|
May 2000
Supplement to the
May JEMS article on
Heart Failure and
Acute Pulmonary
Edema |
By Connie J. Mattera, MS, RN, EMT-P |
Editor's note: In May JEMS, Connie Mattera, MS, RN, EMT-P, discussed heart failure and
acute pulmonary edema. The information below is intended to supplement the information
provided in the original article.
|
Heart failure affects 4.8 million people in the United States and
represents the only cardiovascular disease with increasing
prevalence. Improved survival rates in those sustaining an acute
myocardial infarction (MI) and the demographic shift to an aging
society have both contributed to this increase.
Heart failure is a state of impaired cardiac function in which the heart
cannot pump sufficient blood to meet the body's metabolic demands.
It occurs when the workload demand exceeds the pump's ability to
supply blood, when the heart's ability to pump effectively decreases
or when blood flow through the heart is impeded (sclerosed heart
valves) and compensatory mechanisms activate. Several factors
including ischemia, hypertension, alcohol abuse, smoking and
infections in the heart or its valves may predispose a patient to heart
failure.
Primary Causes of Heart Failure
- Myocardial infarction
- Dysrhythmias
- Cardiomyopathies (form of myocardial disease related to viral
infections, injury from toxic effects of alcohol and malnutrition)
- Myocarditis (inflammatory process in myocardium often
associated with a bacterial or viral infection)
- Ruptured chordae tendineae
- Acute papillary muscle dysfunction
- Acute aortic insufficiency
- Prosthetic valve dysfunction
- Ruptured intraventricular septum
- Congenital/acquired valve and septal defects
- Hypertensive cardiovascular disease
Secondary Causes of Heart Failure
- Drugs that alter cardiac function
- Cardiac tamponade
- Pulmonary embolism
- Atrial myxoma (benign primary tumor covered by thrombus
formation arising from the lining of the atria; may simulate
mitral or tricuspid stenosis)
- Superior vena cava syndrome
|
Physiology of normal pump function
The heart is composed of two pumps in a series; the pulmonary
pump and the systemic pump. Cardiac output (CO) is a measure of
the strength of contractions ejecting a volume of blood with each
systole (stroke volume or SV) multiplied by the heart rate (HR) in one
minute (CO = SV x HR) with normal values ranging from 3.5 to 8.0
L/minute.
Stroke volumes are typically 60 to 100 ml (70 mean), but a healthy
heart has the capacity to increase this volume greatly. In reality,
stroke volume equals the end diastolic volume minus the end systolic
volume (systolic remainder).
- End diastolic volume (EDV) is the amount of blood in the
left ventricle LV just before contraction (approximately 130 to
150 ml). Factors affecting EDV are diastolic filling pressures
(preload, venous return), heart rate, atrial contraction and
ventricular compliance (distensibility).
- End systolic volume (ESV) is the amount of blood
remaining in the heart after systole (approximately 24 to 36
ml/m2 or 60 ml). Factors affecting ESV are contractility and
afterload.
- Ejection fraction is the percentage of the end diastolic
volume that is ejected. Usually over 50%.
Heart rate is under autonomic nervous system (NS) control. The
sympathetic NS speeds heart rate (chronotropic effect), increases
contractility (inotropic effect) and speeds conduction through the
electrical conduction system (dromotropic effect) via stimulation of
ß-1 receptors. The parasympathetic system slows heart rate via
stimulation of the vagus nerve, which heavily influences the sinoartial
(SA) and atrioventricular (AV) nodes with few fibers extending into
the ventricles.
In normal circulation, the inhibitory parasympathetic influence on
heart rate and vascular tone is greater than the excitatory
sympathetic effects. The normal heart rate in adults is 60 to 100
beats per minute (BPM) based on intrinsic pacing rates of the SA
node modified by vagal tone. CO can be increased to three times
normal output by increasing rate alone. An increase in HR plus SV
can increase CO by about five times.
As with any pump, the heart's performance is influenced by inflow
and outflow pressures and/or volumes. Stroke volume, for example,
is determined by preload (inflow), afterload (outflow), and contractility
factors (see Table 1). |
|
Table 1
DETERMINANTS OF STROKE VOLUME |
Preload |
Preload is the effective distending or filling pressure
of the ventricle (wall tension) at the end of diastole
proportional to the resting muscle length. Created in
great measure by the venous return to the heart,
normal is 4 to 12 mmHg. Beyond the optimum
preload, myocardial performance levels off or
declines.
Pulmonary congestion and edema are likely beyond
preload levels of 18 to 20 mmHg.
