Transcript Cardiac Medications

Cardiac Medications
Hypertension
Learning Objectives
 Students will be able to:
 Discuss the major categories of drugs as
they relate to the treatment of Cardiac
Disease.
 Describe the major effects of various
medications on cardiac function.
 Discuss major nursing implications when
administering above medications.
New Zealand Statistics:
 Maori die almost a decade earlier than
non-Maori in New Zealand.
 Cardiovascular disease is a major
contributor to this statistic (NZGG, 2003).
 Maori should therefore be assessed for
risk 10 years earlier than non-Maori.
Hypertension
 Defined as a consistent elevation of the
systolic or diastolic blood pressure above
140/90mm Hg
 On two elevated readings (sitting and
supine) on separate office visits
 Two types hypertension
 Primary: no known cause
 Secondary: consequence of underlying
disease or condition
Goal with hypertension:
 Two primary regulatory factors:
 Blood flow (volume)
 Peripheral Vascular Resistance (PVR)
 Goal is to optimise these two in order to get
pressure below 140/90 mm Hg
 Primary groups of drugs are used:
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Diuretics
Adrenergic inhibitors (Beta-blockers)
Vasodilators
ACE inhibitors
Calcium antagonists
Diuretics: to reduce overall
volume of blood
 Thiazides - block sodium
reabsorption in nephron’s
distal segment
 Water is excreted with
sodium, producing decreased
blood volume
 Loop diuretics – potent loop
diuretic that inhibits sodium
and chloride reabsorption at
proximal and distal tubules
and ascending loop of Henle
 Indicated for acute
pulmonary oedema
MedlinePlus Medical
Encyclopedia
Diuretics Cont’d
 Nursing Interventions:
 Monitor K+ routinely (depleted here)
 Monitor weight daily and intake/output
 Give in am so avoid nocturia
Potassium-sparing diuretics
(Aldactone or Spironolactone)
 Potassium sparing diuretic
 Antagonises aldosterone in the distal tubules
which increases sodium and water excretion
 Need to watch for hyperkalemia and don’t give
potassium supplements
 Monitor electrolytes and fluid intake/output
 Monitor blood pressure and daily weights
 Less potent than thiazide and loop diuretics but
useful as an adjunct to other diuretic therapy
Vasodilators
 Hydralazine hycrochloride (Apresoline)
 Dilate peripheral blood vessels by directly
relaxing arteriolar smooth muscle
 Usually used in combination with other
antihypertensives as they increase
sodium and fluid retention
Calcium Antagonists
 Felodipine, Nifedipine, Diltiazem
 Inhibit the influx of calcium into muscle
cells; act on vascular smooth muscle
(primary arteries) to reduce spasms and
promote vasodilatation
 May enhance serum Digoxin levels
Cardiac Medications
Coronary
Artery
Disease
New Zealand Statistics
 Cardiovascular disease is the leading
cause of death in New Zealand (NZGG,
2003).
 1998 N.Z. had age-standardised mortality
rate from CAD of 111/100,000 people
 CAD death rates for Maori less than 75
yrs old are 2-3X higher than non-Maori
and 2X as high for Pacific peoples.
So what is the overall goal in
managing CAD?
 To reduce 5-year cardiovascular risk to
less than 15% with medications
(NZGG, 2003).
 Ensure individuals with total
cholesterol greater than 8mmol/L
undergo risk assessment and lipid
modifying treatment.
 Ensure BP less than 170/100 drug
treatment
Different drug effects:
 Inotropic: relating to or
influencing the force of
contraction
 Chronotropic:
influencing the rate;
especially the heart beat
 Dromotropic: affecting
the conductivity of
cardiac muscle -- used
of the influence of
cardiac nerves
Jarvis, 2000, Figure 17-8. p. 505.
Overview of Pulmonary/Systemic Circulation
Carolyn Jarvis, Physical Exam and
Health Assessment 3rd Ed. 2000.
Figure 17-1. p. 498.
Copyright by W.B. Saunders
So what is the goal of medical
management of heart disease?
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Dissolve clots (save muscle)
Maximize blood flow to heart muscle
Maximize preload
Minimize the afterload
Maximize cardiac contractility (inotropic effect)
Reduce chances clot formation
Reduce overall blood volume if overload
Heart rate between 60-80 beats/min to maximize
cardiac output and filling pressures
 Treat arrhythmias
Preload/Afterload in Heart
Carolyn Jarvis, Physical Exam and Health Assessment 3rd Ed. 2000.
Copyright by W.B. Saunders
So what drugs help meet
these goals?
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Dissolve existing clots quickly—TPA, Urokinase
Maximize preload— I.V. fluids, volume expanders
Minimize afterload—Ace inhibitors, IABP
Maximize cardiac contractility—Digoxin,
Dopamine
Decrease preload, increase coronary circulation,
and reduce pulmonary congestion—Nitrates
Reduce chances clot formation—ASA or other
anti-platelet medications
Reduce overall fluid volume in overload--diuretics
Keep heart rate between 60-80/min (Beta
blockers and Calcium-channel blockers)
Arrhythmias—Atropine, Lidocaine, etc.
