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F1 anesthetics > Ward 11 (heart failure pt.2 > Flashcards

Ward 11 (heart failure pt.2 Flashcards

1
Q

What patient diseases should raise suspicions of possible heart failure

A

Particularly in patients who are at increased risk, including older patients
with underlying cardiovascular disease and those with comorbidities such
hypertension, diabetes, and chronic kidney disease.

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2
Q

X ray findings in heart failure

A
  • Major abnormalities on chest imaging associated with left HF include enlarged cardiac silhouette (cardiothoracic ratio >0.5) and pulmonary venous congestion
    A good mnemonic to remember these principles is ABCDE:
    A - alveolar oedema (bat wing opacities)
    B - Kerley B lines (horizontal lines in the periphery of the lower posterior lung fields)
    C - cardiomegaly
    D - dilated upper lobe vessels
    E - pleural effusion
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3
Q

Biomarkers for HF

A

BNP and N-terminal pro-BNP
(NT-proBNP)

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4
Q

Where is BNP and N-terminal pro-BNP released form and why

A

Are released from the atria and ventricles in response to
increased wall stress.

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5
Q

AHA/ACC classification of heart failure

A

Stage A: At high risk for HF but
without structural heart disease,
symptoms of HF, or HF biomarkers
Stage B: Structural heart disease but without signs and symptoms of HF
Stage C: Structural heart disease with prior or current symptoms of HF
Stage D: Refractory HF

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6
Q

Main goals of treatment in each stage of heart failure

A

Therapeutic interventions in each stage aim to modify risk factors (stage A), treat risk and structural heart disease to prevent HF (stage B), and reduce symptoms, morbidity, and mortality (stages C and D)

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7
Q

Which patients would fit in stage B?

A
  • previous MI
  • Ventricular remodeling
    including ventricular
    hypertrophy and low
    ejection fraction
  • Evidence for increased filling pressures
  • Patients with risk factors and Increased levels of BNPs* or Persistently elevated cardiac troponin in the absence of competing diagnoses resulting in such biomarker elevations such as acute coronary syndrome, CKD, pulmonary embolus, or myopericarditis
  • asymptomatic
    valvular disease
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8
Q

Which patients would fit stage A?

A

Patients with:
- hypertension
- atherosclerotic disease
- diabetes mellitus
- obesity
- metabolic syndrome

or

Patients:
-using cardiotoxic drugs
-with family history of
cardiomyopathy

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9
Q

Which patients fit stage C?

A

Patients with:
- known structural
heart disease
- HF signs and
symptoms

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10
Q

Which patients would fit stage D?

A

Patients with:
- marked HF
symptoms at rest
- recurrent
hospitalized despite
guideline-directed
medical therapy

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11
Q

Diagnostic algorithm for patients with suspected HF

A
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12
Q

Causes of HF

A

The common causes of HF include ischemic heart disease and myocardial infarction (MI), hypertension, and valvular heart disease (VHD). Other causes can include familial or genetic cardiomyopathies; amyloidosis; cardiotoxicity with cancer or other treatments or substance abuse such as alcohol, cocaine, or methamphetamine; tachycardia, right ventricular (RV) pacing or stress-induced cardiomyopathies; peripartum cardiomyopathy; myocarditis; autoimmune causes, sarcoidosis; iron overload, including hemochromatosis; and thyroid disease and other endocrine metabolic and nutritional causes

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13
Q

Goals and drugs for Stage A patients

A

Goals:
Heart healthy lifestyle
Prevent vascular, coronary disease
Prevent LV structural abnormalities
Drugs:
ACEi or ARB in appropriate patients for vascular disease or DM
Statins as appropriate

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14
Q

Goals and drugs for Stage B patients

A

Goals
- Prevent HF symptoms
- Prevent further
cardiac remodeling
Drugs
- ACEI or ARB in
appropriate patients
- Blocker in
appropriate patients
In selected patients
- Implantable
cardioverterdefibrillator
(ICD)
- Revascularization or
valvular surgery as
appropriate

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15
Q

Drugs for patients in Stage C

A

Drugs for use in patients
with preserved EF
- Diuretics
- Treat comorbidities
(HTN, AF, CAD, DM)
Drugs for routine use in
patients with reduced EF
- Diuretics
- ACEI or ARB
- ARNI
- beta Blocker
- Aldosterone antagonist
- Ivabradine
Drugs for use in selected
patients with reduced EF
- Hydralazine/ISDN
- ACEI and ARB
- Cardiac glycoside

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16
Q

Effects of Ang2

A

Has four major cardiovascular actions that are all mediated
by the AT1 receptor:
* vasoconstriction
* stimulation of aldosterone release from the adrenal glands
* direct hypertrophic and proliferative effects on cardiomyocytes and
fibroblasts, respectively
* stimulation of NE release from sympathetic nerve endings and the
adrenal medulla

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17
Q

How is ANG2 formed?

