6 - Chronic Heart Failure Flashcards
(161 cards)
1
Q
When does HF occur?
A
When the heart is unable to deliver adequate supply of oxygenated blood to meet the metabolic demands of the organs
2
Q
What causes decreased contractility?
A
- Rheumatic heart disease
- Cardiomyopathy
- Coronary heart disease/MI
3
Q
What causes increased afterload?
A
- Hypertension
- Aortic stenosis
4
Q
What causes increases preload?
A
- Increased sodium/water retention
- Malfunction of aortic valve
- Drugs (steroid, NSAIDs)
5
Q
What is a direct cardiotoxic drug?
A
ex. Adriamycin
6
Q
What can cause high output failure?
A
anemia
7
Q
What 2 factors affect Cardiac Output?
A
- Heart Rate
- Stroke Volume
8
Q
What 3 factors affect Stroke Volume?
A
- Preload
- Contractility
- Afterload
9
Q
What is the ejection fraction (EF)?
A
Fraction of blood ejected from left ventricle
10
Q
What is the formula for EF?
A
EF = (EDV-ESV)/EDV
11
Q
What is a normal EF for healthy patients?
A
50-70%
12
Q
EF > ___% is considered normal
A
40
13
Q
Preload
A
Degree of filling from left atrium (venous return, end-diastolic volume)
14
Q
Afterload
A
Arteriolar resistance the heart must pump against to eject stroke volume
15
Q
Contractility (inotropy)
A
Intrinsic ability of cardiac myocytes to contract
16
Q
What is cardiac remodelling?
A
Usually begins as compensatory process that results in maladaptive complications:
- Complex process that occurs at the structural, functional, cellular, molecular level
- Systemic factors affecting remodelling can be attributed to changes in hemodynamic load, neurohormonal activation and metabolic status
17
Q
What are the 3 general patters of remodelling?
A
- concentric ventricular remodelling
- eccentric left ventricular hypertrophy
- mixed concentric/eccentric hypertrophy
- concentric hypertrophy = adding of myocardium
- eccentric hypertrophy = sarcomeres are being added, no change in wall thickness
18
Q
Describe the compensatory mechanisms that the body tries to maintain CO & BP by?
A
1) Increase preload
- Increase venous return in an attempt to increase CO
- Sodium/water retention
- Activation of RAAS
2) Vasoconstriction
- Increases after load
- Increase systemic vascular resistance
- Sympathetic stimulation
- Activation of RAAS
3) Tachycardia and increased contractility
- Sympathetic stimulation
4) Neurohormonal Activation
- Compensatory release of hormones in response of hypovolemia - renin, NE, ADH
- In the long term, these contribute to progression of structural abnormalities (ex. Angiotensin 2: increase protein synthesis, cardiac myocyte hypertrophy)
19
Q
HFrEF
A
Heart failure with reduced ejection fraction
20
Q
Describe HFrEF
A
- commonly referred to as systolic heart failure
- low output (congestive) failure
- hypofunctioning left ventricle; decreased contractility
- EF < 40%
- ventricles enlarge (dilate as retain blood)
21
Q
HFpEF
A
Heart failure with preserved ejection fraction
22
Q
Describe HFpEF
A
- diastolic heart failure
- normal contractility and heart size
- impaired left ventricular filling during diastole
- left ventricular stiffness and inability to relax during diastole
- results in increased resting pressure within the ventricle
- the increased pressure impedes ventricular filling, therefore reducing stroke volume (EF preserved)
- can see with thickened left ventricle (hypertrophic cardiomyopathy) or stiff ventricle (restrict cardiomyopathy)
23
Q
What are some signs and symptoms of compensatory mechanisms kicking in?
A
Vasoconstriction - leads to decreased CO
Increased HR - leads to increased oxygen utilization
Increased preload - leads to peripheral and pulmonary edema
Decreased exercise tolerance
24
Q
Signs and symptoms of left-sided heart failure (pulmonary congestion)?