Fibrolytic Drugs
 TPA-tissue
plasminogen
activators
 Streptokinase
Image from site
http://www.americanheart.org/presenter.jhtml?identifier=4751
Nitrates
 GTN
 Cause vasodilatation reducing the amount of
blood returning to the heart from the venous
system, thus decreasing preload.
 This decreases the work of the heart and the
demand of the myocardium for oxygen.
 Also dilate the peripheral arteries, decreasing
the resistance against which the left ventricle
must pump (decreases afterload).
 Increases coronary vasodilation
ACE Inhibitors
 (pril)
 Used to treat both hypertension and ACS
 Inhibit the conversion of angiotension I to
angiotension II, thus blocking the release
of aldosterone, thereby reducing sodium
and water retention
 Potassium-sparing so watch for
hyperkalemia
 Reduce afterload of heart
Inotropes
 Digitalis
 Inhibits the sodium-potassium pump, causing
an increase in intracellular sodium levels
 Increased sodium levels force sodium out of
the cell in exchange for calcium
 Higher intracellular calcium levels increase the
force of contraction, increasing cardiac output
 Digoxin also blocks the slow calcium channels
of the AV nodes, slowing the HR
Antiplatelet Agents
 Low dose Aspirin
 Aspirin blocks the formation of
thromboxane A2 , inhibiting platelet
aggregation
 A single daily dose of around 80mg can
effectively sustain the desired antiplatelet
effect
Anticoagulants
 Heparin (Clexane)
 Binds to anti-thrombin, inactivating
coagulation factors and thrombin,
 thereby blocking the conversion of
fibrinogen to fibrin
Side Effects:
Anticoagulants, Fibrolytics and Antiplatelets
 Bleeding
 What symptoms would you see?
 INR
Beta-blockers
 Block beta-adrenergic receptors of CNS
 Blockage of beta-1 receptors causes a
decrease in the force of contraction, a
slowing heart rate, and a slowing of impulse
of conduction (negative inotrope,
chonotrope, dromotrope)
 These 3 mechanisms of action combine to
decrease myocardial oxygen demand
Calcium-channel blockers
 Action: thought to inhibit calcium ion influx
across cardiac and smooth muscles,
decreasing contractility and oxygen
demand. May also dilate coronary arteries.
 Nursing implication: monitor for rapid drop
in BP (especially if given intravenously).
Cholesterol Lowering Agents:
hypolipidaemic drugs
 Statins
 Reduce plasma lipids and lipoproteins
 Block the production of LDLs and increase
receptor activity that removes LDLs
 Take other drugs 1 hour before or 4-6 hours
after Questran to avoid blockage of
absorption
Cardiogenic shock:
 Inability of the impaired ventricle to perfuse and
oxygenate body tissues
 Common in MI that damages 40% or more of
the left ventricle.
 Signs:
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Systolic BP less than 90 mmHg
Anxiety, restlessness, confusion, coma
Cool, moist, clammy skin
Rales in lungs, decreased (<30ml/hour) urine output
S3 and S4 heart sounds
Coma and death
Cardiac Medications
Congestive Heart Failure
Congestive Heart Failure
Table 17-10. p. 548.
What can cause CHF?
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CAD multiple heart attacks
High BP
Faulty heart valves
Cardiomyopathy
Myocarditis
Congenital heart defects
Cardiac arrhythmias
Aims of treatment CHF:
 Relieve symptoms
 Improve quality of life
 Prevent readmission to hospital, and/or
recurrent ischaemic events
 Reduce mortality
(Lonn & McKelvie, 2000)
Drugs used to treat CHF
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ACE Inhibitors
Beta Blockers
Diuretics
Vasodilators
Inotropes (e.g. Dopamine)
Digitalis
Inotropes
 Digitalis
 Inhibits the sodium-potassium pump, causing
an increase in intracellular sodium levels
 Increased sodium levels force sodium out of
the cell in exchange for calcium
 Higher intracellular calcium levels increase the
force of contraction, increasing cardiac output
 Digoxin also blocks the slow calcium channels
of the AV nodes, slowing the HR
Dopamine
 Stimulates dopamine receptors in the
renal vessels, increasing renal blood
flow, increasing diuresis
 Net result is an increase in cardiac output
 Increase in systemic arterial pressure
Anti-arrhythmic Drugs
 Ventricular arrhythmias
 Amiodarone
Treatment of tachyarrhythmias –
supraventricular nodal and ventricular
tachycardias, atrial flutter and fibrillation.
 Lignocaine
Decreased the depolarisation and excitability
in the ventricles.
Potassium Chloride
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Intracellular ion
Transmission of nerve impulses
Contraction of cardiac muscles
Levels 4.0-4.5
Hypokalaemia=potassium deficit
Nursing implications CHF:
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Daily weights
Strict intake/output records
May be on fluid restriction (1500ml/24hrs)
Teaching regarding medications
Elevate feet to avoid stasis ulcers
Oxygen on at all times
Monitor BP, heart rate, respiratory rate, pulse
oximetry frequently (every 2-4 hours)
 Monitor labs (electrolytes, troponin-T)
 Auscultate lung fields to assess for change every
4 hours!