Heart Failure 2 Flashcards
Goals of Therapy for HFpEF Management:
- Reduce HF symptoms
- Increase functional status (NYHA class)
- Reduce hospitalization risk
— lifestyle modification, congestion control, rhythm control, BP and comorbidity management
no evidence that pharm, diet, etc reduce mortality risk for these patients
Ongoing evaluation and monitoring for HFpEF
- F/u every 1-6 months, depending on comorbid conditions, medication response, etc.
- HTN, CAD, CKD, obesity - Chronic disease management
- Exercise, diet, weight loss, and cardiac rehab
what therapy is most effective providing symptomatic relief to pts with HF
Improves both dyspnea and fluid overload
diuretics
what diuretic is used for mild fluid retention in HF?
thiazides
- Hydrochlorothiazide
- Metolazone
- Chlorthalidone
Monitor renal function and potassium
what diuretic therapy is used for severe fluid retention / symptoms in HF?
oral loop diuretic
- Furosemide
- Torsemide
- Bumetanide
MUST monitor renal function and potassium
what is the Rule Of 2s for HF?
no more than 2L of fluids
no more than 2g of Na
if a pt has continued sx from diuretic therapy, what could you do?
- combine thiazide + loop
- Caution - massive diuresis and electrolyte abnormalities
- Metolazone and furosemide MC combo - Oral potassium replacement
- Potassium chloride (KCl, Klor-con, Kdur) - Monitoring
- Daily weights
- BMP within 1 wk of diuretic therapy initiation or dosage change
what medication reduces the risk of cardiovascular death and hospitalization for heart failure, regardless of diabetes status
SGLT2i
Dapagliflozin (Farxiga), empagliflozin (Jardiance), canagliflozin (Invokana), Sotagliflozin (Inpefa)
how do SGLT2i help with HF?
- osmotic diuresis and natriuresis → decreasing arterial pressure and stiffness → shifts to ketone-based myocardial metabolism
- Additional benefits d/t reduction of preload and afterload, blunting of cardiac stress/injury with less hypertrophy and fibrosis
The exact mechanism remains uncertain
what are the Recommended Pharm Classes for HFrEF?
- Loops - sx relief d/t fluid overload
- ACEi or ARBs (1)
- BB (1) - additive to ACEi
- Aldosterone antagonists (1)
- SGLT2i (1)
- Entresto (1)
- Hydralazine/Nitrate combination (1)
- Corlanor (2a)
- Digoxin (2b)
class indications for ARBs
- Class I indication for patients who do not tolerate ACE inhibitors
- Class IIA indication to continue if pt already on an ARB at time of dx of HF
- Class IIB indication to add to ACE inhibitor if aldosterone antagonist is contraindicated
- Class III (harmful) to add to ACE inhibitor and aldosterone antagonist
which BB is LA and is the most effective for HF?
Metoprolol succinate
indication for aldosterone antagonist for HF?
Class I indication - Prolong survival and reduce cardiac remodeling
CI for Aldosterone Antagonists
patients with K > 5 and eGFR < 30
Combination sacubitril and valsartan
a neprilysin inhibitor, which limits the breakdown of natriuretic peptides (ANP, BNP)
what medication is this?
Entresto
indications for Entresto
pts with continued sx after on appropriate doses of ACEI and BB
Used in place of the ACEI or ARB
what is needed before starting entresto?
Will need a 36 hr washout period of ACEI prior to starting Entresto
Start low dose and titrate to max dose over 4-6 weeks
CI to entresto
h/o angioedema with ACEI
SE of entresto
hypotension and hyperkalemia
indication for Hydralazine / Nitrate
in HF?
Class I as addition to ACEi and BB for black pts
In non-black pts, Class IIA as replacement for ACEi or ARB d/t drug intolerance, renal failure
what med inhibits the If channel in the sinus node → specifically slows sinus rate
Ivabradine (Corlanor)
indication for Ivabradine (Corlanor)
Class IIA indication Approved by the FDA for use in stable patients w/ HF
in order to take Ivabradine (Corlanor), the pt must have:
HR ≥70
sinus rhythm
Are taking the max tolerated dose of BB or in pts in whom BB are CI
Class IIB indication – beneficial to add after ACEi, BB, and aldosterone antagonist
Greater negative chronotropic effects than ionotropic
May improve HF sx and control ventricular rate in pts with afib
what med?