A
- dyspnea on exertion
- orthopnea (dyspnea that occurs when lying flat)
- paroxysmal nocturnal dyspnea
- pulmonary edema
25
Signs and symptoms of right-sided heart failure (systemic venous congestion)?
- organomegaly (enlargement of organs) (ex. hepatomegaly)
- jugular venous distension
- hepatojugular reflex
- lower extremity peripheral edema
26
What are some non-specific findings in patients with HF?
- weakness
- exercise intolerance
- fatigue
- CNS
- cold, pale, clammy skin
27
Describe NYHA Class 1 HF
- Uncompromised.
| - Able to perform ordinary physical activity.
28
Describe NYHA Class 2 HF
- Slightly compromised.
| - Ordinary physical activity results in symptoms.
29
Describe NYHA Class 3 HF
- Moderately compromised.
| - Less than ordinary physical activity results in symptoms.
30
Describe NYHA Class 4 HF
- Severely compromised.
| - Symptoms may be present at rest.
31
Describe ACC/AHA Stage A
At high risk for HF but without structural heart disease or symptoms of HF.
(Risk factors: HTN, CAD, DM, obesity, metabolic syndrome)
32
Describe ACC/AHA Stage B
Structural heart disease but without signs or symptoms of HF
33
Describe ACC/AHA Stage C
Structural heart disease with prior or current symptoms of HF
34
Describe ACC/AHA Stage D
Refractory HF requiring specialized intervention
35
What tools can we use to diagnose HF?
1) Symptoms (weakness, fatigue, exercise tolerance)
2) Signs on clinical exams
- auscultation of heart and lung - S3 gallop, rales
- edema
- jugular vein distention
- hepatojugular reflux
- dyspnea
3) Echo - ejection fraction
4) Chest X-ray
5) Cardiac MRI
6) CV risk assessment
36
Goals of therapy for HF?
- Minimize disabling symptoms
- Decrease hospitalization
- Improve quality of life
- Minimize disease complications
- Slow progression of disease
- Improve survival
37
The drugs we have now are only for alleviating symptoms, but we cannot reverse the disease. The only way to have a healthy heart again = ________
transplant
38
What are some strategies for medical management of HF?
- Eliminate exacerbating factors
- Control associated diseases
- Restrict activity when acute
- Sodium restricted diet
- Exercise conditioning when stabilized to strengthen heart
- Drug therapy
39
What drug therapy options do we have for HF?
1) Diuretics - Excretion of excess water
2) Inotropic agents - Increase myocardial contractility
3) Vasodilators - Decrease cardiac work
4) ACEi - neurohormonal modulators
40
What do diuretics do?
- Relieve breathlessness and deem in patients with symptoms and signs of congestion
- Reduce intravascular volume, edema, preload and pulmonary congestion
- Achieve diuresis through inhibiting reabsorption of sodium in thick ascending limb (loop diuretics), and distal convoluted tubule (thiazide diuretics)
41
What diuretics are more efficient: loop or thiazide?
LOOP
42
What is the dosing regimen for diuretics for HF?
- Start with low dose and adjust to achieve positive diuresis with daily body weight reduction of 0.75 - 1 kg until euvolemia (normal body weight)
* it is essential to know their dry weight
- Aim to maintain patients on dry weight with lowest possible dose
43
Furosemide is a _____ diuretic
loop
44
Dose for furosemide
Initiate at 20-40mg daily, increase dose accordingly to achieve edema free state (dry weight); once symptoms relieved, use lowest possible maintenance dose
45
How do you treat diuretic resistance is severe, refractory HF with furosemide?
- try furosemide IV
| - add metolazone (usually given 30 mins prior to furosemide)
46
Thiazides are usually in combo with ??
loop diuretic
47
Thiazides are unlikely to be effective in patients with CrCl < ___
30
48
What is the dose of HCTZ (thiazide)?
