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Flashcards in CHF Deck (46)
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1
Q
LV failure
A
Symptoms due to low cardiac output and congestion, including dyspnea
2
Q
Optimal management for LV failure includes
A
ACE-I/ARB, BB, aldosterone inhibitors
3
Q
RV failure
A
cor pulmonale or more likely due to LV failure

symtoms: peripheral congestion
4
Q
High-output heart failure is a heart condition that occurs when the cardiac output is higher than normal, examples are:
A
beri beri (nutritional deficit in vitamin B1 (thiamine), and hyperthyroidism
5
Q
Causes of systolic CHF
A
-Ischemic cardiomyopathy
-HTN
-hypo/hyperthyroid
-HIV
-ETOH
-viral
-dilated
-cardiotoxins
-infectious (Chagas)
-hemochromatosis
-sarcoid, amyloid
-valvular
-tachycardia-mediated
-peri-partum
6
Q
Causes of diastolic CHF
A
-HTN
-hypertrophic
-restrictive
-DM
-pericardial disease
-aging (causes diastolic heart failure)
7
Q
Neurohormonal activation is partially responsible for ________
A
mechanical changes in heart failure
8
Q
Vasopressin secretion-
A
promotes water absorption by kidney
9
Q
Renin-angiotensin-aldosterone axis (RAAS)
A
-maintains cardiac output (CO) and tissue perfusion
-stimulates arterial vasoconstriction with angiotensin II
-expands intravascular volume with Na+ and water retention
10
Q
Left ventricular end diastolic pressure (preload right before cardiac output) is important when patient may have heart failure and is presenting with
A
SOB

-Need to know if LVEDP is high or low
-LVEDP is the last pressure right before it pumps blood out to body
11
Q
If LVEDP is high, _______
A
will have congestion and backing up into lungs

LVEDP is about the same as central venous pressure and jugular venous pulsation
Need to know if they’re “wet” (congested, fluid overload) or “dry” (Euvolemic, fluid status is stable, SOB from lung problems)
12
Q
Decreased CO leads to increased HR, increased contractility, vasoconstriction (all raise bp, increase CO)
Low CO also causes increased renin angiotensin, increased ADH and blood volume
Problem with this, you’ll have __________
A
pulmonary edema
13
Q
Classification by
A
stages A-D

(NYHA uses FC class 1-4)
14
Q
general S/S and physical exam findings
A
Tachycardia, Palpations, S3/S4, S3 indicates systolic dysfunction, murmurs, HJR (hepatojugular reflex, press on liver, may see increase in jugular venous pressure), JVP, edema
15
Q
Labs
A
-BNP (BNP becomes physiologically elevated, increases in response to left vent wall stress increase, triggers atrium to release ANP)
16
Q
What do you use to assess LV function?
A
Echo (best way overall, no radiation, easy), MUGA (Multi Gated Acquisition Scan-BEST WAY to look at EF, intervention), angiogram
17
Q
Treatments
A
Target any potential reversible causes (CAD, tachycardia, ETOH, etc..)
18
Q
When do you biopsy?
A
-if pt has acute fulminant myocarditis (pt comes in with flu like illness and then crash, have arrhythmias, pt needs biopsy to rule out giant cell myocarditis, worst type but is treatable)

-Acute presentation (symptoms are new and just started), hemodynamic compromise at initial presentation, new AVB, VT
19
Q
S/S of CHF caused by venous congestion (right sided)
A
-hepatomegaly
-ascites
-pleural effusion--> edema, jugular venous distension
20
Q
S/S of CHF caused by low cardiac output
A
-fatigue/low energy
-pallor
-sweating
-cool extremities
-poor growth
-dizzy
-altered consciousness
-syncope
-tachypnea, nasal flaring/grunting (indicates left sided)
-retractions; pulmonary edema
21
Q
Other etiologies of CHF
A
-Infectious myocarditis
-Dilated cardiomyopathy
-Tako-Tsubo (apical ballooning)
-Hypertrophic
-Restrictive
-Drug induced (chemo/toxic)
22
Q
Dilated cardiomyopathy
A
ARVD (arrhythmiogenic RV dysplasia also called Uhl Cardiomyopathy; fattiness of R vent and can lead to death in young people), non-compaction (massive trabeculation;
tx: defibrillator)
23
Q
Tako-Tsubo (apical ballooning)
A
Stress cardiomyopathy; typically in females, older, emotional stress can trigger sympathetic surge, hypercontratility of base of left vent and base will dilate (balloon), must rule out coronary disease; usually reversible
24
Q
Hypertrophic heart
A
CHF and risk of sudden death (at risk for myopathy, put defibrillator on heart); hypertrophy of left vent, blood cant get out
25
Q
Diastolic heart
A
-“little old lady heart”; very small, has low volume
-SOB; LVEDV is low; JV distension; edema (reflected with elevated central vein pressures)
-BNP increases (EF is greater than 45)

