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Cardiovascular > Heart Failure Part 2 > Flashcards

Heart Failure Part 2 Flashcards

1
Q

What are the goals of therapy for HFpEF

A
  • Reduce HF symptoms
  • Increase functional status (NYHA class)
  • Reduce hospitalization risk

No clear evidence that pharmacologic therapy, diet, or other therapies reduce mortality risk for these patients

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2
Q

How is hospitalization risk reduced?

A
  • Lifestyle modification (exercise, decreased fat and sodium diet)
  • Congestion control
  • Rhythm control
  • BP and comorbidity management
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3
Q

What are the key components of management of HFpEF?

A
  • Ongoing evaluation and monitoring
  • Follow up visits every 1-6 months, depending on comorbid conditions (HTN, CAD, CKD, obesity), medication response, etc.
  • Chronic disease management
  • Lifestyle changes
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4
Q

Overall, what recommendations would you make for a patient with HFpEF?

A
  • Weight and blood pressure log
  • Exercise training
  • Caloric restriction (specifically sodium following rule of 2s–> <2 mg Na, <2 L fluid)
  • Coronary revascularization in presence of significant disease
  • Appropriate pharmacologic therapy
  • Cardiac rehab
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5
Q

What medications can be considered for management of HFpEF?

A
  • Diuretics for congestion and edema
  • SGLT2i
  • ACEi, ARB, thiazides, MRAs, ARNis (for HTN)
  • BBs for HTN, HR, and rhythm control
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6
Q

How would you manage common comorbidities of HFpEF?

A
  • Ischemia –> appropriate management
  • Dyslipidemia–> statins
  • DM –> appropriate agent
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7
Q

What are the SGLT2i?

A
  • Jardiance
  • Farxiga
  • Invokana
  • Inpefa
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8
Q

According to the AHA/ACC guidelines, what medication should be started first as needed for HFpEF?

A

Diuretics –> thiazides or loops

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9
Q

A patient with an ejection fraction of >50% who is symptomatic is started on a thiazide diuretic and maxed out. The provider is now thinking about adding another medication. Which medications could be added that are 2a recommendations?

A

SGLT2i
* Jardiance
* Farxiga

If a patient has an ejection fraction >50%, they have HFpEF

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10
Q

A patient with an ejection fraction of >50% who is symptomatic is maxed out on Jardiance and a thiazide diuretic. The provider is now considering adding another medication to their regimen. Which medications are 2b recommendations and could be added?

A

ARNis
* Entresto

MRA
* Spironolactone
* Eplerenone

ARB
* -sartans

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11
Q

What medication is the most effective means of providing symptomatic relief to patients with heart failure through improvement of dyspnea and fluid overload

A

Diuretic therapy

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12
Q

What diuretics should be used for mild fluid retention?

A

Thiazides
* Hydrochlorothiazide
* Metolazone
* Chlorthalidone

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13
Q

What should be monitored with thiazide diuretics?

A
  • Renal function
  • Potassium
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14
Q

What diuretics should be used with severe fluid retention/symptoms?

A

Oral loop diuretics
* Furosemide
* Torsemide
* Bumetanide

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15
Q

What is the BBW for loop diuretics?

A

Profound diuresis and electrolyte abnormalities

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16
Q

What do you need to monitor with use of loop diuretics?

A
  • Renal function
  • Potassium
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17
Q

If symptoms continue and you have a patient on a diuretic, what can you do? What should you be aware of when doing this?

A
  • You can combine a thiazide with a loop if continued symptoms
  • Be cautious of massive diuresis and electrolyte abnormalities
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18
Q

What is the most common combo of loop and thiazide diuretics for severe HFpEF?

A
  • Metolazone and furosemide
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19
Q

What should be initiated with diuretic therapy?

A

Oral potassium (potassium chloride)

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20
Q

What needs to be monitored with diuretic therapy?

A
  • Daily weight to assess diuresis
  • BMP within 1 week of diuretic therapy initiation or dosage change
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21
Q

What are the SGLT2is?

A

-gliflozins
Dapagliflozin, Empagliflozin, canagliflozin, sotagliflozin

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22
Q

What is the function of SGLT2i in HF?

A

Reduces risk of CV death and hospitalization for HF regardless of diabetes status through uncertain mechanism

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23
Q

What is the mechanism of action of SGLT2i in HF?

