Cardiac Medications

Cardiac Medications

Medication Classification	Medication Used
Anti-hytertensives	Diuretics, Alpha Blockers, Beta Blockers, Ca Channel Blockers, ACE inhibitors, Angiotensin Receptor Blockers, Vasodilators, Centrally acting agents.
Anti-anginals	Beta- Blockers, Calcium channel blockers, Coronary vasodilators (nitrates).
Antidysrythmics	Cardiac glycosides, Beta-blockers, Ca channel-blockers, Various – adenosine, procainamide, quinidine, lignocaine and others
Cardiac Sympathomimetics	Dobutamine, dopamine, adrenaline, nor-ad, isoptroterenol
CCF	ACE inhibitors, Cardiac glycosides, diuretics, inotropes.

Medication by Therapeutic Classification

Therapeutic Classification	Medication
Diuretics	Loop diuretic – frusemide Osmotic diuretic – mannitol Potassium sparing – spironlactone, amiloride. Thiazide diurectic – hydrochorothiazide
Beta Blockers	Propanalol, atenolol, metoprolol, labetolol, esmolol, etc.
Calcium Channel Blockers	Nifedipine, diltiazem, verapamil, amlodipine, feodipine, etc
ACE inhibitors	Captopril, enalapril, fosinopril, ramipiril, etc
Angiotensin II receptor antagonists	Iosartan, valsartan, telmisartan, d’irbesartan (avapro)
Vasodilators	Diazoxide, hydralazine, nitroglycerin, sodium nitroprusside
HMG Co-A Reductase Inhibitors	Iovastatin, fluvastatin, pravastatin

Beta Blockers

n Remember the sympathetic nervous system is activated at two adreno-receptor sub-types:

n Alpha

¨ Alpha 1 receptors

¨ Alpha 2 recptors

n Beta

¨ Beta 1 receptors

¨ Beta 2 receptors

n Stimulation of beta 1 receptors leads to:

n Increase in Heart Rate

n Increase in Cardiac Output

n Stimulation of beta 2 receptors leads to:

n  Dilation of Small Airways in the Lungs

n  Dilation of Small Arteries and Arterioles

n Action –  block the effect of the Sympathetic Nervous System potentially producing:

n  Reduction in Heart Rate

n  Reduction in Cardiac Output

n  Reduction in Blood Pressure

n  Bronchoconstriction

n  Control of Cardiac Arrhythmias

Contra-indications:

n Asthma/Obstructive Pulmonary Disease

n Heart Block ( Unless PPM in-situ)

n Peripheral Vascular Disease

Commonly Used Beta-Blockers:

n Cardioselective: Act mainly on beta1 receptors

¨  Atenolol

¨  Bisoprolol

¨  Metoprolol

n Non-Cardioselective: Act on beta1 and beta2 receptors

¨ Labetolol

¨ Propanolol

NURSING MONITORING

( BETA – BLOCKER)

   Patients can develop heart failure and should be closely observed

·       BP and HR

·        ECG RHYTHM

   H/O Asthma or COPD.

·       SPO2

·       C/O SOB

   H/O diabetics. Symptoms of a Hypoglycaemic attack recognized by Sweating, Tremor and Tachycardia may not be felt by patients.

Cardioselective Beta-blockers, less likely to have this effect.

·       HGT

   Can be stored at room temperature.

Ca Channel Blockers

ACTION:

n  Calcium is an essential part of the mechanism of cardiac and smooth muscle contraction.

n  Blocks influx of calcium ions into cells.    

n  Relaxes the muscle in the walls of arteries (dilation) → lowers blood pressure and improves blood supply to the heart.

n  Relaxes heart muscle → allows heart to make do with a reduced blood supply and reduces symptoms of angina.

USED:

¨ Angina

¨ Hypertension

¨ Improve peripheral vascular insufficiency

¨ Dysrhythmias

COMMONLY USED Ca Channel Blocker:

¨ Amilodipine

¨ Diltiazem

¨ Nifedipine

¨ Verapamil

                                                                              

SIDE – EFFECTS/CONTRAINDICATION:

¨ A-V block

¨  hypotension,

¨ Bradycardia

¨ Oedema

SIDE – EFFECTS/CONTRAINDICATION:

¨  nausea, headache, rash.

¨ Sick-sinus syndrome

¨ 2^nd or 3^rd degree A-V block,

¨ hypotension

¨ severe CCF

¨  acute MI with pulmonary congestion.

NURSING MONITORING

Ca Channel Blocker

Glyceryl Trinitrate

(GTN)

ACTION:

n   mechanism - releases nitric-oxide, a vasodilator.

Reduces the Work of the Heart by:

¨  Venous Dilation: reduces the amount of blood returning to the right Side of the heart (pre-load) and peripheral resistance (afterload).

¨  Coronary artery dilation: increases blood supply to cardiac muscle.

¨  Therefore decreases myocardial O₂ consumption and increases myocardial O₂ supply.

USE:

¨   Anti-anginal: more effective as a preventor.

¨   Heart Failure

n  Routes of administration:

¨   Sublingual – Tablets / Spray

¨   Oral – Tablets (chewable / SR)

¨   Skin Patches

¨   Intra-venous Infusion

¨   Ointment

n  Onset:

¨  Sublingual Tablets/Spray/IV – Within Mins

¨  SR Tablets/Patches/Ointment – 1-3hrs

n  Duration:

¨  Sublingual Tablets/Spray – 20-30 mins

¨  Ointment – 3-5hrs

¨  SR Tablets – 8-12 hours

¨  Patches – 24 hours

Nurse Monitoring

GTN

n Observe for side effects of flushing, headaches, syncope, tachycardia and hypotension.

n Anticoagulant effect of Heparin is reduced by GTN infusion

n Alcohol enhances the vasodilator effects of Nitrates.

n When administering IV GTN to pts with chest pain, rate should be carefully titrated against pain level and BP.

