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Clinical Practice Guidelines for the Prevention.29

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From the Society of Critical Care Medicine

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Hold your TEN for at least an hour prior to extubation

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CVP: mean the a wave at the end of expiration

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CVP: mean the a wave at the end of expiration

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Taken from open pediatrics video.

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"Interpreting Central Venous Pressure Waveforms" by James DiNardo, MD, for OPENPediatrics

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"Interpreting Central Venous Pressure Waveforms" by James DiNardo, MD, for OPENPediatrics

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Jugular Venous Pressure (JVP) Waveform Mnemonic

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Jugular Venous Pressure (JVP) Waveform Mnemonic

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Catheter Associated Urinary Tract Infections (CAUTIs)

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Catheter Associated Urinary Tract Infections (CAUTIs)

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Dorsata gives healthcare providers the tools to quickly build, share, and then use defined workflows for efficient decision-making, documentation, and order entry. By using Dorsata, providers are able to document more efficiently and robustly at the point-of-care without detracting attention from patients. This decreases the time providers spend in the EHR while increasing practice collections.

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Central Line Associated Blood Stream Infections (CLABSIs)

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Central Line Associated Blood Stream Infections (CLABSIs)

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Endotracheal Tube (ETT) Removal with Comfort Care

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Endotracheal Tube (ETT) Removal with Comfort Care

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Jugular Venous Pulse (JVP) Explained Clearly - Evaluation, Waveforms, Interpretation

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MedCram - Medical Lectures Explained CLEARLY

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Jugular Venous Pulse (JVP) Explained Clearly - Evaluation, Waveforms, Interpretation

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Dorsata gives healthcare providers the tools to quickly build, share, and then use defined workflows for efficient decision-making, documentation, and order entry. By using Dorsata, providers are able to document more efficiently and robustly at the point-of-care without detracting attention from patients. This decreases the time providers spend in the EHR while increasing practice collections.

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Clinical Update on Vasopressors and Titration Strategies 2021

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Don't tug back on syringe.
Don't lock the balloon to quickly - you might trap air.

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GDMT (Goal Directed Medical Therapy) in Heart Failure

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GDMT (Goal Directed Medical Therapy) in Heart Failure

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Medical Treatment Options For Cardiogenic Shock

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See formulary for full details

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DAPT with Statin is standard therapy

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Percutaneous coronary intervention with intracoronary stents_ Overview - UpToDate

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Good tables that explain the use of DOACs.

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The tables and charts on this site are very helpful

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The table below categorizes vasoactive medications. This might seem like a lot, but grouping drugs together into classes can simplify things.

classic inodilators (milrinone, dobutamine)

Physiologic effect

Primary effect is positive inotropy, with positive chronotropy as well.

Secondary effect is peripheral vasodilation.

Cardiac output is increased due to both inotropic effect and vasodilation.

Effect on blood pressure is variable, depending on how responsive the heart is to inotropy. If the heart responds strongly (with increased stroke volume and heart rate), it is possible for these drugs to increase blood pressure. However, if the heart is already working as hard as it can, then the vasodilator effect may be dominant, causing a drop in blood pressure. Overall, the effect on blood pressure is unpredictable.

Clinical use

(1) Low-output cardiogenic shock. Care is required for patients with hypotension, since there is a risk of exacerbating hypotension.

(2) Septic shock with inadequate cardiac output (as an add-on agent). However, epinephrine could be a superior choice in that situation, if blood pressure is tenuous.

Pro/con of different agents?

Milrinone causes a bit more vasodilation, so it might be better for cardiogenic shock. However, milrinone is renally eliminated, which can make it difficult to titrate in patients with renal failure.

Dobutamine is easier to titrate due to its short half-life, so it is often a preferred agent if the patient's response to inotropy isn't entirely predictable.

Prolonged infusion of dobutamine may cause desensitization of beta-receptors and reduced efficacy. This may be a problem, but it can also help wean the patient off dobutamine once the infusion has been running for a long time (it may be easier to wean off than would be expected).

isoproterenol

Mechanism: Pure beta-agonist.

Physiologic effect: Very powerful chronotrope, with positive inotropic effects as well.

Clinical use: Bradycardia (will work in some patients who are refractory to epinephrine).

How to titrate: typically, against heart rate.

Pro/Con?

Isoproterenol is probably the most powerful chronotrope.

It doesn't cause vasoconstriction, so it's safe to give peripherally.

Its main drawback is pricing & availability: in the United States the price is astronomical and some hospitals don't have it. If you don't have it, epinephrine can usually be used as an alternative agent.

vasopressin

Mechanism: Stimulates V1 and V2 receptors, causing vasoconstriction and renal water retention.

Physiologic effects:

It increases systemic vascular resistance (SVR).

It does cause venoconstriction, which may increase preload.

Its dominant effect on cardiac output is often to cause a reduction (but this may depend on the heart's ability to tolerate increased afterload).

Clinical use:

Vasodilatory shock (particularly sepsis). Typically given in low doses (0-0.06 U/min), either as primary or secondary agent (27483065).

Front-line agent for hepato-renal syndrome (HRS) in countries lacking terlipressin (such as the United States).

Central diabetes insipidus (very low doses needed, e.g. 0.01 units/minute or less).

Variceal gastrointestinal hemorrhage (theoretically an attractive agent, but pragmatically it's impossible to titrate adequately).

How to titrate: typically, against blood pressure.

