CONTENTS
- Rapid Reference 🚀
- Intro: what this chapter is about
- Hemodynamic evaluation & risk stratification
- Causes of heart failure decompensation
- Investigations
- Treatment
- Related topics
- Podcast
- Questions & discussion
- Pitfalls
evaluation
- EKG & echocardiography.
- CBC (consider transfusion for HgB <7-8 mg/dL).
- Electrolytes including Ca/Mg/Phos.
- Troponin.
- Lactate & liver function tests if shock is suspected.
- Consider:
- TSH (thyroid stimulating hormone).
- Digoxin level.
- Ferritin and transferrin saturation.
1) treat the lungs 📖
- Cardiogenic pulmonary edema ➡️ Consider BiPAP (vs intubation).
- Large effusion(s) may be drained if causing acute distress.
- Consider inhaled epoprostenol for intubated patients with right ventricular failure or pulmonary hypertension.
2) optimize the MAP 📖
- HTN/normotension with HFrEF ➡️ Consider afterload reduction. Options include:
- Hypotension (severe or w/ organ dysfunction) ➡️
- Norepinephrine is usually a good choice.
- Epinephrine is an option in HFrEF with hypoperfusion.
3) optimize the volume 📖
- Fluid challenge if: hypoperfusion, no pulmonary congestion (no B-lines on ultrasound), assessment suggests total body hypovolemia.
- Diuresis if: significant systemic/pulmonary congestion, assessment suggests total body volume overload.
4) consider dobutamine in HFrEF if either: 📖
- (a) Normotensive patient plus organ hypoperfusion.
- (b) Refractory cardiogenic pulmonary edema in hypotensive patient.
5) consider digoxin if: 📖
- HFrEF with chronic atrial fibrillation.
6) treat underlying etiology 📖
- New-onset tachyarrhythmia causing heart failure: cardioversion, antiarrhythmics.
- Bradycardia or inappropriately slow heart rate: treat.
- Ischemic cardiomyopathy: Revascularization, treatment for acute MI if present.
7) mechanical circulatory support 📖
- Consider for persistent organ failure – device of choice is patient/institution specific.
8) things to avoid 📖
- Nephrotoxins (e.g., NSAIDs, ACE-inhibitors, angiotensin receptor blockers).
- Initiation of beta-blocker in decompensated heart failure.
- Any beta-blocker or calcium-channel blocker (e.g., diltiazem) in a patient with cardiogenic shock.
this chapter is about LV failure
- LV failure spans a spectrum of severity which ranges from mild heart failure decompensation to frank cardiogenic shock.
- Cardiogenic shock isn't necessarily a discrete entity, but rather may be conceptualized as the most severe form of heart failure. (30072134)
- Patients with severe heart failure may go in and out of cardiogenic shock, depending on their management.
this chapter is not about:
- SCAPE (Sympathetic Crashing Acute Pulmonary Edema), a distinct form of rapid-onset heart failure which is associated with hypertension.📖 The basic principles in this chapter will apply to SCAPE. However, the chapter on SCAPE will be more clinically applicable to that scenario.
- Isolated right ventricular failure (cor pulmonale) – this requires a unique approach.📖 However, many patients with LV failure also have some RV failure as well (i.e., biventricular failure) – such patients are included in this chapter.
- Less common types of heart failure with unique physiology (e.g., acute valvular regurgitation, hypertrophic cardiomyopathy, dynamic LV outflow tract obstruction 📖).
bedside hemodynamic assessment
- Noninvasive hemodynamic assessment is essential for the initial diagnosis and management of cardiogenic shock (table above). Some comments on various findings are included below.
- Cardiac index (systemic perfusion)
- Normal mentation doesn't prove that perfusion is adequate, as some patients with cardiogenic shock may have preserved mentation until very late in the disease process. For example, some patients in occult cardiogenic shock may have normal mentation despite malperfusion of other organs (e.g. shock liver and acute kidney injury).
- Elevated shock index (heart rate divided by systolic blood pressure) above ~0.8 is concerning for impending or present shock. However, shock index may be insensitive in the presence of negative chronotropic medications (e.g., beta-blockers) or conduction system disease.
- Pulmonary capillary wedge pressure (pulmonary congestion)
- High wedge pressure is suggested by pulmonary edema (dyspnea, edema on chest X-ray, and B-lines on lung ultrasound).
- The best test to determine wedge pressure is lung ultrasonography. Bilateral diffuse B-lines imply elevated wedge pressure, whereas bilateral A-lines suggest a low or normal wedge pressure. Ultrasonography is more sensitive than chest X-ray or exam to detect mild cardiogenic pulmonary edema.