-Starting dose of 25 mg, usual dose up to 100 mg/day
49
What is the dose of metolazone (thiazide)?
-Starting dose of 2.5mg, usual dose of 2.5-10 mg/day
50
What is the reasoning behind adding a thiazide diuretic to a loop diuretic?
You will achieve water loss in both the ascending limb and the distal tubule
51
What are some adverse effects/monitoring for diuretics?
1) Volume depletion - leads to dehydration and reduction in BP and CO (check for signs of hypovolemia and symptomatic hypotension)
2) Loss of K+ and Mg2+ (hypokalemia can induce digoxin toxicity)
* aim to keep K+ > 4 mmol/L
3) Renal impairment - want to monitor SCr
52
What things can we monitor to determine diuretic efficacy?
- daily weight
- input/output
- jugular venous distention
- peripheral edema
- sitting/standing HR & BP
- organ congestion (pulmonary rales and hepatomegaly)
53
When should renal function and electrolytes be checked when on diuretics?
1-2 weeks after initiation and after dose increase
54
Rationale of using BB in HF
Long term sympathetic activation may contribute to:
- Disease progression
- Augmented activation of RAAS
- Peripheral vasoconstriction
- Remodelling of cardiac myocytes (i.e. fibrosis, apoptosis)
**BB block sympathetic activation and all these things from occuring
55
Are BB considered useful in HF?
YES - 1ST LINE THERAPY (in addition to ACEi)
56
Beta blockers are indicated for all _____
HFrEF
57
Beta blockers are first line treatment along with ??
ACEi and MRA (mineralocorticoid receptor antagonist - ex. spironolactone) if NYHA 2 or above
58
Why are BB 1st line in HF?
proven to reduce mortality
59
Metoprolol SR:
| Initial dose
12.5mg SR daily
| or 12.5 mg BID
60
Metoprolol SR:
| Target HF dose
200 mg SR daily
| or 100 mg BID
61
Bisoprolol:
| Initial dose
1.25 mg daily
62
Bisoprolol:
| Target HF dose
10 mg daily
63
Carvedilol:
| Initial dose
3.125 mg BID
64
Carvedilol:
| Target HF dose
25 mg BID
65
Nebivolol:
| Initial dose
1.25 mg daily
66
Nebivolol:
| Target HF dose
10 mg daily
67
Why do we start BB at such low doses in HF?
Want to start with low dose bc they already have affected contractility, don't want to push them into acute HF.
They are on BB to reduce oxygen demand.
68
Describe the dosing approach of BB in HF
- Used in all stages of NYHA 1 - 4
- Initiate when patients are stable and not in acute decompensated heart failure
- Start with very low dose
- Increase dosage approximately every 2 weeks
- Try to attain target doses (alternatively, aim for highest dose tolerated)
- If hypotensive - consider decreasing dose of other meds or change timing of meds
- Avoid large dose reduction or abrupt withdrawl
- Decrease dose if on inotropes (in-hosp); discontinue if patient is in cariogenic shock
69
What are some side effects of beta blockers?
- postural hypotension
- headache
- dizziness
- bradycardia
- bronchospasm
- fatigue
- decreased exercise tolerance, fluid retention (on initiation)
- insomnia, vivid dream
- sexual dysfunction
- PAD, cold extremity
- caution in diabetic bc they mask the symptoms of hypoglycaemia
70
What do we need to monitor for BB?
