
climb the stairs and super winded
91
Class IV
Symptoms at rest
92
ECG findings
i. Sinus tachycardia usually present
ii. Atrial enlargement (when the P wave gets wide) may be present
iii. LVH or RVH may be present
1. If V1 and V2 have more than 35 boxes of QRS then they probably have LVH
iv. Conduction delays, such as left bundle branch block may be present
1. Changing the architecture of the heart by making it bigger
93
CXR
i. Cardiomegaly
ii. Upper lung redistribution of flow (cephalization - dilation of vessels in the upper parts of the lungs)
iii. Interstitial fluid (if pulmonary edema present)
iv. Kerley B lines = HALLMARK
v. Pleural effusion
94
Labs
i. Elevated BNP
| 1. B-type natriuretic peptide
95
Pts with known LVSD have BNP
o BNP 80 - 200 (uncertain clinical significance).
96
Elevated BNP may also result from:
o PE.
o Lung CA.
o Pulmonary TB.
97
ABG findings
" Hypoxemia.
| " Respiratory acidosis.
98
BMP or CMP findings
Hyponatremia.
Elevated liver enzymes, especially AST if liver is congested
99
ECG
Sinus tachycardia usually present.
Atrial enlargement (wide P wave) may be present.
LVH or RVH may be present.
Conduction delays may be present (ex. LBBB)
Cardiomegaly.
Upper lung redistribution of flow (cephalization).
100
De Rosa: fave indicator of HF on a Ekg
35 boxes height of QRS complex V1/V5 or V2/V6 (still note 100% accurate)
101
shock
Extreme version of HF
| Life threatening condition of hypoperfusion and hypoxia.
102
cardiogenic shock criteria
" Low output condition.
| " SBP < 90 mm Hg for 30 minutes with adequate volume (i.e., not hypovolemic).
103
types of shock
o Hypovolemic - hemorrhaging
o Anaphylactic - allergic reaction í vasodilation
o Septic - infection í widespread vasodilation
o Cardiogenic.
104
pump failure leading to HF
Caused by lactic acidosis
NA/K pumps don't work well
Become hypoxic
p