- Total body volume status (systemic congestion)
- Note that it's possible for patients to have an elevated pulmonary capillary wedge pressure without total body volume overload (e.g., euvolemia plus an acutely deteriorating left ventricle). Alternatively, patients with marked peripheral edema and systemic congestion often have some degree of right ventricular dysfunction (often combined with left ventricular dysfunction).
- Clinical history can be very useful here: is there a history of volume loss (e.g. gastroenteritis, over-diuresis) or volume gain (e.g. diuretic nonadherence, iatrogenic fluid administration)? Weight gain or loss?
- Echocardiographic assessment of the inferior vena cava and jugular veins may allow estimation of the central venous pressure.
- Peripheral pitting edema suggests systemic congestion.
Forrester classifications
- Based on the pulmonary capillary wedge pressure and the cardiac index, patients may be categorized as shown above. These categorizations have direct implications for prognosis and treatment. (790191)
- First, imagine overlaying cardiac output curves over this classification system (shown below).
- Green curve: normal cardiac output function
- Orange curve: moderate heart failure
- Red curve: severe heart failure
- Patients who are warm/wet may often be managed with volume removal and/or vasodilation to reduce their afterload (vasodilation shifts fluid out of the lungs without affecting the total body volume).
- Patients who are cold/dry may often be managed by fluid administration:
classic presentation of cardiogenic shock: patients who are cold & wet
- Cardiogenic shock may be roughly conceptualized as requiring two components:
- (1) Systemic hypoperfusion due to low cardiac output (cold).
- (2) Filling pressures are elevated (wet).
- Patients in cardiogenic shock cannot be fixed with volume administration or removal.
- Giving volume will worsen their pulmonary congestion (making them wetter).
- Removing volume will worsen their systemic hypoperfusion (making them colder).
- Management of cardiogenic shock usually requires interventions to improve cardiac function (e.g., inotropic medications, revascularization, or a mechanical support).
- Cardiogenic shock patients may look deceptively OK, but they are indeed critically ill.
- Early recognition facilitates appropriate ICU management.
- The patient with unrecognized cardiogenic shock will generally fail to respond to non-intensive therapy, running in circles (typically the patient is initially diuresed, then develops worsening renal failure, then is given fluid back, then develops pulmonary edema, then transferred to ICU).
vasodilated cardiogenic shock
- To make things confusing, cardiogenic shock may trigger a systemic inflammatory response with elevated cytokine levels and reduced systemic vascular resistance. This may occur later in the course of cardiogenic shock, possibly due to ischemic tissue damage. This condition will mimic septic shock. (28923988)
- To add further to the confusion, some patients with septic shock will develop a sepsis-induced cardiomyopathy. So, advanced-stage septic shock and advanced-stage cardiogenic shock can look clinically quite similar (e.g., shock, vasodilation, reduced systolic heart failure, systemic inflammation).
- This may represent a final common pathway of the dying patient.
HFpEF vs. HFrEF
- Heart failure patients may be classified as heart failure with reduced ejection fraction (<40%, HFrEF, a.k.a “systolic failure”) vs. heart failure with preserved ejection fraction (HFpEF, a.k.a. “diastolic dysfunction”).
- Differentiating HFpEF vs. HFrEF can be done with bedside echocardiography.
- HFrEF: reduced ejection fraction.
- HFpEF: preserved ejection fraction. Presence of heart failure is suggested by dilated left atrium, left ventricular hypertrophy, and pulmonary congestion (B-lines on lung ultrasonography). Doppler measurements can also be used to diagnose diastolic dysfunction (E/E’, etc). In most cases, however, the diagnosis of diastolic HF can be made based on history, physical exam, EKG, CXR, and basic 2-dimensional ultrasonography of the heart and lungs.
- Treatment of these disorders is generally similar, with a few differences:
- HFpEF patients shouldn't be treated with inotropes.
- HFpEF patients may be more preload-dependent, thus at higher risk for hypotension following diuresis.
volume alteration
- Acute volume overload (e.g., diuretic nonadherence, dietary indiscretion).
- Acute hypovolemia (e.g., over-diuresis, reduced oral intake, gastroenteritis).
acute reduction in LV ejection fraction
- Acute MI (the cause of ~75% of cardiogenic shock). (31262417)
- Takotsubo cardiomyopathy 📖, post-cardiac arrest stunning.
- Tachymyopathy.
- Peripartum cardiomyopathy.
- Myocarditis (e.g., viral, SLE, giant-cell, eosinophilic, checkpoint inhibitors).
arrhythmia
- Bradyarrhythmia.
- Tachyarrhythmia (most often new-onset atrial fibrillation).
- Decreased cardiac resynchronization therapy (CRT) pacing. (Irwin & Rippe, 9th ed.)