A
  • Largely derived from angiotensinogen in two proteolytic steps.
  • First, renin, an enzyme released from the kidneys, cleaves the decapeptide AngI from the amino terminus of angiotensinogen (renin substrate).
  • Then, ACE removes a carboxy-terminal dipeptide (His9-Leu10) from AngI, yielding the active
    octapeptide, AngII
18
Q

What do ace inhibitors do?

A
  • lower the circulating level of AngII
  • Thus, ACEIs not only act as
    vasodilators but also reduce aldosterone levels and thereby act as an indirect
    diuretic, have direct antiremodeling effects on the heart, and produce
    sympatholytic effects (thus moderating the reflex tachycardia that accompanies
    vasodilation and the lowering of blood pressure).
  • Important renal functions
  • ACEIs favor hyperkalemia, which can be detrimental in patients with renal insufficiency but is normally beneficial for patients with heart failure who more often present with hypokalemia, a
    condition that promotes cardiac arrhythmias
19
Q

ACE inhibitors renal function

A

When renal perfusion pressure
is reduced, AngII constricts renal efferent arterioles, and this serves to
maintain glomerular filtration pressure and GFR. Thus, under circumstances
in which renal perfusion pressure is compromised, inhibition of
the RAAS may induce a sudden and marked decrease in GFR. For this
reason, ACEIs are contraindicated in bilateral renal artery stenosis. Likewise,
because patients with heart failure often have low renal perfusion
pressures, aggressive treatment with ACEIs may induce acute renal failure.
To avoid this, for patients with heart failure patients, ACEIs should be
initiated at very low doses; blood pressure, blood creatinine, and K+ levels
should be monitored; and the ACEI dose slowly increased over weeks
toward target levels . The potentially dangerous acute effects become
beneficial with long-term use of ACEIs because the (small) chronic
lowering of glomerular pressures protects the glomerulus from fibrotic
degeneration.
- ACEIs shift the balance of
vascular smooth muscle tone toward vasodilation and thereby increase
renal blood flow, another reason for their chronic protective effects on
the kidney. This effect also explains why NSAIDs, which reduce the production
of vasodilating prostaglandins, antagonize effects of ACEIs and
should be avoided in patients with heart failure.

20
Q

Angiotensin other effects

A
  • Angiotensin-converting enzyme
    has other actions, including the inactivation of bradykinin and substance
    P. ACEIs increase bradykinin and substance P levels, with two prominent
    consequences: cough, the most frequent ADR (~5%); and angioedema, a
    rare (~0.7%), but life-threatening condition presenting with swelling of
    the skin and mucous membranes of the throat and asphyxia (three times
    more common amongst African Americans).
  • Experimental evidence suggests
    that increases in bradykinin contribute to the therapeutic efficacy
    of ACEIs and may explain why ARBs, which do not increase bradykinin
    (and therefore cause no cough), have not been consistently associated with
    improved survival in patients with HFrEF
21
Q

Combination of drugs in heart failure

A

ACEi (1st choice) or ARB (2nd choice), beta blocker. mineralocorticoid receptor antagonist, and diuretic
- Angiotensin Receptor and Neprilysin Inhibitors is the latest option

22
Q

Neprilysin inhibitor used in HF

A

The latest addition to standard combination therapy of heart failure is
sacubitril/valsartan. It is made by cocrystallizing the well-known ARB
valsartan with sacubritril, a prodrug that, after deesterization, inhibits
neprilysin, a peptidase mediating the enzymatic degradation and inactivation
of natriuretic peptides (ANP, BNP, CNP), bradykinin, and substance
P. Thus, the drug combines inhibition of the RAAS with activation of a
beneficial axis of neurohumoral activation, the natriuretic peptides

23
Q

Aldosterone effects

A

promotes Na+ and fluid retention, loss of K+ and Mg2+, sympathetic
activation, parasympathetic inhibition, myocardial and vascular fibrosis,
baroreceptor dysfunction, and vascular damage, all adverse effects in the
setting of heart failure.

