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Cardiology (Fall 2023) > Lecture 14: Heart Failure Part 2 > Flashcards

Lecture 14: Heart Failure Part 2 Flashcards

1
Q

What are the classes for intervention recommendations in HF

A
  • 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
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2
Q

what are the general goals of therapy for HFpEF

A
  • 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:(
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3
Q

what are the key components of HFpEF management

A
  • 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
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4
Q

what is slide 15 saying

A
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5
Q

what is the most effective means of providing symptomatic relief of HF

A

diuretic therapy! improves both dyspnea and fluid overload

very hard to manage fluid retention s/s w/o a diuretic

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6
Q

what diuretics do you use for mild vs severe fluid retention

A

Mild fluid retention -> Thiazides!!
- hydrochlorothiazide
- metolazone
- chlorthalidone
Severe fluid retention -> oral loop diuretic
- furosemide (lasix)
- torsemide (demadex)

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7
Q

If you put a patient on a thiazide for fluid retention, what labs MUST you monitor

A

renal function and potassium

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8
Q

If fluid retention does not responding to thiazides or loops what should you do? what are the cautions of this therapy?

A
  • 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
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9
Q

why are SGLT-2 inhibitors used in HF

A

they reduce the risk of cardiovascular death and hospitalization for HF regardless of diabetes status!

Dapagliflozin (Farxiga) and Empagliflozin (Jardiance)

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10
Q

What are the MOA of SGLT-2 inhibitors in HF?

A
  • 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
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11
Q

What are the goals of therapy for HFrEF management

A
  • clinical improvement, stabilization and reduction in risk of morbidity and mortality
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12
Q

What is HFrEF management based on

A

Extensive ACCF/AHA guidelines in place based on multiple clinical trials assessing outcomes of HFrEF with different management options

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13
Q

what are the 3 aspects of HFrEF management

A
  • 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
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14
Q

what are the goals of __pharmacologic__ management of HFrEF

A
  • 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
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15
Q
A
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16
Q

what are the reccomended classes of pharm therapy for HFrEF

A
  • 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)
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17
Q

what are loops used for in HFrEF? what are the MC loops used?

A
  • symptom relief d/t fluid overload
  • furosemide, torsemide, bumetanide
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18
Q

what is the use of ACE inhibitors in HFrEF

A
  • Class I indication
  • Improve survival
  • Common Medications: Enalapril, Captopril, Lisinopril, etc.
    Begin with low dose and titrate over one to two week intervals
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19
Q

what do you have to monitor if a patient takes ACE inhibitors

A

BMP to evaluate potassium level and renal function

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20
Q

what are the indications for ARBs in HFrEF

think about class I, II, and III indications

A
  • 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
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21
Q

what is the indication for BB in HFrEF

A
  • 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!
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22
Q

who should you use caution with BB

A
  • Use cautiously with bradycardia, first degree AVB, hx of asthma or symptomatic hypotension
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23
Q

what are the indications for ARBs in HFrEF

A

Class I indication
Prolong survival and reduce cardiac remodeling
Common medications: Spironolactone and Eplerenone

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24
Q

Who are Aldosteron Antagonists CI in?

A

Contraindicated in patients with potassium > 5 and eGFR < 30

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25
Q

what is entresto, what does it do?

A
  • Combination sacubitril and valsartan
  • Sacubitril is a neprilysin inhibitor, which limits the breakdown of natriuretic peptides (ANP, BNP)
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26
Q

what are the indications for Enestro in HFrEF?

A
  • 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
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27
Q

What are SE of Entresto

A

hypotenstion and hyperkalemia

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28
Q

what are the indications for Hydralazine/nitrate in HFrEF?

A
  • 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
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29
Q

what are the indications for Ivabradine (corlanor) in HFrEF?

A
  • 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
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30
Q

what are the indications for Digoxin in HFrEF?

A
  • 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
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31
Q

what are the indications for CCB in HFrEF?

A
  • 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)
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32
Q

what medications should be AVOIDED in HFrEF

A
  • Antiarrhythmics (amiodarone and fofetilide are okay, all others are NOT)
  • NSAIDS
  • thiazolidinediones - actos (pioglitazone), avandia (rosiglitazone)
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33
Q

when is exercise training reccomended in HFrEF? what are the benefits?

A
  • 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
34
Q

what is Cardiac resynchronization therapy (CRT) and what are its benefits in HFrEF

A
  • 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
35
Q

when is CRT reccomended in HFrEF

A

LVEF < or = 35%, QRS > 120ms with NYHA class III or IV symptoms

36
Q

what can be used to prevent sudden cardiac arrest in patients with HF

A

implantable cardioverter defribrillator

primary or secondary reccomendations vary based on etiology

37
Q

who is primary prevention of SCA reccomended in

A
  • people who havent had SCD
  • After optimal medical therapy
38
Q

when is secondary prevention used in SCA

A
39
Q

what do patients use while they wait for the implantation of their defibrillator

A
  • LifeVest - wearable defibrillator
  • only indicated as a bridge to ICD
40
Q
A
41
Q

what is Acute decompensated HF

A
  • 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
42
Q

What could cause acute decomensation of HF

A
  • med noncomplaince
  • MI
  • tachyarrhythmias
  • excessive salt intake
43
Q

how does acute decompensated HF present?