Digoxin
what CCBs have been shown to be safe with use in HF, but not beneficial?
which are harmful in pts with HF and should be avoided?
Amlodipine and Felodipine
Verapamil and Diltiazem - Myocardial depressants / negative inotropic effects
what meds to avoid in HF?
- Antiarrhythmics - Flecainide, Propafenone, Sotalol
- NSAIDs
- Thiazolidinediones – Actos (pioglitazone), Avandia (rosiglitazone)
what are the preferred antiarrhythics in HF
Amiodarone and dofetilide (Tikosyn)
Non-Pharmacologic Management
for HF
- exercise training - cardiac rehab
- Cardiac Resynchronization Therapy (CRT)
what non-pharm management is recommended in patients with stable NYHA class II to III HF
Lessens sx, increases exercise capacity, improves quality of life, reduces hospitalizations and improves survival
cardiac rehab
An effective therapy in patients with HF and ventricular dyssynchrony identified as a prolonged QRS
Cardiac Resynchronization Therapy (CRT)
Can improve exercise tolerance, NYHA functional class, and reduce morbidity and mortality
recommendations for Cardiac Resynchronization Therapy (CRT)
LVEF < or = 35%
QRS > 120ms
NYHA class III or IV sx
what is used to prevent Sudden Cardiac Arrest (SCA)
implantable cardioverter defibrillator (ICD)
vary based on etiology of cardiomyopathy and whether for primary or secondary prevention
what arrhythmia is common in pts with HF and cardiomyopathy
ventricular arrhythmias
what is classified as primary prevention for SCA
For those who have not suffered SCD
After optimal medical therapy
primary prevention for Ischemic CM and Nonischemic CM
- ICD is recommended for LVEF < 35% with class II or III HF sx and >40 d post-MI or revascularization
- LVEF < 35% with NYHA class II or III HF symptoms, > 90 days post dx, and reasonable likelihood of > 1 yr survival
Secondary Prevention for Sudden Cardiac Arrest (SCA)
- Pts with HF and cardiomyopathy who have survived an episode of SCD or have sustained VT without obvious reversible causes are recommended for ICD
- Unexplained syncope - pts with LVEF < 30% and unexplained syncope, recommend ICD
What to do while waiting the 90 days in SCA?
- LifeVest – a wearable defibrillator
- Indicated as a bridge to ICD during the waiting period
A common and potentially fatal cause of acute respiratory distress
Acute Decompensated HF
May be new HF or an exacerbation of chronic HF
Causes of acute decompensations include medication noncompliance, myocardial ischemia/infarction, tachyarrhythmias, excessive salt intake
Acute Decompensated HF is characterized by ?
acute dyspnea with rapid accumulation of fluid
Requires rapid assessment and stabilization
Acute Decompensated HF Presentation
acute pulmonary edema
Severe dyspnea, production of pink, frothy sputum
Diaphoresis and cyanosis
inspiratory rales
Wheezes and rhonchi
diagnostics for Acute Decompensated HF
- echo
- cxr
- BNP
- CMP
- cardiac enzymes
- CBC
- EKG
Stabilization/management measures for acut decompensated HF?
Airway/oxygenation assessment
VS
Cardiac monitoring
IV access
Diuretic therapy
Vasodilator therapy
Urine output monitoring
is Supplemental Oxygen needed for Acute Decompensated HF? how to deliver?
- Provide if needed, NOT in the absence of hypoxia
- O2 sat >94% is goal - Keep pt seated upright
- Non-rebreather facemask with high-flow O2
-
NPPV for rsp distress, rsp acidosis and/or hypoxia
- If fail NPPV or don’t tolerate, intubate
Diuretic Therapy for Acute Decompensated HF?
