Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Clinical 2.0 > Chronic Heart Failure > Flashcards

Chronic Heart Failure Flashcards

(101 cards)

Start Studying
1
Q

what is heart failure

A

clinical syndrome with subsets of conditions due to cardiac dysfunction
occurs when heart is unable to deliver adequate supply of oxygenated blood to meet metabolic demands of the organ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what causes decreased contractility

A

rheumatic heart disease
cardiomyopathy
coronary heart disease/mi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what causes increased afterload

A

hypertension

aortic stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what causes increase preload

A

increased sodium/water retention
malfunction of aortic valve
drugs - nsaids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

causes of heart failure

A 
decreased contractility 
increased afterload 
increased preload
direct cardiotoxic drugs
high output failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is cardiac output

A

SV x HR

volume of blood pumped by the heart per minute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is ejection fraction

A

fraction of blood ejected from LV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

define preload

A

degree of filling from the left atrium (venous return)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

define afterload

A

arteriolar resistance the heart must pump against to eject stroke volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

describe contractility

A

intrinsic ability of cardiac myocytes to contract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are the 3 general patterns of remodeling

A

concentric ventricular remodeling (thickening)
eccentric left ventricular hypertrophy (sacromeres being stretched)
mixed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how does the body maintain CO and BP

A

increase preload
vasoconstriction
tachycardia and increased contractility
neurohormonal activation- renin, NE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how does the body increase preload

A

increase venous return
sodium water retention
activation of renin angiotensin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how does vasoconstriction help in heart failure

A

increases afterload

increases systemic vascular resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

describe heart failure with reduced ejection fraction

A 
low output 
hypofunctioning left ventricle, decreased contractility 
ejection fraction <40%
ventricles enlarge  
systolic heatr failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

describe hert failure with preserved ejection fraction

A

diastolic heart failure
normal contractility and heart size
impaired LV filling during diastole
thickened LV or stiff ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what can be the result of a LV stiffness and inability to relax during diastole

A

increased resting pressure within the ventricle

increased pressure impedes ventricular filling therefore reducing stroke volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is hpertrophic cardiomyopathy

A

thickened LV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is restrictive cardiomyopathy

A

stiff ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

bad effects of the following compensatory mechanisms
vasoconstriction:
increased HR:
increased preload:

A

vaso - decreased cardiac output
hr - increased oxygen utilization
preload - peripheral and pulmonary edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

signs of left sided heart failure (pulmonary congestion)

A

dyspnea (difficult breathing) on exertion
orthopnea (SOB when lying down)
paroxysmal nocturnal dyspnea (SOB that awakens the patient)
pulmonary edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

signs of right sided heart failure (systemic venous congestion)

A

organomegaly
jugular venous distention
hepatojugular reflex
lower extremity peripheral edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

other signs of heart failure

A 
weakness 
exercise tolerance 
fatigue 
cns
cold, pale, clammy skin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

