Download Antianginals and Medications Used in Shock

Angina pectoris is clinical syndrome with
primary s/s of chest
pain/pressure/discomfort
 Results from deficit of supply and
demand
 Most often 2ndary to atherosclerotic
plaque formation
 Can also be secondary to vasospasm

Caused by development and
progression of atherosclerotic plaque
 Plaque narrows the vessel lumen,
decreases elasticity and impairs dilation
of coronary arteries
 Result is impaired blood flow to the
myocardium

Classic angina
 Variant angina
 Unstable angina

From obstruction of coronary arteries
secondary to athersclerotic plaque
deposition
 Chest discomfort is usually precipitated
by factors that increase workload of the
heart like physical activity, exposure to
cold and emotional upset
 Pain is usually relieved by rest,
nitroglycerine or both

Described as substernal chest pain of a
constricting, squeezing or suffocating
nature
 May radiate to jaw, neck, shoulder, back or
down left arm
 Sometimes mistaken for arthritis or
indigestion especially because discomfort is
accompanied by nausea & vomiting;
dizziness, diaphoresis, shortness of breath
and feeling of impending doom may also
be present







Also called Prinzmetal’s
Caused by spasms of the coronary artery
that decreases blood flow to myocardium
Spasms occur in vessels already partially
obstructed by plaque
Usu. occurs at rest and at night, often
occurs same time each day
Relieved by nitroglycerine
Tx is by avoiding precipitants, taking antianginals
Rest, preinfarction and crescendo
angina
 On continuum falls between classic
angina and MI
 Occurs in advanced CAD
 Often leads to MI

Women have atypical s/s such as
epigastric or back discomfort
 Older adults may have atypical s/s and
may experience “silent” ischemia
 Individuals with diabetes mellitus may
present w/o typical s/s

Begins with accumulation of lipid filled macrophages=foam cells
on inner lining of coronary arteries
Foam cells develop secondary to elevated cholesterol levels
White blood cells attach to endothelium and move into subendothelial
spaces , ingest lipids and become foam cells
Early lesions progress to plaques containing foam cells and covered by
smooth muscle cells and connective tissue
Advanced lesions also contain hemorrhages, ulcerations and scar tissue
Commonly develops in coronary arteries
Plaque lesions develop over time and
enlarge, extend deeper into lumen of artery
 Eventually plaques rupture, thrombus
formation occurs that largely occludes
vessel lumen with resultant compromised
blood flow
 Stenosis >80% blood flow cannot increase
with increased demands
 If gradual, can develop collateral
circulation


Occurs when coronary arteries are
unable to provide sufficient blood and
oxygen for normal cardiac functions
 May occur as acute coronary syndrome
w/three consequences
1. Unstable angina
2. Silent MI diagnosed by markers only
3. MI w/or w/o ST segment elevation

Endothelium of normal coronary arteries
synthesizes various substances that
protect against vasoconstriction and
vasospasm, bleeding, clotting,
inflammation and excessive cell growth
 Impaired endothelium or hypertension
leads to vasoconstriction, vasospasm,
clot formation, plaque formation and
growth of smooth muscle in blood vessels

Endothelium derived relaxing factor (NO) is
produced by the endothelium of coronary
arteries
 Released by shear stress on endothelium,
sympathetic stimulation of exercise and
interactions with various chemical
mediators
 NO relaxes vascular smooth muscle and
inhibits adhesion and aggregation of
platelets
 With endothelial damage, vasodilatory and
antithrombotic effects are lost

Also, production of strong
vasoconstrictors (endothelin1,
thromboxane A2 and angiotensin II) are
increased
 Inflammatory cells enter injured area,
growth factors stimulate growth of
smooth cells
 Result—blockage of coronary arteries

Age, race, gender and family history
 Smoking, hypertension, hyperlipidemia,
obesity, sedentary lifestyle, stress and use
of drugs that increase workload of heart
 Diabetes mellitus

Lifestyle modification
 Weight loss
 Smoking cessation
 PTCA with intracoronary stents
 Laser therapy
 CABG