Pro/Con

Vasopressin may preferentially cause vasoconstriction of post-glomerular arterioles in the kidney, causing improvement in renal function.

It may cause some pulmonary vasodilation, which can be helpful in the context of pulmonary hypertension.

Vasopressin shouldn't generally be given peripherally (if it extravasates, there is no antidote).

Vasopressin can cause digital ischemia, especially when combined with norepinephrine - must pay careful attention to perfusion of hands and feet; shut off vasopressin at first sign of ischemic digits.

phenylephrine

Mechanism: Pure alpha-agonist, causes arterial and venous vasoconstriction.

Physiologic effect

Increased systemic vascular resistance (SVR).

Venoconstriction increases the preload.

Effect on cardiac output depends on preload-responsiveness versus ability of the heart to handle increased afterload. For example, in a patient with systolic heart failure and volume overload, added preload won't help, whereas the heart may be unable to tolerate afterload - so the net effect is to reduce the cardiac output. Alternatively, for a patient who is preload-responsive with a stronger ejection fraction, phenylephrine could cause a net increase in cardiac output.

Available evidence in sepsis suggests that phenylephrine has a very similar physiologic effect compared to norepinephrine (reviewed here). Both agents are predominantly alpha-agonists.

Phenylephrine can cause a mild reflex bradycardia due to elevation in blood pressure.

Clinical use:

Vasodilatory shock.

Useful in patients with critical aortic stenosis (who have a fixed afterload imposed on the left ventricle by the stenotic valve).

Atrial fibrillation with fast ventricular response (increases blood pressure while causing reflex reduction in heart rate).

How to titrate: typically, against blood pressure.

Pro/Con

It has classically been feared that phenylephrine would drop the cardiac output. This seems to occur with phenylephrine boluses, but not with infusions (available evidence indicates that a phenylephrine infusion functions pretty similarly compared to a norepinephrine infusion).

It is safe to give peripherally.

Phenylephrine is about ten times less potent than norepinephrine (i.e. 10 mcg/min phenylephrine is roughly equivalent to 1 mcg/min norepinephrine). Phenylephrine is generally supplied as a fairly dilute solution, which can make this logistically problematic for patients requiring high-dose vasoconstriction. Thus, phenylephrine monotherapy is largely restricted to patients with mild to moderate vasodilatory shock due to logistic constraints.

norepinephrine

Mechanism: Predominantly an alpha-agonist, with some beta-agonism as well.

Physiology

Increases systemic vascular resistance (SVR), causes venoconstriction (increasing preload), and has an inotropic/chronotropic effect.

Increases blood pressure and may increase urine output.

Tends to cause cardiac output to increase or remain stable (depending on how responsive the heart is to preload, afterload, and inotropy).

How to titrate:

Pro/Con
Strong track record in septic and cardiogenic shock.

epinephrine

Mechanism: At lower doses the beta-agonist effects may predominate; with ongoing up-titration there are increasing alpha-agonist effects as well.

Physiology

Causes chronotropy and inotropy, thereby increasing the cardiac output.

Increases systemic vascular resistance and also causes venoconstriction (increasing preload).

Stabilizes mast cells, blocking the pathophysiology of anaphylaxis.

Beta-2 agonist stimulation causes bronchodilation, decreases potassium levels, and stimulates the generation of aerobic lactate production by the liver. This is often feared, but lactate may be used as a metabolic fuel by the heart, so this mechanism of action is probably beneficial (in the absence of profound pre-existing metabolic acidosis).

Clinical uses

(1) Bradycardia and bradycardic shock (given inotropic effects).

(2) Septic shock (shown in the 🐱CAT trial to be an adequate alternative to norepinephrine). It seems to work especially well in patients with inappropriately low heart rate and/or low cardiac output, who likely have a poor sympathetic response to sepsis (more on this here).

(3) At low doses (below 5-10 mcg/kg/min), the predominant effect is as an inotrope, so it can be used for patients with low-output cardiogenic shock. Compared to dobutamine/milrinone, low-dose epinephrine has a touch of alpha-activity which will tend to prevent hypotension.

(4) Push-dose epinephrine is useful for patients crashing from a variety of causes (e.g. bradycardic peri-arrest). Epinephrine is generally a good choice for the nearly-dead patient.

(5) First-line agent for anaphylaxis. Note that epinephrine may be indicated for treatment for anaphylaxis even if the hemodynamics are stable (see IBCC anaphylaxis chapter).

How to titrate: depends on clinical application.

Pro/Con

Epinephrine is a powerful drug with established efficacy in sepsis, also useful in bradycardia and cardiogenic shock.

The main concern is that at high doses for long periods of time, it may promote a stress cardiomyopathy.

It causes lactate production which isn't dangerous (may be physiologically beneficial). However, practitioners must be aware of this issue; otherwise they may senselessly chase lactate values.

Epinephrine causes a small decrease in potassium, which is generally not a problem. Effects on potassium may be useful in patients with hyperkalemia and bradycardia (BRASH syndrome).

dopamine

Mechanism/physiology

Dopamine hits a variety of receptors at different dose ranges ("dirty" drug).

It's often difficult to figure out what it is doing to your patient. For example, low-dose dopamine can actually cause hypotension (due to a predominant effect of vasodilation), which can make it difficult to wean off the dopamine.

Reasons dopamine should be abandoned:

1. Dopamine increases mortality in RCTs: Dopamine increased mortality compared to norepinephrine in the subgroup of patients with cardiogenic shock (De Backer 2010). It also increased mortality compared to epinephrine among septic children (Ventura 2015).