*NOTHING REDUCES MORTALITY- NO MEDS TO IMPROVE MORTALITY FOR DIASTOLIC; little bit of lasix, try and lower BP, but still wont decrease mortality*
26
Q
Systolic heart
A
-heart is dilated, it’s very big; has many liters of volume
-SOB; LVEDP is low; JV distension; edema (reflected with elevated central vein pressures)
-BNP increases because of stretch, wall tension, vol or P, whatever makes left V work harder; If you hear S3 its systolic (EF is less than 45)

*LOWER MORTALITY FOR SYSTOLIC: ACE inhibitors, ARBs, beta blockers (metropalol or carbatolol only); aldosterone antagonists*
27
Q
If you hear an S3 the problem is
A
systolic (Not diastolic)
28
Q
EF, ejection fraction is less than _______ you GET A DEFRIBILATOR, ICD (implantable cardioverter defibrillator)
A
35
29
Q
What can be used in African Americans to reduce mortality?
A
hydrolazine nitrate combo reduces mortality
30
Q
Besides S3, only way you can tell the difference (systolic vs diastolic) is _______
A
from an Echo (can’t rely on S/S because they’re the same)
31
Q
1. Heart failure presentation (clinical)- Patient comes into ER presenting with
A
SOB, sitting upright, JVP is to mandible, cool, clammy, sweaty, respiratory distress and edema

-Patient is probably in heart failure, appears that they aren’t profusing well
32
Q
2. Heart failure presentation (clinical)- First drug to give a patient like this?
A
Give Lasix (IV, not PO) immediately
33
Q
3. Heart failure presentation (clinical)- O2 sat is 91%, give O2 also
In triage, patient with SOB should have EKG, it shows
A
No ST elevation indicating MI, so you know its not a stmi
34
Q
4. Heart failure presentation (clinical)- BP is 190/100, patient is not on any medications, patient probably has an S3 but they are very hard to hear. Do a Chest Xray and see
A
cardiomegaly and pulmonary vascular congestion
35
Q
Need to lower BP: Imodapine is a
A
CA blocker for long term BP management
36
Q
You CAN'T use Imodapine for 1st time acute decompensated heart failure if pt __________
A
isn't on a beta blocker (Metropalol) already
-can give it to them once they are stabilized, so DON'T give when they 1st come into ER if they arent already on a B-blocker
37
Q
What can you give patient first to lower BP?
A
Nitroglycerine drip- can use this; it's a venodilator, some vasodilation, dilates pulmonary vessels, preload decreases, pulmonary congestion decreases, afterload decreases some, this clears up congestion and decrease BP
38
Q
Additional treatment
A
Noninvasive ventilation with BiPAP machine, measure output carefully so may use foley cath
39
Q
During CHF, EKG may show
A
QRS duration > 120
LBBB
Abnormal QS pattern
Broad R wave with deep S wave and inverted T wave
40
Q
Frank Starling Curve shows that
A
stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end diastolic volume) when all other factors remain constant
41
Q
LVAD (Left Ventricular Assist Device) is a treatment method that
A
sucks blood out of left vent and dumps it back into aorta; takes the place of your left vent
-Bridge in between transplantation, end of life care, etc.
42
Q
OMM treatments
A
1. Lymphatic Pump: fluid mobilization
2. Diaphragmatic Techniques: abdominal and thoracic
3. Effluerage: mobilize peripheral fluid
4. Clavicular releases: promote thoracic duct drainage
5. CV4: fluid homeostasis and decrease stress
6. OA, thoracics, lumbar, Chapman pts, fascia
43
Q
2 types of dilated cardiomyopathies are
A
1. Systolic Dysfunction
2. Eccentric hypertrophy (sarcomeres added in series)
44
Q
Causes of dilated cardiomyopathies
A
-ETOH
-chronic cocaine
-beri-beri (lack of vitamin B1/thiamine)
-coxsackie virus
-chagas (tropical parasitic disease)
-doxorubicin (chemo for cancer)
-hemochromotosis (iron overload)
-sarcoid
-peripartum-(PPCM) is a form of dilated cardiomyopathy that is defined as a deterioration in cardiac function presenting typically between the last month of pregnancy and up to six months postpartum; heart muscle can't contract forcefully enough to pump adequate amounts of blood to the body
45
Q
Hypertrophic Cardiomyopathy
A
-60-70% inherited as auto dominant
(Beta-myosin heavy-chain mutation)
-Can be a/w friedrich ataxia
-Syncope during exercise and sudden death in athletes due to VT
-Tx: cessation of high-intensity athletics
(BB, CCB, ICD if high risk)
46
Q
Examples of Restrictive/infiltrative cardiomyopathy
A
-Sarcoid
-amyloid
-postradiation fibrosis,
-Loffler (endocardial fibroelastosis w/ eosinophilic infiltrate)
-hemochromotosis (dilated can also occur)