Unit 1: ADHF, HF, AKI

Common factors the precipitate ADHF

non-adherence to HF regimen, sodium restriction, acute MI, uncorrected HTN, Afib, recent negative inotropics, drugs that increase salt retention, EtOH and illicit drug use, endocrine issues (DM/thyroid), infections

ADHF definition

new or worsening heart failure requiring hospitalization usually with symptoms of dyspnea, edema and

fatigue

Signs of congestion (wet)

increased JVD, Positive HJR, peripheral edema, DOE/SOB, crackles/rales, recent weight gain, increased BNP/NT-proBNP, abdominal distention

Signs of low perfusion

cool extremities, low urine output, altered mental status, lack of response to IV diuretic, hypotension, tachycardia, pallor, fatigue

Forrester classifications

Dry and warm (normal), Wet and warm, dry and cold, wet and cold (bad)

Treatment for Wet and Warm patients

IV loop diuretics, add IV/oral thiazides if needed, nitrates can be used for fast onset if needed

Treatment for cold and dry patients

If PCWP <15- IV fluids, IF PCWP 15-18 and SBP < 90- IV inotropes maybe with vasoconstrictor, if SBP > 90, use IV vasodilator

PCWP

Pulmonary capillary wedge pressure, tells us state of congestion of patient (18 is middle cutoff)

CI

cardiac index, Cardiac output adjusted for BSA, tells us state of perfusion, 2.2 is middle cutoff

Wet and Cold treatment in ADHF

if SBP < 90- IV inotrop plus/minus vasopressor and IV diuretic, if > 90- IV diuretic plus/minus vasodilator

Why D/C meds in ADHF

if it caused the exacerbation, BBs d/c if it causes fluid overload, ACEIs and ARBs/Aldosterone if renal function decreased

CO formula

Heart rate x stroke volume

What meds can decrease CO leading to ADHF

BBs, NDHP-CCBs, anti-arrhythmics, Cardiotoxic agents

What meds can cause Na/Water retention leading to ADHF

NSAIDs, Corticosteroids, TZDs, DPP4is, salt-containing drugs

What does high BNP or NT-proBNP tell us?

tells us that HF may be cause of symptoms/issues

Goals of therapy in ADHF

control symptoms (hypoperfusion or volume overload), maintain/improve hemodynamic stability, reduce short-term M&M, address precipitating factors

Monitoring for Loop diuretics in ADHF

symptomatic relief, adequate urine output, K+ and Mg levels, Scr and BUN for overdiuresis

Dosing of Loops in ADHF

Loop-naive gets 20-40 mg IV furosemide, loop experienced gets at least 2-3 times equivalent home dose

Strategies for when diuretic resistance develops

increase intermittent IV dose, change to continuous, combo therapy with thiazide diuretic

Nitroglycerin mainly affects what kind of dilation?

venous vasodilation

Nitroprusside affects what kind of dilation

arterial and venous vasodilation equally

Dobutamine MOA and use in ADHF

beta 1 and 2 agonist, used for cold patients to increase CO

milrinone MOA and use in ADHF

PDE3 inhibitor, increases CO in cold patients but can decrease BP so don’t use if patient is hypotensive

what is heart failure?

condition caused by an abnormality that affects cardiac systolic or diastolic function, and has pulmonary/systemic congestion, increased natriuretic peptides, and presents as fatigue, dyspnea and volume overload

HFrEF

HF with reduced ejection fraction, LVEF less than 40%

HFpEF

HF with preserved ejection fraction, LVEF greater than 50%

HFmrEF

HF with mildly reduced ejection fraction, LVEF 41-49%

Risk factors of Heart Failure

ischemic heart disease, HTN, Diabetes, Obesity, smoking,

Causes of heart failure

Ischemic heart disease, HTN, Valvular heart disease, genetic variant or FH of cardiomyopathy, exposure to cardiotoxic agents, metabolic disorders

Factors that affect preload

atrial contractility, heart rate, aortic pressure, ventricular compliance, TBV

Define preload

stretch of the heart’s ventricles before contraction

Define afterload

pressure the heart must overcome to push blood out of ventricles

factors that influence afterload

pulmonic/aortic valve disease, arteriolar tone, viscosity of blood

Higher preload does what to CO

increases it

higher afterload does what to CO

decreases it

Symptoms of HF

dyspnea, coughing/wheezing, edema, fatigue, nausea, confusion, high HR

Signs of HF

JVD, edema, pulmonary rales, cardiomegaly, S3 gallop, weight gain (>2 kg/week)

Labs that can be performed to diagnose HF

BNP, CMP, CBC, thyroid test, ECG, chest x-ray,

how does RAAS affect cardiac function?