A
  • Leads to osmotic diuresis and natriuresis –> decreasing arterial pressure and stiffness –> shifts to ketone-based myocardial metabolism
  • Reduction of preload and afterload, blunting of cardiac stress/injury with less hypertrophy and fibrosis
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24
Q

What are the goals of therapy for HFrEF?

A
  • Clinical improvement, stabilization, and reduction in risk of morbidity and mortality
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25
Q

How is HFrEF managed overall?

A
  • Correction of systemic disorders or underlying causes (thyroid, DM, HTN, COPD, valvular disease, CAD)
  • Lifestyle modifications/nonpharmacologic therapies
  • Pharmacologic management
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26
Q

What are lifestyle modifications/nonpharmacologic therapies for HFrEF management?

A
  • Tobacco and alcohol cessation
  • Sodium restriction
  • Daily weight monitoring
  • Weight loss in obese patients
  • Increase exercise/cardiac rehab
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27
Q

What are the goals of pharmacologic management of HFrEF?

A
  • Improve symptoms
  • Slow or reverse deterioration in myocardial function
  • Reduce mortality
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28
Q

How should pharmacologic therapy be initiated for HFrEF?

A
  • Initiated at low doses and titrated to target doses based on tolerability
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29
Q

What is the first step in pharmacologic treatment of HFrEF (LVEF <40%)?

A

Establish diagnosis, address congestion, and initiate GDMT–> all class I and can start all at once or add over time
* ARNi in NYHA II-III; ACEi or ARB in NYHA II-IV
* Beta blocker
* MRA
* SGLT2i
* Diuretics as needed

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30
Q

A patient is initiated on one of the class I recommendations previously mentioned for HFrEF and now has a LVEF >40, what should you do?

A

Reassess and optimize dosing, compliance and patient education

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31
Q

A patient is initiated on one of the class I recommendations for HFrEF and still has a LVEF of <40%. What should you do now?

A
  • Give a nitrate if AA
  • If >1 year survival and LVEF <35%, NYHA 1-III recommend ICD
  • If NYHA II-III; ambulatory IV; LVEF <35%; NSR and QRS >150 ms with LBBB CRT-D

CRT-D = cardioresynchronization therapy

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32
Q

If a patient is started on 1st line medications for HFrEF and specific patient scenarios are considered and they continue to have refractory HF stage D, what will you do?

A
  • Durable MCS
  • Cardiac transplant
  • Palliative care
  • Investigational studies

MCS = mechanical circulatory support

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33
Q

What are recommended classes in HFrEF pharmacologic therapy that are class 1?

A
  • Loop diuretics
  • ACE inhibitors or ARBs
  • Beta blockers
  • Aldosterone antagonists
  • SGLT2i
  • Entresto
  • Hydralazine/nitrate combination
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34
Q

What are recommended drugs for HFrEF that are class 2 recommendations?

A
  • Corlanor (2a)
  • Digoxin (2b)
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35
Q

What is the use of loop diuretics in HFrEF?

A

Symptom relief due to fluid overload

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36
Q

What are the common loop diuretics used in HFrEF?

A
  • Furosemide
  • Torsemide
  • Bumetanide
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37
Q

What is the function of ACE inhibitors in HFrEF?

A

Improve survival (class I indication)

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38
Q

What are common ACE inhibitors that are used for HFrEF?

A
  • Enalapril
  • Captopril
  • Lisinopril
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39
Q

How should you dose ACE inhibitors for HFrEF?

A
  • Start low and titrate over one to two week intervals
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40
Q

What should be monitored with ACE inhibitor use in HFrEF?

A

BMP at baseline to evaluate potassium level and renal function, then again in 1-2 weeks

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41
Q

When are ARBs a class I indication in HFrEF?

A

Only if patients do not tolerate ACE inhibitors

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42
Q

When are ARBs a class II indication?

A
  • If patient already on an ARB at time of diagnosis of HF (IIA)
  • IIB to add to ACE inhibitor if aldosterone antagonist contraindicated
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43
Q

When are ARBs a class III (harmful) indication?

A

To add to ACE inhibitor and aldosterone antagonist

WILL CAUSE KIDNEY FAILURE DO NOT DO THIS

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44
Q

What is the function of BB in HFrEF?

A

Improves survival, class I indication, as additive to ACE inhibitors

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45
Q

Which beta blockers are used in HFrEF?