2. It's often impossible to figure out what dopamine is doing (given the variety of different effects at different doses in different patients). This makes it impossible to titrate in any rational fashion (up-titration may cause dopamine to function via a different mechanism entirely).

3. Dopamine has unique adverse endocrine effects.

4. Dopamine may directly stimulate diuresis via action on dopamine-receptors, thereby falsely suggesting that renal perfusion is adequate.

5. There is a relatively high risk of tissue necrosis if it extravasates.

6. Better agents exist: there is nothing dopamine does that can't be achieved with the use of norepinephrine and/or epinephrine.

7. Dopamine may cause greater malperfusion of the gut compared to norepinephrine.

peripheral IV line

Hemodynamic stabilization should never wait until central access is obtained. Thus, peripheral vasopressors should be started immediately if the blood pressure or perfusion is inadequate.

Norepinephrine is safe for short periods of time through a large peripheral vein. Ongoing peripheral infusion also appears safe, but this should ideally be done within the context of a well-designed protocol involving frequent monitoring of the extremity and preparation for management of extravasation reaction (more on this here). Ongoing infusion should be avoided in deep ultrasound-guided peripheral IVs, where it may be impossible to monitor the tissue surrounding the end of the IV cannula.

Phenylephrine and epinephrine have not been reported to cause tissue necrosis. Peripheral infusion of these agents appears to be generally safe, although this should still ideally be done via a well-functioning cannula proximal to the wrist (more on this here).

Vasopressin should arguably be avoided for peripheral administration, because if it extravasates there is no vasodilatory agent which can counteract its action.

midline catheter

These are catheters placed in the arm, similar to a PICC, but shorter (typically 10-20 cm in length, terminating before the shoulder).

Clinician-placed midlines are evolving as an alternative to either ultrasound-guided peripheral IVs or central lines.

This is a rapidly emerging topic. Overall, vasopressor administration via midline catheters appears to be safe.

More on midline catheters: see EMCrit RACC Midlines part 1 & part 2.

basics

Oral alpha-1 agonist, which acts as a pure vasopressor.

Overall behavior is similar to that of phenylephrine (may be conceptualized as "oral phenylephrine").

more common clinical indications in critical care:

Cirrhosis & hepatorenal syndrome

Midodrine is a component of oral therapy for hepatorenal syndrome.

Some evidence suggests that ongoing midodrine therapy in patients with cirrhosis may support renal perfusion (given that these patients suffer from chronic vasodilation).

dose

The usual starting dose is 10 mg PO q8hr. Make sure the drug is dosed q8hr and not "three times daily with meals," which is what the computer may default to.

Dose range is 5-40 mg q8hr (26953217).

Midodrine is cleared by the kidney, so exercise caution in renal dysfunction.

contraindications/cautions

Reflex bradycardia can occur.

The major limitation is that midodrine should be weaned off after the patient is discharged from the ICU to the ward. Failure to wean off midodrine in a timely fashion could potentially lead to harm. One study showed that midodrine was commonly continued and administered alongside antihypertensives. Although this may be justifiable in patients with heart failure and reduced ejection fraction, in many cases it was likely an error (31107279, 31524705).

more on midodrine:

PulmCrit blog here.

Mayo Clinic experience with 1,119 patients treated with oral midodrine (Rizvi 2018).

mechanisms of action

(1) Methylene blue causes vasoconstriction by inhibiting nitric oxide synthase.

This is a potentially dangerous way to increase blood pressure, because it could potentially impair microvascular perfusion.

Historically, a nitric oxide synthesis inhibitor was shown to increase mortality in septic shock .

(2) Methylene blue inhibits the conversion of guanine triphosphate to cGMP (an intracellular signaling molecule which increases vasodilation).

(3) Methylene blue may be able to accept electrons from NADH and transfer them to cytochrome C in the mitochondria, thereby bypassing parts of the electron transport chain. This could restore mitochondrial function in some situations where parts of the electron transport chain are dysfunctional, for example metformin toxicity (28840449).

more common indications

Refractory vasoplegic shock of any etiology.

Especially following cardiothoracic surgery.

Possibly also: septic shock, anaphylaxis.

Metformin poisoning

dosing

potential adverse effects / contraindications

1. Inhibition of cGMP may increase pulmonary vascular resistance, thereby impairing right ventricular function and impairing oxygenation. This may be more of a problem at higher doses.

2. High levels of methylene blue can interfere with pulse oximetry (a problem mostly when giving the bolus dose).

3. Methylene blue can act as an oxidizing agent at high doses (e.g. >7 mg/kg). This may cause methemoglobinemia. In patients with G6PD deficiency, this could also cause hemolytic anemia.

4. Methylene blue inhibits monoamine oxidase A (MAO), thereby increasing brain serotonin levels. This could cause serotonin syndrome in the presence of other serotonergic agents.

5. Methylene blue may inhibit CYP enzyme metabolism, leading to accumulation of some medications (e.g. digoxin, warfarin, fentanyl).

6. Methylene blue is contraindicated in pregnancy (due to a potential for placental vasoconstriction and fetal hypoxemia).

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Any use of dopamine (there are better agents).

Failure to aggressively up- and down-titrate vasopressors to determine the physiologic effect of each on any specific patient. Medications may not behave as described in a textbook (even this book!). By continually adjusting infusion rates, it is often possible to get a sense of which agents are most effective. The goal is always to use the minimal total dose of vasopressors necessary to achieve hemodynamic targets, so if a drug doesn't seem to be having any effect then wean it off.