Clinical significance
- Determines the amount of blood the ventricles
will have to circulate during systole
- Influences fiber length/stretch of the
myocardium
|
Afterload |
Resistance or pressure the ventricle must overcome
to eject blood, resulting from vascular resistance.
RV afterload: pulmonary vascular resistance
LV afterload: systemic vascular resistance
Clinical significance
- Influences ventricular isovolumetric
contractions. The greater the afterload, the
harder the heart will have to pump to overcome
the increased resistance.
- Influences myocardial venous O2 extraction
(MVO2)
|
Contractility |
Inherent contractile function of the heart muscle
measured by the degree of myocardial fiber
shortening achieved. Refers to changes in the force of
myocardial contraction and is a function of the
interaction between the contractile elements of the
muscle cells independent of preload and afterload.
Related to the isovolumetric contraction capacity,
which influences MVO2.
Determinants:
- Sympathetic nervous system (SNS) activity
- Circulating catecholamines
- Rate and rhythm of cardiac contractions
- Drugs: positive inotropes, §-1 stimulants (i.e.,
dopamine), Ca++
- Ionic environment (Na, Ca, K, Mg)
- Myocardial oxygenationa Functional myocardium
|
FRANK-STARLING'S LAW
Establishes that the length of the ventricular fiber before contraction
(fiber stretch caused by end diastolic volume) determines the
strength and velocity of contraction.
increased stretch = increased force of contraction
In a normal Starling's curve, very slight changes in fiber length
produced by small changes in LV end diastolic pressure are
associated with significant increases in SV.
Can increase cardiac output by 2 to 2 1/2 X normal through this
mechanism.
Gains in contraction fall off when the myocardial fibers are stretched
beyond physiological limits.
At that point, further stretching fails to produce a positive effect on
the force of contraction. |
Preload & Afterload |
Decreased Preload |
Increased Preload |
Volume changes
- Hemorrhage
- Diaphoresis
- Vomiting, diarrhea
- Third space losses
- Rapid tachycardia (>150 BPM
- shortened diastole,
decreased filling time)
|
Volume changes
- IV fluids
- Blood products
- Renal failure
- Bradycardia
|
Venous dilation
- Hyperthermia
- Drugs: alpha blockers, NTG,
nitrates, nitroprusside
- Shock: septic, neurogenic,
anaphylactic
|
Venous/arterial constriction
- Hypothermia
- Drugs: alpha stimulants
|
Decreased Afterload |
Increased Afterload |
Arterial dilation
- Decreased 02, hypoxemia
- Shock: septic, neurogenic,
anaphylactic
- Increased potassium (K)
- Drugs: alpha blockers, ACE
inhibitors, NTG in high doses,
Ca antagonists, nitroprusside
|
Arterial constriction
- Shock: hemorrhagic,
cardiogenic; gross volume
deficits
- Drugs: alpha stimulants -
norepinephrine, epinephrine.
- Arteriosclerosis;
atherosclerosis
|
Decreased
Contractility |
Increased
Contractility |
- Hypoxemia, hypercapnia
- Acidosis
- Pharmacologic depressors: §
blockers, quinidine,
procainamide (Pronestyl),
lidocaine and barbiturates
- Electrolyte imbalances
- Myocardial depressant factor
(MDF) released from ischemic
pancreas
- Intrinsic changes with chronic
volume overload
|
- Sympathetic stimulation (§1)
- inotropic effect
- Exogenous stimulation -
Dopamine, calcium chloride
|
Pathophysiology of atherosclerosis &
acute ischemic coronary syndromes
(AICS)
In a healthy artery, the inner wall is smooth and elastic, producing
endothelial relaxant factor (EDRF). This enables the vessel
to dilate and constrict based on regional demands and for blood to
flow freely.
Arterial disease usually evolves over a lifetime, typically starting
when something injures the lining of the artery and the body tries to
repair the damage.
Atherosclerosis is a progressive disease that develops when the
lining of the artery degenerates from the buildup of fatty substances
and scar tissue. It affects the aorta, coronary, cerebral as well as
other arteries of the body and is the most common cause of
arteriosclerosis (hardening of the arterial walls). |
Genesis of atherosclerosis
A blood-borne irritant, such as homocysteine (derived from the
protein in our diets), produces toxins on contact with plasma, and
those toxins injure the arterial wall.
Fatty substances (LDL - low density lipoprotein) cholesterol
infiltrates the arterial intima (inner layer) at the points of intimal
injury.
Monocytes (circulating immune cells) rush to the site of injury,
burrow into the blood vessel walls, mature into macrophages ("big
eaters"), gorge themselves on oxidized fatty substances (lipid
peroxidation) and die, causing inflammation (Slyper, 1994).
