Transcript Cardiac Medications #2

CARDIAC MEDICATIONS
Why they do what they do (2014)
LEARNING OBJECTIVES
Students will be able to:
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Review the pathological process of Hypertension,
Coronary Artery Disease and Heart Failure
Discuss the major categories of drugs used for the
treatment of Cardiac Disease.
Describe the effects of these medications on
cardiac function.
Describe nursing considerations when administering
above medications.
WHAT CAN GO WRONG ?
Circulation could be impaired by a weakened
pumping action (CCF)
 Irregular heart beat (Arrhythmias )
 Narrowed or clogged blood vessels due to fatty
deposits - atherosclerosis ( CAD, Hypertension ,
Stroke ,MI )
 Loss of elasticity of vessel walls and increase in
pressure of circulating blood on vessel walls
(Hypertension)
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CARDIAC DRUGS AND HYPERTENSION
(2013)
REGULATION OF BLOOD PRESSURE
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Blood pressure is the force exerted by the blood
against walls of the blood vessells
Arterial BP = CO x SVR
Regulation involves nervous system, cardiovascular
system, renal and endocrine systems
Vascular endothelium - endothelin
SDL
Lewis pg. 832
SDL - HYPERTENSION
Major groups of first–line antihypertensives can
Can be arranged in order of the first four letters
of the alphabet.
A - ACE inhibitors , angiotensin 11 receptor antagonists
B - β- blockers *****
C - Calcium channel blockers (antagonists)
D - diuretics
Discuss the above under the headings ,example,
mechanism of action, risk factors, precautions, and side
effects .
Lewis pg : 841
DIURETICS
Prescribed to treat Hypertension or to eliminate
oedema caused by Heart Failure
 Most diuretics increase urine output by blocking
reabsorption of sodium and chloride
 They are classified into four categories
- Loop
- Thiazides
- Potassium Sparing
- Osmotic
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THE NEPHRON
DIURETICS: TO REDUCE OVERALL
VOLUME OF BLOOD
Thiazides (chlorothiazide)
 Inhibit
Na reabsorption in the distal
convoluted tubule
 Slow acting
 Use with caution with Digoxin
LOOP DIURETICS
(Frusemide)
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Inhibit sodium and chloride reabsorption at
proximal and distal tubules and ascending loop
of Henle
Promote excretion of water, sodium, chloride
and potassium
Indicated for acute pulmonary oedema
Frumil – loop and K+ sparing
POTASSIUM-SPARING DIURETICS
( Amiloride)
 Act
in the distal and collecting renal tubules either
directly or by inhibiting aldosterone to inhibit
sodium reabsorption and potassium 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
 Contraindicated in renal failure.
ALDOSTERONE RECEPTOR BLOCKERS
(Spironolactone)
 Also classed as potassium sparing
 Inhibits Na retaining and K+ excretion effects
of aldosterone in distal and collecting tubules.
 Watch for hyperkalaemia
 Monitor use with ACE inhibitors
 Do not combine with other PSD’s
OSMOTIC DIURETICS - MANNITOL
Elevate osmotic pressure of the glomerular
filtrate to hinder reabsorption of solutes and
water and promote excretion of water, sodium,
potassium, chloride, calcium, phosphorus,
magnesium and uric acid
 Mannitol(Osmitrol)
 Used mainly for reducing intracranial and
intraocular pressure.
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DIURETICS
NURSING INTERVENTIONS
Monitor for dehydration - confusion
 Monitor for electrolyte imbalances especially
hypokalaemia which can trigger arrhythmias
 Monitor for hypotension – teach signs of
orthostatic hypotension
 Monitor weight daily – report weight gain and
oedema
 Listen to chest sounds –> crackles -> overload
 Take diuretic in morning preferably as need to
urinate increases for 6 to 8 hrs.
VASODILATORS
Dilate peripheral blood vessels by directly
relaxing arteriolar smooth muscle
 Usually used in combination with other
antihypertensives as they increase sodium and
fluid retention
 Several classes include Calcium antagonists,
nitrates, ACE inhibitors and sympatholytics
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CALCIUM ANTAGONISTS
CALCIUM CHANNEL BLOCKERS
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Felodipine, Nifedipine, Diltiazem, Verapamil
Inhibit the influx of calcium ions into muscle cells;
act on vascular smooth muscle (primary arteries)
to reduce spasms and promote vasodilatation
Decrease contractility, workload and Oxygen
demands
May enhance serum Digoxin levels
Watch for rapid drop in BP if given IV
Avoid grapefruit if on Nifedipine
CARDIAC MEDICATIONS
Coronary
Artery
Disease
CASE STUDY
Jane Hart 55, has a history of hypertension
and hyperlipidaemia. She is admitted to the
emergency unit with chest discomfort. A 12 lead
ECG shows atrial fibrillation, and ST
elevation in in the inferior leads. She has
bilateral crackles in her lung bases with an
S3 heart sound. Cardiac enzymes are raised and a
diagnosis of ACS with AF and heart failure is
made.