A
  • acute pulmonary edema
  • severe dyspnea
  • production of pink frothy sputum
  • diaphoresis and cyanosis likely
  • lung exam = inspiratory rales (could also see wheezes and rhonchi)
44
Q

what are diagnostics for acute decomponsated HF

A
  • Echo
  • CXR
  • BNP
  • CMP
  • Cardiac Enzymes
  • CBC
  • EKG
45
Q

what is the management for acute decomensated HF

A
  • Airway/oxygenation assessment
  • Vital signs
  • Cardiac monitoring
  • IV access
  • Diuretic therapy
  • Vasodilator therapy
  • Urine output monitoring
46
Q

what are the parameters of supplemental oxygenation in Acute decomensated HF

when do you give it, how do you give it, ect?

A
  • 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
47
Q

what is the preferred route and type of diruetic in acute decompensated HF

A
  • IV recc d/t greater and more consistent drug bioavailability
  • loops are first line (furosemide, torsemide, bumetanide)
48
Q

what are effects of diuretic therapy in acute decomensated HF on renal function

A
  • 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.)
49
Q

if a patient is not responding to diuretic therapy, what should you do

A
  • 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.
50
Q

wen is vasodilator therapy used in Acute decompensated HF? what is the vasodilators used and how are they given?

A
  • recommended in patients w/o hypotension and severe symptomatic fluid overload
  • continuous IV infusion of nitroglycerin or nitroprusside or morphine.
  • MUST monitor BP frequently!!!!
51
Q

what is the MOA of nitroglycerin

A
  • Reduces LV filling pressures via venodilation
  • At higher doses, lowers systemic afterload
52
Q

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

A

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!

53
Q

what vasodilator therapeutic med is highly effective in pulmonary edema? How does this med work?

A

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

54
Q

what vasodilator therapeutic med has a longer half life? what does this mean?

A

nesiritide
* longer half life means hypotension and arrhythmias persist longer
* not commonly used or reccomended

This is recombinant BNP

55
Q

when should you hold BB therapy in acute decompensated HF

A
  • if on chronic therapy
  • severely decompensated
  • hypotensive patients

can reinitiate therapy prior to discharge once patient is stable

56
Q

when would you hold, continue or initiate ACE inhibitors and ARBs

A
  • 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
57
Q

when is it indicated to use inotropic agents in acute decompensated HF

A

indicated for pts with severe LV systolic dysfunction to maintain systemic perfusion and preserve end-organ performance

58
Q

what are the inotropic agents that we use in acute decompensated HF? what is the MOA of each of these

A
  • milrinone - PDE3 inhibitor with inotropic properties but can also cause vasodilation
  • Dobutamine - stimulates B1 receptors to increase BP, HR, but also has vasodilation effects
59
Q

what are the SE of inotropic agents

A

May lead to hypotension (Milrinone), hypertension (Dobutamine), and tachyarrhythmias

60
Q

what is included in venous thromboembolism prophylaxis and when would we use it in acute decompensated HF

A
  • Heparin, LMWH, or fondaparinux
  • SCDs of A/C is contraindicated
  • indicated in Hospitalized pts
61
Q

what is ultrafiltration?

A
  • 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
62
Q

what is mechanical cardiac assistance and who is it considered for

A
  • 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).
63
Q

What is cardiogenic shock

A

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)

64
Q

What is cardiac index

A
  • 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
65
Q

what are causes of cardiogenic shock

A
66
Q

what is the prinicple feature of shock

A

hypotension w evidence of end-organ hypoperfusion

67
Q

What is the typical response to low cardiac output in cardiogenic shock

A
  • sympathetic stimulation to increase cardiac performance and maintain vascular tone
  • results in tachycardia and increase myocardial contractility and peripheral vasoconstriciton
68
Q

what isthe typical presentation of cardiogenic shock pt

A

peripheral vasoconstriction (cool, clammy skin) and tachycardia

69
Q

what labs are seen in cardiogenic shock?

A
  • 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
70
Q

what diagnostic studies can be done in assessment of cardiogenic shock

A
  • EKG for underlying cause (MI, arrhythmia)
  • Stat transthoracic echocardiogram
  • CXR for cardiomegaly, pulmonary congestion
71
Q

what procedures should be done in management of cardiogenic shock

A
  • 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
72
Q

what is the treatment plan for cardiogenic shock

A
73
Q

How do you check pulmonary capillary wedge pressure

A
  • 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
74
Q

what do inotropic vasopressor agents do

A
  • Increase the contractility of the heart, HR, and peripheral vascular tone
  • increase myocardial oxygen demands
75
Q

Whar is the differences between B-agonists and A-agonists

A

B-agonist - can precipitate tachyarrhythmias
a-agonists - can lead to dangerous vasoconstriction and ischemia in vital organ beds

76
Q

What does dopamine do at difference doses in cardiogenic shock

A
  • 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
77
Q

what does dobutamine do as an inotropic agent in cardiogenic shock

A
  • strong B1 and B2a efffects = increased CO, BP, HR and decreased PVR
78
Q

how does dobutamine differ from dopamine

A

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.

79
Q

what does NE (levophed) do in cardiogenic shock

A
  • 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
80
Q

what must a patient be on with an intra-aortic balloon pump? what are the benefits of this device?

A
  • Patient’s must be anticoagulated with IV heparin due to risk of thrombosis
  • Benefits of decreased afterload without increases in myocardial demand
81
Q

what device is typically used as a bridge to cardiac transplant?

A

LVAD

Cardiology (Fall 2023) (45 decks)

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