Fatty streaks form inside the large- and medium-size arteries, often
at stress points and where branching occurs or where the wall is
already damaged.
These deposits thicken, forming an atheroma (a hard mass of fatty
tissue) that gradually erodes the wall, narrows the arterial pathway
and impairs the flow of blood.
An atheroma builds up to form a harder mass called plaque. The
fibrous cap of the plaque contains smooth muscle cells, collagen, and
intra and extracellular lipids. The lipid-filled "foam cells" are believed
to be either monocytes or modified smooth muscle cells. The
necrotic core contains cell debris, cholesterol esters and crystals, and
calcium.
Budging of the plaque into the vessel lumen produces significant
obstruction of blood flow causing a marked disparity between O2
supply and demand in watershed tissues. This results in a continuum
of events grouped under the umbrella of acute ischemia
coronary syndromes (AICS) ranging from stable to unstable
angina (ischemia due to > 70% occlusion) to acute myocardial
infarction (necrosis). In some cases, such stenosis is capable of
precipitating an MI without total occlusion of the vessel. |
RISK FACTORS FOR
ATHEROSCLEROSIS & AICS |
Primary
Cigarette smoking: Cigarette by-products are potent oxidizing
agents that damage the intimal (inner) lining of arterial walls. This
exposes collagen and results in platelet aggregation (clumping).
Nicotine increases circulating fibrinogen and catalyzes the entry of
LDL-cholesterol, which increases the risk of plaque formation in
coronary arteries. Smoking has been found to interfere with vitamin
B12 synthesis, elevating plasma homocysteine levels (Wile-Curtis,
2000) and impairs secretion of EDRF.
Uncontrolled hypertension (systolic and/or diastolic): stronger
predictor in elderly women than in men.
Hyperlipidemia: lipid profile includes HDL; dense LDL; VLDL,
& total cholesterol. Low levels of HDL (under 45 mg/dl) are better
predictors of CHD in women than men. Total cholesterol > 265 mg/dl
and triglyceride levels > 400 mg/dl increase risk.
Hyperhomocysteinemia is estimated to account for 10% of
coronary artery disease (CAD) in the United States. Homocysteine is
a sulfur amino acid. Elevations are typically caused by a genetic
defect in the enzyme responsible for homocysteine metabolism. High
levels cause thromboembolism and severe premature
atherosclerosis. A major factor implicated in elevated levels is a
deficiency in vitamins B6, B12, and folic acid. Elevations are also
seen with chronic renal failure, hypothyroidism, pernicious anemia,
certain cancers (breast, pancreas, ovaries), and acute lymphoblastic
leukemia. Normal levels: < 14 micromoles/L. There is a 40%
increased risk of CAD with 4 micromoles/L above normal levels.
May predict heart disease 1.2-3.1 times as well as
hypercholesteremia; 8-18 times as well as hypertension; and 3.5
times as well as cigarette smoking (Wile-Curtis, 2000). |
Secondary
- Heredity; family history of CAD
- Glucose intolerance; diabetes mellitus
- Left ventricular hypertrophy: CO
|
Contributory
- Obesity
- Inactivity
- Stress
- Personality type "A"
- Rheumatic heart disease
- Lung disease
- Gender: Premenopausal secretion of estrogen in women boosts
HDL levels in the liver, decreasing activity of hepatic lipase that
degrades HDL into an inactive form and inhibits the deposition
of LDL cholesterol into the arterial walls. It also has a direct
vasodilating effect on arterioles (keeps BP down), resulting in
increased blood flow. Post-menopausal women are at equal risk
as men. Women are generally 5-10 years older than men when
diagnosed with CHD.
- Age over 50: Senescent (aging) hearts/blood vessels lose
residual capacity and show longer term effects of
atherosclerosis.
- New research reveals that heart/vascular disease may be
triggered by infectious agents and may possibly be impacted by
the use of antibiotics.