- Increased isolated right ventricle pacing. (Irwin & Rippe, 9th ed.)
valvular dysfunction
- LV outflow tract obstruction (LVOTO). 📖
- Prosthetic valve dysfunction (e.g., thrombosis).
- Native valve dysfunction (e.g., endocarditis, ruptured papillary muscle 📖).
other
- Thyroid disease (hypothyroidism or hyperthyroidism).
- Medications/substances:
- Toxicity (e.g. excess beta-blocker, digoxin toxicity).
- Adverse medication effect (e.g. NSAIDs, diltiazem, pioglitazone).
- Medication nonadherence.
- Sympathomimetic abuse.
- Uncontrolled hypertension.
- Uncontrolled sleep-disordered breathing.
- Hypophosphatemia.
- Iron deficiency (with or without anemia).
is a pulmonary artery catheter (PAC) helpful?
- Hemodynamic assessment can generally be made non-invasively as described above. Furthermore, high-quality echocardiographic images with doppler can provide substantial hemodynamic information (e.g. cardiac output based on the velocity-time integral). (28595621)
- Reasons for avoiding a PA catheter include:(29796916)
- 1) PA catheterization is an invasive procedure which carries risk of pneumothorax, line infection, arrhythmia, pulmonary artery perforation, and heart block. These risks aren't merely academic; I've seen all of these complications.
- 2) PA catheterization will always reveal abnormal numbers, but it's unknown what we should do with this data. (7555127) Specifically, there is no defined goal for cardiac output or systemic vascular resistance. A cardiac index which may be adequate for one patient will leave another patient in cardiogenic shock.
- 3) PA catheterization tends to encourage fluid management based on static filling pressures. However, these pressures (even the hallowed pulmonary capillary wedge pressure) do not predict fluid-responsiveness. (24286266)
- 4) Numerous studies have failed to show benefit from Swan-Ganz catheterization both in critically ill patients overall and also specifically in heart failure patients. (14645314, 12510037, 16714768, 16084255) The ESCAPE trial, a multicenter RCT in heart failure, showed that Swan-Ganz catheterization increased adverse events without offering benefit. (16204662)
- 5) Over time, there has been steady improvement in echocardiography. Meanwhile, physicians and nurses are becoming less skilled at insertion and troubleshooting of PA catheters. Altogether, this means that the added value of PA catheter beyond echocardiography is continuously declining. Given that the Swan-Ganz catheter had dubious value in its heyday (the 1990s), it's even less beneficial currently.
- Routine use of PA catheterization is not recommended by AHA guidelines, even in cardiogenic shock. (28923988) Reasons to consider PA catheterization may include:
- Documentation of hemodynamics to determine candidacy for cardiac transplantation or ventricular assist device.
- Uncertain nature of shock with no alternative source of hemodynamic information (e.g., poor transthoracic echocardiographic windows and inability to perform a transesophageal echocardiogram).
- ⚠️ Contraindications to PA catheter insertion include:
- Bundle branch block (especially left bundle branch block), since PA catheterization may cause right bundle branch block. (30947630)
- Arrhythmia or hyperkalemia (insertion may trigger arrhythmias).
- Risk of displacing other devices (e.g., transvenous pacemaker, pacemaker inserted within <1 month). (36017548)
- Mechanical right heart valve, or status post tricuspid valve clip (TriClip).
- Significant stenosis of the tricuspid or pulmonic valves.
- Known thrombus or tumor in the RV or RA
interpretation of the mixed venous oxygen saturation
- The mixed venous oxygen saturation is potentially the most accurate way to assess the cardiac output. This is particularly true in patients in whom PA catheter thermodilution measurements may be limited (e.g., due to tricuspid regurgitation).🌊
- The Fick Equation 🧮 allows for estimation of the cardiac output using the mixed venous oxygen saturation. This is reasonably accurate for most cardiac patients, but it does require estimations regarding the metabolic rate. For patients with unusual metabolic rates (e.g., due to hypothermia or systemic inflammation), the estimated cardiac output may be inaccurate.
- Note that there are numerous factors which affect the mixed venous oxygen saturation. Random flux in these factors may cause the mixed venous oxygen saturation to vary over time. Avoid assuming that changes in the mixed venous oxygen saturation necessarily reflects an improvement or decrement in the cardiac output.🌊
interpretation of the hemodynamic data
- A table of normative values for hemodynamic data are provided below, but these should be interpreted very cautiously.
- Shock is defined in a relative fashion, as a state wherein cardiac output is insufficient to provide adequate tissue oxygenation. Thus:
- Some patients with chronic heart failure adapt to having a low cardiac output, allowing them to avoid shock despite having a cardiac output below “normal” values.
- There is no known cardiac output which should necessarily be targeted for critically ill patients.