- Mainstay d/t fluid overload
- Start ASAP
- IV > oral
- Loop first line
dosing tips for diuretic therapy in acute decompensated HF?
- Individualize and titrate based on response
- If on chronic oral therapy, IV should be at least equal if not greater
- Peak diuresis occurs 30 min after administration
- No single regimen has been shown to be superior
- Bolus vs continuous infusion
- High vs low dose
diuretic effect on renal function in acute decompensated HF?
- R/o other causes of AKI
- If severely sx, diuresis is indicated regardless of GFR
- Reduce dose/hold if elevation and signs of intravascular volume depletion
-
Cardiorenal Syndrome
- D/t elevated venous pressure and reduced CO
- Renal function may actually improve with diuresis
what is the next step if pt with acut decompensated HF is having inadequate response to diuretic
- Sodium restriction
- Water restriction in patients with hyponatremia
- Addition diuretic
- Chlorothiazide – only IV thiazide diuretic
- HCTZ – oral thiazide
- Metolazone – oral diuretic addition of choice with renal failure
— Inhibits reabsorption of Na in distal tubules, thereby increasing excretion of water, Na, K and H
- Aldosterone antagonist – enhances diuresis and minimizes K wasting
what is recommended for pts without hypotension and severe symptomatic fluid overload in acute decompensated HF?
Vasodilator Therapy
- Frequent BP monitoring required
- Continuous IV Nitroglycerin or Nitroprusside, or morphine
— nitroglycerin: Short half-life, well tolerated, Reduces LV filling pressures via venodilation
which vasodilator
Potent with both venous and arteriolar effects
Used when pronounced afterload reduction is needed - HTN emergency, acute AR, acute MR
Nitroprusside
cautions with nitroprusside
- Metabolizes to cyanide, accumulation/toxicity can be fatal
- reflex tachycardia
- rebound vasoconstriction upon d/c
- Limit to 24 to 48 hrs, esp with renal failure
which med for acute decompensated HF
- Highly effective in pulmonary edema
- increases venous & arterial dilation, lowering LA pressure, and relieves anxiety, which can reduce the efficiency of ventilation
morphine
Morphine may lead to ? by reducing the ventilatory drive.
CO2 retention
Recombinant BNP
Vasodilator with no benefits over nitroglycerin or nitroprusside
Longer half-life, so hypotension and arrhythmias persist longer
Not common - Costly and not sufficient data to support its use
which med?
Nesiritide (Natrecor)
additional therapy for Acute Decompensated HF
- ACEi and ARBs
- Continue if already on, unless pt has hypotension, AKI or hyperkalemia
- Initiate new therapy once pt is stable - BB
- If on chronic therapy, and severely decompensated or hypotensive, hold therapy - Otherwise, may continue
- Initiate new therapy prior to discharge, once pt is stable - Inotropic Agents - milrinone, dobutamine
- Venous Thromboembolism Prophylaxis
- Heparin, LMWH or Fondaparinux - Ultrafiltration
- Mechanical Cardiac Assistance - Considered for cardiogenic shock
Milrinone MOA
phosphodiesterase inhibitor (PDE3) with mostly inotropic properties, but also causes vasodilation
Dobutamine MOA
stimulates B1 receptors to increase BP, HR, but also has vasodilation effects
indications for inotropic agents?
Indicated for severe LV systolic dysfunction to maintain systemic perfusion and preserve end-organ performance
SE of inotropic agents
hypotension (Milrinone), HTN (Dobutamine), and tachyarrhythmias
Effective method to remove excess fluid without major hemodynamic compromise and no effect on serum electrolytes in acute decompensated HF
Ultrafiltration
Uses peripheral venous access and small blood volume, compared to hemodialysis
2 major Mechanical Cardiac Assistance devices:
Intraaortic balloon counterpulsation
Internally implanted left ventricular assist device
indications for Mechanical Cardiac Assistance
Cardiac index (CI) <2.0 L/min per m2
systolic arterial pressure (SAP) <90 mmhg
PCWP >18 mmhg
Clinical signs of reduced CO in cardiogenic shock
Cool extremities, weak distal pulses, altered mental status, and diminished urinary output (< 30 mL/h)
Hemodynamic findings in cardiogenic shock include:
Hypotension
PCWP > 15 mmHg which excludes hypovolemia
Cardiac index < 2.2 L/min/m2
What is Cardiac Index?
