P H A R M AC OT H E R A P Y
F O R C A R D I AC A N D
R E L AT E D P RO B L E M S .
SISTER M. SOCHIMA MGBOKWERE (DMMM), PHD., RN
MIAMI DADE COLLEGE
LIPOPROTEINS
• Lipoprotein is a complex combination of lipids in various
amounts along with a protein component called
apoprotein to enable transport through the blood.
• HDL: Contains the most apoprotein up to 50%.
Greater than 60mg/dL is desirable. (Good Cholesterol)
• LDL: Contains the highest amount of cholesterol.
Less than 100mg/dL is optimal. (Bad Cholesterol)
• VLDL: Primary carrier of triglycerides in the blood.
Reduced to LDL through a series of steps.
TERMS FOR LIPID DISORDERS
• Hyperlipidemia
• High levels of lipids in the blood
• Hypercholesterolemia
• Elevated blood cholesterol
• Dyslipidemia
• Abnormal levels of lipoproteins, excess
or deficient
LDL & HDL
NONPHARMACOLOGIC METHODS FOR
CHOLESTEROL REDUCTION
 Reduce saturated fats in diet.
 Reduce total fat intake to 30% or
less of caloric intake.
 Reduce cholesterol intake to 300
mg/day or less.
 Exercise as possible.
 Stop smoking.
 Increase in soluble fiber in diet
PHARMACOLOGIC APPROACH
• TYPES OF ANTILIPIDEMICS
1. HMG-CoA REDUCTASE Inhibitors (STATINS)
2. BILE ACID SEQUESTRANTS
3. NIACIN/NICOTIC ACID(VITAMIN B3)
4. FIBRIC ACID AGENTS
5. CHOLESTEROL ABSORPTION INHIBITORS AND
MISCELLENEOUS DRUGS
HMG-COA REDUCTASE INHIBITORS
(STATINS)
• Nursing interventions
• Mechanism of Action:
Monitor liver enzymes.
Interferes with an enzyme HMG-CoA
reductase in the synthesis of
Report unexplained
cholesterol
muscle tenderness or
• First line drugs for lipid disorder
weakness, fever, and
treatment
malaise.
• Slows the progression of CAD
• All are contraindicated in pregnancy
Teach patient importance
• All are given Orally, administer with food to
of compliance with health
decrease GI discomfort.
care regimen.
• The primary goal of therapy is to reduce the
risk of MI and Stroke.
SIDE EFFECTS AND INTERACTIONS
HMG-CoA REDUCTASE INHIBITORS
(STATINS)
ATORVASTATIN
(LIPITOR)
• SIDE EFFECTS
•
H/A, Fatigue, Muscle or joint pains
•
Heartburn, severe myopathy,
/Rhabdomyolysis—rare but possible.
–Interaction: with
SIMVASTATIN
(ZOCOR)
PRAVASTATIN
(PRAVACHOL)
ROSUVASTATIN
(CRESTOR)
Macrolide
antibiotics, Azole antifungals,
Fibric acid agents, and some
immunosuppressants, Grapefruit
juice, contraindicated in serious
liver disease.
BILE ACID SEQUESTRANTS
• Bind bile acids to increase the excretion of cholesterol in stool.
• Cause more frequent side effects than statins
• They are not absorbed into the systemic circulation therefore
effects are limited to the GI tract.
• Interfere with absorption and minerals
• Extended use can cause nutritional deficiency
• Can cause bloating, abdominal pain, N/V and constipation
– Cholestyramine (Questran), Colesevelam (Welchol),
Colestipol (Colestid).
NICOTINIC ACID (NIACIN)
• It is B-complex vitamin (Vitamin B3)
• Much larger doses needed to reduce cholesterol 23gm/day
• Rarely used because of side effects
• Primary effect is to decrease VLDL levels also reduces
triglyceride levels and increase HDL levels
• Flushing and hot flashes present in almost all patients
• Nausea, excess gas, and diarrhea are common.
Hepatotoxicity and gout have been reported.
• Will elevate FBS in patients with DM
• Rarely used in monotherapy.
FIBRIC ACID AGENTS
• Used for severe hypertriglyceridemia.
• Mechanism of Action: Activates the enzyme lipoprotein
lipase which increases the breakdown and elimination of
triglycerides from the plasma.
• Adverse effects: GI distress, watch for bleeding with
patients on anticoagulants
• Specific Agents:
• Gemfibrozil (Lopid), Fenofibrate (Tricor, Antara).
• Administer with meals to reduce GI distress
• Pregnancy category B.
CHOLESTEROL ABSORPTION
INHIBITOR
• ezetimibe (Zetia)
• Mechanism of action: inhibits absorption of cholesterol
in the small intestine.
• Primary use: modest reduction in LDL
 It must be combined with a statin for optimum effect.
• Adverse effects: Serious side effects are uncommon.
Nasopharyngitis, myalgia, upper respiratory tract
infection, anthralgia, and diarrhea are possible adverse
effects.
• Zetia is pregnancy category C.
DIURETICS
• KIDNEYS
• Primary regulator of fluid and
electrolyte balance
• Acid base balance
• Secrete Renin
• Secrete Erythropoietin
• Production of calcitriol (active
form of Vitamin D)
REABSORPTION
• Filtrate in Bowman's capsule is same composition as
plasma minus large proteins.
• Some substances in filtrate cross wall of nephron and
reenter blood process called tubular reabsorption.
• Most of water in filtrate is reabsorbed.
• Glucose, amino acids, sodium, chloride, calcium, and
bicarbonate are reabsorbed.
SECRETION
• Some substances pass from blood through walls
of nephron and become part of filtrate.
• Potassium, phosphate, hydrogen, ammonium ion,
and some acid drugs are secreted into filtrate.
• Reabsorption and secretion are critical to
pharmacokinetics of many drugs.
THE NEPHRON
NEPHROTOXIC DRUGS
DIURETICS
• Diuretics are drugs that alter the volume and/or
composition of body fluids. They are given to
increase the rate of urine flow
• Goal of most diuretic therapy is to reverse abnormal
fluid retention in the body.
•
•
•
•
•
INDICATIONS
HTN
HEART FAILURE
LIVER FAILURE AND CIRHOSIS
PULMONARY EDEMA
DIURETICS
• Most common mechanism of action is by blocking the reabsorption of Na+ ion
in the nephron.
• CLASSIFICATIONS
• LOOP DIURETICS
• THIAZIDE DIURETICS
• POTASSIUM SPARING DIURETICS
• CARBONIC ANHYDRASE INHIBITORS
• OSMOTIC DIURETICS
ADVERSE EFFECTS OF DIURETIC THERAPY
•
•
•
•
Fluid and electrolyte disturbances
Dehydration
Orthostatic hypotension