- When approaching hemodynamic data, beware of the normalization fallacy (the incorrect belief that any values should be adjusted towards normal). For example, a patient with chronic compensated heart failure may be doing well clinically with an elevated systemic vascular resistance (SVR). The elevated systemic vascular resistance functions here as a compensatory mechanism, allowing maintenance of an adequate blood pressure. Aggressive intervention to “normalize” the systemic vascular resistance could destabilize the patient by causing hypotension.
CT scan isn't generally used as a diagnostic test for heart failure. Consequently, we often don't think much about what heart failure looks like on CT scan. However, this becomes important, because heart failure may mimic a variety of other disorders on CT scan.
#1/3: CT scan findings in heart failure
direct findings reflective of hydrostatic pulmonary edema
- Septal thickening (generally smooth and bilateral).
- Kerley B-lines.
- Thickening of the interlobar fissures (may be more easily discernible on chest X-ray).
- Airway filling:
- Initially: GGO (ground glass opacities).
- Severe edema may eventually cause bilateral consolidation.
- This tends to be distributed in a central (e.g., perihilar) and/or gravitational fashion (favoring the lower lung zones).
- Central (“batwing”) distribution tends to occur in acute left ventricular failure, or renal failure. (Muller 2019)
- Pleural effusion(s) may be seen.
- The presence of bilateral effusions may be especially suggestive of heart failure.
indirect findings which may be seen (depending on the etiology):
- Dilation of cardiac chambers:
- Left ventricular dilation suggests chronic systolic heart failure.
- Left atrial dilation may occur with various etiologies of chronic left ventricular failure (including systolic or diastolic dysfunction).
- Engorgement of the inferior vena cava.
#2/3: radiologic findings in sympathetic crashing acute pulmonary edema (SCAPE)
- Normally, interstitial pulmonary edema (i.e., septal thickening) occurs early and precedes the development of alveolar edema (i.e., ground glass opacities). Thus, ground glass opacities should be accompanied by septal thickening.
- Very abrupt pulmonary edema may produce ground glass opacities without septal thickening. This occurs if alveolar filling rapidly occurs, before enough time has passed for interstitial edema to develop. (Fishman 2023)
#3/3: asymmetric pulmonary edema
causes of asymmetric pulmonary edema
- (1) Patient sleeps on their side, creating a gravitational gradient.
- (2) Underlying parenchymal lung disease (e.g., due to asymmetric COPD or sarcoidosis).
- (3) Mitral regurgitation:
- Usually right-sided (may involve upper right, middle/lower right, or entire right side).
- Rarely, left-sided pulmonary edema can occur. (36566029)
- (4) Focal disease of the pulmonary veins:
- Pulmonary vein stenosis following AF ablation.
- Compression by aortic dissection, tumor, or granulomatous infection. (36566029)
radiological differential diagnosis
causes of hydrostatic pulmonary edema include:
- Left ventricular failure:
- Systolic or diastolic dysfunction.
- Valvular heart disease.
- Fluid overload.
- Iatrogenic fluid administration.
- Renal failure (often in combination with heart failure).
- Obstruction of the pulmonary veins:
- Fibrosing mediastinitis.
- Status post AF ablation.
- Pulmonary vein compression by malignancy.
- Pulmonary veno-occlusive disease (PVOD).
- Neurogenic pulmonary edema. 📖
heart failure mimics on CT scan
- Heart failure mimic may be suggested by:
- (1) Findings suggestive of heart failure (e.g., septal thickening, pleural effusions, ground glass opacities).
- (2) Findings inconsistent with heart failure:
- Normal left atrial size. 📖
- Age and/or clinical context inconsistent with heart failure.
- Diagnostic considerations include:
- Acute heart failure (left atrium has not yet dilated, for example due to acute valvular regurgitation).
- Heart failure mimics, especially:
- Infections, such as:
- Hantavirus.
- Pneumocystis jirovecii pneumonia.
- AEP (acute eosinophilic pneumonia).
- Pulmonary veno-occlusive disease (suggested by findings of pulmonary hypertension).
- Pulmonary vein stenosis s/p atrial fibrillation ablation.
- Lymphangitic carcinomatosis.
- Infections, such as:
- Related differential diagnoses:
- Full differential diagnosis of septal thickening: 📖
- Other causes of hydrostatic pulmonary edema are listed above ☝️.
BiPAP (noninvasive ventilation)
- Patients in respiratory distress due to heart failure often respond nicely to BiPAP. This is strongly supported by evidence in heart failure:
- BiPAP has been shown to reduce intubation and mortality.
- BiPAP reduces cardiac preload and afterload (physiologic effects similar to an ACE inhibitor).