- Clinical improvement
- BP, HR (If symptomatic bradycardia, discontinue/adjust other HR reducing meds if possible. ex. amiodarone, CCBs, digoxin)
- Worsening symptoms
71
MOA of ACEi
1) Hemodynamic effects
- Increase CO
- Decrease preload
- Decrease systemic vascular resistance
- Decreased BP
2) Hormonal effects (Inhibit RAAS)
- Decrease angiotensin 2
- Decrease aldosterone
- Slow ventricular remodelling
72
Who are ACEi indicated for?
all patients with HFrEF along with BB (regardless of what NYHA class)
73
Benefit of using ACEi in HF patients?
reduces mortality, cardiac death and hospitalization
74
Ramipril:
| Initial dose
1.25-2.5 mg BID
75
Ramipril:
| Target HF dose
5 mg BID
76
Lisinopril:
| Initial dose
2.5-5 mg daily
77
Lisinopril:
| Target HF dose
20-40 mg daily
78
Perindopril:
| Initial dose
2 mg daily
79
Perindopril:
| Target HF dose
4 mg daily
80
Enalapril:
| Initial dose
1.25 - 2.5 mg BID
81
Enalapril:
| Target HF dose
10 mg BID
82
Captopril:
| Initial dose
6.25 - 12.5 mg TID
83
Captopril:
| Target HF dose
25 - 50 mg TID
84
Trandolapril:
| Initial dose
0.5 - 1 mg daily
85
Trandolapril:
| Target HF dose
4 mg daily
86
Adverse effects of ACEi
- Hypotension
- Renal impairment
- Hyperkalemia
- Cough
- Rash (more common with captopril)
- Taste alterations
- Angioedema (swelling of face, lips, tongue, larynx)
87
Monitoring for ACEi efficacy?
- Right and left sided symptoms
- Exercise tolerance
- Weight/fluid balance
88
How do you monitor for adverse reactions of ACEi?
- check renal fcn and electrolytes at baseline
- monitor blood chemistry 1-2 weeks after dose initiation and 1-2 weeks after final dose citation, then monitor every 3-4 months thereafter
- new cough
89
Rationale for using MRAs (minteralcorticoid receptor antagonists) in HF ?
-Aldosterone contributes to sodium/water retention, sympathetic activation , myocardial and vascular fibrosis and other pathophysiologic effects seen in HF
90
Who are MRAs indicated for?
All HF patients NYHA 2-4 in addition to ACEi and BB
91
Evidence for using MRAs in HF?
yes - reduce mortality
92
Examples of MRAs?
- Spironolactone
| - Eplerenone
93
Spironolactone:
| Initial dose
25 mg daily
94
Spironolactone:
| Target dose
50 mg daily
95
Eplerenone:
| Initial dose
25 mg daily
96
Eplerenone:
| Target dose
50 mg daily
97
What types of patients would you caution use of MRAs in?
- Hyperkalemic pts
- Scr > 220 and K+ > 5
- If on digoxin (hyperkalemia ay precipitate digoxin toxicity)
- Male pts uncommonly develop breast discomfort of gynecomastia (spironolactone - 10%) - consider switching to eplorenone
98
What does an ARB do?
blocks AT1 receptor
99
______ shown to reduce CV mortality
candesartan
100
______ shown to improve hospitalization rate due to HF
valsartan
101
When would you choose an ARB?
if someone got a cough using ACEi
102
Valsartan:
| Initial dose
40 mg BID
103
Valsartan:
| Target HF dose
160 mg BID
104
Candesartan:
| Initial dose
4 mg daily
105
Candesartan:
| Target HF dose
32 mg daily
106
Losartan:
| Initial dose
25 mg daily
107
Losartan:
| Target HF dose
150 mg daily ???
| **no clinical trials in HF
108
What does Hydralazine/Nitrate Combo do?
significant reduction in mortality and improvement in exercise
109
_____ is superior to Hyd/ISDN
ACEi
110
Is an ACEi with Hyd/ISDN better than ACEi alone?
Yes
111
Hyd/ISDN:
| Target dose
Hyd 75 mg/ISDN 40 mg TID-QID
112
Rationale of using Hydralazine/Nitrate Combo?
- Vasodilation decrease cardiac work by overcoming detrimental effects of compensatory mechanisms
- Achieved through reduction of preload (nitrates) and after load (hydrazine)
113
When is Hydralazine/Nitrate Combo recommended?