Potassium and sodium imbalances
LOOP DIURETICS
• Blocks the reabsorption of Na+ and Cl- in the loop of
Henle.
• Na and H20 are lost together with potassium,
calcium and magnesium.
• THE MOST EFFECTIVE DIURETIC
• USED TO REDUCE EDEMA ASSOCIATED
WITH HEART FAILURE, PULMONARY
EDEMA, LIVER CIRRHOSIS & CRF.
• LESS EFFECTIVE AS ANTI HYPERTENSIVE AGENTS.
• Highly protein bound, can displace other drugs
e.g., warfarin.
ADVERSE EFFECTS &CONTRAINDICATIONS
 MONITOR FOR SIGNS OF DEHYDRATION
– THIRST, DRY MOUTH, WEIGHT LOSS, H/A.
 AND ELECTROLYTES IMBALANCE
• Hypokalemia, hyponatremia, hypocalcemia,
• hypomagnesemia, hypochloremia
• USE CAREFULLY WITH DIGOXIN
• USE CAREFULLY WITH OTOTOXIC
DRUGS
• May diminish hypoglycemic effect of
sulfonylureas and insulin.
•
•
•
Not used with ANURIC PATIENTS
DECREASES THE ELIMINATION OF LITHIUM IF
GIVEN CONCURRENTLY
WATCH FOR CROSS-SENSITIVITY TO SULFA
DRUGS.
LOOP DIURETICS
FUROSEMIDE
(LASIX)
BUMETANIDE
(BUMEX)
TORSEMIDE
(DEMADEX)
ETHACRYNIC ACID
(EDECRIN)
THIAZIDE DIURETICS
• Blocks Na+ reabsorption in the distal
tubule and increase potassium and
water excretion.
• Less effective than the loop diuretics.
• Sometimes raise the blood glucose
level.
• Contraindicated in preeclampsia or other pregnancy
induced hypertension.
• Increases the risk of renal toxicity
from NSAIDs.
• SPECIFIC AGENTS
• Chlorothiazide (Diuril)
• Hydrochlorothiazide (HCTZ)
• Bendroflumethiazide with nadolol
(Corzide)
• Methyclothiazide (Enduron)
• Chlorthalidone (Thalitone)
• Indapamide (Lozol)
• Metolazone (Zaroxolyn)
THIAZIDE AND THIAZIDE-LIKE DIURETICS
• Increased potassium loss may occur which enhances the action of
digoxin.
• Thiazides enhance the action of lithium and lithium toxicity can occur.
• Thiazides induce hypercalcemia which enhances the action of digoxin.
• Monitor for signs of digitalis toxicity (Bradycardia, N/V, visual changes).
• Allergies to sulfa-based medications can indicate hypersensitivity.
• Use with caution in pregnant women
• Do not administer to lactating women
• Use sunscreen to decrease photosensitivity
• Take potassium supplements, if ordered
• Consume potassium-rich foods(fruits, fruit juices, and vegetables)
• Report any tenderness or pain in joints
POTASSIUM SPARING DIURETICS
• Mechanism of Action: ACTS IN THE LATE DISTAL, AND
COLLECTING TUBULE TO PROMOTE NA+ AND H20 EXCRETION
AND K+ RETENTION. (blocks the action of aldosterone at the
Na+-K+ pump, inhibiting the pump).
• Advantage: diuresis without affecting blood potassium levels
• Spironolactone may decrease effectiveness of anticoagulants.
• Patients taking lithium or digoxin may be at increased risk for toxicity.
• Triamterene contraindicated for lactating women
• Specific Agents: spironolactone (Aldactone)
• Triamterene (Dyrenium), amiloride (Midamor)
NURSING IMPLICATIONS
• Give with food to improve absorption
• Do not give potassium supplements
• PREGNANCY CATEGORY D
• RISK OF HYPERKALEMIA INCREASED IF TAKEN WITH ACE INHIBITORS
–
MUSCLE WEAKNESS, FATIGUE, BRADYCARDIA
• Can cause gynecomastia, diminished libido
• ASA and other salicylates may decrease effects
• Acidosis may occur if combined with ammonium chloride
• Avoid use of potassium-based salt substitutes
• When in direct sunlight, use sunscreen
• Do not eat excess amount of foods high in potassium
MISCELLANEOUS DIURETICS—CARBONIC
ANHYDRASE INHIBITORS
• Examples: acetazolamide (Diamox),
dichlorphenamide, ethoxzolamide, and
methazolamide
• Mechanism of action: to inhibit
formation of carbonic acid
• Primary use: to decrease intraocular
pressure(IOP) in patients with open
angle glaucoma, used in the
management of edema secondary to
HF that is refractory to other diuretics.
• Adverse effects:
Allergic
reaction (contain sulfa), fluid and
electrolyte imbalances,
• Metabolic acidosis, nausea, vomiting,
anorexia, confusion, orthostatic
hypotension, crystalluria, hemolytic
anemia, and renal calculi
• Contraindicated in severe renal and
hepatic impairment.
MISCELLANEOUS DIURETICS—OSMOTIC
DIURETICS
• Example: mannitol
(Osmitrol)
• Also used to maintain urine flow in
prolonged surgery, acute renal failure,
or severe renal hypoperfusion
• Mechanism of action: Increase the
osmolality (concentration) and Na
reabsorption in the proximal tubule
and loop of Henle.
 Monitor for electrolyte imbalance.
• Primary use: to reduce intracranial
pressure (ICP) due to cerebral edema
and to decrease intraocular pressure
(IOP) e.g., in glaucoma.
 Do not use if crystals are present in
the vial.
 Warm to dissolve crystals first or,
give immediately after drawing up.
CARDIOVASCULAR DISORDER DRUGS
REGULATORS OF BLOOD PRESSURE
 Baroreceptors in the aorta and
carotid sinus
 Vasomotor center in the
medulla
 Hormones: antidiuretic
hormone (ADH), atrial
natriuretic peptide (ANP),
brain natriuretic peptide (BNP)
PHYSIOLOGIC RISK FACTORS
Excessive intake of saturated fat and simple
carbohydrates
Alcohol: increases renin secretions
GUIDELINES FOR DETERMINING HYPERTENSION
Category
Systolic Pressure
Diastolic Pressure
Normal
Less than 120 mm Hg
Less than 80 mm Hg
Prehypertension
120 to 139 mm Hg
80 to 89 mm Hg
Stage 1 hypertension
140 to 159 mm Hg
90 to 99 mm Hg
Stage 2 hypertension
Greater than 160 mm Hg
Greater than 100 mm Hg
Primary Factors Affecting Blood Pressure
RENIN-ANGIOTENSIN-ALDOSTERON SYSTEM
A NON PHARMACOLOGIC MANAGEMENT OF HTN
THERAPEUTIC/POSITIVE LIFESTYLE CHANGES
•
•
•
•
•
•
•
•
Limit alcohol intake
Restrict sodium
Reduce intake saturated fat/cholesterol
Increase intake of fresh fruits/vegetables
Increase physical activity
Learn coping strategies
Maintain optimum weight
Discontinue tobacco use
PHARMACOLOGIC MANAGEMENT OF HTN