A
  • Carvedilol
  • Metoprolol succinate
  • Bisoprolol
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46
Q

When would you use caution with beta blockers?

A
  • Bradycardia
  • First degree AVB
  • Hx of asthma or symptomatic hypotension
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47
Q

How should you dose beta blockers for HFrEF?

A

start low and titrate up

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48
Q

This medication is a class I indication and prolongs survival and reduces cardiac remodeling

A

Aldosterone antagonists

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49
Q

What are common aldosterone antagonists used in HFrEF?

A

Spironolactone and eplerenone

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50
Q

When are aldosterone antagonists contraindicated?

A
  • Patients with potassium >5 and eGFR <30
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51
Q

What is entresto?

A
  • Combination sacubitril and valsartan
  • Neprilysin inhibitor, which limits breakdown of natriuretic peptides
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52
Q

When is entresto contraindicated?

A

If h/o angioedema with ACEI

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53
Q

When would entresto be added to a drug regimen for HFrEF?

A
  • For patients with continued symptoms after an appropriate dose of ACEI and BB
  • Used in place of ACEI or ARB
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54
Q

How long do you have to wait after use of ACEI to start entresto?

A
  • 36 hour washout period prior to starting entresto
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55
Q

What are benefits and risks of entresto?

A
  • Reduces hospitalizations and HF death
  • Can lead to hypotension and hyperkalemia
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56
Q

When could hydralazine/nitrate be added to a drug regimen for HFrEF?

A
  • Class I indication as addition to ACE inhibitor and beta blocker therapy for black patients
  • Class IIa indication as replacement for ACEi or ARB due to drug intolerance or renal failure in non-black patients
57
Q

What hydralazine/nitrate medications could be added for black patients with HF?

A
  • Hydralazine
  • Isosorbide dinitrate
58
Q

What is the mechanism of action of ivabradine (corlanor)

A

Inhibits the If channel in the sinus node to slow the sinus rate

59
Q

When could ivabradine be used for HFrEF?

A
  • Class IIA indication for stable patients with HF
60
Q

What must patients have before initiation of Ivabradine (Corlanor)?

A
  • Heart rate >70 bpm
  • Sinus rhythm
  • Taking maximally tolerated dose of beta blockers or in patients in whom beta-blockers are contraindicated
61
Q

What is the benefit of ivabradine (corlanor)?

A

Shown to reduce hospitalizations and CV death

62
Q

When could digoxin be considered as a therapy?

A
  • Class IIB indication
  • Can be beneficial to add to therapy after ACE inhibitor, BB, and aldosterone antagonist
63
Q

What effect does digoxin have on HF?

A
  • Negative chronotropic effects greater than ionotropic
  • May improve symptoms and control ventricular rate in patients with afib
64
Q

What medications should you use caution with HF?

A
  • CCB: amlodipine and felodipine are safe, but not beneficial
  • Verapamil and diltiazem are harmful in HF and should be avoided due to myocardial depression/negative inotropic effects
  • Certain antiarrhythmics
  • NSAIDs
  • Thiazolidinones
65
Q

What are the preferred antiarrhythmics in HF? Which ones should be avoided?

A
  • Preferred: amiodarone and dofetilide
  • Avoid: flecainide, propafenone, sotalol
66
Q

What thiazolidinediones can be used in HF?

A
  • Actos
  • Avandia
67
Q

What non-pharmacologic therapy can be considered in HF?

A
  • Exercise training
  • Cardiac resynchronization therapy
  • ICD/lifevest
68
Q

What are guidelines for cardiac rehab in HF?

A
  • Recommended in stable NYHA class II to III HF
69
Q

What are benefits of cardiac rehab in HF?

A
  • Lessens symptoms
  • Increases exercise capacity
  • Improves quality of life
  • Reduces hospitalizations
  • Improves survival
70
Q

When would cardiac resynchronization therapy be indicated?

A
  • HF and ventricular dyssynchrony identified as prolonged QRS
  • LVEF < or = 35%
  • QRS >120 ms
  • NYHA class III or IV
71
Q

What are benefits of cardiac resynchronization therapy in HF?

A
  • Improved exercise tolerance and NYHA functional class
  • Reduced morbidity and mortality
72
Q

What ventricular arrhythmias are common in patients with HF and cardiomyopathy?