- Chlamydia penumoniae: causes respiratory illness
and may also damage arteries
- Pophyromonias gingivalis: People with chronic gum
disease may have more heart attacks
- Cytomegalovirus: Common herpes virus seems to
exacerbate vascular conditions
|
Conditions That May Result From
Atherosclerosis |
- Hypertension
- Angina
- Acute myocardial infarction
(AMI)
- Left ventricular dysfunction
- Congestive heart failure
(CHF)
- Pulmonary edema
- Cardiogenic shock
|
- Cardiac arrest
- Aortic aneurysm
- Peripheral vascular
disease
- Arterial occlusions
- Renal stenosis
- Stroke
- Transient ischemic attack
(TIA)
|
Clinical Hemodynamic Subsets of
Patients with AMI
- Subset I: Patients who are normotensive and have adequate
peripheral perfusion
- Subset II: Patients with pulmonary congestion
- Subset III: Patients with systolic hypertension
- Subset IV: Patients with peripheral hypoperfusion but no
pulmonary congestion
- Subset V: Patients who have both pulmonary congestion and
peripheral hypoperfusion (i.e., pump failure).
|
Examples of continuous positive airway
pressure (CPAP) candidates (all are
patients you may normally expect to
intubate)
> Cardiogenic pulmonary edema with hemodynamic
stability;
> Status asthmaticus;
> Chronic obstructive pulmonary disease (COPD) with
acute or chronic exacerbation;
> Patients with "do not intubate" orders (palliative care in
terminal patients) or those with advance directives and
pneumonia;
> Post-extubation rescue for acute respiratory failure (if a
patient wakes up enough to extubate themselves, try
CPAP rather than reintubating).
|
Limitations of non-invasive support
> It does not give definitive control of the airway. Patients
with airway impairment or aspiration risk must be
intubated;
> It does not control ventilation. If apneic or inadequate
respiratory drive is present, the patient must be intubated;
and/or
> The patient who fails to promptly stabilize or who
deteriorates despite CPAP should be considered for
immediate intubation.
|
Hazards/complications of CPAP
Equipment related:
> Loss of oxygen supply can affect your ability to continue
treatment;
> Equipment can become disconnected from the circuit;
> TA leak can be experienced in the mask.
Associated with the patient:
> The treatment requires patient cooperation;
> High alveolar pressures can cause an over distention of
alveoli resulting in lung overdistention (barotrauma
resulting in pneumothorax) and/or an increase in
intrapulmonary shunting;
> Overdistention of the lungs can reduce the ability of the
lungs to move easily (decreases compliance);
> Positive pressure may increase secretions or dry upper
airways;
> Impedance of pulmonary blood flow may cause CO2
retention w/ increased work of breathing;
> Gastric distention (rare with CPAP < 30 cm H2O); use
caution in aerophagia sensitive patients (i.e., gastric
stapling, upper gastointestinal surgery);
> Aspiration with very high gas flow and gastric distention;
> Facial skin necrosis at the site of mask contact if used
long-term;
> Intracranial pressure (ICP): if a possible cause of ICP
present; observe closely.
|
What to monitor after CPAP is applied
to a patient
- Patient tolerance: comfort, mental status;
- Respiratory rate/depth; subjective feeling of dyspnea/distress;
- Lung sounds; SPO2; use of accessory muscles;
- BP; pulse; ECG rhythm;
- Complications such as: gastric distention; coughing or
vomiting.
|
Criteria to use to discontinue CPAP in
the field
- Inability to tolerate the mask due to discomfort or pain;
- Need for ET intubation to manage secretions or protect the
airway;
- Hemodynamic instability;
- ECG instability with evidence of ischemia or clinically significant
ventricular dysrhythmias.
|
First-line drug profiles
Treat suspected ischemia with aspirin |
Profile: ASA |
Generic name |
Aspirin - acetylsalicylic acid |
Brand names |
Multiple based on manufacturer |
Action |
- Blocks formation of thromboxane A2.
Thromboxane A2 causes platelets to
aggregate and arteries to constrict.
Prevents platelets from forming a thrombus
or prevents an existing clot from expanding.
- This reduces overall mortality from AMI;
reduces nonfatal reinfarction; and reduces
nonfatal stroke.
|
Indications |
EMS: Myocardial ischemia. Thrombolytic therapy
and aspirin improve short-term and long-term
survival by 20-25% with an additive effect
(Leizorovicz, 1994). Long-term aspirin therapy
now recommended for every patient who has a
history of MI, stroke, angina, TIA, arterial
bypass surgery or angioplasty (British Medical
Journal, 1994). |
Onset of action |
Within 5 minutes |
Duration of
action |
Life of the platelet |
Contraindications |
Known hypersensitivity to ASA, bleeding
disorder, active ulcer disease, > 6 mos pregnant,
recent GI bleed/surgery |
Precautions |
Ask patient w/ asthma if they are ASA sensitive |
How supplied |
Baby ASA in 81 mg tabs or adult tabs 325 mg |
Dose and route |
160-325 mg (2-4 baby aspirin) chewed and
swallowed ASAP. ASA taken at 75-325 mg/day
decreases risk of AMI and stroke by 25%.