Diuretics
Angiotensin-converting enzyme (ace)inhibitors
Angiotensin II receptor blockers
Calcium channel blockers
Beta adrenergic blockers (antagonists)
SECONDARY ANTIHYPERTENSIVE AGENTS.
Alpha1-adrenergic antagonist
Alpha2-adrenergic agonists
Direct-acting vasodilators
Direct renin inhibitors
ACE INHIBITORS AND ACE RECEPTOR BLOCKERS
ACE INHIBITORS/RECEPTORS BLOCKERS

African-American adults
and some older adults



Do not respond with ACEI
monotherapy
Do respond when taken with
diuretic
Side effects

Irritating cough, insomnia,
hyperkalemia, tachycardia,
angioedema, postural
hypotension…
• Contraindications



Pregnancy
Potassium-sparing diuretics
such as spironolactone
(Aldactone)
Salt substitutes that contain
potassium
ACE
INHIBITORS
ACE RECEPTOR
BLOCKERS
DIRECT
RENIN
INHIBITORS
ENALAPRIL
(VASOTEC)
CANDESARTAN
(ATACAND)
ALISKIREN
(TEKTURNA)
BENAZAPRIL
(LOTENSIN)
LOSARTAN
(COZAAR)
CAPTOPRIL
(CAPOTEN)
OLMESARTAN
(BENICAR)
LISINOPRIL
(ZESTRIL)
TELMISARTAN
(MICARDIS)
RAMIPRIL
(ALTACE)
VALSARTAN
(DIOVAN)
•
CALCIUM CHANNEL BLOCKERS
Mechanism of Action:
Blocks calcium ions from
entering the cell limiting
muscle contraction.
•
Used to treat angina, dysrhythmias,
and HTN.
•
Considerations:
•
Obtain ECG, heart rate, and B/P prior
to therapy
During therapy, monitor heart rate
and B/P regularly
•
•
•
Signs of CHF and reflex tachycardia
At low doses, relaxes vascular smooth
muscles thereby reducing peripheral
vascular resistance
•
Side Effects:
•
Dizziness, headache, flushing,
hypotension
Grapefruit juice may enhance the
absorption of CCBs.
•
•

•
•
•
•
Works more in the elderly and
African American population
Specific Agents:
AMLODIPINE (NORVASC)
NICARDIPINE (CARDENE)
NIFEDIPINE (ADALAT,
PROCARDIA XL)
DILTIAZEM (CARDIZEM)
MORE ACTIONS OF CALCIUM CHANNEL BLOCKERS
Relax coronary artery spasm (variant angina)
 Relax peripheral arterioles (stable angina)
 Decreases cardiac oxygen demand
 Decrease cardiac contractility (negative inotropic effect that
relaxes smooth muscle)
 Decrease afterload
 Decrease peripheral resistance
 Reduce the workload of the heart