A
  • Asymptomatic PVCs to sustained VT or VF
73
Q

what determines recommendations for implantable cardioverter defibrillator to prevent sudden cardiac arrest?

A
  • etiology of cardiomyopathy
  • whether for primary or secondary prevention
74
Q

What are primary prevention recommendations for ICD?

A
  • For those who have not suffered SCD to prevent sudden cardiac arrest
  • After optimal medial therapy
  • Ischemic CM: ICD recommended for LVEF <35% with class II or III HF symptoms and >40 days post-MI or revascularization
  • Nonischemic CM: LVEF <35% with NYHA class II or III HF symptoms, >90 days post dx, and reasonable likelihood of >1 year survival
75
Q

What are indications for ICD for secondary prevention of SCA?

A
  • Patients with HF and cardiomyopathy who have survived an episode of SCD
  • OR sustained VT without obvious reversible causes
76
Q

What is an additional indication for an ICD in HF other than primary or secondary prevention?

A
  • Patients with LVEF <30% an unexplained syncope
77
Q

What should be done while waiting 90 days for an ICD?

A
  • Lifevest: wearable defibrillator as bridge to ICD
78
Q

What is acute decompensated HF?

A
  • Common and potentially fatal cause of acute respiratory distress
  • May be new HF or exacerbation of chronic HF
79
Q

What are causes of acute decompensated HF?

A
  • Medication noncompliance
  • Myocardial infarction/ischemia
  • Tachyarrhythmias
  • Excessive salt intake
80
Q

What are characteristics of acute decompensated HF?

A
  • Rapid accumulation of fluid that requires rapid assessment and stabilization
81
Q

What is the presentation of acute decompensated HF?

A
  • Acute pulmonary edema
  • Severe dyspnea
  • Production of pink, frothy sputum
  • Diaphoresis and cyanosis likely present
  • Inspiratory rales
  • Wheezes and rhonchi also common
82
Q

What are diagnostic tests that can be performed in acute decompensated HF?

A
  • Echo
  • CXR
  • BNP
  • CMP
  • Cardiac enzymes
  • CBC
  • EKG
83
Q

How is acute decompensated HF managed?

A

Stabilization/management measures:
* Airway/oxygenation assessment
* Vital signs
* Cardiac monitoring
* IV access
* Diuretic therapy
* Vasodilator therapy
* Urine output monitoring

84
Q

How/when should supplemental oxygen be administered in acute decompensated HF?

A
  • If needed, not in absence of hypoxia ox sat >94% goal
  • Keep patient upright
  • Non-rebreather with high-flow O2
  • Noninvasive PPV preferred for respiratory distress, acidosis, or hypoxia
  • If fail NPPV or don’t tolerate, intubate and initiate mechanical ventilation
85
Q

How should a patient with acute decompensated HF be managed with diuretic therapy?

A
  • Start ASAP
  • IV recommended bc greater availability
  • Loop diuretics are first line (furosemide, torsemide, bumetanide)
86
Q

What are dosing tips for diuretics in acute decompensated HF?

A
  • Individualize and titrate based on response
  • If on chronic oral therapy, IV should be equal or greater
  • Peak diuresis = 30 mins after admin
  • No single regimen is superior (bolus vs continuous or high vs low dose)
87
Q

What should be monitored while a patient with acute decompensated HF is on diuretic therapy?

A
  • Vital signs
  • Fluid status: daily weights and Is/Os
  • Renal function
  • Electrolytes
88
Q

What should be kept in mind with diuretic therapy and renal function?

A
  • Diurese regardless of changes in GFR if severely symptomatic
  • Reduce dose or hold if elevation and signs of intravascular volume depletion
  • Cardiorenal syndrome can occur due to elevated venous pressure and reduced cardiac output but is actually improved with diuresis
89
Q

What can you do if there is an inadequate response to diuretic therapy?

A
  • Sodium restriction
  • Water restriction in patients with hyponatremia
  • Addition of a second diuretic
90
Q

What additional diuretics can be added if there is an inadequate response to loop diuretic therapy in acute decompensated HF?

A
  • Chlorothiazide (IV)
  • HCTZ
  • Metolazone
  • Aldosterone antagonist
91
Q

Which additional diuretic is the addition of choice with renal failure because it inhibits reabsorption of Na in distal tubules, thereby increasing excretion of water, Na, K, and H

A

Metolazone

92
Q

What is the benefit of adding an aldosterone antagonist to a loop in acute decompensated HF?