Long-term therapy with 75-81 mg/day offers as
much protection as the larger doses, without the
side effects. |
Side effects
(common) |
Bleeding, GI distress |
Profile: NITROGLYCERINE |
Generic name |
nitroglycerine |
Brand names |
Nitrostat, Nitrogard |
Action |
- Increase venous capacitance by dilating the
veins
- Pools blood in the periphery, resulting in
reduced ventricular preload and pulmonary
blood flow.
- At higher doses it dilates the arteries,
decreases afterload and facilitates cardiac
emptying.
- Dilates epicardial conductance arteries
(especially collaterals) and increases
collateral blood flow. This limits infarct size
and as shown by enzyme studies and
improves LV function.
- Increases myocardial oxygen supply and
decreases myocardial oxygen demands
- Questionable as to whether it improves
long-term survival in AMI but studies show
that it does improve outcomes in chronic
congestive heart failure (CHF) (ESPRIM
trial, 1992).
|
Indications |
- Acute ischemic chest pain if SBP > 90
mmHg
- Cardiogenic pulmonary edema if SBP >
90-100 mm Hg
- Hypertension (HTN) associated with AMI
- To limit infarct size in AMI without chest
pain
|
Onset of action |
2-5 minutes SL peaks at 4 minutes |
Duration of
action |
5-30 minutes |
Contraindications |
Hypotension (BP < 90 mmHg), hypovolemia,
increased ICP |
Precautions |
- Administer carefully in an inferior wall MI
and use with caution (if at all) in right
ventricular MI. These patients are
dependent on RV preload to maintain CO
and can experience extreme hypotension
during NTG administration.
- Limit mean BP drop to 10% if patient is
normotensive and 30% if hypertensive.
|
How supplied |
Tablets, spray, paste, patch, solution for IV
drips. |
Dose and route |
1-2 0.4 mg tabs SL q. 5-10 minutes as long as
systolic BP > 90-100 mmHg. |
Side effects
(common) |
Decreased BP, tachycardia, worsening ischemia,
headache, burning sensation under tongue. |
Profile: CAPTOPRIL |
Generic name and
Brand names |
Capoten (captopril), Vasotec (enalopril) (have
best documented mortality benefit). Others
include Prinivil or Zestril (lisinopril), quinapril
(Accupril), ramipril (Altace), trandolapril (Mavik),
fosinopril (Monopril), moexipril (Univasc) |
Action |
Neurohormonal modulating properties:
Inhibits the conversion of angiotensin I to
angiotensin II, therefore preventing arteriolar
constriction (decreases PVR). Prevents
remodeling, decreases afterload, increases
ejection fraction and CO, decreases LV wall
tension, increases LV relaxation (so improves
diastolic dysfunction as well) and allows the
left ventricle to empty, reducing
myocardial dysfunction. Sympatholytic actions
cause a decrease in bradykinin. PCWP decreases
within 10 minutes, thereby reducing dyspnea and
the work of breathing. In one study,
administration of ACE inhibitors decreased
intubation rates in pulmonary edema from 25%
to 5%. Limits infarct size, preserves viable
myocardium. |
Indications |
Treatment mainstay for systolic dysfunction with
nitrates |
Benefits |
Increases exercise intolerance, improves clinical
symptoms, reduces mortality in patients with
overt heart failure, delays the onset of symptoms
in those with symptomatic left ventricular
dysfunction (Bancroft, 1997). The greater the
impairment and the lower the ejection fraction,
the more clearly beneficial ACE inhibitors
become. |
Onset of action |
10-30 minutes |
Duration of
action |
6 hours |
Contraindications |
- Pregnant women due to the inhibitory effect
on protein synthesis and fetal development;
may be lethal to fetus.
- Patients with bilateral renal artery stenosis,
unilateral renal artery stenosis in a single
kidney, renal insufficiency with
hyperkalemia (> 5.5 mEq/L), and
symptomatic hypotension.
- Allergy
|
Precautions |
Non-oliguric patients with renal insufficiency can
take an ACE inhibitor with appropriate dose
adjustment (i.e., half the usual recommended
dose). |
How supplied |
Captopril: 12.5 mg and 25 mg tabs |
Dose and route |
Captopril: 12.5 mg SL immediately after or
simultaneously with NTG as soon as acute
pulmonary edema is suspected. May repeat X 1
with next NTG to a total dose of 25 mg as long as
hemodynamically stable. |
Side effects
(common) |
Angioedema, decreased BP. Cough induced by
increased bradykinin levels in the lungs. ACE is
the enzyme required to break down bradykinin (a
bronchospastic and vasodilating agent). Women
are more susceptible to the bronchospastic
effects of bradykinin than men, so ACE-induced
cough is more prevalent in women after longer
use |
Second-line drug profiles
Loop diuretics |
Profile: furosemide (Lasix) |
Generic name |
Furosemide |
Brand names |
Lasix |
Action |
Loop diuretic; venodilator will decrease preload |
Indications |
Cardiogenic pulmonary edema |
Onset of action |
5 minutes; peak effect in 30-60 minutes |
Duration of
action |
2-8 hours |
Contraindications |
Hypovolemia, dehydration |
Precautions |
- Adrenergic response to decreased CO
causes peripheral and target organ
vasoconstriction i.e., kidneys and lungs.