nyha class 1

A

cardiac function uncompromised

able to perform ordinary physical activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
nyha class 2
slightly compromised cardiac function | ordinary physical activity results in symptoms
26
nyha class 3
moderately compromised cardiac function | less than ordinary physical activity results in symptoms
27
nyha class 4
severely compromised cardaic function | symptoms may be present at rest
28
acc/aha class a
at righ for hf but without structural heart disease of symptoms of hf ex. diabetes
29
acc/aha stage b
structural heart disease without signs or symptoms of HF
30
acc/aha stage c
structural heart disease with prior or current symptoms of HF
31
acc/aha stage d
refractory HF requiring specialized intervention
32
signs on clinical exams of HF
``` auscultation of heart and lung - rales, S3 gallop edema jugular vein distention hepatojugular reflux dyspnea ```
33
goals of therapy
``` minimize disabling symptoms decrease hospitalization improve quality of life minimize disease complications slow progression of disease improve survival ```
34
what are some medical management strategies
``` elminate exacerbating factors control associated diseases restrict activity when acute sodium resticted diet exercise condition when stabilized drug therapy ```
35
what are the four types of drugs used in hf
diuretics - excrete excess water inotropic agents - increase myocardial contractility vasodilators - decrease cardiac work acei - neurohormonal modulators
36
how do diuretics help in hf, any evidence
relieve breathlessness and edema in patients with congestion | no evidence for reduced mortality
37
use of diuretics in hf
use loop start with low dose and adjust to achieve body weight reduction of .75-1kg until euvolemia (normal water volume) try to maintain ppatients dry weight with the lowest possible dose can alter dose based on volume status
38
furosemide dosing
20-40 daily then increase to acheive edema free state, once symptoms relieved use lowest possible maintenance dose
39
when would you initiate metolazone
in combo with loop diuretic if not enough, given 30 min before furosemide
40
metoalzone dosing
start 2.5 mg, usual dose 2.5-10mg/d
41
AE of diuretics
volume depletion - dehydration, reduced bp and co loss of K and Mg renal impairment
42
do thiazides work in renal impairment
no
43
monitoring of diuretics
signs of hypovolemia, symptomatic hypotension electrolytes K>4 renal function before initiating, SCr, eGFR check renal function and electrolytes 1-2 weeks after initiation or dose increase
44
how to monitor the efficacy of diuretics
``` daily weight input/output jugular venous distention peripheral edema HR/BP organ congestion ```
45
which hf are beta blockers along with acei indicated for
HFrEF
46
metoprolol SR dosing
12.5mg daily target 200
47
bisoprolol dosing
1.25 daily | target 10mg
48
carvediol dosing
3.125mg bid | target 25 bid
49
when and how do you initiate beta blockers
when stable not in acute decompensated HF start with very low dose, increase every 2 weeks to attain target dose or highest tolerated avoid abrupt withdrawal
50
AE of beta blockers
``` postural hypotension headache dizzines bradycardia bronchospasm fatigue decreased exercise tolerance insomnia sexual dysfunction PAD, cold extremities caution in diabetic ```
51
monitoring fo rbeta blockers
BP HR worsening symptoms
52
hemodynamic effects of acei
increase co decrease preload decrease systemic vascular resistance decrease BP
53
hormonal effects of acei
inhibit raas decrease angiotensin II decreases aldosterone slow ventricularremodelling
54
ramipril dosing
1.25-2.5 bid | target 5 bid
55
perindopril dosing
2mg daily | target 4
56
lisinopril dosing
2.5-5 daily | target 20-40
57
adverse effects of acei
``` hypotension renal impairment hyperkalemia cough rash taste alteration angioedema ```
58
why do you caution low salt subs
have high K content
59
monitoring of acei
check renal function and electrolytes at baseline monitor blood chemistry 1-2 weeks after initiation and final dose titration then every 3-4 months after new cough efficacy
60
what does aldosterone do
sodium/water retention sympathetic activation myocardial and vascualr fibrosis
61
what are mras indicated in
HFrEF nyha class 2-4 in addition to acei and bb
62
spironolactone dosing
start 25mg daily | target 50
63
dosing of eplerenone and advantage
25mg target 50 has less hormonal side effects
64
who should you caution the use of mras in
hyperkalemia renal failure digoxin (hyperkalemia precipitates digoxin toxicity) male may develop gynecomastia
65
when do you use arb should you use it in combo with acei
alternative if acei cough | no more adr
66
valsartan dosing
40 bid | target 160 bid
67
candesartan