A
  • Enhances diuresis and minimizes potassium wasting
93
Q

When is a vasodilator recommended in acute decompensated HF?

A
  • No hypotension
  • Severe symptomatic fluid overload
94
Q

How is vasodilator therapy for acute decompensated HF administered and what is monitored?

A
  • Continuous IV infusion of nitroglycerin or nitroprusside or morphine
  • Frequent BP monitoring required
95
Q

What is the MOA of nitroglycerin?

A
  • Reduces LV filling pressures via venodilation
  • Lowers systemic afterload at higher doses
96
Q

What are the effects of nitroprusside?

A
  • Vasodilator with venous and arteriolar effects
97
Q

When is nitroprusside used?

A
  • When pronounced afterload reduction is needed
  • HTN emergency, acute AR, acute MR
98
Q

Why could nitroprusside be dangerous?

A

Metabolizes to cyanide, accumulation/toxicity can be fatal
May cause reflex tachycardia

99
Q

How much nitroprusside can be given?

A

Limit to 24-48 hrs especially with renal failure

100
Q

What is morphine highly effective as a vasodilator in treating for acute decompensated HF?

A

Pulmonary edema

101
Q

What is the mechanism of action of morphine in acute decompensated HF?

A
  • Increases venous and arterial dilation, lowering LA pressure
  • Relieves anxiety which can reduce efficacy of ventilation

However, may reduce ventilatory drive

102
Q

What is the mechanism of action of nisiritide?

A
  • Recombinant BNP
  • Vasodilator with no benefits over nitro or nitroprusside
103
Q

What are some things to keep in mind with nesiritide use?

A
  • Longer half-life, so hypotension and arrhythmias persist longer
  • Costly and not sufficient data to support use
104
Q

What are 2 medications that can be initiated for acute decompensated HF once the patient is stable?

A
  • ACE inhibitors/ARBs
  • Beta blockers (hold if severely decompensated or hypotensive and on chronic therapy)
105
Q

What inotropic agents are indicated for patients with severe LV systolic dysfunction ot maintain systemic perfusion and preserve end-organ performance?

A
  • Milrinone
  • Dobutamine
106
Q

What is the MOA of milrinone?

A
  • PDE3
  • Inotropic
  • Vasodilation
107
Q

What is the MOA of dobutamine?

A
  • Stimulates B1 receptors to increase BP, HR, but also vasodilate
108
Q

What are side effects of milrinone and dobutamine (inotropic agents for acute decompensated HF)?

A
  • May lead to hypotension (milrinone)
  • Hypertension (dobutamine)
  • Tachyarrhythmias
109
Q

Patients with ADHF who are hospitalized are at a higher risk for what vascular event? What will you give them for this?

A
  • VTE
  • Heparin, LMWH, or fondaparinux
  • SCDs if A/C contraindicated

SCD = sequential compression device

110
Q
A
111
Q

What is an additonal therapy for acute decompensated HF that is used to remove excess fluid without major hemodynamic compromise or impact on electrolytes

A
  • Ultrafiltration
112
Q

What is an additional therapy for acute decompensated HF that is considered for patients in cardiogenic shock?

A
  • mechanical cardiac assistance
113
Q

What are the 2 major devices used in mechanical cardiac assistance?

A
  • Intraaortic balloon counterpulsation
  • Internally implanted left ventricular assist device
114
Q

What criteria do patients have to meet to get mechanical cardiac assistance?

A

cardiac index less than 2.0 L/min
Systolic artery pressure <90 mmhg
pulmonary wedge pressure >18 mmHg

114
Q
A
115
Q

What is the definition of cardiogenic shock?

A
  • Signs of reduced cardiac output and hemodynamic findings
116
Q

What are the clinical signs of reduced cardiac output?

A
  • Cool extremities
  • Weak distal pulses
  • Altered mental status
  • Diminished urinary output
117
Q

What are hemodynamic findings of cardiogenic shock?

A
  • Hypotension
  • PCWP of >15 mmHg which excludes hypovolemia
  • Cardiac index <2.2 L/min/m2
118
Q

What is a cardiac index?

A
  • Cardiac output per square meter of body surface area
  • Provides info on left ventricular function
  • Normal ranges from 2.6-4.2
  • CO/BSA = CI
119
Q

What are causes of cardiogenic shock?