THE OVERALL GOAL IN MANAGING
CORONARY ARTERY DISEASE
 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:
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Inotropic: relating to or
influencing the force of
contraction
Chronotropic: influencing
the rate; especially the
heart beat
Dromotropic: affecting
the rate of electrical
impulses in the heart
muscle. Affects
conduction velocity of the
AV node
Jarvis, 2000, Figure 17-8. p. 505.
WHAT IS THE GOAL OF MEDICAL
MANAGEMENT OF CAD
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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 of clot formation
Reduce overall blood volume if overloaded
Heart rate between 60-80 beats/min to maximize
cardiac output and filling pressures
Treat arrhythmias
WHAT DRUGS HELP MEET THESE
GOALS?
Dissolve existing clots quickly—tPA, Metalyse
(TNK) - Streptokinase ->Thrombolytics
 Maximize preload— I.V. fluids, volume
expanders
 Minimize afterload — Ace inhibitors,
 Maximize cardiac contractility— Digoxin,
Dopamine
 Maximize blood flow to heart— vasodilators Nitrates
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CONTINUED ………….
Inhibit factors necessary for platelet
aggregation - antiplatelets (aspirin)
 reduce overall fluid volume in overload –
diuretics
 Keep heart rate between 60 -80 b/min –
(Beta blockers and Calcium-channel blockers )
 Antiarrhythmics – amiodarone, lignocaine,
atropine
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CLOTTING MECHANISM
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Platelets accumulate
release chemicals that
activate blood clotting
factors
factors together with
vit K act on fibrinogen
convert to fibrin
fibrin enmeshed with
platelets form clots
http://www.youtube.com/watch?v=xNZEERMSeyM
THROMBOLYTIC DRUGS
(CLOT BUSTERS)
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tPA - tissue plasminogen
activators
Increase blood level of
plasmin
Breaks down fibrin threads
Metalyse – New
Streptokinase not drug of choice
Alteplase - (rt-PA) can be
given if pt had
Streptokinase
http://www.bioportfolio.com/leaddiscovery/thrombolysis.gif
ANTIPLATELET AGENTS
Low dose Aspirin
 Clopidogrel (Plavix )
 Aspirin blocks the formation of thromboxane A2
inhibiting platelet aggregation (sticking
together)
 A single daily dose of around 80mg can
effectively sustain the desired antiplatelet
effect
 Risk of bleeding
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ANTICOAGULANTS
Heparin IV, Clexane, warfarin
 Binds to anti-thrombin, inactivating coagulation
factors and thrombin, thereby blocking the
conversion of fibrinogen to fibrin
 Prevent formation of a clot or stabilize existing
clots so that they do not break away and
cause embolism
 Do not dissolve clots
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SIDE EFFECTS:
ANTICOAGULANTS, THROMBOLYTICS AND
ANTIPLATELETS
Bleeding
 Stroke
 Reperfusion arrhythmias
 Hypotension
 Allergic reactions
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SDL- THROMBOLYTICS, ANTIPLATELETS
AND ANTICOAGULANTS
Discuss the above drugs under the following
headings :
 Examples
 Mechanism of action
 Risk factors
 Precautions and nursing considerations
 Side effects
ACE INHIBITORS
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(pril) Accupril, Captopril
Used to treat both hypertension and ACS
Inhibit the conversion of angiotensin I to angiotensin II,
thus blocking the release of aldosterone, thereby
reducing sodium and water retention
Decrease pulmonary congestion and peripheral
oedema
Potassium-sparing so watch for hyperkalemia
Discontinue if pt complains of dry irritating cough (
caused by inhibiting breakdown of bradykinins and
kinins
ANGIOTENSIN 11 RECEPTOR ANTAGONISTS (ARB’S)
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Selectively bind to Angiotensin 11
receptors in vascular smooth blood
vessels to prevent vasoconstriction.