It is a standard add-on for individuals of African descent.
Can be given to all patients if:
- Ongoing symptoms with ACEi and BB
- Unable to tolerate neither ACEi or ARB
114
What is an ARNI?
Angiotensin receptor neprilysin inhibitor:
sacubitril & ARB
*new class of combination agents (sacubitril/valsartan) that act on RAAS and natriuretic peptides
115
Rationale of using an ARNI in HF?
- Increase circulation of a-type natriuretic peptide (ANP) and BNP by inhibiting neprilysin
- ANP and BNP enhances diuresis, natriuresis, myocardial relaxation, anti-remodelling
- ANP and BNP also inhibit RAAS
- AT1 receptor blockade by ARB reduces vasoconstriction, sodium/water retention and myocardial hypertrophy
116
ARNI's have a higher risk of what side effect than ACEi?
symptomatic hypotension
117
Who are ARNIs recommended for?
- May be considered as a replacement for ACEi in patients with HFrEF who remain symptomatic despite optimal treatment with an ACEi, a BB and an MRA
- In patients with HFrEF NYHA class 2 or 3 who tolerate an ACEi or ARB, replacement by an ARNi is recommended to further reduce morbidity and mortality
118
Sacubitril/valsartan:
| Starting dose
49/51 mg BID
**valsartan 51 mg in Entresto is approx valsartan 80 mg.
119
Sacubitril/valsartan:
| Target dose for HF
97/103 mg BID
120
If switching from ACEi to ARNI, how long should you space it out?
ARNI should not be given concomitantly with ACEi or within 36 hours of last dose of ACEi.
121
What is Ivabradine and how does it work?
f-channel inhibitor
* inhibit f-channels within SA node resulting in disruption of I(f) ion current flow, thereby prolonging diastolic depolarization and reducing heart rate
* no effects on BP, myocardial contractility or AV conduction
122
Who is Ivabradine recommended for?
Ivabradine can be beneficial to reduce HF hospitalization for patients with symptomatic (NYHA class 2-3) stable chronic HFrEF (LVEF < 35%) who are receiving guideline directed evaluation and management, including a BB at max tolerated dose and who are in sinus rhythm with a HR of 70 ppm or greater at rest.
123
Ivabradine:
| Starting dose
5mg BID
124
Ivabradine:
| Target dose
Up to 7.5 mg BID
125
How does digoxin work?
Increases force and velocity of contraction through inhibition of Na-K-ATPase (positive ionotrope)
126
Describe the clinical use of digoxin in HF
- effective in heart failure associated with fast atrial rate, severe HF, S3 gallop, low EF and enlarged heart size
- no mortality benefit
- decrease rate of hospitalization
- improves symptoms, expertise performance, decrease hospitalizations
- improve QOL
127
Describe the role of digoxin in HF
-use in patients with persistent symptoms despite maximized use of vasodilators and diuretics
128
Elimination of digoxin is primarily ______
renal
129
Digoxin:
| ___% found in skeletal muscle
50
130
Digoxin:
| _____ distribution time
long
131
Digoxin:
| Normal half life
1.5 days
132
Digoxin:
| Half life for someone with kidney failure?
>5 days
133
Digoxin:
| Therapeutic range?
Historically 0.5 - 2.0 mcg/L
*Current data supports targeting conc of < 1.0 mcg/L to gain neurohormonal modulating effects without enhancing adverse outcome
134
Digoxin:
| Dosing for CrCl > 20
0.125 mg/day
135
Digoxin:
| Dosing for CrCl < 20 or weight < 40 kg
0.0625 mg/day
136
Digoxin:
| What are some signs of toxicity?
Noncardiac: N/V, confusion, altered color vision, weakness, dizziness
Cardiac: AV conduction disturbances
137
Digoxin:
| What are some factors affecting digoxin activity or toxicity?