A
  • AMI
  • End-stage severe cardiomyopathies
  • Acute myocarditis
  • Stress cardiomyopathy
  • Endocarine disease: brady or tachyarrhthymias
  • Secondary to medications
  • Posttraumatic
120
Q

What is the pathophysiology of cardiogenic shock?

A
  • Principle feature = hypotension with evidence of end-organ hypoperfusion
  • Low cardiac output –> sympathetic stimulation –> tachycardia and increased myocardial contractility and peripheral vasoconstriction
121
Q

What is the classic presentatio of a cardiogenic shock patinet?

A
  • Peripheral vasoconstriction (cool, moist skin) and tachycardia
122
Q

What are diagnostic labs in cardiogenic shock?

A
  • Elevated cardiac enzymes (if 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
123
Q

What are imaging studies for cardiogenic shock?

A
  • EKG for underlying cause (MI, arrhythmia)
  • Stat transthoracic echo
  • CXR for cardiomegaly, pulmonary congestion
124
Q

What procedures can be considered for management of cardiogenic shock?

A
  • UA with insertion of foley catheter for UO measurement
  • +/- pulmonary artery catheter placement (if diagnosis questionable, pt on inotropes/pressors, or patient not responding to treatment)
  • +/- left heart catheterization
  • Pulmonary capillary wedge pressure with Swanz Ganz catheter: if elevated, supports pulmonary edema diagnosis
125
Q

What is the treatment of cardiogenic shock?

A
  • Oxygen supplementation; intubation, ventilation
  • Vasopressors/inotropes
  • +/- intra-aortic balloon pump
  • Suspected MI –> ASA, Heparin, urgent cath, revascularization
126
Q

what should you consider with vasopressors/inotropes in cardiogenic shock?

A
  • IV fluids arterial line and pulmonary artery catheter insertion to guide management
  • correct underlying causes of acidemia
127
Q

What is the function of inotropic/vasopressor agents in cardiogenic shock?

A
  • Increase contractility of heart, HR, and peripheral vascular tone
  • Can also increase myocardial oxygen demand
128
Q

What should you keep in mind when using inotropic/vasopressor agents?

A
  • beta agonists can precipitate tachyarrhythmias
  • alpha agonists can lead to dangerous vasoconstriction and ischemia in vital organ beds
  • attention should be given to patient as whole not desired arterial pressure
129
Q

What are the inotropic/vasopressor agents used in cardiogenic shock?

A
  • Dopamine
  • Dobutamine
  • Norepinephrine
130
Q

How does dopamine work as an inotropic/vasopressor agent?

A
  • Catecholamine with varying effect at different doses
  • Low doses: dilate renal arterioles/vascular bed
  • Intermediate doses: B1 receptor stimulation and enhanced myocardial contractility
  • High doses: alpha receptor stimulation in addition to B1 stimulation and tachycardia
131
Q

What is the MOA of dobutamine?

A

Strong B1 and weak B2 effects resulting in increased cardiac output, blood pressure, and heart rate, decreased peripheral vascular resistance

132
Q

What are the 2 ways dobutamine differs from dopamine?

A
  • Does not cause renal vasodilation
  • Stronger B2 effect
133
Q

What is the MOA of norepinephrine (Levophed)?

A
  • Strong B1 and alpha-adrenergic effects and moderate B2 effects
  • Increases CO and HR, decreases renal perfusion, decreases peripheral vascular resistance
  • BP effects vary
134
Q

How is norepinephrine usually used?

A

Typically added to dopamine if patient still hypotensive

135
Q

How do you choose a inotropic/vasopressor agent?

A
  • Choose based on need, while looking at HR, MAP, and patient clinical status
  • Titrate single agent to max tolerate dose before adding additional agent
  • Most should be administered through a central line because peripheral extravasation into surrounding tissue can lead to vasoconstriction and skin necrosis
136
Q

What are the 2 circulatory support devices used in cardiogenic shock?

A
  • Intra-aortic balloon pump and left-ventricular assist device (LVAD)
137
Q

How is intra-aortic balloon pump used in cardiogenic shock?

A
  • Temporary support system
  • Patient anticoagulated with IV heparin due to risk of thrombosis
  • Benefits of decreased afterload without increases in myocardial demand
138
Q

How is Left-ventricular assist device usually used in cardiogenic shock?

A

As bridge to cardiac transplant

Cardiovascular (17 decks)

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