24
Q

Aldosterone levels with ACEIs or ARBs

A

Aldosterone plasma levels decrease under therapy with ACEIs or ARBs, but quickly increase again, a phenomenon called aldosterone escape. It is likely explained by incomplete blockade of the
RAAS (e.g., AngI can be converted to AngII by chymase, in addition to
ACE; see Figure 26–1) and by the fact that aldosterone secretion is regulated
not only by AngII but also by sodium and potassium plasma Na+ and
K+

25
Q

Mechanism of action of MRAs

A

The MRAs act as antagonists of nuclear receptors of aldosterone.
- They are K+-sparing diuretics (see discussion that follows) but gained more importance in the treatment of heart
failure for their additional efficacy in suppressing the consequences of
neurohumoral activation
- MRAs inhibit all the effects of aldosterone, of which the reduction in
fibrosis is most pronounced in animal models

26
Q

Effect of beta blockers in heart failure

A

In a simple view, β blockers protect the heart from the adverse long-term consequences of adrenergic overstimulation, for example, increased energy consumption,
fibrosis, arrhythmias, and cell death. Lower heart rates not only save
energy but also improve contractile function because the failing heart,
in contrast to the healthy human heart, has a negative force-frequency
relation (Pieske et al., 1995). In addition, β blockers improve perfusion
of the myocardium by prolonging diastole, thereby reducing ischemia

27
Q

Beta blockers used in heart failure

A
  • Metoprolol (less favored due to short half life and metabolization differences)
  • Bisoprolol
  • Carvedilol
  • Nebivolol
28
Q

How many times should the beta blockers be taken?

A
  • Bisoprolol once daily (half life of 10-12 hours)
  • Metoprolol (should be prescribed as zero-order prolonged release formulation since half life is too short 3-5 hours, even extended release formulations do not suffice)
  • Carvedilol (twice daily due to half life of 6-10 hours). An advantageous
    peculiarity of carvedilol is that it dissociates only slowly from β receptors
    and therefore acts longer than its plasma t1/2 suggests.
  • Nebivolol once daily (not approved in USA for heart failure)
29
Q

Examples of MRAs used in heart failure

A

Spironolactone and eplerenone

30
Q

Adverse effects of MRA

A

Hyperkalemia

31
Q

Spironolactone vs Eplerenone

A
  • Spironolactone is a nonspecific steroid hormone receptor antagonist with similar affinity for progesterone and androgen receptors; it causes gynecomastia (painful breast swelling, 10% of patients) in men and dysmenorrhea in women.
  • Eplerenone is selective for the mineralocorticoid receptor and therefore does not cause gynecomastia
32
Q

What is fluid overload a consequence of in heart failure?

A

Fluid overload with increased filling pressures (increased preload) and
dilation of the ventricles in heart failure is the consequence of decreased
kidney perfusion and activation of the RAAS

33
Q

What do diuretics do in heart failure?

A

Diuretics increase Na+ and water excretion by inhibiting transporters in
the kidney and thereby improve symptoms of CHF by moving patients to
lower cardiac filling pressures along the same ventricular function curve

34
Q

When should diuretics not be given in patients with heart failure?

A

Diuretics should not be given
to patients without congestion because they activate the RAAS and may
accelerate a vicious downward spiral.

35
Q

Diuretics used in heart failure and dosing)

A

Loop diuretics (furosemide, bumetanide) twice a day or more

36
Q

Diuretics impact on heart failure

A

Diuretics improve symptoms but studies showing mortality benefit are lacking.

37
Q

Heart failure treatment targeted to a certain race

A

Hydralazine–Isosorbide Dinitrate has shown marked benefits in African Americans/Blacks

38
Q

Lusitropy meaning

A

Ability of the heart to relax

39
Q

How do cardiac glycosides function and effects on heart failure?

A
  • It has positive inotropic effects and negative chronotropic and dromotropic action
  • Increases parasympathetic stimulation
40
Q

Is digoxin prescribed in heart failure?

A

Rarely prescribed, very narrow therapeutic index and mixed results on mortality (some showing increased moratlity in both HF and AF)

41
Q

Digoxin in AF

A
  • The major “indirect” electrophysiological effects of cardiac
    glycosides are hyperpolarization, shortening of atrial action potentials,
    and increases in AV nodal refractoriness. - The last action accounts for
    the utility of digoxin in terminating reentrant arrhythmias involving
    the AV node and in controlling ventricular response in patients with
    atrial fibrillation

F1 anesthetics (39 decks)

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