Ongoing infusion of vasopressin despite evidence of malperfused digits.

Excess use of vasopressors (especially the combination of norepinephrine and vasopressin), which can lead to a phenomenon of iatrogenic vasoconstrictive shock in patients with poor cardiac function (wherein excessive vasoconstriction causes a drop in cardiac output, causing low cardiac output and shock). Beware of this phenomenon. When encountered, consider the addition of epinephrine and down-titration of vasoconstrictors.

Use of agents with beta-agonist activity in patients with atrial fibrillation and rapid ventricular response.

Failure to up-titrate norepinephrine beyond arbitrary "upper limits" imposed by hospitals or local culture (there is actually no upper limit on the norepinephrine dose).

Fear of using epinephrine due to concerns that it may increase the lactate (increased lactate levels due to epinephrine are probably beneficial in most cases).

Delaying vasopressor initiation until central access is obtained (instead, peripheral vasopressor infusion should be used to immediately stabilize the patient).

Pressor overview

Pure pressors

Epinephrine & lactate

Titration & selection issues

Peripheral pressors & midlines

Vasopressin

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CONTENTS Pressor Overview Core agents Inodilators (milrinone, dobutamine, isoproterenol) Pure vasopressors Inopressors (norepinephrine, epinephrine, dopamine) Peripheral vasopressors Midodrine Methylene Blue Podcast Questions & discussion Pitfalls PDF of this chapter (or create customized PDF) The table below categorizes vasoactive medications. This might seem like a lot, but grouping drugs together into classes can simplify things.

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Sympathetic Crashing Acute Pulmonary Edema (SCAPE)

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Treatment Priorities for this clinical scenario

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CONTENTS

SCAPE dx & rx checklist ✅

1. Rapid onset of severe dyspnea.

2. Hypoxemia.

3. Hypertension (SBP >160 mm and/or MAP > 120 mm).

4. Diffuse rales (sometimes with pink frothy sputum).

5. POCUS shows diffuse B-lines.

Either works fine (the key is a high expiratory pressure).

Rapidly uptitrate pressures, to target:

CPAP of ~15-18 cm.

BiPAP of ~18/15 cm.

If not tolerated, consider IV fentanyl.

(1) Bolus of 1,000-2,000 mcg over ~2 minutes (e.g., 400-800 mcg/min for 2.5 min).

(2) Start infusion at ~100-300 mcg/min.

(3) Aggressively uptitrate to 800 mcg/min if needed, targeting Bp reduction (SBP <~140 mm).

(4) After SCAPE episode breaks, aggressively wean down nitroglycerine to avoid hypotension.

Rapid reduction in Bp is essential (e.g., SBP <~140).

CPAP/BiPAP plus nitroglycerine infusion are usually adequate. If not, then consider:

(#1) Clevidipine gtt (preferably) or nicardipine gtt.

(#2) Enalaprilat, 1.25 mg IV (may repeat q15 minutes to a maximal dose of 5 mg).

(#3) Low-dose fentanyl (if uncontrolled pain or air hunger).

physiology of sympathetic crashing acute pulmonary edema (SCAPE)

SCAPE occurs due to a vicious spiral involving increasing sympathetic outflow, excessive afterload, and progressively worsening heart failure. Since SCAPE is a vicious spiral, this may develop very rapidly (hence the terminology "flash pulmonary edema"). With aggressive therapy, it may resolve very rapidly as well.

The central, defining pathophysiological feature of SCAPE is pathologically elevated afterload due to systemic vasoconstriction and hypertension.

SCAPE patients may be euvolemic or hypovolemic. The problem is a shift of fluid into the lungs, rather than hypervolemia.

fluid overload subacute pulmonary edema (FOSPE)

FOSPE occurs in patients who develop gradual volume overload. This is compared with SCAPE in the table above.

SCAPE and FOSPE aren't mutually exclusive. For example, some patients can have SCAPE superimposed upon FOSPE (i.e., gradual volume accumulation over time, which eventually reaches a tipping point and triggers an acute episode of SCAPE). Some authors have proposed that SCAPE and FOSPE represent two extreme forms of pulmonary edema, with some patients lying in between.

Differentiating SCAPE vs. FOSPE is clinically important, because the treatment is different.

nomenclature

SCAPE is known by a variety of different terms throughout the scientific literature, most notably:

Flash pulmonary edema (this is becoming less popular).

Hypertensive acute heart failure (preferred terminology in hypertension journals).

SCAPE (increasingly utilized in emergency medicine and critical care journals).

SCAPE is currently the preferred terminology, since it is clear and unique.

SCAPE patients often meet the criteria for "hypertensive emergency" (i.e., severe hypertension plus target organ dysfunction). However, SCAPE represents a unique entity which requires uniquely tailored therapy. For example, SCAPE develops very rapidly so patients can be promptly lowered to their baseline blood pressure (unlike many patients with hypertensive emergency, who have more gradual elevation of blood pressure and consequently require a more gradual therapeutic reduction). More on hypertensive emergency .

defining clinical features of SCAPE (34215472)

Rapid onset of respiratory distress (e.g., usually within <6 hours).

Marked tachypnea and dyspnea.

Hypoxemia.

Hypertension (generally SBP>160 mm and/or MAP>120 mm).

Diffuse rales on auscultation.