BETA BLOCKERS
•
•
•
•
•
•
•
•
•
Actions/side effects:
Decrease HR & contractility
Reduce cardiac workload ease
symptoms of angina
Slows conduction through the
myocardium
Used in the treatment of migraines,
MI, and HF
Cardio-selective contraindicated in
patients with COPD.
Rebound HTN when stopped
abruptly…
Possible hypoglycemia in patients with
DM.
May cause male sexual dysfunction(
erectile dysfunction, decreased libido)

Specific Agents:

metoprolol
(Lopressor)

atenolol (Tenormin)

nadolol (Corgard)

nebivolol (Bystolic)

propranolol (Inderal)

•
•
•
ALPHA 1 BLOCKERS
Mechanism of Action: Lowers BP
directly by blocking sympathetic
receptors in arterioles causing
vasodilation.
Also used in treatment of benign
prostatic hypertrophy(BPH).
Side Effects: Dizziness, nausea,
nervousness and fatigue.
•
•

•
•
Can cause orthostatic hypotension
Can cause Na and H20 retention
therefore are prescribed with diuretics
ALPHA 2 AGONISTS
Inhibit the outflow of sympathetic
impulse from CNS to target organs and
tissues.
Can cause sedation and dizziness,
leukopenia, thrombocytopenia,
hemolytic anemia, lupus.
ALPHA 1 & ALPHA 2
ALPHA 1 BLOCKERS
ALPHA 2 AGONISTS
(CENTRALLY ACTING)
DOXAZOSIN (CARDURA)
CLONIDINE (CATAPRESS)
PRAZOSIN (MINIPRESS)
METHYLDOPA (ALDOMET)
TERAZOSIN (HYTRIN)
ALPHA 1 & BETA 1 BLOCKERS
Labetalol(Normodyne,
trandate)
DIRECT ACTING VASODILATORS
•
•
•
•
Mechanism of Action:
Cause vasodilation by direct
relaxation of arterial smooth
muscle
Only for severe hypertension
and hypertensive crisis
Adverse effects: reflex
tachycardia, sodium and fluid
retention
Specific Agents:
•
Hydralazine (Apresoline),
Minoxidil (Loniten),
•
Sodium nitroprusside
(Nitropress, Nipride)
•
•
Treatment of Hypertansive
emergency:
Sodium Nitroprusside
(Nitropress, Nipride)
•
•
•
•
•
•
Used for hypertensive crisis,
very potent
Half-life of 2mins.
Must be covered in a dark
plastic or foil to avoid
decomposition by light during
use.
Can cause cyanide toxicity.
Discard if drug color changes
Cannot be used for >24hrs
DRUGS FOR HEART FAILURE




Inability of ventricles to pump enough
blood for body's needs;
Weakening of heart muscle due to aging
or disease
The goals of pharmacotherapy are to
remove the underlying cause whenever
possible
Treat the symptoms of HF, so that the
patient’s quality of life can be improved.

BRIEF OVERVIEW
•
CARDIAC OUTPUT
PRELOAD
CONRACTILITY
AFTERLOAD
RIGHT AND LEFT SIDED HF
POSITIVE AND NEGATIVE INOTROPES
(contractility)
•
•
•
•
•

Laboratory tests

Atrial natriuretic peptide (ANP) 20 to 77 pg/mL;
20 to 77 ng/L (SI units)

Brain natriuretic peptide (BNP)–Desired
value: less than 100 pg/mL; positive
value: greater than 100 pg/mL
Left and right sided Heart failure
LEFT SIDED HEART
FAILURE
•
•
•
•
•
Blood accumulates in left ventricle
Blood backs up into lungs
Left ventricle thickens and
enlarges: hypertrophy
Cardiac remodeling
Cough and shortness of breath
result
RIGHT SIDED HEART
FAILURE
•
•
•
•
Blood accumulates in the right
ventricle
Blood backs up into jugular
veins
Causes peripheral edema and
organ engorgement
Less common than left-sided
HF
Pathophysiology of heart failure
ACC/AHA & NEW YORK HEART ASSOCIATION (NYHA)
CLASSIFICATION
NYHA
ACC/AHA

FOUR FUNCTIONAL CLASSES

Stages

I:
Patients with cardiac disease but with
no symptoms during physical activity

A High risk for HF without symptoms
or structural disease

B Some levels of cardiac changes (e.g.,
decrease ejection fraction without
symptoms of heart failure)

C Structural heart disease with
symptoms of HF (e.g., fatigue, SOB,
edema, decreased physical activity)

D Severe structural heart disease and
marked symptoms of HF at rest

II:
Patients with cardiac disease who have
slight limitations on physical activity, with
symptoms such as fatigue, palpitations,
dyspnea, or angina

III:
Patients with cardiac disease who have
marked limitations during physical activity

IV:
Patients with cardiac disease who are
unable to perform physical activity, and who
have symptoms at rest.
Characteristics
PHARMACOLOGIC MANAGEMENT OF HEART FAILURE
Preload,
Afterload, Contractility
Mechanisms




Slowing the heart rate
Increasing contractility
Reducing myocardial workload
PHARMACOLOGIC MANAGEMENT OF HF
ACE INHIBITORS
Reduce afterload, Drug of choice for heart failure
Enhance excretion of sodium and water, Lowers peripheral resistance
and reduces blood volume
Increases cardiac output
ANGIOTENSIN II RECEPTOR
BLOCKERS
Actions very similar to ACE inhibitors
Usually used for patients who are unable to tolerate the adverse
effects of ACE inhibitors
DIURETICS
Increase urine flow, Reduce blood volume and cardiac workload, Reduce
edema and pulmonary congestion
Prescribed in combination with other drugs
BETA ADRENERGIC
BLOCKERS
Slow heart rate and reduce blood pressure, Inotropic effect
Reduce workload of heart
DIRECT VASODILATORS
Minor role in heart-failure treatment, Lower blood pressure
Relax blood vessels, Decrease oxygen demand on the heart
CARDIAC GLYCOSIDES
Increase cardiac output by increasing the force of myocardial contraction.
CARDIAC GLYCOSIDES
Digitalis preparations (digoxin)


Actions

Positive inotropic


Negative chronotropic


Decreases heart rate
Negative dromotropic


Increases myocardial contractility
Decreases conduction
Increase stroke volume

Increases cardiac output
CARDIAC GLYCOSIDES

•
•
DIGOXIN
POSITIVE INOTROPE, NEGATIVE
CHRONOTROPE, NEGATIVE
DROMOTROPE
Improved contractility, Reduced HR,
Decrease in Cardiac workload, Increase in
CO
•
*Narrow safety margin
•
Check pulse one full minute prior to
administration must be 60b/m or >
•
*CHECK DIGOXIN LEVEL PRIOR TO
ADMINISRATION therapeutic level
usually 0.8-2ng/mL
•
IMPAIRED RENAL FUNCTION and
HYPOKALEMIA INCREASES TOXICITY
•
•

•
•
•
Use carefully with diuretics
Contraindicated in AV-Blocks
ADVERSE EFFECTS:
N/V, fatigue, anorexia, visual
disturbances (such as seeing halos, a
yellow-green tinge, or blurring,
when toxic)
Overdose can be fatal
Treatment for overdose:
•
DIGOXIN IMMUNE FAB (DIGIBAND).
DRUGS FOR ANGINA PECTORIS AND MYOCARDIAL
INFARCTION (MI)

ANGINA PECTORIS: Acute chest pain caused by insufficient oxygen
to the myocardium

Stable : Occurrences are predictable as to intensity, frequency
and duration, pain usually subsides with rest.

Unstable: Arise more frequently, pain more intense,
unpredictable, occurs even at rest

Prinzmetal or vasospastic: Unpredictable as a result of spasms
of coronary arteries related decreased blood flow. Unrelated to
rest or activity, occurs mostly during rest periods.
ACUTE CORONARY SYMDROME (ACS)

MYOCARDIAL INFARCTION (MI)

Complete occlusion of a coronary artery causing death of cardiac muscle.

UNSTABLE ANGINA

Partial occlusion of the coronary artery by a thrombus causing severe chest
acute pain.
Goal of pharmacotherapy is to reduce
Myocardial O2 Demand by:




Slowing heart rate
Reducing preload
Reducing
contractility
Reducing afterload)
•
SELECTED DRUGS






Organic Nitrates,
Beta Blockers,
CCB,
Anti-Platelets/
Anticoagulants,
Thrombolytics.
:


•
•
•
•
•
NITRATES
nitroglycerin (Nitrostat)
Sublingual, topical (ointment, transdermal patch), buccal
extended-release tablet, oral extended-release capsule
and tablet, aerosol spray (inhalation), and IV
Mechanism of Action:
Relaxes both arterial and venous smooth muscle; dilate
coronary arteries
Reduce myocardial workload, lower myocardial oxygen
demand
Assist diagnosis of MI: pain that persists 5–10 mins after
administration, may indicate MI.
Arterial and venous dilation; relieve coronary artery
vasospasm
NITRATES
IV nitrates have greatest risk for
severe hypotension
• Educate patients that alcohol is
contraindicated with nitrates
• If hypotension occurs, withhold
nitrates
 SIDE EFFECTS
• H/A, postural hypotension,
flushing, dizziness, tolerance, rash.

CONTRAINDICATIONS: Hypotension,
increased intracranial pressure or head
trauma, pericardial tamponade,
constrictive pericarditis, glaucoma.

SPECIAL CONSIDERATIONS:
Administer in glass bottle and special
nitroglycerin tubing
Cover bottle to avoid degradation
Use gloves when applying
Do not apply over hairy area
Change sites when applying topical
preparations.
Initial, date and time
•






SHOCK
•
•
•

•
•
Inadequate blood flow to meet body's
needs
Considered medical emergency
Can lead to irreversible organ damage
and death
Classified by:
Underlying pathological condition
Organ system causing the disease
OVERVIEW OF SHOCK
TYPE OF SHOCK
DEFINITION
UNDERLYING PATHOLOGY
ANAPHYLACTIC
ACUTE ALLERGIC REACTION
Severe reaction to an allergen such as
penicillin, nuts, shellfish, or animal
proteins
CARDIOGENIC
FAILURE OF THE HEART TO PUMP
SUFFICIENT BLOOD TO THE TISSUES
Left heart failure, myocardial ischemia,
MI, dysrhythmias, pulmonary embolism,
myocardial or pericardial infection
HYPOVOLEMIC
LOSS OF BLOOD VOLUME
Hemorrhage, burns, excessive diuresis, or
severe vomiting or diarrhea
NEUROGENIC
Vasodilation due to overstimulation
of the PSNS or under stimulation of
the SNS
Trauma to the spinal cord or
medulla, severe emotional stress or
pain, or drugs that depress the CNS
SEPTIC
Multiple organ dysfunction as a
result of pathogenic organisms in the
blood, often a precursor to acute
respiratory distress syndrome and
DIC
Wide spread inflammatory
response to bacterial, fungal, or
parasitic infection.
SYMPTOMS OF A PATIENT IN SHOCK
PHARMACOLOGIC MANAGEMENT OF SHOCK




