The following is a question about ACLS submitted by JMEDIC22, answered by the professionals at AMRI.

Q: For a long time, our EMS protocols included IV morphine for treating CHF (Congestive Heart Failure). Following a recent discussion, our department’s medics had these observations:

• The CHF patients getting IV morphine ended up intubated far more often than the patients who didn't receive morphine.
• We always believed that the patients looking more relaxed, and often with easier breathing, demonstrated the benefits of morphine.
• Our medics remember that most of the patients getting intubated ended up dying, many during transport to the ER.

Can your experts comment?

Evolution of CHF Treatment

Traditionally, many prehospital protocols included the use of morphine IV, high-loop diuretics, rotating tourniquets, and inhaled bronchodilators. Today, some or all of these protocols have fallen into disfavor. When considering underlying cardiovascular and pulmonary physiology and pathophysiology, it’s clear why many of these protocols failed to benefit the patient.

Congestive heart failure (CHF) or cardiogenic pulmonary edema often causes severe respiratory dysfunction, as well as:

• Severe shortness of breath
• Severe increases in work of breathing
• Severe hypoxemia and hypoxia
• Many more conditions

The proximate cause of this pulmonary crisis is related to heart failure. As the pressures in the failing heart increase (cardiac filling pressures), the failing ventricle becomes more "after loaded" which worsens cardiac performance, and may lead to complete heart failure and cardiac arrest.

Alternate Approaches

With this in mind, what does the administration of morphine (a potent respiratory depressant) accomplish in this group of critically ill patients? Although morphine may have certain mild effects of vascular tone, administering to a patient with respiratory failure is unappealing to most.

If the patient has high filling pressures as a result of worsening ventricular function, the obvious goal should be their reduction and improvement in ventricular function. Some approaches to this include:

• Vasodilators - Clinicians may in some cases administer a carefully titrated vasodilator such as nitroglycerin (NTG) or sodium nitroprusside (SNP) while dynamically monitoring the patient. Look for decreased respiratory frequency, decreased work of breathing, improvement in arterial pressure and general perfusion. Because these agents have a very rapid half-life compared to morphine, the infusion can be stopped immediately if improvement is not observed. Most studies report a high rate of positive response to these agents.
• CPAP/BiPAP - The pulmonary dysfunction is largely caused by the high intravascular pressures moving water into the lung tissue, causing the lungs to become stiff and non-compliant. This increased interstitial pressure causes a loss of Functional Residual Capacity (FRC), a reduction in tidal volume, and collapse of small airways. Rather than intubation and mechanical ventilation, the use of continuous positive airway pressure (CPAP) or Bilevel positive airway pressure (BiPAP), again carefully titrated, has been shown to improve the compliance curve for the patient, resulting in a reduction in rapid respiratory rate, increase in tidal volume, and recruitment of collapsed alveoli. Of course, this is respiratory support, still dependent on restoring cardiac function as the primary therapeutic goal.

Other Considerations for CHF Treatment

Because these CHF patients have severely diminished renal function (due to decreased cardiac output leading to degradation of renal blood flow), when filling pressures are normalized and adequate perfusion is restored, these patients are often hypovolemic. For years some practitioners thought these patients were "fluid-overloaded" when in fact the intravascular water was trapped in their lung tissue via the high hydrostatic pressure gradients. If that is the case, loading patients with hundreds of milligrams of furosemide would be a poor choice.

Treating scattered wheezing in the acute CHF patient is not indicated. We know that it is the increased interstitial pressure of the lung tissue, not bronchospasm, that is responsible for the audible pulmonary sounds.

Final Thoughts

In summary, although these patients presented acutely ill, the root of these malignant cascades is both primarily and secondarily cardiac in nature. Current critical care literature recommends aggressively addressing the underlying pathophysiology rather than focusing on the dramatic symptoms of acute cardiac failure.

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