CO/min/BSA
Provides info on LV function
Normal CI ranges from 2.6 to 4.2 L/min/m²x
The principle feature of cardiogenic shock is
hypotension with evidence of end-organ hypoperfusion
main pathophys of cardiogenic shock is a result of ?
tachycardia and increased myocardial contractility and peripheral vasoconstriction
labs for cardiogenic shock (not diagnostics)
- Elevated cardiac enzymes in presence of MI
- Elevated CR, ALT, AST in renal and hepatic hypoperfusion
- coag abnormalities in hepatic congestion / hypoperfusion
- Anion gap acidosis and / or serum lactate elevation
- BNP for degree of fluid overload
diagnostics for cardiogenic shock
EKG for underlying cause (MI, arrhythmia)
Stat TTE
CXR for cardiomegaly, pulmonary congestion
procedures for Cardiogenic Shock
- UA w/ insertion of foley catheter for UO measurement
- +/- Pulmonary artery catheter placement
- Consider if dx is questionable, pt on inotropes/pressors, or pt not responding to tx - +/- L heart cath
tx for cardiogenic shock
- Oxygen; intubation, ventilation
- Vasopressors/inotropes; consider careful IV fluids, arterial line and pulmonary artery catheter insertion to guide management; correct underlying causes of acidemia
- +/- Intra-aortic balloon pump
- Suspected MI → ASA, Heparin, Urgent Cath, Revascularize (PCI, CABG, Fibrinolysis)
Utilizes a Swan Ganz Catheter which is placed through a central line in the internal jugular, subclavian, or femoral veins
Provides an indirect estimate of left atrial pressure (LAP)
(cardiogenic shock)
Pulmonary Capillary Wedge Pressure
Invasive and associated with risks, so not always done
what med Increases the contractility of the heart, the heart rate, and peripheral vascular tone
also increase myocardial oxygen demand
Inotropic/Vasopressor Agents
which Inotropic/Vasopressor Agents can precipitate tachyarrhythmias
B-agonists
which inotropic/vasopressor agents can lead to dangerous vasoconstriction and ischemia in vital organ beds
α-agonists
Dopamine is qualitatively different effects at varying doses
- Low doses (< 3 mcg/kg/min) → predominantly dilate the renal arterioles/ vascular bed
- Intermediate doses (3-6) → β1-receptor stimulation and enhanced myocardial contractility
- Higher doses → α-receptor stimulation (peripheral vasoconstriction) in addition to continued β1 stimulation and tachycardia
Dobutamine has strong β1 and weak β2/α effects, which results in
increased cardiac output, blood pressure, and heart rate, as well as decreased peripheral vascular resistance
Dobutamine, a synthetic sympathomimetic agent that differs from dopamine in two important ways:
It does not cause renal vasodilation
It has a much stronger β2 (arteriolar vasodilatory) effect
which Inotropic/Vasopressor Agents
Strong β1 and α-adrenergic effects and moderate β2 effects
Increases CO and HR, decreases renal perfusion, decreases peripheral vascular resistance
BP effects are variable
Typically added to another Inotropic/Vasopressor Agents
if pt continues to be hypotensive
Norepinephrine (Levophed)
Typically added to Dopamine if patient continues to be hypotensive
Inotropic/Vasopressor Agent should be administered through what?
consequences if not?
central line
Peripheral extravasation into surrounding tissue can lead to vasoconstriction and skin necrosis
which circulatory support device
Temporary support system
pt must be anticoagulated with IV heparin d/t risk of thrombosis
Benefits of decreased afterload without increases in myocardial demand
Intra-aortic Balloon Pump (IABP)
which circulatory support device is typically used as a bridge to cardiac transplant
LVAD