Giving a first-line drug that is to act on one
of the poorly perfused organs is
counterproductive. Either much higher
doses than normal must be used or the
anticipated effects are likely to be blunted.
- Once the nitrates and ACE inhibitors have
opened up peripheral blood flow, moderate
or low doses of Lasix will cause diuresis.
- 50% of these patients are not volume
overloaded; use of Lasix may be
questionable as it may activate the Reninn
Angiotensin, Aldosterone cascade and
further add to volume and sodium overload.
|
Side effects
(common) |
Decreased potassium |
How supplied |
Preloads, ampules for IVP administration |
Dose and route |
1 mg/kg intravenous push (IVP); if already taking
oral furosemide give 2 times the daily oral dose
IVP |
Analgesics/anxiolytic (anti-anxiety) |
Profile: MORPHINE |
Generic name |
morphine sulfate (MS) |
Action |
Narcotic analgesic; CNS depressant; sedative;
weak venodilator decreases preload |
Indications |
Pain, anxiety w/ pulmonary edema. MS use in
pulmonary edema will fade as clinicians become
more familiar with superior vasodilators and
inotropes |
Onset of action |
2-3 minutes |
Duration of
action |
30-60 minutes |
Contraindications |
Respiratory depression, hypotension. |
Precautions |
Some discourage use of MS in pulmonary edema
(PE) due to respiratory depressant effects. May
use naloxone 0.4-0.8 mg IV to reverse
respiratory depression after narcan
administration |
Side effects
(common) |
Sedation, respiratory depression, hypotension
(especially with volume depleted patients);
nausea/ vomiting; bradycardia; itching and
bronchospasm (uncommon). |
How supplied |
Ampules, tubex, preloads for IVP administration. |
Dose and route |
1-3 mg increments q. 5 minutes IVP usually to a
total of 8-10 mg. |
Vasopressor use in cardiogenic shock |
Profile: DOPAMINE |
Generic name |
Dopamine hydrochloride |
Brand name |
Intropin |
Classification |
Sympathetic agonist |
Action |
Dopamine is a naturally occurring catecholamine
that is a precursor of norepinephrine. It is
chemically related to both epinephrine and
norepinephrine and increases BP by acting on
both alpha and beta-1 (§) receptors. There are
also dopaminergic receptors.
Action is dose dependent.
- Dilates renal and mesenteric blood vessels
at low doses (1-2 mcg/kg/min)
- Acts as a § agonist by stimulating
adenocyclase in the cell which converts ATP
to cyclic AMP. Cyclic adenosine
monophosphate (C-AMP) is activated by a
protein kinase (phosphokinase) which allows
or increases calcium entry into the cell
allowing the cross bridging of myosin and
actin in the sarcomere. This causes a
positive inotropic effect (
increases myocardial
contractility). It does not increase
myocardial O2 demand as much as
isoproterenol (Isuprel) and epinephrine and
does not have the same powerful
chronotropic effects.
- Acts on the alpha adrenergic receptors
causing peripheral vasoconstriction. Unlike
norepinephrine, when used in therapeutic
dosages, dopamine maintains renal and
mesenteric blood flow because of its effect
on the dopaminergic receptors. For these
reasons, dopamine is the most commonly
used vasopressor. It will increase both the
BP and pulse pressure (difference between
systolic and diastolic BP), but there is
generally less effect on the diastolic
pressure.
|
Indications |
- Hemodynamically significant hypotension
(systolic BP of 70-100) not resulting from
hypovolemia
- Cardiogenic shock (low doses); anaphylactic,
neurogenic shock (higher doses).
|
Onset of action |
5 minutes |
Duration of
action |
10 minutes IV |
Contraindications |
- Should not be used as the sole agent in
hypovolemic shock unless fluid volume
resuscitation is underway.
- Pheochromocytoma (tumor of the adrenal
gland).
- Presence of tachydysrhythmias.
|
Precautions |
- Treat rate problem first (severe
brady/tachycardias - HR > 150) if present.
