Transcript ACE Inhibitor Training

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.
The City of Allentown, the author, and the Eastern PA EMS
Council assume no responsibility for the use or misuse of this
material. All images are presumed to be free of copyright and
the use of this material is strictly for non-commercial use.
The author has allowed the use of this material on a free and
unencumbered basis for educational purposes only as long as
this message, the logo of City of Allentown, and proper
citation of authorship is provided.
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Objectives
(focused to Congestive Heart Failure in the emergency setting)
Understand the gross epidemiology of Heart Failure
Review the basic pathophysiology of CHF
Become familiar with ACE Inhibitors
Plan a course of treatment based on BLS/ALS protocols
Interface with Medical Command through MedCom
Recognize and prepare for adverse side effects
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Heart Failure Incidence
and Prevalence
♥ Prevalence
Worldwide – 22 million
United States – 5 million
♥ Incidence
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)
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Define - Heart Failure:
Heart failure, the inability of the
circulatory system to meet the metabolic demands of the body.
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
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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.
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Heart Failure is caused by:
 Narrowing of the coronary arteries (coronary artery
disease)
 Heart attack
 Heart valve damage
 High blood pressure
 Disease of the heart muscle itself (cardiomyopathy)
 Defects in the heart present at birth (congenital heart
defects)
 Infection of the heart valves and/or heart muscle itself
(endocarditis and/or myocarditis).
According to the AMERICAN HEART ASSOCIATION
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Heart Failure is classified as:
Class I
Class II
Class III
Class IV
Asymptomatic
heart failure
ejection fraction
(EF) <40%
Mild symptomatic
heart failure
with ordinary
exertion
Moderate
symptomatic
heart failure
with less than
ordinary exertion
Symptomatic
heart failure
at rest
We often meet our patient’s when they are in Class IV heart failure!
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Reduce
Hypertension
Oxygen and
position
Use CPAP to
reverse alveolar
fluid shift
In many cases,
acute heart failure
is associated with a
hypertensive crisis.
Correct the hypertension
and you can often mitigate
the emergent symptoms.
Tip: CPAP works better with lowered
pulmonary vascular pressures!
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Fluid shift is a significant problem in the
patient with acute Heart failure
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!
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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!
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Right sided failure vs. Left sided failure
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.
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Right sided failure vs. Left sided failure
Image shows enlarged
heart and an significant
accumulation of fluid in
both lungs.
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.
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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.
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Nitroglycerin – Step One in
reducing blood pressure.
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 ‘screendoor’ 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)
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ACE Inhibitors
(a possible Command Only additional treatment)
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.
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ACE Inhibitors – How do they work?
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:
1. renin
2. angiotensin
3. aldosterone.
This system can be a potent vasoconstrictor – interrupt any
portion of the system and you can cause vasodilatation and
thus reduce systemic blood pressure.
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The ACE inhibitor or angiotensinconverting 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
http://endo.endojournals.org/cgi/reprint/144/6/2179.pdf
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Pharmacology of ACE Inhibitors
By blocking the ACE enzyme, ACE inhibitors decrease circulating levels of
angiotensin II which decreases peripheral vascular resistance, and despite this
fall in peripheral resistance, there is little effect on heart rate.
Drug names end in –’pril’
•Captopril
•Lisinopril
•Fosinopril
•Quinapril
•Enalapril
PA State protocols allow
pre-hospital use of only
Captopril and Enalapril
IMPORTANT! ACE INHIBITOR THERAPY IS NOT A FIRST LINE
MEDICATION.
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Pharmacology of ACE Inhibitors:
Captopril (brand name Capoten)
First ACE Inhibitor developed for use in control of blood pressure
Widely used
Administered SL (per protocol) or PO (no IV preparations)
Dose 25mg SL – one time.
Best used for patients who are suffering hypertension with peripheral edema
(right side heart failure) as the medication requires an adequate airway and
moist mouth.
Onset via SL – within 5 minutes peaking in one hour.
Packaged as 12.5mg or 25mg tablets
NOT normally available in the ER for replacement.
Required to carry at least 50mg on ALS ambulances.
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Pharmacology of ACE Inhibitors:
Enalapril - ENALAPRILAT INJECTION (brand name Vasotec)
Second generation ACE inhibitor
Also widely used
Administered IV (per protocol) or PO
Dose 0.625mg – 1.25mg – one time.
Slow IV push – followed by flush.
Best used for patients who are suffering hypertension with pulmonary
edema (left side heart failure).
Onset via IV – actions begin almost immediately peaking in 30 minutes
Packaged as 1.25mg per ml in vials of 1ml or 2ml
Normally available in the ER for replacement.
Required to carry at least 2.5mg on ALS ambulances.
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Cautions of ACE Inhibitor use
Use may cause:
Hypotension (quickly in sodium or volume depleted patients) – report
diuretic use, renal insufficiencies or dialysis to medical command. Starting
doses for patients on diuretics is usually 0.625mg. Be prepared to provide
careful fluid bolus should hypotension occur while assessing for pulmonary
edema.
Angioedema (rare, but in the event of anaphylactoid response, treat with
SQ Epi 1:1000)
Syncope
Cough
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Contraindications of ACE Inhibitor use
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.
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Treatment of the acute CHF patient
 First do a complete assessment and uncover the medical history of the
patient.
 Follow PA State Protocol 5002 – ALS
 Position patient for ease of breathing – usually Fowler’s
 Provide high flow oxygen while assessing for edema.
 Frequent repeat assessments of lung sounds are needed
 If blood pressure is elevated, begin NTG treatment per protocol
 Provide CPAP for those patients who qualify for the treatment
 Contact Medical Command through MedCom and provide report and ETA.
Advise Medical Command that you have the option of administering either
Captopril SL or Enalapril IV at their discretion
 Monitor airway and cardiovascular systems constantly
 Rapid but safe transport to appropriate facility
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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”