Pink, frothy sputum may be seen.

Clinical features of sympathetic activation:

Diaphoresis, pallor, appearing extremely unwell.

Tachycardia.

Agitation.

Patients may have a history of recurrent episodes of SCAPE.

POCUS

Aside from history and examination, POCUS is the most powerful tool for the diagnosis of SCAPE.

Lung sonography:

Cardiogenic pulmonary edema generates a pattern of diffuse B-lines throughout the chest, with a thin pleural interface (unlike non-cardiogenic pulmonary edema, which often causes a patchy distribution of B-lines and a thickened pleural interface including patches of subpleural consolidation). Small bilateral pleural effusions may further support the diagnosis of cardiogenic pulmonary edema.

Ultrasonography is extremely sensitive for cardiogenic pulmonary edema. If a diffuse pattern of B-lines is not seen in a patient with acute dyspnea, cardiogenic pulmonary edema may be immediately and confidently excluded as the cause of the patient's dyspnea.

Cardiac ultrasonography should generally reveal some form of heart failure, for example:

Systolic heart failure, with reduced left ventricular ejection fraction.

Diastolic heart failure may be suggested by left ventricular hypertrophy and a dilated left atrium.

⚠️ Note that SCAPE patients may be hypovolemic, hypervolemic, or euvolemic. Therefore, the IVC will not necessarily be distended (nor will the patient necessarily have distended jugular veins).

chest X-ray

Chest X-ray may also be used as a diagnostic tool. However, X-ray is less sensitive for acute pulmonary edema compared to thoracic ultrasonography. Some patients with SCAPE may not have an unequivocally abnormal chest X-ray.

Chest x-ray findings may include:

Bilateral, fluffy infiltrates centered in the hila ("bat wing pulmonary edema").

Kerley B lines (fluid in the interlobular septa causing fine lines perpendicular to the pleura).

Pleural effusion(s).

Lack of an alternative diagnosis (e.g., absence of pneumothorax or lobar pneumonia).

⚠️ diagnostic pitfall: other forms of respiratory distress cause hypertension

Any form of severe respiratory failure may lead to distress and hypertension. Therefore, don't assume that the combination of respiratory failure plus hypertension necessarily implies a diagnosis of SCAPE.

In uncertain situations, it is reasonable to initiate treatment for SCAPE while simultaneously investigating for other problems.

One of the hallmarks of SCAPE is rapid improvement with therapy. For patients who aren't turning around rapidly, evaluate carefully for alternative or additional problems, for example:

Wrong diagnosis (patient has ARDS, not cardiogenic pulmonary edema).

Underlying problem (cardiogenic edema is due to acute STEMI or valvular regurgitation)

brain natriuretic peptide (BNP)

There is no evidence that BNP testing adds clinical information above and beyond the combination of clinical judgement and POCUS for patients with heart failure.This is particularly true of SCAPE patients, wherein the diagnosis is generally not subtle.

Pragmatically, the turn-around time of the BNP test is too long to be clinically useful for the immediate bedside management of SCAPE.
💡 SCAPE is a bedside clinical diagnosis which must be reached within minutes (on the basis of history, examination, and POCUS).

SCAPE usually results from the combination of an underlying substrate plus an acute trigger. Even after a diagnosis of SCAPE is clear, an acute process causing SCAPE should be considered as well (e.g., myocardial infarction or acute valve dysfunction).

there is usually an underlying substrate of SCAPE:

Chronic left ventricular failure (especially diastolic heart failure).
On the contrary, preserved right ventricular function might also predispose patients to have SCAPE (if the right ventricle is outperforming the left ventricle, this will cause fluid to accumulate in the lungs).

History of hypertension in ~90% of patients (especially labile hypertension).
Renal artery stenosis in particular predisposes to SCAPE (a combination known as Pickering syndrome).

acute triggers of SCAPE may include:

Nonadherence with antihypertensives (especially vasodilators such as ACE inhibitors or angiotensin receptor blockers).

Volume overload (e.g., missed hemodialysis sessions, nonadherence with diuretics).

Sympathomimetic intoxication.

Withdrawal (e.g., from clonidine).

Acute MI.

Exertion, stress, or anxiety.

Rare causes of acute heart failure (e.g., acute valve dehiscence or viral cardiomyopathy).

The hallmark of SCAPE is rapid deterioration, but aggressive treatment can rapidly reverse this process. Four core principles may be helpful to guide the overall management strategy.
principle #1: the primacy of positive pressure

The most important intervention is BiPAP or CPAP (which have equivalent efficacy). From an evidentiary standpoint, these interventions are superior to any other intervention for SCAPE.
These therapies have been demonstrated in multiple RCTs and meta-analyses to avoid intubation and mortality (table below).

All possible efforts should be made to use CPAP/BiPAP, for example:

Coaching the patient to encourage adherence.

Initially gently holding the mask on the patient's face.

Medication use to reduce air hunger and improve CPAP/BiPAP tolerance.

principle #2: blood pressure (afterload) control

Excessively high blood pressure increases the afterload on the left ventricle, promoting fluid backup into the lungs. This is fundamental to the pathophysiology of SCAPE. Therefore, one of the essential goals of treatment is to rapidly reduce the blood pressure.

There is no well-defined blood pressure goal, but a common target may be to reduce the systolic Bp to <~140 mm rapidly.However, the MAP or diastolic Bp may actually be superior targets, since they are more closely correlated with systemic vascular resistance.