- It's not merely enough to place the patient on BiPAP – for maximal benefit the pressures should be up-titrated as tolerated (figure below). The most important parameter is the expiratory pressure, which should be ramped up rapidly if possible. An alternative and equally effective strategy is simply to use CPAP.📖
- 🛑 Ongoing use of BiPAP is generally not advisable in patients with true cardiogenic shock and multiorgan failure (e.g., delirium, renal failure).
intubation
- Often needed for frank cardiogenic shock (especially patients with delirium due to brain hypoperfusion).
- Advantages:
- Provides full support for the work of breathing, which may allow shunting of blood away from the diaphragm and towards vital organs.
- Stabilizes patients for procedures that require lying flat (e.g. cardiac catheterization)
- Disadvantage: intubation in cardiogenic shock carries risks of hypotension/arrest, so be careful.
- When in doubt about the need for intubation: initiate BiPAP without delay, optimize other factors as rapidly as possible (e.g. Rx #2-5). Continually re-evaluate and intubate if necessary.
- 🛑 Even if the patient does eventually require intubation, it's often safer to resuscitate them before intubation.
drainage of large effusions
- If the patient isn't in respiratory distress, then effusions should be managed with diuresis and optimization of heart failure. However, it can take large effusions a long time to resorb. If the patient has large effusion(s) and this is causing significant respiratory distress or hypoxemia, then therapeutic drainage may be beneficial.
- (Note that even if the effusion is drained, the underlying heart failure must still be optimized. If the effusion is drained without management of the underlying heart failure, it will soon recur. Draining the effusion doesn’t fix the heart failure, it just temporarily stabilizes respiratory function.)
inhaled pulmonary vasodilator
- Inhaled epoprostenol or nitric oxide may be considered for an intubated patient with biventricular failure or severe hypoxemia. Physiological benefits include:
- (1) Reduction in right ventricular afterload may improve cardiac output among patients with right ventricular failure.
- (2) Inhaled pulmonary vasodilators will improve perfusion:ventilation matching and thereby improve the oxygen saturation.
- There is a risk that improved RV function will dump more blood into the left ventricle, thereby increasing the pulmonary capillary wedge pressure and exacerbating cardiogenic pulmonary edema. However, in the intubated patient this generally isn't a major problem.
For a patient with decompensated heart failure, the blood pressure needs to be high enough to perfuse the organs. However, if the pressure is too high, this will increase the workload on the heart (excessive afterload). Often an ideal blood pressure will be in the low-normal range (e.g., MAP 60-65 mm).
hypertension (or high-normal Bp) should be managed with afterload reduction
- Afterload reduction is highly beneficial for patients with HFrEF and sufficient blood pressure to tolerate it. Afterload reduction may improve cardiac output, decongest the lungs, and reduce the myocardial workload.
- ⚠️ Unfortunately, patients with preserved ejection fraction may benefit less from afterload reduction (with a higher risk of hypotension). (22281246) However, vasodilators may remain useful in such patients with the context of hypertensive emergency (i.e., SCAPE 📖).
- In the acute phase, a high-dose nitroglycerine infusion is the safest vasodilator.
- High doses may be needed to achieve arterial vasodilation, titrated against the patient's blood pressure (up to 800 mcg/min, often with dosing in the 50-200 mcg/min range).📖
- Once the patient has stabilized a bit, this may be transitioned to an oral agent:
- An ACE-inhibitor or ARB is good at afterload reduction. However, this increases the risk of renal failure, especially in a tenuous patient who is being actively diuresed.
- The combination of hydralazine plus isosorbide dinitrate has similar physiologic effects compared to an ACE-inhibitor without the nephrotoxicity.💉 (3520315)
hypotension may be managed with an inopressor (e.g., epinephrine or norepinephrine)
- Hypotension requires treatment to defend coronary and end-organ perfusion.
- Norepinephrine is widely recommended as a front-line agent for cardiogenic shock. Norepinephrine will improve the blood pressure, but there is a risk that excessive afterload could drop the cardiac output.
- Epinephrine could be a reasonable choice for a patient with reduced ejection fraction, hypotension, and poor cardiac output. At low doses (e.g., 0-5 mcg/min) epinephrine acts predominantly as an inotrope. However, unlike dobutamine, epinephrine doesn't cause vasodilation.
- At very low doses, it seems that the epinephrine causes some vasodilation by acting on beta-2 receptors, but also some vasoconstriction by acting on alpha-receptors. The net effect on systemic vascular resistance seems to be relatively neutral. The net effect of low-dose epinephrine is often an improvement in blood pressure and cardiac output, without affecting systemic vascular resistance much.
- Epinephrine may be especially helpful in patients with bradycardia or inappropriately normal heart rates.
- Vasopressin may be useful in patients with tachycardia or pulmonary hypertension.