- The patient is often maximally
sympathetic-nervous-system (SNS)
stimulated, resulting in a feedback
mechanism which creates more
phosphodiesterase (the enzyme that breaks
down C-AMP) and dopamine may not work.
- Dopamine will increase HR and can induce or
worsen supraventricular and ventricular
dysrhythmias.
|
Side effects
(common) |
Nervousness, headache, tachycardia, palpitations,
chest pain, dysrhythmias, dyspnea, nausea &
vomiting. Many of these SE are dose-related. |
Interactions |
- Like all catecholamines, can be deactivated
by alkaline solutions (sodium bicarbonate).
- Because monoamine oxidase (MAO)
inhibitors (type of antidepressant) potentiate
dopamine, reduce dose.
- May cause hypotension if used with
phenytoin (Dilantin).
|
How supplied |
Comes in prefilled syringes, ampules, and
premixed bags. Standard preparation is 200 mg/5
ml of solvent; 400 mg preparations in 5 ml of
solvent are also available. Drips are typically
mixed at 800 mg/500 ml or 400 mg/250 ml IVPB
(1600 mcg/ml). |
Dose and route |
Beta predominates: 2-10 mcg/kg/min; Alpha
predominates > 10 - 20 mcg/kg/min Often start
at 2.5-5 mcg/kg/min IVPB and titrate upwards
until BP improves. Pediatric dose: 2-20
mcg/kg/min |
Notes on quick dosing of Dopamine:
Obtain the patient's weight in pounds. Take first 2 numbers of weight
in pounds. Ex: 200 pound patient. Subtract 2 from that number: (20 -
2 = 18) The drip is run at 18 microdrops per minute to administer 5
mcg/kg/min. Sample exercises:
- If a patient weighs 125 pounds: You should begin a Dopamine
drip at a rate of _______ microdrops/minute (5 mcg/kg/min
dose);
- If after 5 minutes there is no response, you should increase the
rate to_______ microdrops/minute (10 mcg/kg/min dose);
- If there is still no response, you can increase to a maximum
of_______ microdrops/minute (20 mcg/kg/min dose).
DOPAMINE Dose by Weight |
BODY WEIGHT |
DOSE RANGES |
Start at 5
mcg/kg/min
§
predominates |
Do not
exceed 20
mcg/kg/min
alpha
predominates |
100 lbs |
45 kg |
8 mcgtts/min |
32
mcgtts/min |
121 lbs |
55 kg |
10
mcgtts/min |
40
mcgtts/min |
143 lbs |
65 kg |
12
mcgtts/min |
48
mcgtts/min |
165 lbs |
75 kg |
14
mcgtts/min |
56
mcgtts/min |
187 lbs |
85 kg |
16
mcgtts/min |
64
mcgtts/min |
210 lbs |
95 kg |
19
mcgtts/min |
76
mcgtts/min |
240 lbs |
109 kg |
22
mcgtts/min |
88
mcgtts/min |
260 lbs |
118 kg |
24
mcgtts/min |
96
mcgtts/min |
|
Long-term therapies for heart failure
- Calcium channel blockers:
- If the BP remains disproportionately elevated after an AMI or
once the patient is out of pulmonary edema and they are already
taking ACE inhibitors, physicians may prescribe amlodipine
(Norvasc), felodipine (Plendil) or other Ca blockers to treat
refractory angina or hypertension (Michael & Parnell, 1998).
Beta blockers
- (Selective §1 antagonists): Benefits include decreased
cardiotoxic effects of chronically elevated levels of
norepinephrine, improvement in cardiac function and exercise
performance, delayed deterioration in left ventricular function,
improvement in symptoms, and prolongation of survival
(Michael & Parnell, 1998). When used long-term for dilated
cardiomyopathy, should see alleviation of tachycardia, increased
ejection fraction, decreased third heart sounds, and
improvement in orthopnea and dyspnea.
Digoxin:
- Positive inotropic agent derived from the foxglove plant.
Foxglove has five leaves in the shape of fingers sprouting off of
a single stem...thus the name "DIGIT-alis (Bancroft, 1997).
Currently used for treating systolic heart failure in patients
whose symptoms persist after ACE inihibitors and diruretics.
Major benefit is to improve symptoms; it has not been shown to
improve morbidity or mortality. Agents known to increase
digoxin levels are quinidine, verapamil, amiodarone, and
antibiotics (aminoglycosides, erythromycin and tetracycline).
Observe for signs of digitalis toxicity.
Angiotensin II receptor blockers:
- losartan (Cozaar), candesartan (Atacand), irbesartan (Avapro),
valsartan (Diovan), telmisartan (Micardis), eprosartan (Teveten).