BLOOD OR BLOOD
PRODUCTS
To restore volume depending on
the clinical situation
COLLOIDS- Increase volume by
increasing plasma oncotic pressure
 Albumin
 Hetastarch (hespan)
CRYSTALLOIDS- Used to replace
fluid that have been lost and
increase urine output



NS,
Lactated ringers
Hpyertonic saline

VASOCONSTRICTORS/VASOPRESSORS

Used to maintain BP when vasodilation has caused
hypotension but fluids have not been lost (e.g.
anaphylactic shock)

They are considered critical medications,
infusions are always via a pump
Require continuous monitoring and titration
as necessary
Discontinuation is gradual




Dopamine, Norepinephrine, Neo-synephrine,
Epinephrine
DOPAMINE is considered both vasopressor and
inotropic drug
PHARMACOLOGIC MANAGEMENT OF SHOCK

INOTROPIC DRUGS
•
Increase the force of myocardial contraction
Used in shock to increase cardiac output
•
•
•
•

•
Medical emergency
•
Goal of therapy is to prevent further hyper
response by body defenses and support the
cardiovascular system.
•
Epinephrine 1:1000
Colloids/Crystalloids
Benadryl
Bronchodilators (Ventolin)
DIGOXIN –Increases myocardial contractility
and cardiac output
DOBUTAMINE (DOBUTREX) Selective beta 1
used in cardiogenic shock to increase myocardial
contractility. GIVEN AS IV INFUSION ONLY
DOPAMINE- Both alpha 1 and beta 1 agonist.
GIVEN AS IV INFUSION ONLY
•
Phentolamine (Regitine) administered to area
of infiltration if extravasation occurs.
ANAPHYLAXIS:
•
•
•
DRUGS FOR DYSRHYTHMIAS
•
Lack of synchronization of the atria and/or ventricles or of the right
and left sides of the heart will cause dysrhythmias
Dysrhythmias named according to the type of rhythm
produced and its location e.g. Atrial or Ventricular
fibrillation
•
DYSRHYTHMIAS ARE ASSOCIATED WITH:
 HTN, Cardiac Valve Disease, CAD, Medications e.g.
Digoxin, Hypokalemia, MI, Stroke, DM, HF.
 Goals of therapy are to prevent or terminate dysrhythmias
in order to reduce the risks and resultant complications
•
TYPES OF DYSRHYTHMIA
•
•
•
•
•
•
Atrial or ventricular tachycardia
Atrial flutter
Atrial or ventricular fibrillation
Heart block
Premature atrial or premature
ventricular contractions (PVCs)
Sinus bradycardia
TYPES OF DYSRHYTHMIA
Atrial or ventricular tachycardia
 Atrial flutter
 Atrial or ventricular fibrillation
 Heart block
 Premature atrial or premature
ventricular contractions (PVCs)
 Sinus Bradycardia

NON PHARMACOLOGIC THERAPY
•
•
•
Catheter ablation—Identify and destroy aberrant
cardiac cells that cause dysrhythmias
Cardiac pacemaker—Paces heart at set rate
Implantable cardioverter defibrillator (ICD)—
combination of pacemaker and defibrillator
PHARMACOLOGIC MANAGEMENT OF DYSRHYTHMIAS

Most antidysrhythmic drugs act by interfering myocardial action potentials by
blocking: potassium, sodium or, calcium channels
•
•
Blocking flow through the ion channels (conduction) or
Altering autonomic activity (automaticity)

Anti dysrhythmics divided into 4 classes

CLASS I: SODIUM CHANNEL BLOCKERS
CLASS II: BETA ADRENERGIC ANTAGONISTS
CLASS III: POTASSIUM CHANNEL BLOCKERS
CLASS IV: CALCIUM CHANNEL BLOCKERS
Some antidysrhythmics produce their effect by prolonging the refractory period
(potassium channel blockers)




SODIUM CHANNEL BLOCKERS (CLASS I)
:Specific Agent: procainamide (Pronestyl)
 Mechanism of action: to block sodium ion channels,
which slows rate of impulse conduction across heart
 Primary use: to correct atrial and ventricular
dysrhythmias


Adverse effects: Creates new dysrhythmias or worsens
existing ones, Lupus effect, nausea, vomiting, abdominal pain,
headache, high doses can produce CNS effects.



procainamide (Pronestyl) 1A,
lidocaine 1B,
Flecainide 1C
BETA-ADRENERGIC BLOCKERS
(CLASS II)
Specific Agents:: propranolol (Inderal)
 Acebutolol (Sectral)
 Esmolol (Brevibloc)
 Sotalol (Betapace)




Mechanism of action: Blocks beta receptors, which reduces
automaticity and slows conduction velocity across myocardium
Primary use: to treat atrial dysrhythmias associated with heart
failure
Adverse effects: bradycardia, hypotension with dizziness and
fainting, Bronchospasms, hypoglycemia, diminished libido
POTASSIUM CHANNEL BLOCKERS
(CLASS III)
drug: amiodarone (Cordarone)
 Mechanism of action: Blocks potassium-ion channels in
myocardial cells, which prolongs refractory period of the
cardiac cycle.
 Primary use: to treat resistant ventricular tachycardia,
atrial dysrhythmias with heart failure
 Adverse effects: blurred vision, pneumonia-like syndrome,
bradycardia, hypotension, Can create new dysrhythmias or
worsen existing ones
 Hypokalemia and Hypomagnesemia should be corrected
prior to initiating therapy.
 Pregnancy category D.