Nitrates
 Beta blockers
 Calcium channel blockers

Relax smooth muscle in blood vessel
walls==vasodilation
 Reduce venous pressure and venous
return to heart, thus, preload
 this decreases cardiac workload and
oxygen demand
 Increase blood flow to ischemic areas
 Decrease afterload

Prototype is nitroglycerine
 Nitrates are converted to nitric oxide in
vascular smooth muscle. Activates
guanylate cyclase affecting cAMP.
Decreases calcium levels in smooth
muscle thus decreased contraction of
smooth muscle. End result: vasodilation.
 Contraindications are: Increased ICP,
males taking phosphodiesterase enzyme
type 5 inhibitors

Nitroglycerine—IV, SL, topical. For acute
angina, prevent exercise induced
angina
 Isordil (Isorsorbide dinitrate )acts in 2’,
lasts 2-3 hours.
 Imdur (mononitrate). Imdur is metabolite
of Isordil. Onset one hour, peaks
between 1-4 hours, prophylaxis of angina

Block beta 1 receptors which increase
heart rate and force of myocardial
contraction, so increase MVO2
consumption.
 Reduce heart rate and contractility.
Enhance blood flow.
 Block response to sympathetic
neurotransmitters
 Caution in asthmatics and those with
COPD

Inderal (propranolol) is prototype.
Metabolized by liver.Need greater doses
po due to liver metabolism.
 Tenormin (Atenolol), Lopressor
(metoprolol )and Corgard (nadolol)—
long half lives so given once daily.
 Usually end in -ol

Act on contractile and conductive
tissues of heart and on vascular smooth
muscle
 Accomplished by blocking calcium
channels, preventing movement of
extracellular calcium into the cell. Thus,
coronary and peripheral arteries are
dilated, myocardial contractility is
decreased and conduction system is
depressed

Improve blood supply to myocardium by
dilating coronary arteries
 Decrease workload of heart by dilating
peripheral arteries
 Reduce coronary vasospasm
 Slow rate of ventricular response in atrial
fibrillation, flutter and supraventricular
tachydysrhythmias
 Lower blood pressure by dilating
peripheral arteries

Most have short half-lives so need
frequent dosing
 90% protein bound
 Peak within 1-2 hours
 Two types—dihydropyridines and
nondihydropyridines
 Procardia (Nifedipine) is prototype of
dihydropyridines-vascular smooth muscle
to produce vasodilation

Nondihydropyridines—Cardizem (diltiazem)
and Calan (verapamil)—better for heart
rate management in SVTs, work on
conduction system
 Nimodipine-use in subarachnoid
hemorrhage to decrease cerebral
vasospasm
 Contraindications—3rd degree heart blocks,
cardiogenic shock, severe bradycardia,
hypotension, heart failure or renal
impairment.

Many end in –ipine
 Plendil (Felodipine), DynaCirc
(isradipine), Cardene (nicardipine),
Procardia (nifedipine), Nimotopp
(nimodipine), Sular (nisoldipine), Norvasc
(amlodipine)

Aspirin
 Antilipemics—statins, Zetia, Niacin,
Lovasa
 antihypertensives

Use shorter acting ones to decrease
tolerance or
 Use long acting ones but omit during
night

Caution with nitrates in elderly due to
potential hypotension
 For relief of acute angina, nitroglycerine
is usually drug of choice
 Nitrates, beta blockers and calcium
channel blockers are metabolized in
liver, use with caution in patients with
hepatic impairment

Obtain BP and heart rate before each
dose on antianginal medication. Hold if
BP<90 systolic
 Give antianginals on regular schedule
 If oral nitrates and topical agents being
used also, stagger administration times
 Nitro SL—keep in cool, dry place;
observe expiration date


IV nitro must be hung with special tubing
and in delivered in glass bottle,
medication otherwise is adsorbed onto
tubing
Characterized by decreased blood
supply to body tissues
 Common signs and symptoms include:
hypotension, oliguria, heart failure,
mental confusion, cool extremities,
coma
 In a previously hypertensive individual, a
drop in BP of 50mm Hg or greater can
result in shock, even if BP is considered
“normal”