4 daily | target 32
68
when is hydralazine/nitrate combo recommended
in african americas add on wiht acei other patients unable to tolerate acei and BB
69
what is the rationale for using hydralazine(vasodilator) and nitrate combo in heart failure
vasodilation decreased cardiac work, afterload reduction | nitrates reduce preload
70
target dose for hydralazine/nitrate combo
hyd 75mg / isdn 40 mg tid-qid
71
how does an angiotensin receptor neprilysin inhibitor (sacubitril) work
inhibit neprilysin which is an enzyme that breaks down anp and bnp to increase the circulation of ANP and BNP anp and bnp enhance diureses, natriureses, mayocardial relaxation, antiremodeling, and inhibit RAAS
72
is there any evidence of a sacubitril/valsartan combo, when should it be used
reduction in mortality, higher symptomatic hypotension | replacement for acei in people with HFrEF who are still symptomatic on acei, BB, and mra
73
sacubitril/valsartant (entresto) dosing
starting 49-51 bid target 97/103 bid (higher bioavalabilty of valsartan in the form)
74
entresto should not be given with acei or within how many hours of the last dose of an acei
36
75
ivabradine moa
inhibit f channels within sa node resulting in disruption of If ion current flow prolonging diastolic depol and reducing heart rate no effects on BP, myocardial contractility or AV conduction
76
in what patients did ivabradine decrease heart rate but not affect mortality
HFEF with LVEF <35 in normal sinus rthym, nyha class 2-4, hospirtalized in the past 12 months
77
ivabradine dosing
5mg big up to 7.5 bid
78
digitalis glycosides- digoxin moa
increase force and velocity of contraction through inhibition of NAKATPase decrease av conduction
79
when is digoxin used
heart failure with fast atrial rate, severe, S3 gallop, low EF, enlarged heart size improves the quality of life not mortality persistent symptoms despite maximized meds
80
distribution of digoxin adn when you should collect samples
50% in skeletal muscle, dependent of body weight long distribution time have to collect samples >6 hours post dose
81
digoxin elimination and half life
renal so normal half life 1.5 days and with kidney failure increase to >5 days
82
target digoxin concentration
<1mcg/L to gain neurohormonal modulating effects without enhancing adverse outcome
83
digoxin dosing
.125mg/day | CRCL<20 or weight <40kg give .0625mg/day
84
signs of digoxin toxicity
``` NV confusion altered color vision weakness dizziness av conduction disturbances - arrthymia ```
85
factors affecting digoxin activity/toxicity
electrolyte disturbances - potassium renal function -decreased elimination elderly hypothyroidism
86
digoxin drug interaction
increase bioavail-tetracycline, erythromycin decrease bioavil - antacids, cholestyramine, metoclopramide decrease elimination - quinidine, verapamil, spironolactone, amiodarone drugs that increase K Mg - diuretics
87
treatment of digoxin toxicity
``` withdrawal of digoxin correction of electrolyte abnormalities antiarrhythmic agents pacemake digoxin specific antibodies oral activated charcoal ```
88
properties and evidence of hawthorn extract
inotropic, vasodilating, lipid lowering, antioxidant, antiinflammatory modest increase in exercise tolerance but not really good trials
89
Lcarnitine role in myocardial energy production
chronic replacement to increase exercise tolerance and decrease cardiac dimensions improved 3 yr survival in dilated cardiomyopathy
90
fish oild for heart failure
small but sig mortality benefit
91
coenzyme Q10 properties and evidence
component of the electron transport chain decreased levels in heart failure mixed results
92
why avoid antiarrhythmic agents in HF
proarrhythmia negative inotropic effects increased mortality
93
why avoid nonDHP calcium antagonists in HF
direct negative inotropic agents | CI in systolic heart failure
94
why avoid tricyclic antidepressants in HF
proarrhythmic potential
95
why avoid nsaids in HF
inhibit effects of diuretics and acei cause salt and water retention can worsen cardiac and renal function
96
why avoid corticosteroids in HF
AE on salt and water retention
97
why avoid doxorubicin and tratuzamab in HF
dose dependent cardio toxicity | can cause HF
98
exercise recommendation in HF
``` aerobic 3-5x per week 30-45 min for class 1-3 ```
99
salt and fluid restriction in HF
no added salt diet <2g per day limit fluid intake to 1.5L-2L per day include jello, soup....
100
non pharms for HF
``` exercise limit salt and fluids monitor daily morning weight no more than 1 alcoholic drink a day smoking cessation influenza and pneumococcal vaccine ```
101
when is left ventricular assist device used
end stage HF or as bridging to heart transplant

Clinical 2.0 (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions