Lecture 14: Heart Failure Part 2 Flashcards
What are the classes for intervention recommendations in HF
- Class I - treatment is recommended/is indicated
- Class IIa - treatment should be considered
- Class IIb - treatment may be considered
- Class III - treatment is not reccomended
what are the general goals of therapy for HFpEF
- reduce HF symptoms
- increase functional status
- reduce hospital risk
- There is NO clear evidence that pharmacologic therapy, diet or other therapies reduce mortality for these patients:(
what are the key components of HFpEF management
- ongoing eval and monitoring (FU every 1-6mo depending on comorbs such as HTN, CAD, CKD)
- chronic disease management
- exercise, diet, weight loss, cardiac rehab
what is slide 15 saying
what is the most effective means of providing symptomatic relief of HF
diuretic therapy! improves both dyspnea and fluid overload
very hard to manage fluid retention s/s w/o a diuretic
what diuretics do you use for mild vs severe fluid retention
Mild fluid retention -> Thiazides!!
- hydrochlorothiazide
- metolazone
- chlorthalidone
Severe fluid retention -> oral loop diuretic
- furosemide (lasix)
- torsemide (demadex)
If you put a patient on a thiazide for fluid retention, what labs MUST you monitor
renal function and potassium
If fluid retention does not responding to thiazides or loops what should you do? what are the cautions of this therapy?
- combine loops and thiazides (MC is metolazone and furosemide)
- causes massive diuresis and electrolyte abnormalities
- must initiate oral potassium
- monitor daily wieght to assess diuresis and BMP within one week of therapy initiation or dosage change
why are SGLT-2 inhibitors used in HF
they reduce the risk of cardiovascular death and hospitalization for HF regardless of diabetes status!
Dapagliflozin (Farxiga) and Empagliflozin (Jardiance)
What are the MOA of SGLT-2 inhibitors in HF?
- Leads to osmotic diuresis and natriuresis → decreasing arterial pressure and stiffness → shifts to ketone-based myocardial metabolism
- Additional benefits may be due to reduction of preload and afterload blunting of cardiac stress/injury with less hypertrophy and fibrosis
What are the goals of therapy for HFrEF management
- clinical improvement, stabilization and reduction in risk of morbidity and mortality
What is HFrEF management based on
Extensive ACCF/AHA guidelines in place based on multiple clinical trials assessing outcomes of HFrEF with different management options
what are the 3 aspects of HFrEF management
- correction of systemic disorders or underlying causes (thyroid, DM, HTN, COPD, valvular disease, CAD)
- LIfestyle modification/nonpharm therapy (smoking/alcohol cessation, Na restriction, weight monitoring, weight loss, increase exercise)
- pharm management
what are the goals of __pharmacologic__ management of HFrEF
- Goals are to improve symptoms, slow or reverse deterioration in myocardial function, and reduce mortality
- Therapy should be initiated at low doses and titrated to target doses based on tolerability
what are the reccomended classes of pharm therapy for HFrEF
- Loop diuretics (1)
- ACE inhibitors or ARBs (1)
- Beta blockers (1)
- Aldosterone antagonists (1)
- SGLT2i (1)
- entresto (1)
- Hydralazine/Nitrate combination (1)
- Corlanor (2a)
- Digoxin (2b)
what are loops used for in HFrEF? what are the MC loops used?
- symptom relief d/t fluid overload
- furosemide, torsemide, bumetanide
what is the use of ACE inhibitors in HFrEF
- Class I indication
- Improve survival
- Common Medications: Enalapril, Captopril, Lisinopril, etc.
Begin with low dose and titrate over one to two week intervals
what do you have to monitor if a patient takes ACE inhibitors
BMP to evaluate potassium level and renal function
what are the indications for ARBs in HFrEF
think about class I, II, and III indications
- 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
what is the indication for BB in HFrEF
- class I indication
- Improves survival, as additive to ACE inhibitors
- Carvedilol (Coreg), Metoprolol succinate (Toprol XL), and Bisoprolol (Zebeta) are the recommended beta blockers
- start low and titrate up!
who should you use caution with BB
- Use cautiously with bradycardia, first degree AVB, hx of asthma or symptomatic hypotension
what are the indications for ARBs in HFrEF
Class I indication
Prolong survival and reduce cardiac remodeling
Common medications: Spironolactone and Eplerenone
Who are Aldosteron Antagonists CI in?
Contraindicated in patients with potassium > 5 and eGFR < 30
what is entresto, what does it do?
- Combination sacubitril and valsartan
- Sacubitril is a neprilysin inhibitor, which limits the breakdown of natriuretic peptides (ANP, BNP)
what are the indications for Enestro in HFrEF?
- Added to patients with continued symptoms after on appropriate doses of ACEI and BB
- Used in place of the ACEI or ARB
- Will need a 36 hr washout period prior to starting
- Start low dose and titrate to max dose over 4-6 weeks
- Shown to reduce hospitalizations and HF death
What are SE of Entresto
hypotenstion and hyperkalemia
what are the indications for Hydralazine/nitrate in HFrEF?
- Class I indication as addition to ACE inhibitor and beta blocker therapy for black patients
- Class IIA indication as replacement for ACE inhibitor or ARB due to drug intolerance, renal failure
- Hydralazine – Initiate at 25 mg TID and titrate to 75 to 100 mg TID
- Isosorbide dinitrate (Isordil) – Initiate at 10 to 20 mg TID and titrate up to 40 mg TID
what are the indications for Ivabradine (corlanor) in HFrEF?
- Inhibits the If channel in the sinus node → specifically slows sinus rate
- Use in stable pts w/ HR>70 who are maxxed out on BB or cannot tolerate BB
- Shown to reduce hospitalizations and cardiovascular death
what are the indications for Digoxin in HFrEF?
- Class IIA indication – can be beneficial to add to therapy after ACE inhibitor, beta blocker, and aldosterone antagonist
- May improve HF symptoms and control ventricular rate in patients with afib
- Usual dose is 125 mcg daily
- Titration is not recommended
what are the indications for CCB in HFrEF?
- Amlodipine and Felodipine have been shown to be safe with use in HF, but not beneficial
- Verapamil and Diltiazem are harmful in patients with HF and should be avoided (Myocardial depressants / negative inotropic effects)
what medications should be AVOIDED in HFrEF
- Antiarrhythmics (amiodarone and fofetilide are okay, all others are NOT)
- NSAIDS
- thiazolidinediones - actos (pioglitazone), avandia (rosiglitazone)
when is exercise training reccomended in HFrEF? what are the benefits?
- Cardiac rehab is recommended in patients with stable NYHA class II to III HF
- lessens symtpoms, increases exercise capacity, improves QOL, reduces hospitalizations, improves survival
what is Cardiac resynchronization therapy (CRT) and what are its benefits in HFrEF
- An effective therapy in patients with HF and ventricular dyssynchrony identified as a prolonged QRS
- Can improve exercise tolerance, NYHA functional class, and reduce morbidity and mortality
when is CRT reccomended in HFrEF
LVEF < or = 35%, QRS > 120ms with NYHA class III or IV symptoms
what can be used to prevent sudden cardiac arrest in patients with HF
implantable cardioverter defribrillator
primary or secondary reccomendations vary based on etiology
who is primary prevention of SCA reccomended in
- people who havent had SCD
- After optimal medical therapy
when is secondary prevention used in SCA
what do patients use while they wait for the implantation of their defibrillator
- LifeVest - wearable defibrillator
- only indicated as a bridge to ICD
what is Acute decompensated HF
- a common and potentially fatal cause of acute respiratory distress.
- may be new HF or exacerbation of chronic HF
- Characterized by acute dyspnea and rapid accumulation of fluid
What could cause acute decomensation of HF
- med noncomplaince
- MI
- tachyarrhythmias
- excessive salt intake
how does acute decompensated HF present?
- acute pulmonary edema
- severe dyspnea
- production of pink frothy sputum
- diaphoresis and cyanosis likely
- lung exam = inspiratory rales (could also see wheezes and rhonchi)
what are diagnostics for acute decomponsated HF
- Echo
- CXR
- BNP
- CMP
- Cardiac Enzymes
- CBC
- EKG
what is the management for acute decomensated HF
- Airway/oxygenation assessment
- Vital signs
- Cardiac monitoring
- IV access
- Diuretic therapy
- Vasodilator therapy
- Urine output monitoring
what are the parameters of supplemental oxygenation in Acute decomensated HF
when do you give it, how do you give it, ect?
- only give if hypoxic (goal o2 is 94%)
- keep patient seated upright
- nonrebreather facemask with high-flow O2
- noninvasive positive pressure ventilation (NPPV) is preferred for respiratory distress, respiratory acidosis and/or hypoxia
- if they fail/dont tolerate NPPV = INTUBATE
what is the preferred route and type of diruetic in acute decompensated HF
- IV recc d/t greater and more consistent drug bioavailability
- loops are first line (furosemide, torsemide, bumetanide)
what are effects of diuretic therapy in acute decomensated HF on renal function
- changes in GFR may occur, but if HF is severely symptomatic diuresis is indicated regardless
- if intravascular volume depletion is seen then reduce/hold diuresis
- cardiorenal syndrome may be seen (d/t elevated venous pressure and reduced CO.)
if a patient is not responding to diuretic therapy, what should you do
- restric sodium
- restrict water in patients w/ hyponatremia
- add second diuretic (thiazide or aldosterone antagonist)
- if in renal failure, Metolazone is choice for second diuretic.
wen is vasodilator therapy used in Acute decompensated HF? what is the vasodilators used and how are they given?
- recommended in patients w/o hypotension and severe symptomatic fluid overload
- continuous IV infusion of nitroglycerin or nitroprusside or morphine.
- MUST monitor BP frequently!!!!
what is the MOA of nitroglycerin
- Reduces LV filling pressures via venodilation
- At higher doses, lowers systemic afterload
What is the vasodilator is used when pronounced afterload reduction is needed? what is the cautions with this medication?
HTN emergency, acute AR, acute MR
Nitroprusside
* metabolizes into cyanide which can accumulate and become toxic/fatal
* SE = rebound tachycardia
* if discontinued can cause vasoconstriction
* limit to 24-48 hrs especially in renal failure!
what vasodilator therapeutic med is highly effective in pulmonary edema? How does this med work?
morphine
* increases venous and arterial dilation, lowering LA pressure and relieves anxiety which can reduce the efficiency of ventilation
* morphine may lead to CO2 retention d/t decreased ventilation
what vasodilator therapeutic med has a longer half life? what does this mean?
nesiritide
* longer half life means hypotension and arrhythmias persist longer
* not commonly used or reccomended
This is recombinant BNP
when should you hold BB therapy in acute decompensated HF
- if on chronic therapy
- severely decompensated
- hypotensive patients
can reinitiate therapy prior to discharge once patient is stable
when would you hold, continue or initiate ACE inhibitors and ARBs
- If patient is already on them then continue
- Hold if pt has hypotension, AKI or hyperkalemia
- Only initiate new ACEI or ARB therapy if pt is stable
when is it indicated to use inotropic agents in acute decompensated HF
indicated for pts with severe LV systolic dysfunction to maintain systemic perfusion and preserve end-organ performance
what are the inotropic agents that we use in acute decompensated HF? what is the MOA of each of these
- milrinone - PDE3 inhibitor with inotropic properties but can also cause vasodilation
- Dobutamine - stimulates B1 receptors to increase BP, HR, but also has vasodilation effects
what are the SE of inotropic agents
May lead to hypotension (Milrinone), hypertension (Dobutamine), and tachyarrhythmias
what is included in venous thromboembolism prophylaxis and when would we use it in acute decompensated HF
- Heparin, LMWH, or fondaparinux
- SCDs of A/C is contraindicated
- indicated in Hospitalized pts
what is ultrafiltration?
- AKA continuous renal replacement
- Effective method to remove excess fluid without major hemodynamic compromise and no effect on serum electrolytes
- Uses peripheral venous access and small blood volume, compared to hemodialysis
what is mechanical cardiac assistance and who is it considered for
- considered for pts in cardiogenic shock after acute decompensated HF
- considered for Cardiac index (CI) less than 2.0 L/min per m2, systolic arterial pressure less than 90 mmhg, and a pulmonary capillary wedge pressure above 18 mmhg
- can either use intraaortic balloon counterpulsation or interanlly implanted left ventricular assist device (LVAD).
What is cardiogenic shock
Defined by both the clinical signs of a reduced cardiac output and associated hemodynamic findings:
* clinical signs of reduced cardiac output - cool extremities, weak distal pulses, altered mental status, diminished urinary output.
* hemodynamic findings include - hypotension, pulm cap wedge pressure of >15mmHg which excludes hypovolemia, cardiac index <2.2L/min/m2)
What is cardiac index
- cardiac output per minute per square meter of body surface area.
- provides info on LV function
- Normal CI ranges from 2.6 to 4.2 L/min/m2x
what are causes of cardiogenic shock
what is the prinicple feature of shock
hypotension w evidence of end-organ hypoperfusion
What is the typical response to low cardiac output in cardiogenic shock
- sympathetic stimulation to increase cardiac performance and maintain vascular tone
- results in tachycardia and increase myocardial contractility and peripheral vasoconstriciton
what isthe typical presentation of cardiogenic shock pt
peripheral vasoconstriction (cool, clammy skin) and tachycardia
what labs are seen in cardiogenic shock?
- Elevated cardiac enzymes in presence of MI
- Elevated CR, ALT, AST in renal and hepatic hypoperfusion
- Coagulation abnormalities in hepatic congestion / hypoperfusion
- Anion gap acidosis and / or serum lactate elevation
- BNP for degree of fluid overload
what diagnostic studies can be done in assessment of cardiogenic shock
- EKG for underlying cause (MI, arrhythmia)
- Stat transthoracic echocardiogram
- CXR for cardiomegaly, pulmonary congestion
what procedures should be done in management of cardiogenic shock
- UA w/ insertion of foley catheter for UO measurement
- +/- pulm artery catheter placement (questionable dx, pt on inotropes, or not responding to tx)
- +/- left heart cath
what is the treatment plan for cardiogenic shock
How do you check pulmonary capillary wedge pressure
- Utilizes a Swan Ganz Catheter which is placed through a central line in the internal jugular, subclavian, or femoral veins
- Invasive and risky so not always done
- provides estimate of left atrial pressure (8-10)
- if elevated suspect pulmonary edema
what do inotropic vasopressor agents do
- Increase the contractility of the heart, HR, and peripheral vascular tone
- increase myocardial oxygen demands
Whar is the differences between B-agonists and A-agonists
B-agonist - can precipitate tachyarrhythmias
a-agonists - can lead to dangerous vasoconstriction and ischemia in vital organ beds
What does dopamine do at difference doses in cardiogenic shock
- Low doses (less than 3 mcg/kg/min) → predominantly dilate the renal arterioles/ vascular bed
- Intermediate doses (between 3 and 6) → β1-receptor stimulation and enhanced myocardial contractility
- Higher doses → α-receptor stimulation (peripheral vasoconstriction) in addition to continued β1 stimulation and tachycardia
what does dobutamine do as an inotropic agent in cardiogenic shock
- strong B1 and B2a efffects = increased CO, BP, HR and decreased PVR
how does dobutamine differ from dopamine
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.
what does NE (levophed) do in cardiogenic shock
- Strong β1 and α-adrenergic effects and moderate β2 effects
- Increases cardiac output and heart rate, decreases renal perfusion, decreases peripheral vascular resistance
- BP effects are variable
- Typically added to Dopamine if patient continues to be hypotensive
what must a patient be on with an intra-aortic balloon pump? what are the benefits of this device?
- Patient’s must be anticoagulated with IV heparin due to risk of thrombosis
- Benefits of decreased afterload without increases in myocardial demand
what device is typically used as a bridge to cardiac transplant?
LVAD
