ALS PROTOCOL UPDATE EASTERN PA EMS COUNCIL PREPARED BY: DAVID K. VAN ALLEN, NREMT-P, FP-C BUREAU MANAGER, CITY OF ALLENTOWN PARAMEDICS JANUARY 2009. ACE Inhibitor Training. Captopril SL. Enalapril Injection.
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This training is not designed to replace the need of your service’s medical director to assure that you, the ALS practitioner, are trained to use this medication.
This presentation is only an adjunct to other more complete training that is needed to ensure that you fully understand the uses, effects and contraindications of the medication discussed.
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Worldwide – 22 million
United States – 5 million
Worldwide – 2 million new cases year
United States – 500,000 new cases year
♥ Afflicts 10 out of every 1,000 people over age 65 in the United States
(Stats from American Heart Association - 2002)
It is a multifaceted disease state involving several organs including the heart, kidney, vascular and respiratory systems - and there are several forms of heart failure with multiple etiologies. The treatment of chronic or acute heart failure is a particularly difficult therapeutic problem with no single drug or drug class adequate to provide complete relief from the symptoms of the disease.
Sadly, regardless of the treatment, 50 % of individuals die within 5 years of developing CHF. In an era where morbidity and mortality from other cardiovascular diseases are decreasing, deaths from CHF are increasing.
American College of Cardiology Web Site www.acc.org
Our local elderly population is higher than in some other areas. This means that we as paramedics will encounter a patient in some stage of heart failure more frequently – and often when they are experiencing emergent acute failure symptoms.
According to the AMERICAN HEART ASSOCIATION
Asymptomatic heart failureejection fraction (EF) <40%
Mild symptomatic heart failure
symptomatic heart failure
with less than
Symptomatic heart failure
We often meet our patient’s when they are in Class IV heart failure!
Correct the hypertension and you can often mitigate the emergent symptoms.
Tip: CPAP works better with lowered pulmonary vascular pressures!
The acute phase of heart failure is almost always is associated with higher blood pressures resulting in fluid shift from the capillary vascular spaces to the surrounding interstitial tissue.
Think of capillaries in your body as a screen door. There are holes that are big enough to naturally pass nutrients, oxygen and CO2 through the openings, but the holes are normally small enough to keep the formed elements of blood (red blood cells, etc) and plasma (90% water) from shifting out under normal pressure.
It is easy to see that if you simply increase pressure, that water would pass right through!
Increased pressure in the capillaries can cause a shift of fluids into the limbs, hands, feet, toes and fingers, as well as the abdomen and lungs – depending on which side of the heart is failing!
Partial failure of the right ventricle’s ability to eject its full load of blood leads to congestion of systemic capillaries. This is caused by increased venous blood pressure which pushes against the walls of small capillaries in the limbs. This excess pressure helps to generate excess fluid accumulation in the tissues of extremities by forcing plasma from the blood, past the walls of the capillaries and into the surrounding tissue. The lymphatic system becomes overwhelmed and cannot collect and remove the excess fluid. This causes swelling under the skin or peripheral edema and usually affects the dependent parts of the body first (causing foot and ankle swelling in people who are standing up, and sacral edema in people who are predominantly lying down). In progressively severe cases, ascites (fluid accumulation in the abdominal cavity causing swelling) and hepatomegaly (painful enlargement of the liver) may develop.
Partial failure of the left ventricle’s ability to eject its full load of blood leads to congestion and high blood pressures in the pulmonary vasculature. The symptoms of left sided heart failure are therefore predominantly respiratory in nature. The patient will have dyspnea on exertion and in severe cases, dyspnea at rest. They may also experience breathlessness when lying flat, called orthopnea, or paroxysmal nocturnal dyspnea, which is a sudden nighttime attack of severe breathlessness. Just like in right side failure, the higher blood pressures (this time in the pulmonary circuit) cause water to leak through the capillaries surrounding the alveoli, which then fills them up reducing or stopping the ability to transfer oxygen and CO2 to the blood. This creates the sensation of trouble breathing that we so often see in these patients.
Image shows enlarged heart and an significant accumulation of fluid in both lungs.
One of the goals in the emergency treatment of CHF is to reduce the systemic and therefore the pulmonary blood pressures to help get those ‘screen door’ capillary beds working correctly again.
Reminder: Heart failure can affect both sides of the heart at the same time.
Nitro is used in the CHF patient when blood pressures are high to help bring those pressures down as quickly and as safely as possible. NTG primarily causes venous dilation which results in a reduction of pre-load to the heart.
The reduction in preload helps to reduce venous return pressures to the heart and can help to lower systemic blood pressure. This helps with our ‘screen-door’ effect, and reduces workload of the heart. To be effective in the patient presenting with acute heart failure, the dosing of NTG may need to be aggressive and carefully monitored. (See PA State Protocol 5002-ALS)
Recent research has shown that adding ACE Inhibitors to the emergent treatment of the patient in CHF may reduce mortality and morbidity by providing a second immediate mechanism to reduce blood pressure. ACEi does this by relaxing and dilating mainly the arterioles and thereby reducing cardiac ‘after-load’; allowing the heart to work against a lower systemic resistance. (Recall, NTG works mostly to reduce pre-load)
Adding ACEi to the immediate treatment of a class IV heart failure patient may help lower blood pressure (one of the goals) and also lower the work of the heart. ACE Inhibitor therapy has a longer therapeutic life per dose, over medications such as NTG and has been a commonly used maintenance medication for patients in failure.
Title: Effects of long-term enalapril therapy on left ventricular diastolic properties in patients with depressed ejection fraction. SOLVD Investigators.
The renin-angiotensin-aldosterone system (RAAS) in the body plays an important role in regulating blood volume and systemic vascular resistance, which together influence cardiac output and mostly arterial pressures.
As the name implies, there are three important components to this system:
This system can be a potent vasoconstrictor – interrupt any portion of the system and you can cause vasodilatation and thus reduce systemic blood pressure.
The ACE inhibitor or angiotensin-converting enzyme inhibitor interrupts or blocks production of an enzyme (the ACE) that helps convert the protein angiotensin I into angiotensin II – A-II is a protein that makes blood vessels constrict and promotes retention of fluid, raising blood pressure.
ACE inhibitors act to widen the blood vessels and make it easier for the heart to pump blood through the body.
For a mini-review of the Renin-Angiotensin System (RAS) please see
PA State protocols allow pre-hospital use of only Captopril and Enalapril
IMPORTANT! ACE INHIBITOR THERAPY IS NOT A FIRST LINE MEDICATION.
ACE Inhibitors are contraindicated in patients who are hypersensitive to any component of the product and in patients with a history of angioedema related to previous treatment with an angiotensin converting enzyme inhibitor and in patients with hereditary or idiopathic angioedema.
Always be ready to adjust your treatments to take care of adverse condition changes. The patient in class IV heart failure is at risk for cardiac arrest.
Johnny says: “You must be on your game”