- electrolyte disturbances (hypo and hyperkalemia)
- renal function - renal impairment will cause decreased elimination
- drug interactions
- elderly
- hypothyroidism
138
What drugs increase bioavailability of digoxin?
tetracycline, erythromycin
139
What drugs decrease bioavailability of digoxin?
antacids, cholestyramine, metoclopramide
140
What drugs decrease elimination of digoxin?
quinidine, verapamil, spironolactone, amidoarone
141
What drugs decrease K+ or Mg2+ leading to electrolyte disturbances?
diuretics
142
How do we treat digoxin toxicity?
- withdrawal of digoxin
- correction of electrolyte abnormalities
- antiarrhythmic agents
- pacemaker
- digoxin specific antibodies
- oral activated charcoal
143
Hawthorn extract is a natural product for HF: describe it's properties
inotropic, vasodilating, lipid-lowering, antioxidant, anti-inflammatory
144
Evidence for hawthorn extract?
- modest increase in exercise tolerance
| - one randomized trial showed decrease in mortality
145
L-carnitine is a natural product for HF: describe it's properties
- plays a role in myocardial energy production
| - thought to increase exercise tolerance and decrease cardiac dimensions
146
Are fish oils of benefit to HF patients?
small but significant mortality benefit
147
Coenzyme Q10 is a natural product for HF: describe it's properties
- component of the electron transport chain in the mitochondria
- micronutrient
- there are decreases levels of coenzyme Q10 in patients with HF
148
What drugs should be avoided in HF?
- AAD (anti-arrthymic drugs)
- non-DHP CCB
- TCA's
- NSAIDs
- corticosteroids
- doxorubicin, trastuzamab
149
Why should AAD (anti-arrthymic drugs) be avoided in HF?
- proarrhythmia
- negative inotropic effects
- increased mortality
150
Why should non-DHP CCB's be avoided in HF?
-direct negative inotropic agents, CI in patients with systolic chronic heart failure
151
Why should TCAs be avoided in HF?
-pro arrhythmic potential
152
Why should NSAIDs be avoided in HF?
-inhibits effects of diuretics and ACEi, cause salt and water retention, can worsen both cardiac and renal fcn
153
Why should corticosteroids be avoided in HF?
adverse effects on salt and water retention
154
Why should doxorubicin and trastuzamab be avoided in HF?
dose-dependent cardiotoxicity
155
Non-pharms for HF:
| Exercise
- recommended for all patients with stable HF symptoms & impaired LV systolic fcn
- aerobic exercise 3-5x/week, 30-45 min per session for NYHA Class 1-3
156
Non-pharms for HF:
| Salt & Fluid restriction
- No added salt diet (<2-3 grams of salt per day, equivalent of 1/4 tsp)
- Limit fluid intake to 1.5-2L/day for patients with fluid retention or congestion that is not easily controlled with diuretics or in patients with significant renal dysfunction or hyponatremia
* *All fluid counts (coffee, soup, jello)
157
List some more non-pharos for HF
- monitor daily weight (without clothes and after voiding)
- no more than 1 alcoholic drink per day
- smoking cessation
- influenza and pneumococcal vaccination
- aggressive risk reduction
- patient education is key for drug adherence and fluid/salt restriction
158
What is an ICD and who is it recommended for?
```
Implantable Cardioverter Defibrillator:
-indicated for primary prevention of sudden cardiac death in selected patients with nonischemic dilated cardiomyopathy or ischemic heart disease > 40 days post MI with LVEF 35% or less and NYHA class 2 or 3
```
159
What is CRT and who is it recommended for?
Cardiac Resynchronization Therapy:
-indicated for patients with LVEF < 35%, left bundle branch block with a QRS duration of 150 ms or greater, NYHA 2, 3, or 4 symptoms
160
Who is a heart transplant indicated for?
end stage heart failure
161
What is LVAD and who is it recommended for?
Left ventricular assist device:
| -for end stage heart failure or as bridging to heart transplant