These agents avoid the effects ACE inhibitors have on
bradykinin and prostaglandins which likely contribute to the
cough, angioedema, and renal dysfunction seen with the "prils".
Action: dose-dependent vasodilation, decreased BP, decreased
systemic vascular resistance and decreased aldosterone and
norepinephrine secretion. Shows promise for those who are
unable to tolerate ACE inhibitors.
Aldosterone inhibitors:
- In addition to sodium and water retention, aldosterone causes
depletion of magnesium and potassium, which may contribute to
ventricular dysrhythmias. Other potential adverse effects
include potentiation of the catecholamine effects in the vessels
and myocardium, myocardial fibrosis, and baroreceptor
dysfunction (Michael & Parnell, 1998). Ace inhibitors lower
aldosterone levels but need high doses to achieve normal
values. Spironolactone (Aldactone) is the most potent
adosterone inhibitor currently available.
Endothelin receptor antagonists:
- The endothelin system potentiates the effects of
norepinephrine, serontonin, renin, angiotensin II, aldosterone,
and epinephrine. Agents such as phosphoramidon, BQ-123, and
bosentan are under investigation to determine their efficacy.
Bipyradines
- are true phosphodiesterase inhibitors that allow cyclic
adenosine monophosphate (C-AMP) to remain active longer
thus strengthening cardiac contractility, increasing cardiac index
by 20%, decreasing pulmonary capillary wedge pressures by
20%; and peripherally dilating the patient to reduce afterload.
Two approved drugs are Amrinone 0.75 mg/kg then
5-15 mcg/kg/min and milranone. Vesnarinone
(OPC-8212) is investigational and demonstrates only positive
inotropic effects. While not commonly used in the
out-of-hospital environment, they may become a bridge to
definitive care in the E.D.
Amiodarone:
- Patients with severe heart failure are prone to malignant
ventricular dysrhythmias which should not be treated with other
agents due to their proarrhythmic and negative inotropic
effects. Amiodarone has shown to decrease risk of sudden
death and improve functional heart failure class in some studies,
but has demonstrated less positive outcomes in others. It may
show promise for those with severe heart failure, but needs
further study.
|
|
Suggested Reading |
ACEP: Implementation of Early Defibrillation/Automated External
Defibrillator Programs. Policy Statement. Dallas, October 1992.
American College of Cardiology and American Heart Association
Task Force Report. ACC/AHA guidelines for the early management
of patients with acute myocardial infarction. Circulation, 82(2);
664-707, 1990.
Bersten AD, Holt AW, Vedig AE, et al: "Treatment of severe
cardiogenic pulmonary edema with continuous positive airway
pressure delivered by face mask." New England Journal of Medicine,
325(5), 1825-1830, 1991.
Connors AF, et al: "The effectiveness of right heart catheterization in
the initial care of critically ill patients." JAMA, 276, 889-897, 1996.
Grauer K, Cavallaro D: "Acute myocardial infarction." In ACLS: A
Comprehensive Review Vol II (pp. 342-366). St. Louis: Mosby, 1993.
Grauer K: "What's new with acute myocardial infarction."
Audio-Digest Emergency Medicine. 14(11), June 1, 1997.
Leizorovicz L: "The ESPRIM trial: short-term treatment of acute
myocardial infarction with molsidomine." The Lancet, 34; pp. 91-96,
1994.
Ornato JP, Cannon CP, Gibler WB, et al: "Clinical Pathways for the
Evaluation and Treatment of Chest Pain." Monograph from The
Center for Long Term Care Research & Education, The School of
Medicine, Medical College of Virginia/Virginia Commonwealth
University, April 1, 1997.
Place B: "Using airway pressure." Nursing Times, 93(31), 42-44,
1997. Rosen SD, Paulesu E, Frith, C et al.: "Central nervous
pathways mediating angina pectoris." The Lancet, 344: 147-150, July
16, 1994.
Sanders M: "Pathophysiology and management of cardiovascular
disease." In Mosby's Paramedic Textbook (pp. 636-646). St. Louis:
Mosby, 1995.
Slyper AH: "Low-density lipoprotein density and atherosclerosis."
JAMA, 272(4), 305-307, 1994. Staff: "To gauge the risk of MI and
stroke." Emergency Medicine, pp. 156-163, Jan. 15, 1992.
Wile-Curtis A: "New independent risk factor for coronary artery
disease found in homocysteine." Nursing Spectrum, pp. 26-27, Jan.
10, 2000.
Yacone LA: "Cardiac assessment: what to do, how to do it." RN, pp.
42-48, May 1987. |