Frontline therapies to control hypertension are to maximize BiPAP/CPAP pressure and to maximize the nitroglycerine infusion dose. The vast majority of SCAPE patients can be rendered normotensive with optimization of these two therapies.

Nicardipine or clevidipine are useful in refractory hypertension:

These vasodilators are more potent arterial vasodilators than nitroglycerine, so they may work in patients who are failing to respond to nitroglycerine. They may also be useful options in patients on phosphodiesterase type-5 inhibitors (e.g., sildenafil), who have contraindications to nitroglycerine.

Clevidipine is ideal, due to its shorter half-life and stronger evidentiary basis in acute heart failure.

Nicardipine has a longer half-life, so there is a risk of causing overshoot hypotension (especially when the underlying SCAPE abates).

(IV Enalaprilat (1.25 mg, may repeat q15 minutes to a maximal dose of 5 mg) is another option for refractory hypertension, but it would be uncommon to actually need this.28032307, 8822986, 27262665) Oral captopril is less desirable, since it would require removal of the BiPAP or CPAP mask.

principle #3: beta-blockers are contraindicated

Beta-blockers will impair pump function, so they are generally contraindicated in the context of acute decompensated cardiogenic pulmonary edema (which includes SCAPE). Reduced contractility could cause the ventricle to fail even more, leading to worsening pulmonary edema.

Beta-blockers should not be administered in efforts to control blood pressure in SCAPE patients.
The key pathophysiologic problem in SCAPE is excessive afterload, which requires treatment with vasodilators.

💡 Remember that positive inotropes (e.g., dobutamine) are sometimes used for the management of cardiogenic pulmonary edema! Inotropes are used for patients with lower blood pressure than SCAPE patients (such patients usually have more of a pump problem, rather than an afterload problem). Nonetheless, this should underscore the concept that beta-blockers aren't beneficial in decompensated cardiogenic pulmonary edema (including SCAPE).

principle #4: watch for when the SCAPE breaks

If treated appropriately, the SCAPE will break rapidly - the vicious spiral will stop and the patient will improve. The most obvious way to tell this is happening is often when the blood pressure starts to drop precipitously. Management involves:

(1) Rapidly down-titrate the nitroglycerine infusion and CPAP/BiPAP pressures (while watching for recurrent SCAPE).

(2) Consider any triggers of SCAPE and treat them (e.g., nonadherence to antihypertensives, volume overload).

(Further discussion of this phenomenon here.)

basics

Positive airway pressure achieves an immediate and titratable reduction in both cardiac preload and afterload.

Either CPAP or BiPAP may be used - the key intervention is an increase in the mean airway pressure (the time average of pressure in the airway).

CPAP: Mean airway pressure is equal to the pressure setting of the CPAP.

BiPAP: Mean airway pressure is a bit over the expiratory pressure (ePAP). For example, with BiPAP set at 15 cm/10 cm, the mean airway pressure might be somewhere around ~12 cm.

BiPAP is often used as this gives the patient a bit of mechanical support, which may improve comfort (patients perceive the machine as giving them support). However, either BiPAP or CPAP are equally effective.

nuts and bolts

CPAP: Start at a low pressure (e.g., 5-8 cm), up-titrate rapidly as tolerated to a maximal pressure of ~15-18 cm.

BiPAP: Start at a low pressure (e.g., 12 cm/6 cm). Up-titrate rapidly as tolerated, with a goal of increasing the expiratory pressure (e.g., titrate up to ~18 cm/15 cm).

The maximal safe pressure is not precisely defined, but pressures above ~20 cm may increase the risk of gastric insufflation.

make sure to optimize the CPAP or BiPAP

CPAP or BiPAP is the most important, evidence-based therapy for SCAPE - so the first priority should be utilizing this treatment and optimizing it.

Higher airway pressure will more effectively reduce preload and afterload in a dose-dependent fashion.

Airway pressures should generally be rapidly up-titrated, while monitoring patient comfort and hemodynamics (higher pressures may cause a reduction in blood pressure - which is generally a welcome effect).

⚠️ Perhaps the most common pitfall in management of SCAPE is failure to up-titrate CPAP or BiPAP settings. Up-titrating the airway pressure will cause an instantaneous reduction in preload and afterload, which might be faster and more reliably effective than any medication.

if the patient can't tolerate the usual mask

(1) Basic techniques:

Start by holding the mask gently to the patient's face.

Start with lower pressures, then ramp up the pressure as the patient adapts to it.

(2) Medication:

may be ideal here to reduce anxiety and work of breathing (more on this below). Patients often have difficulty tolerating the mask because they are very air hungry, leading to flow starvation (the patient wants to take a breath faster than gas can be provided from the CPAP/BiPAP machine). Fentanyl directly treats underlying air hunger and eliminates this problem. Don't worry about causing respiratory suppression - these patients generally have excessive respiratory drive with profound tachypnea.

IV haloperidol or IV droperidol may also be a reasonable choice here.

IV benzodiazepines work in some patients, but commonly cause confusion and disinhibition in other patients. They may be beneficial among patients on chronic benzodiazepines, who are known to respond well to them.

(3) Other interfaces:
Helmets and nasal interfaces are both potentially effective. Some patients may tolerate these better than the usual orofacial mask. Both of these interfaces may be safer among patients who are at risk of emesis and subsequent aspiration.