- Dopamine should be avoided, given evidence of harm compared to norepinephrine in the SOAP-II trial. (20200382)
fluid administration
- Consider giving a fluid challenge if the following conditions are met:
- (1) There is insufficient end-organ perfusion (e.g., acute kidney injury).
- (2) No evidence of pulmonary congestion (e.g., no B-lines on lung ultrasonography).
- (3) Overall assessment suggests true hypovolemia (e.g., no systemic congestion).
- Fluid should be given in boluses of 500-1000 ml fluid challenges, with careful determination of the effect on the patient. If fluid isn't causing clinical improvement, don't give more.
- Be careful – static hemodynamic parameters (e.g., CVP, pulmonary capillary wedge pressure) do not predict fluid-responsiveness and should not be used as the primary determinant of fluid administration. (24286266)
fluid removal
- Consider diuresis if the following conditions are met:
- (1) There is significant pulmonary and/or systemic congestion.
- (2) Overall assessment suggests total body fluid overload.
- For patients who aren't responding adequately to furosemide, consider adding a thiazide diuretic (e.g., metolazone 5 mg q12hr-q24hr). This may enhance sodium excretion, with improved clearance of extravascular edema fluid. (23131078, 26948252, 31838029). Patients with severe systemic congestion may have reduced absorption of some diuretics, so they may require IV diuretics (e.g., IV furosemide plus IV chlorothiazide). More on diuresis: 📖.
- Patients with substantially elevated central venous pressure can experience an improvement in renal function with diuresis, because decreasing venous congestion will increase blood flow through the kidney. The driving pressure through the kidneys is equal to the MAP minus the CVP, so lowering the CVP may increase renal perfusion.
avoid catecholamine inotropes when possible
- Inotropes will cause a short-term improvement in hemodynamics. Unfortunately, available evidence indicates that inotrope use associates with worse outcomes. (28602370) Available prospective RCT data is scanty, but it likewise suggests that inotropes may be harmful. (11911756)
- Inotropes should be used only if necessary, for the following indications:(29806100)
- Hypoperfusion with low-normal blood pressure (e.g. acute kidney injury with poor urine output despite #1-3 above).
- Refractory cardiogenic pulmonary edema: Front-line therapies for cardiogenic pulmonary edema include #1-3 above: BiPAP, nitroglycerine (if blood pressure is adequate), and diuresis (if there is evidence of volume overload). Some patients will fail to respond to these treatments, especially hypotensive patients in whom nitroglycerine or diuresis is contraindicated. In such patients inotropes may be used with a goal of reducing the pulmonary capillary wedge pressure and decongesting the lungs.
dobutamine vs milrinone?
- An RCT comparing dobutamine vs. milrinone in patients with cardiogenic shock found no difference between the two agents. (34347952) Dobutamine has a shorter half-life which makes it more easily titratable, which arguably makes it the preferred agent. Alternatively, milrinone is renally cleared so it may exhibit erratic pharmacokinetics in shocked patients (e.g., accumulating unexpectedly if there is a reduction in renal function). Even with normal renal function, the half-life of milrinone is long (2.3 hours) – making rapid titration impossible.
- Both agents may cause hypotension, so they shouldn't be used in profoundly hypotensive patients. Thus, it's generally preferrable to start with blood pressure control (step #2 above).
- Milrinone may have a niche role among patients with end-stage heart failure, because it can be delivered on a chronic, outpatient basis via a pump.
digoxin
- Digoxin is the only positive inotropic agent whose use doesn't correlate with increased mortality. It's not a particularly powerful inotrope, but it might be the safest (with close monitoring of digoxin levels).
- Digoxin can be considered for patients with long-standing atrial fibrillation and systolic heart failure.
- Patients with new-onset atrial fibrillation might benefit from cardioversion to sinus rhythm instead.
- Digoxin generally isn't used as a front-line agent for heart failure, but can be considered when the patient is failing to respond to other therapies.
- With intravenous loading, improvement may occur over several hours.
arrhythmia treatment
- If shock is caused by new-onset tachyarrhythmia (e.g. atrial fibrillation), then reversion to sinus rhythm may be beneficial. However, if the heart rate isn't very high then be careful – slowing down the heart rate may actually aggravate matters.
- If shock is caused or aggravated by bradycardia, this should be treated accordingly.📖
cardiogenic shock due to MI
- Treat with medical therapies for type-I MI (e.g. aspirin, P2Y12 inhibitor, anticoagulation).
- Revascularization is essential. This is beneficial even at delayed time points. (10460813)
- Thrombolysis works poorly in cardiogenic shock – PCI or CABG is generally necessary.
anemia?
- Although heart failure patients are often anemic, this usually isn't the cause of their decompensation. As a general rule, treatment of the dyspneic patient with blood transfusion in the expectation that this will improve pulmonary status is disappointing.