Prevents the release of aldosterone
in the adrenal cortex caused by the
reaction of these receptors with
angiotensin 11
End in “sartan” eg. Losartan,
candesartan, eprosartan
Results in decrease in blood pressure
due to decrease in peripheral
resistance and blood volume
Used for patients intolerant to ACE
inhibitors
INOTROPES
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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 (cardiac Glycoside ) also blocks the slow
calcium channels of the AV nodes, slowing the HR
CARDIAC GLYCOSIDES
Digitalis (Digoxin) – Lanoxin
 Act by influencing movement of ions in and out
of the myocardial fibres (calcium and sodium)
 Improve pumping action of the heart
 reduce the flow of electrical impulses through
the AV node slowing ventricular contraction
 increase contractility
 improve efficiency of each heart beat
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NITRATES
GTN – Nitroglycerin – relaxes smooth muscle
 Cause vasodilatation reducing the amount of blood
returning to the heart from the venous system
(Venous filling ) thus decreasing preload.
 This decreases the work of the heart and the demand
of the myocardium for oxygen. Demands must not
exceed supply.
 Dilate the peripheral arteries, decreasing the
resistance against which the left ventricle must pump
(decreases afterload).
 Dilates coronary arteries and collateral vessels
SDL – GTN education plan
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NITRATES
The following are categories of medicines that can increase or decrease the effects of nitrates.
Because there are so many kinds of medicines within each category, not every type of medicine is
listed by name. Tell your doctor about every medicine that you are taking, even if it is not listed
below.
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Viagra (sildenafil), Levitra (vardenafil), or Cialis (tadalafil). Do not take Viagra, Levitra, or Cialis
within 24 hours of taking nitrates. When these erectile dysfunction medicines are mixed with
nitrates, the combination can lower your blood pressure and make you dizzy, lightheaded, or
faint. In some cases, patients have died after mixing erectile dysfunction medicines with
nitrates.
Medicines to treat high blood pressure
Certain heart medicines
Over-the-counter cough, cold, and flu medicines
Over-the-counter herbal cough, cold, and flu medicines
While taking nitrates, you should avoid smoking. Smoking can decrease the effect of the
medicine. You should also avoid alcohol, because it can increase the effect of the medicine.
BETA-BLOCKERS (LOLS)
 Block
beta-adrenergic receptors of CNS
 Blockage of beta-1 receptors causes a
decrease in contractility, decrease in heart
rate, blood pressure and a slowing of impulse
of conduction through the AV node (negative
inotrope, chronotrope, dromotrope)
 These 3 mechanisms of action combine to
decrease myocardial oxygen demand helping
to prevent angina
BETA BLOCKERS
CHOLESTEROL (LIPID) LOWERING DRUGS
HYPOLIPIDAEMIC DRUGS
Statins - Simvastatin (Lipex ),Lipitor (common)
 Reduce levels of fats in the blood by
interfering with absorption of bile salts in the
bowel (carry large amounts of cholesterol)
 Prevent conversion of fatty acids to lipids in
the liver
 Reduce plasma lipids and lipoproteins
 Block the production of LDLs and increase
receptor activity that removes LDLs
(SDL)
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CHOLESTEROL (LIPID) LOWERING DRUGS
HYPOLIPIDAEMIC DRUGS
ANTIARRYTHMIC DRUGS
Act by impeding the movement of ions across
the membrane of myocardial cells
 Affects action potential
 Treat ectopic beats
 stabilises the excitable myocardial tissue
 Suppresses automaticity, depresses rate of
depolarisation, slows impulse conduction,
prolongs action potential and increases
refractory period.
( SDL) Amiodarone
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ADRENALINE
Adjunctive in the treatment of cardiac arrest
 Sympathomimetic
 β and α effects
 Influence both BP and tissue perfusion
 stimulation of receptors in myocardium result
in increased rate, and force of contraction
 Increased CO results in increased BP
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Cardiac Medications
Congestive Heart Failure
AIMS OF TREATMENT - CHF
Treat underlying cause
 Relieve symptoms by reducing workload of
the heart.
 Improve quality of life
 Prevent readmission to hospital, and/or
recurrent ischaemic events
 Reduce mortality
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Drugs used to treat CHF
ACE Inhibitors
 Beta Blockers
 Diuretics
 Vasodilators
 Inotropes (e.g. Dopamine)
 Digitalis
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POTASSIUM CHLORIDE
Intracellular ion
 Transmission of nerve impulses
 Contraction of cardiac muscles
 Levels 4.0-4.5
 Hypokalaemia=potassium deficit
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SDL