It is essential to rapidly reduce the blood pressure, perhaps targeting a systolic blood pressure <140 mm (as explored further above). Nitroglycerine is the key intervention used to achieve this.
some key points about nitroglycerine in SCAPE

The dose of nitroglycerine required to achieve arterial vasodilation in SCAPE is about an order of magnitude greater than the usual doses of nitroglycerine required for management of anginal chest pain. This is because higher doses of nitroglycerine are required to achieve arterial vasodilation (whereas lower doses are sufficient to achieve venodilation).

Patients vary widely in their individual sensitivity to nitroglycerine, which underscores the importance of aggressive, empiric dose-titration.

step #1) loading dose of nitroglycerine

Start with an initial loading dose of IV nitroglycerine of ~1,000-2,000 micrograms.This may be provided in one of two ways:

(a) Pushing a bolus of 1,000-2,000 mcg nitroglycerine over ~2 minutes.

(b) Nitroglycerine infusion at 400-800 mcg/min for 2.5 minutes.

Both approaches are equivalent, with the choice depending on logistics.

The main risk of nitroglycerine boluses is hypotension. However, this is unlikely if the diagnosis of SCAPE is secure (since these patients are profoundly vasoconstricted). Several studies have found nitroglycerine boluses to be safe in the context of SCAPE. Occasional patients who have SCAPE along with underlying hypovolemia may develop hypotension that usually responds to observation or administration of small volumes of crystalloid - since the nitroglycerine levels will naturally fall within minutes.

IV nitroglycerine boluses have been shown to be safe, even when administered by paramedics in the (field.33023684, 31900011) Consequently, resuscitationists working within the critical care arena should feel quite comfortable with this as well.

step #2) maintenance infusion of nitroglycerine

The nitroglycerine infusion may be initiated at a rate of ~100-300 mcg/min (depending on the baseline blood pressure and illness severity).( A high dose of nitroglycerine is required to achieve arterial vasodilation, possibly at least ~150 mcg/min. Based on the vicious-spiral physiology of SCAPE, it's generally better to start at a 34215472)high dose, control the blood pressure promptly, and then back down.

If blood pressure isn't controlled promptly, up-titrate the nitroglycerine aggressively. Very high doses (e.g., 800 mcg/min) may be required for limited periods of time, to break the cycle of progressive hypertension.
Re-bolusing nitroglycerine is unnecessary, since a high-dose infusion will provide the same amount (e.g., 800 mcg/min for five minutes is roughly equal to a 4,000 mcg bolus every 5 minutes).

If hypertension is refractory to 800 mcg/min nitroglycerine, then:

Make sure the CPAP/BiPAP pressures are maximized.

Consider the addition of nicardipine, clevidipine, IV enalaprilat, captopril, and/or fentanyl. (More on this above.)

step #3) wean off nitroglycerine as SCAPE resolves

Generally the SCAPE will start resolving rapidly (within minutes to a couple of hours), causing the blood pressure to decrease. As quickly as the storm began, it quietly abates.

Nitroglycerine can usually be titrated off rapidly as SCAPE resolves. In some cases, ongoing hypertension control may require the addition of an oral vasodilator (e.g., ACE inhibitor) - but in many cases this isn't required. (More on oral vasodilators below.)

💡 Watch the blood pressure very carefully and down-titrate the nitroglycerine infusion accordingly, to avoid hypotension.

contraindications to nitroglycerine?

Nitroglycerine is contraindicated among patients who recently received phosphodiesterase type-5 inhibitors (e.g., sildenafil, tadalafil, vardenafil). Nicardipine or clevidipine might be considered in such patients.

Aortic stenosis isn't a contraindication to nitroglycerine in the context of SCAPE. However, some caution is required (with perhaps somewhat lower doses and more gradual dose titration than usual).

sublingual nitroglycerine

This may be utilized if a patient experiences SCAPE in a location unable to provide IV nitroglycerine (e.g., a medicine ward).

The goal of sublingual nitroglycerine is solely to bridge the patient until they are able to receive IV nitroglycerine - not as an alternative or replacement for IV nitroglycerine. Patients should be transported immediately to a location capable of administering definitive therapy (IV nitroglycerine and noninvasive ventilation).

The optimal dose is unclear, but 3-5 sublingual 400-mcg tablets q5 minutes might be reasonable. (Note that the bioavailability of sublingual nitroglycerine is only ~40%.)

background

Opioids offer numerous theoretical benefits for SCAPE patients - including venodilation, sympatholysis, and anxiolysis.

Retrospective studies have correlated the use of morphine with worse outcomes among patients with pulmonary edema. This shouldn't be surprising. Sicker patients are more likely to be air hungry, prompting therapy with morphine. It's also conceivable that morphine could mask the symptoms of pulmonary edema, prompting providers to be less aggressive with other therapies (e.g., patient doesn't look sick enough to need CPAP).

The role of opioids in SCAPE remains controversial. However, opioids may be useful in a selected group of patients, when integrated into an organized treatment strategy.

Fentanyl is probably the best agent here, for the following reasons:

Fentanyl has a rapid onset of action, allowing it to be titrated accurately.

Fentanyl doesn't cause histamine release, making it less likely to promote nausea/vomiting.

potential indications for fentanyl?

(1) Inability to tolerate the CPAP/BiPAP mask.

Marked air hunger may cause patients to have difficulty tolerating noninvasive ventilation.

Fentanyl directly reduces air hunger, so this is a direct physiological approach to the underlying problem.