- Patients should be transfused to standard transfusion targets: >7 mg/dL (>70 g/L) or, in a patient with evidence of active myocardial ischemia, >8 mg/dL (>80 g/L).
Mechanical support is indicated for patients refractory to #1-5 above. Perhaps the most important end-organ to support is the kidneys. If the patient develops severe renal failure, this aggravates matters greatly. Depending on the context, mechanical support may play a variety of different roles:
- Bridge to recovery.
- Bridge to surgically-implanted ventricular assist device (VAD).
- Bridge to cardiac transplant.
- Bridge to re-assessment, ideally following resolution of multi-organ failure (“bridge to bridge”).
Options include aortic balloon pumps, percutaneous centrifugal pumps, and full veno-arterial ECMO. Controversy remains regarding the ideal timing and use of various devices, with relatively little high-quality evidence. Expert consultation is required. One problem with most of these devices is that they constrain the patient to bed with limited mobility. (29478105)
factors involved in determining mechanical support device
- Is support needed for the left ventricle, the right ventricle, or both?
- Ability to tolerate anticoagulation? (This is required for both temporary & durable devices.)
intra-aortic balloon pumps (IABP)
- The most popular devices overall and the most thoroughly investigated. Unfortunately, RCTs consistently fail to show improvement in patient-centered outcomes. (22920912, 21878431)
- Intra-aortic balloon pumps may augment cardiac output by 0.3-0.5 liters/minute. (31374209) However, they may be less effective in the context of tachycardia or irregular rhythms. (32469155)
- Contraindications: Severe peripheral artery disease, moderate-to-severe aortic regurgitation, aortic disease.
impella
- Evidentiary basis?
- LV-Impella failed to show any difference when compared to an intra-aortic balloon pump in the IMPRESS trial. (27810347)
- Recent retrospective registry study compared matched patients treated with impella vs. IABP: patients treated with impella had some improvement in renal function, more bleeding, more peripheral vascular complications, and no difference in mortality. (30586755)
- Contraindications: LV thrombus, prosthetic aortic valve, severe aortic stenosis, moderate-to-severe aortic regurgitation, severe peripheral arterial disease, inability to anticoagulate, ventricular septal defect (VSD). (31374209)
- There is even less evidence regarding other temporary mechanical devices (e.g. RV-impella, TandemHeart, RV-TandemHeart, Thoratec, Aortix, Reitan pump). (29907274)
VA-ECMO
- This seems to show the most promise, as a rapidly deployable strategy capable of supporting the sickest patients (patients with respiratory failure and biventricular heart failure). (29655828)
- Nephrotoxic medications (e.g. NSAIDs, ACEi/ARB).
- Don't try to suppress a sinus tachycardia. This is often a compensatory mechanism that may be keeping the patient alive.
- Avoid using diltiazem for rate control in AF patients with decompensated heart failure and reduced ejection fraction (the negative inotropic effects may be problematic).📖
- Don't treat mild, stable hyponatremia with an infusion of 3% saline or salt tablets. Patients with heart failure commonly have mild hyponatremia. This will generally tend to resolve with treatment of the underlying heart failure (e.g. diuresis with furosemide).
- Fluid and sodium restriction haven't shown benefit in RCTs. (23689381, 17395053) Hospital food often isn't great, so the must humane thing is probably to provide a regular diet. Follow fluid balance and use diuretics if needed.
be very careful with beta blockers in decompensated heart failure
- Beta-blockers are fantastic for chronic, compensated heart failure, but potentially dangerous in decompensated heart failure (negative inotropy may further impair cardiac function).
- Beta-blockers shouldn't be started in the context of decompensated heart failure.
- It is controversial whether beta-blockers should be continued among patients who were previously taking them.
- Beta-blockers should be held in patients with cardiogenic shock.
- For patients who aren't in shock, beta-blockers may be continued (perhaps at a reduced dose initially).
- Please note that a beta-blocker is the opposite to giving an inotrope. So any enthusiasm for using dobutamine in heart failure should translate into an equal and opposite aversion towards beta-blockers.
advantages & general comments
- May be useful in patients with heart failure (the overall physiological effect is similar to an ACE inhibitor, but without a risk of nephrotoxicity).
- Short duration of action may facilitate rapid oral titration.
drawbacks & contraindications
- Contraindications
- Hydralazine is contraindicated in patients with HOCM (hypertrophic obstructive cardiomyopathy), or left ventricular outflow tract obstruction.
- Drawbacks
- Hydralazine may cause reflex tachycardia and fluid retention.
- Renal dysfunction may cause hydralazine to accumulate over time.
onset & duration
- Hydralazine 💊
- Onset within ~1 hour.
- Duration of ~6-8 hours.