CALCIUM CHANNEL BLOCKERS
(CLASS IV)
Specific Agent: verapamil (Calan)
 Mechanism of action: to block calcium ion channels,
which reduces automaticity and slows myocardial (AV)
conduction velocity
 Primary use: to treat supraventricular dysrhythmias
 Adverse effects: bradycardia, hypotension, headache


Verapamil (calan)

Diltiazem (cardizem)
ADENOSINE (ADENOCARD)

Naturally occurring nucleoside

Given as a 1-2 second IV bolus injection

Indicated for persistent PSVT
Half life is 10 seconds
 Pay may experience brief period of systole
after administration

SR. M. SOCHIMA MGBOKWERE (DMMM), PhD., CCRN.
MIAMI DADE COLLEGE
THROMBOEMBOLIC DISORDERS
Conditions in which the body forms undesirable clots
THROMBUS
A stationary clot. Forms in vessels. Grows in size as more fibrin
is added.
EMBOLUS
A travelling clot. Pieces of a thrombus may break off and travel
through the blood stream to affect other vessels.
DEEP VEIN THROMBOSIS (DVT)
Thrombi in the venous system. Usually forms in the vein of the
legs due to sluggish blood flow.
THROMBOCYTOPENIA
A deficiency in platelets. Occurs when platelet count falls below
150,000mm3. May occur as a result of increased platelet
destruction or decreased platelet production.
HEMOPHILIAS A, B & von
Willebrand’s disease (vWD)
Bleeding disorders caused by genetic deficiencies in specific
clotting factors. They are typified by prolonged coagulation
times.
Activated partial
thromboplastin time
(aPTT)
Used to monitor
heparin
pharmacotherapy
Prothrombin time (PT) Used to monitor
warfarin therapy
Platelet count
25-35 secs; 1.5-2tx
higher than the pretreatment value
High values indicate
risk for bleeding and
that heparin dose may
need to be reduced
INR should be 2-3 to
prevent DVT; 2.5-3.5,
to prevent arterial
thrombosis
High values indicate
risk for bleeding and
that anticoagulant dose
may need to be
reduced
Part of complete blood 150,000-350,000
count
Values below 20,000
indicate
thrombocytopenia
Bleeding time
Used for general
2-9mins
diagnosis of
coagulation disorders
Long bleeding count
may indicate a low
platelet count or
anticoagulant therapy
Heparin anti-Xa
Used to monitor
heparin or lowmolecular weight
(LMWH)
pharmacotherapy in
patients with heparin
resistance
High value indicate a
risk for bleeding and
that heparin or
LMWH dose may
need to be reduced
0.3-0.7 international
units/mL for heparin;
0.4-1.1international
units/mL for LMWH
TYPE OF MODIFICATION
MECHANISM OF DRUG
ACTION
DRUG CLASSIFICATION
PREVENTION OF CLOT
FORMATION
Inhibition of specific clotting
factors
ANTICOAGULANTS
Inhibition aggregation of
platelet.
ANTIPLATELETS
Dissolve already formed clots.
THROMBOLYTICS
REMOVAL OF EXISTING
CLOT
Inhibition of fibrin destruction HEMOSTATICS
PROMOTION OF CLOT
FORMATION
Administration of missing
clotting factors
CLOTTING FACTOR
CONCENTRATES

Mechanism of action:

(parenteral) and warfarin
(oral)
inhibit specific clotting factors
to prevent formation or
enlargement of clots


Primary use: to prevent
formation of clots in veins, to
treat thromboembolic
disorders
Specific drugs: heparin


Most serious side effect to
assess is bleeding.
To assess internal bleeding,
Monitor CBC, lumbar pain,
abdominal bulging, guaiac
tests on stool
Essential for patient safety to
assess coagulation studies
•
Monitor intake of vitamin K–rich
foods; limit intake of garlic.
•
Monitor for thrombocytopenia
•
Protamine Sulfate is the antidote
•
transition from heparin to
warfarin.
•
for heparin overdose.
•
•
Monitor for signs and symptoms
Bleeding risk increases during
Do not give warfarin to pregnant
patients.
•
Heparin, low–molecular weight
of Hepatitis
heparin can be given to pregnant
Instruct patients not to take ASA,
patients.
while taking LMWH’s

LMWHs


Mechanism of action is similar to heparin except

inhibition is more specific to Factor X

They are administered parenterally

Duration of action is 2-4X longer than heparin

Less likely than heparin to cause thrombocytopenia


Enoxaparin (Lovenox)

Dalteparin (Fragmin)
Factor Xa Inhibitors

Fondaparinux (Arixtra)

Rivaroxaban (Xarelto)
Direct thrombin inhibitors
Mechanism of Action: Bind to the active site
of thrombin, preventing the formation of
fibrin clots.

Argatroban (Argatroban)

Dabigatran (Pradaxa)
 Warfarin
(Coumadin)

Inhibits the hepatic synthesis of coagulation factors II, VII, IX, and X.