activation leads to fluid retention that can increase preload and cardiac output

How do catecholamines affect cardiac function

5HT and NE increase HR and contractility that then increases cardiac output

Stage A HF classification

at risk for HF, no symptoms, no structural heart disease

Stage B HF classification

Pre-HF, No Sx, structural heart disease, RF and increased BNP, elevated filling pressures

Stage C HF classification

Symptomatic HF, current or prior symptoms, structural heart disease

Stage D HF classification

marked symptoms, despite GDMT

NYHA Stage 1

No Sx or limitation to activity

NYHA Stage 2

Mild Sx, comfortable at rest but slight limitations

NYHA Stage 3

Sx with less than ordinary activity, marked limitation of activity

NYHA Stage 4

Sx at rest, unable to do physical activity

Non-pharm HF treatment

education, sodium restriction (<3 g mild, <2 g moderate), social support, treatment of sleep disorders, weight disorders

MOA of Beta Blockers in HF

decreased heart rate, Decreased activation of RAAS, Decreased sympathetic outflow, Decreased blood pressure, Decreased remodeling

ADRs of Beta Blockers

bronchoconstriction, bradycardia, cold extremities, hypoglycemia, adverse lipid profile

MOA of ACEis and ARBs in HF

inhibit RAAS system

ADRs of ACEis and ARBs

cough, angioedema, hypotension, hyperkalemia, hyponatremia

MOA of Aldosterone Antagonists

competes for aldosterone in binding sites that prevent Na/K ATPase from functioning

ADRs of Aldosterone antagonists

electrolyte imbalances, gynecomastia, hyperkalemia

Step 1 of treatment for HF

establish HFrEF diagnosis, address congestion with loop diuretics, initiate GDMT (ACEs, ARBs, BBs, MRAs, SGLT2is or ARNIs)

MOA of Loop diuretics

acts on Na/K/Cl symporter, leading to increased secretion of Na and Cl and K, reducing blood volume

ADRs of loop diuretics

electrolyte imbalances, dehydration, ototoxicity, hypotension

MOA of ARNI

relax blood vessels, reduce sodium, improve kidney function, increases BNP presence

ADRs of ARNI

angioedema, hyperkalemia, impaired renal function, hypotension

MOA of SGLT2is

block glucose reabsorption in proximal tubule, resulting in increased glucose excretion

ADRs of SGLT2is

increased UTIs, volume depletion, increased ketones

Efficacy Monitoring parameters for ACEs, ARBs, and ARNIs, BBs, Aldosterone antagonists

decreased mortality, hospitalizations, HF symptoms, less exacerbations

Efficacy monitoring parameters for SGLT2is

decreased CV mortality, decreased hospitalizations

Efficacy monitoring parameters for Loop diuretics

Reduction in fluid retention

Beta blockers that can be used in HF

Bisoprolol, carvedilol, metoprolol succinate

SGLT2is that can be used in HF

dapagliflozin and empagliflozin

Which drug classes reduce mortality in HF?

all Step 1 therapies that are indicated except for loop diuretics

ADRs of Hydralazine/ISDN

Hypotension, Headaches, Dizziness, GI complaints

Hydralazine/ISDN is best used in which population for HF?

African Americans; 43% reduction in mortality

Cardiac glycosides MOA

inhibit Na/K ATPase by binding to K site, leading to increased contraction force and lower HR

Cardiac glycoside example

Digoxin

Cardiac glycosides ADRs

tachyarrhythmias, bradyarrhythmias, fatigue, confusion, blurry vision, N/V, SOB,

Step 3/4 treatment for HFrEF patients who are African American

Hydralazine/isosorbide dinitrate

Additional therapies in step 4

Ivabradine, Vericiguat, Digoxin

Hydralazine/ISDN MOA

Direct acting vasodilator; stimulates nitric oxide signaling, activates cGMP, venous dilation and preload reduction

Ivabradine MOA and when do we use

slows spontaneous depolarization, decreases HR; patient optimized on BB therapy and HR >70

Vericiguat MOA

Enhances production of cGMP and enhances sGC sensitivity to endogenous NO resulting in vasodilation and decreased preload

When can Vericiguat be used?

Patients with recent worsening of HF despite appropriate GDMT

When can digoxin be considered in HF?

symptomatic patients or unable to tolerate GDMT

Characteristics/RFs for HFpEF patients

HTN, ischemic disease, older, obesity, metabolic dysfunction, inactivity

HFpEF treatment

SGLT2is first, then Loops, MRAs, ARNIs, ARBs as directed

Which meds are most recommended for HFpEF

SGLT2is, Loops for Sx management, MRAs, ARBs