- Isosorbide dinitrate 💊
- Onset within ~1-2 hours.
- Duration of ~8 hours.
dose
- Hydralazine
- Start 25-37.5 mg q6-8hr. (Irwin & Rippe 9th ed.)
- Max dose 100 mg q6-8hr. (Irwin & Rippe 9th ed.)
- Isosorbide dinitrate
- Start 20 mg q6-8hr. (Irwin & Rippe 9th ed.)
- Max dose 40 mg q6-8hr. (Irwin & Rippe 9th ed.)
- 💡 Doses may be staggered every four hours (i.e., alternating doses of hydralazine and isosorbide dinitrate every four hours) to avoid causing an excessive drop in blood pressure.
basics
- Nitroprusside is a balanced arterial and venous vasodilator with a short half-life. This makes nitroprusside a potentially useful agent for fine titration of afterload. However, clevidipine may be a safer alternative (if it is available).
- Prolonged use of high-dose nitroprusside may lead to accumulation of cyanide or sodium thiocyanate.
- For hypertensive emergency, higher doses of nitroprusside may be needed – so toxicity becomes a substantial issue. Generally, nitroprusside is not a preferred agent for treating hypertensive emergency.
- For heart failure, lower doses of nitroprusside are generally sufficient, so toxicity is less problematic.
contraindications
- Hepatic dysfunction (increases risk of cyanide toxicity).
- Renal dysfunction (increases risk of sodium thiocyanate toxicity).
- Severe hypoxemia (nitroprusside may cause ventilation/perfusion mismatch).
- Active myocardial ischemia (generalized coronary artery dilation may cause a steal phenomenon that draws perfusion away from the infarcted tissue).
- Intracranial pressure elevation (nitroprusside may further increase the intracranial pressure).
- Lack of central access (may cause necrosis if it extravasates).
- Recent use of phosphodiesterase-5 inhibitors (e.g., sildenafil).
metabolic pathway and toxicity
metabolism of nitroprusside (simplified version)
- Nitroprusside rapidly decomposes within the blood into cyanide.
- Cyanide is converted into sodium thiocyanate by the liver.
- Sodium thiocyanate is excreted by the kidneys.
cyanide intoxication 2/2 nitroprusside
- Risk factors:
- Hepatic dysfunction.
- Most often occurs when >5 mcg/kg/min is utilized, but it can occur in some patients on 2 mcg/kg/min for prolonged periods.
- Clinical manifestations may include:
- Neurologic dysfunction (anxiety, restlessness, confusion, headache; eventually stupor and coma).
- Dyspnea, tachycardia, hypertension, diaphoresis, nausea/vomiting.
- Diagnosis:
- Lactic acidosis is a late feature that cannot be used to exclude early toxicity.
- Treatment:
- Consult with poison control.
- May use high-dose hydroxocobalamin.
thiocyanate intoxication 2/2 nitroprusside
- Risk factors:
- Renal dysfunction.
- Prolonged infusion for >24-48 hours (normally, thiocyanate has a half-life of 3-4 days). (18158484)
- Clinical manifestations may include:
- Neurologic dysfunction (altered mental status, tinnitus, paresthesias, seizures, hyperreflexia).
- Anorexia, nausea, fatigue.
- Diagnosis: Elevated thiocyanate levels are diagnostic (if available).
- Treatment: May require dialysis.
other side-effects:
- Thrombocytopenia.
- B12 deficiency.
dosing & pharmacology
- Nitroprusside is very short-acting, making it easily titratable:
- Peak effect occurs within two minutes.
- If discontinued, effect disappears within a few minutes.
- Dosing:
- ⚠️ Avoid prolonged use (>24-48 hours). Prompt efforts should be made to transition to another therapy (e.g., hydralazine plus isosorbide dinitrate, or ACE inhibitors, or temporary use of nitroprusside to facilitate diuresis).
- Monitoring of cyanide and/or thiocyanate levels may be considered if these tests are available. However, routine monitoring of cyanide levels may not be necessary. (25425768)
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- Failure to identify a patient who is cold and wet (Forrester class IV). These patients may not look terrible, but they have cardiogenic shock and generally require ICU admission.
- Treatment plan that focuses on a single intervention (e.g. diuresis), without optimizing other aspects of the patient (e.g. afterload reduction).
- Delayed management of respiratory distress (e.g. with BiPAP, effusion drainage, or intubation).
- Application of an outpatient-style management (e.g. beta-blocker and ACEi/ARB initiation) in a critically ill patient with cardiogenic shock.
Guide to emoji hyperlinks
- = Link to online calculator.
- = Link to Medscape monograph about a drug.
- = Link to IBCC section about a drug.
- = Link to IBCC section covering that topic.
- = Link to FOAMed site with related information.
- = Link to supplemental media.
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