(2) Extreme dyspnea/anxiety?
For patients with profound dyspnea, low-dose fentanyl could be reasonable to promote comfort and reduce anxiety-driven sympathetic activation.

⚠️ Fentanyl should never be used alone as management for air hunger, but solely as an adjunctive agent in combination with CPAP/BiPAP and nitrates.

⚠️ SCAPE will generally start improving rapidly, so fentanyl should be required only initially. If a patient has persistent air hunger over several hours, this suggests an alternative diagnosis - reevaluate for other causes of dyspnea.

⚠️ caution with oral vasodilators

The hallmark of SCAPE is labile blood pressure. Initially patients are profoundly hypertensive, but with resolution of SCAPE they often transition to being normotensive (without requiring any medication).

Be careful about starting long-acting antihypertensives during the acute phase of SCAPE, because this may eventually lead to rebound hypotension after SCAPE has resolved.

when to use oral vasodilators

The best time to initiate oral vasodilators is if the following situation occurs - which is actually infrequent:

(1) Pulmonary edema resolves following treatment with an IV nitroglycerine infusion (e.g., resolution of dyspnea and hypoxemia).

(2) There is a persistent requirement for IV nitroglycerine in order to control the blood pressure.

(3) The nitroglycerine requirement has been relatively stable for a couple of hours.

In this situation, oral vasodilators may be used to wean off the IV nitroglycerine. Continued use of oral vasodilators may also help prevent the recurrence of SCAPE episodes.

💡 In most cases of SCAPE, clinical resolution will allow the IV nitroglycerine to be weaned off without the use of any oral antihypertensive agents.

ACE inhibitors & ARBs

An ACE inhibitor or angiotensin receptor blocker (ARB) is probably the best antihypertensive for these patients, if renal function allows.

Oral captopril may be preferred because it is fast-acting. This allows for rapid assessment of its effects and prompt oral titration. For example, a dose of 12.5-25 mg can be given and this can be repeated in ~2 hours if there is an inadequate effect.

The main drawback of ACE inhibitors and ARBs is potential nephrotoxicity. These agents may not be ideal for patients with acute kidney injury, or multimorbid patients with numerous active medical problems.

oral hydralazine/isosorbide dinitrate

The combination of oral hydralazine plus isosorbide dinitrate produces similar hemodynamic effects compared to an ACE inhibitor, without a risk of nephrotoxicity.

The usual starting dose is isosorbide dinitrate (ISORDIL) 20 mg PO q8hr plus hydralazine 37.5 mg PO q8hr. The dose can be up-titrated to effect.

This combination is useful for acute stabilization. Once the patient has recovered from their acute illness and their volume status has been optimized, the combination will usually be transitioned to a different agent (e.g., an ACE inhibitor).

key concepts regarding fluid management

Diuresis isn't a front-line intervention for SCAPE. The key pathophysiologic problem with SCAPE is uncontrolled sympathetic outpouring and increased afterload. Many patients with SCAPE may be euvolemic or even hypovolemic (merely experiencing a maldistribution of fluid that shifts into the lungs).

approach to fluid management in SCAPE

The initial therapies are positive pressure ventilation and afterload control (usually with high-dose nitroglycerine). These should be instituted immediately, prior to consideration of diuretics.

Assess the patient clinically after initiating nitrates and positive pressure ventilation (e.g., with echocardiography). If there is evidence of hypervolemia, then volume removal may be beneficial (either with diuresis or dialysis). A benefit from volume removal is particularly supported if there is a clinical history suggestive of volume overload (e.g., nonadherence with diuretics, or missed hemodialysis sessions).

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To keep this page small and fast, questions & discussion about this post can be found on another page .

Know your patient's BiPAP pressures, and aggressively up-titrate them. Just starting BiPAP isn't enough; the pressures should be ramped up rapidly. BiPAP at 18cm/15 cm is going to do a lot more than at 10cm/5cm.

DO NOT delay treatment with BiPAP and nitroglycerine while waiting to see if diuresis will work.

DO NOT try to treat the hypertension of a SCAPE patient with beta-blockers. The pathophysiologic problem is excessive afterload, which a beta-blocker won't address. Beta-blockers may reduce pump function, thereby worsening the pulmonary edema.

Try to avoid intubation if possible, because these patients will often improve dramatically and rapidly with BiPAP and high-dose nitroglycerine. Patients who look horrifically ill will often improve within minutes.

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Going further

Imaging credits: Opening image includes figures from PMID 34215472, 32278569, and 29942881 (full references above).

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Sympathetic Crashing Acute Pulmonary Edema (SCAPE)

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CONTENTS Rapid Reference 🚀 SCAPE vs subacute pulmonary edema Diagnosis Triggers of SCAPE Principles of treatment CPAP or BiPAP Nitroglycerine Opioid Oral vasodilators Volume management & diuresis Podcast Questions & discussion Pitfalls SCAPE dx & rx checklist ✅ central clinical findings of SCAPE (more) Rapid onset of severe dyspnea. Hypoxemia.

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Chris Domenico Reviews Pressors and Inotropes

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Jantzen's Grounded Theory of Nursing Well

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Jantzen's Grounded Theory of Nursing Well

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A way for us to think about our individual and group approach to improving our practice. From:
Jantzen, D. (2019). Refining nursing practice through workplace learning: A grounded theory. Journal of Clinical Nursing, 28(13/14), 2565–2576. https://doi.org/10.1111/jocn.14841

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A great video from the New England Journal of Medicine.  You will need your PennKey to view