Given orally

Takes several days to reach maximum therapeutic effect

Pregnancy category X

Regular monitoring of INR is required

Contraindicated in recent trauma, active bleeding, bleeding disorders, severe
hypertension,

Antidote for overdose is Vitamin K.

Mechanism of action: To alter the plasma membrane of platelets
so they cannot aggregate. Prolong bleeding time by interfering
with aggregation of platelets

Primary use: to prevent thrombus formation mostly in the
arteries. Prevent MI, strokes, TIA’s.

Includes:
Aspirin
 ADP receptor blockers
 Glycoprotein 11b/111a receptor antagonists


Prolonged pressure needed to control bleeding at puncture sites


aspirin (ASA)
Dipyridamole (Persantine)

GLYCOPROTEIN IIB/IIIA
Receptors antagonists
eptifibatide (Integrillin)
 tirofiban (Aggrastat)


ADP Receptor Blockers
 Clopidogrel (Plavix)
 Ticagrelor (Brilinta)
 Ticlopidine (Ticlid)

Discontinue at least 7 days prior to surgery

Contraindicated in patients with active bleeding

Monitor platelet count and hematocrit

Monitor for signs of bleeding if used with other anticoagulants

Teach patients about diet ( intake of Vit. K rich food, alcohol)

Mechanism of action: Thrombolytics promote the process of
fibrinolysis by converting plasminogen to plasmin, which
digests fibrin and dissolve clot

Used to dissolve life-threatening clots

Specific Agents:
Alteplase (Activase) commonly called TPA.
Reteplase rPA (Retavase)



Primary uses



To treat acute myocardial infarction, deep vein thrombosis
To treat acute ischemic stroke, pulmonary embolism, arterial
thrombosis
To clear IV catheters

Effective if given within 12 hours of onset of symptoms of MI and 3
hours of symptoms of stroke

Avoid parenteral injections during therapy
Contraindicated in active internal bleeding, history of stroke or head
injury within the past 3 months, recent trauma or surgery within
14days, uncontrolled hypertension, arterio-venous malformation


Mechanism of action: to prevent fibrin from
dissolving (antifibrinolytics)
Primary use: Used mostly to prevent and treat
excessive bleeding from surgical sites
Used to shorten bleeding time.

Specific drug: Aminocaproic


acid (Amicar)

Adverse effects: May cause hyper-coagulation with concurrent
use of estrogen and oral contraceptives

Monitor for clotting

Administer intravenously, monitor site closely

Assess for myopathy and myoglobinuria (reddish-brown urine)

Teach patient to report symptoms of clotting or bleeding

Do not take aspirin

Contraindicated in patients with DIC, severe renal impairment
TRANSFUSION THERAPY
Intravenous administration of whole blood or blood
components for therapeutic purposes.
• To restore volume
• To restore oxygen carrying capacity
• To replace clotting factors or platelets to reverse
coagulopathy
• To replace white blood cells in neutropenic patients
ABO SYSTEM
 Blood type determined by the presence or absence of
certain antigens on the surface of red blood cells.
 Types A, B, AB and O (when neither A or B is present)




Hemolytic Blood Reaction
Antibodies, (Agglutinins)
Foreign Antigens (Agglutinogens)
Blood typing and cross-matching prior to Blood
transfusion (72 hrs)
BLOOD TRANSFUSION
 Obtain blood component from blood
bank following agency protocol
 Correctly verify product and identify
patient with a second person (RN).
 Clearly identify patient per agency
protocol, have patient state first and
last name, and date of birth (if able)
 Verify that component received from
blood bank is component ordered by
physician
 Check that the patients blood type and
Rh type are compatible with the donor
blood type and Rh type. Be sure blood
is not discolored or has clots.
 Check that unit number on unit of
blood and on form from blood bank
match.
 Check expiration date and time of unit
of blood
 Record verification process as directed
by agency policy
TRANSFUSION THERAPY NURSES ROLE
•
•
•
•
•
Review Agency Policy and Procedure regarding BT
Verify order and indication for transfusion
Assess baseline vital signs, medical history
Monitor for signs and symptoms of transfusion reaction
Elevation in heart rate, elevation of temperature, pruritis, sob,
abdominal pain, N/V
CRITICAL POINTS
•
•
•
•
•
NORMAL SALINE is used to prevent coagulation of
the blood product. Solutions that contain dextrose will
cause coagulation donor blood.
A unit of blood should not hang for more than four
hours because of the danger of bacterial growth.
Do not leave patient for the first 15mins after start of
BT (no short cuts)
Medication should never be injected into an IV line with
a blood component infusing.
The transfusion should be stopped immediately and the
physician notified if signs of transfusion reaction occur.
SIDE EFFECTS
•
•
•
•
•
•
Observe for fever with or without chills
Observe for tachycardia and /or tachypnea and dyspnea
Observe client for hives or skin rash
Observe for flushing
Observe for GI Symptoms
Observe for a fall in blood pressure
IN THE EVENT OF TRANSFUSION REACTION
• Stop the transfusion
• Remove tubing containing blood product and replace it with
new tubing, maintain patent IV line using 0.9%NS
• Notify physician
• Notify blood bank
• Obtain blood samples (if needed) from arm opposite
transfusion. Check agency policy regarding number and type
of tubes to be used
• Return remainder of blood to blood bank
• Monitor and document vital signs every 15mins or more
frequently if needed.
• Administer prescribed medications