Hypovolemic—caused by trauma, GI
bleed, ruptured aneurysms, third
spacing, dehydration
 Manifestations—
hypotension,tachycardia, cool, clammy
skin, diaphoresis, oliguria

Cardiogenic—acute MI, cardiac surgery,
cardiomyopathy, dysrhythmias
 S/S—those of heart failure such as
pulmonary edema, tachycardia,
hypotension, cool, moist skin, confusion,
restlessness


1.
2.
3.
Distributive
Neurogenic—spinal cord damage,
spinal anesthesia. S/S—hypotension,
bradycardia, warm, dry skin
Septic—infection. Hypotension , cool or
warm skin, hypothermia or hyperthermia
Anaphylactic shock—contrast dyes,
drugs, insect bites, foods. S/S—hives,
edema, hypotension, bronchospasm
Management may vary according to type
of shock
 Generally will use alpha adrenergics to
increase peripheral vascular resistance
(norepinephrine and phenylephrine)
 Beta adrenergic drugs are used to increase
myocardial contractility and heart rate
(isoproterenol and dobutamine)
 Some drugs have both alpha and beta
activity (dopamine, epinephrine)


Dobutrex (dobutamine)—synthetic
catecholamine. Provides less vascular
activity than dopamine. Acts mainly on
beta1 receptors to increase force of
contraction w/o increasing heart rate.
Most useful when need increased
cardiac output. Short half life of 10
minutes.

Dopamine—stimulates alpha, beta and
dopaminergic receptors. Action is dose
dependent. Low dose stimulate
dopaminergic receptors located in renal
and splanchnic vascular beds. Low doses
will increase renal blood flow and GFR (so
long as cardiac function is improved). 0.510mcg/kg/min provide this effect. At 320mcg/kg/min have effect of increased
heart rate, BP and contractility. 2050mcg/kg/min predominant alpha effect.
Epinephrine—catecholamine. Low doses
stimulates beta receptors (so increases
CO), causes bronchodilation as well.
Larger doses act on alpha receptors.
 Drug of choice in anaphylaxis. Prevents
release of histamine, so reverses
vasodilation and bronchoconstriction.
 Can be given IV,subQ or even via ETT.


Isuprel (isoproterenol)—synthetic
catecholamine. Works exclusively on
beta receptors. Increases heart rate,
myocardial contractility and variable BP
effects. Limited usefulness as vasopressor.
Increases myocardial oxygen
consumption and decreases coronary
flow. Causes cardiac dysrhythmias.

Primacor (milrinone)—used in
combination with other agents in
cardiogenic shock. Increases cardiac
output and decreases SVR w/o
increasing heart rate or myocardial
oxygen consumption. Improved CO then
increases renal perfusion, thus urinary
output with decrease in circulating
volume and decreased cardiac
workload.

Levophed (norepinephrine)—
catecholamine. Primarily alpha 1
stimulation but also beta1 receptors.
Useful in cardiogenic and septic shock.
Does cause reduced renal blood flow so
limits its long term use.

Neosynephrine (phenyleprine)—
adrenergic that stimulates alpha
receptors. Longer duration of action
than epinephrine. Reduction of renal
and mesenteric blood flow limits
prolonged use.
Use large vein for IV access site
 Infusion pump
 Start adrenergic slowly
 Stop drug gradually
 Manage patient, not the monitor.
 Observe for dysrhythmias, tachycardia,
angina, tissue necrosis if extravasation

Hypovolemic shock best managed by fluids
 Cardiogenic shock may be complicated by
pulmonary edema, may need to give
diuretics, limit fluid intake
 Anaphylactic shock often managed with
epinephrine. May also use histamine
receptor blockers like Benadryl and
Tagamet (H1 and H2 receptor blockers).
May also use corticosteroids to increase
tissue responsiveness and for antiinflammatory effects.

Vasopressor agents used in critical care
settings
 Require cardiac and BP monitoring
 May often have hemodynamic
monitoring as well
 Vigilant monitoring is essential