Angiotensin-Converting Enzyme Inhibitors

n  ACE is angiotensin-converting enzyme which is a substance present in the circulation.

n  ACE converts Angiotensin I into  Angiotensin II.

n  Angiotensin is normally produced in response to falling blood pressure and excess sodium loss.

n  Angiotensin II causes profound vasoconstriction and sodium retention by the kidney, therefore supporting the circulation.

n  In hypertension & heart failure, ACE is overactive and causes unwanted vasoconstriction and sodium retention.

n  ACE Inhibitors block the actions of Angiotensin-Converting Enzyme.

n  They therefore block the conversion of Angiotensin I to Angiotensin II.

n  This produces vasodilation and promotes sodium excretion (water follows).

n  In Hypertension this leads to a reduction in peripheral vascular resistance and fall in BP.

n  In Heart Failure it reduces stress on the myocardium by reducing congestion on the right side (reduces pre-load).

n  Reduces energy required to eject blood from the left ventricle, by reducing PVR (reduces afterload).

n  ACE inhibitors are among the Most Important drugs used in the treatment of Hypertension and Heart failure.

Angiotensin II Receptor Blockers

n  Developed after ACE inhibitors.

n  Block the effect of angiotensin II at receptors.

n  Result in vasodilation and reduced BP.

n  Similar side-effects to ACE inhibitors.

n  Complications include angioedema, renal failure.

Nurse Monitoring

ACE INHIBITOR

n A trial of the lowest dose should be carried out before commencing a regular regimen.

n Strict 24hr BP monitoring should occur.

n K⁺ may rise in patients taking ACEI’s, particularly if they are already taking K⁺ supplements or K⁺ sparing diuretics.

n High K⁺ Levels may cause Dysrhythmias.!

                                                       

Diuretics

n  Most act by increasing sodium excretion.

n  Part of renal tubule where they act varies.

n  Loop diuretics act on Loop of Henle by preventing reabsorption of sodium. Also cause vasodlation, reducing BP.

n  K⁺ follows sodium & can cause hypokalaemia, requiring supplements.

n  Fast-acting: used for CCF, cirrhosis & renal failure.

n  Thiazide diuretics prevent reabsorption of Na+ from the convoluted tubules.

n  Vasodilatory effect by desensitizing smooth muscle to Ca++ release.

n  Used in HT.

n  Potassium wasting. Can cause impotence.

n  Osmotic diuretics large molecules not reabsorbed by kidneys post filtration – drag water with them (mannitol).

n  Used for treatment of cerebral oedema.

n  Potassium sparing diuretics decrease sodium reabsorption and suppress activity of aldosterone in collecting tubules.

n  Used in combination with loop diuretics.

n  HT, CCF.

NURSE MONITORING

Diuretics

HMG-CoA Reductase Inhibitors

n HMG-CoA Reductase is an enzyme involved in the production of cholesterol by the liver.

n HMG-CoA Reductase Inhibitors (statins) reduce the production of ‘bad cholesterol’ LDL’s.

n Used in prevention of coronary artery disease.

n Side effects: GI disturbances, headache, rash

¨Rare – myopathy and rhabdomyolisis.

Aspirin

n  Type of drug :

¨  nonsteroidal anti-inflammatory, antipyretic, analgesic.

n  Uses:

¨  Mild painkiller / reduces fever

¨  Reduces inflammation in disease affecting joints, cartiledges and muscles (high dose)

¨  Antiplatelet action – irreversibly blocks the synthesis of a prostaglandin Thromboxane A2 by platelets in response to injury in the vascular epithelium – impedes clotting (AMI or stroke).

n  Dosage:

¨  Varies according to reason for usage

n  Onset:

¨  30-60 mins (regular aspirin)

¨  1.5-8hrs (coated aspirin).

NURSE MONITORING

ASPIRIN

¨Gastrointestinal side effects. (e.g loss of appetite, nausea, vomiting + diarrhoea, gastric bleeding)

¨In asthmatic patients can provoke an asthma attack and worsen existing asthma

¨Not recommended in pregnancy

¨Not recommended in children under 12

¨Avoid with alcohol as increases stomach irritation

¨To prevent gastric irritation, patients should take aspirin with food.

¨Can be stored at room temperature.

Cardiac Sympathomimetics and Antidysrhythmics

n 2 groups of drugs are varied and complex.

n Usually used within the context of resuscitation and cardiac arrest.

n Algorithms for ALS provide specific indications, contra-indications and precautions.

Inotropes

n Adrenaline – naturally occurring catecholamine produced by adrenal medulla.

n Agonist – acts on both ά & ß receptors, but predominantly ß.

n ↑ rate & contractility of heart ↑ CO.

n ↑ depth & rate breathing.

n Systemic vasoconstriction ↑ BP.

Uses:

n Low cardiac output states especially cardiogenic shock.

n Asthma, COPD or anaphylaxis → bronchodilation.

Dosage: varies for use

n 0.3 to 0.5mg s/c for allergic reaction

n 1mg plus for cardiac arrest.

n Presented 2 strengths 1mg/ml or 1mg/10ml

Nor-adrenaline

 is a natural catecholamine released by neural fibers.

n Acts on both ά & β receptors, but predominantly ά.

n ↑ heart rate & contractility ↑ CO.

n Vasoconstriction ↑ SVRI & BP.

Uses:

n Acute low cardiac output states particularly septic and neurogenic shock.

n ADD and depression.

n In high doses can cause limb / tissue ischaemia and death.

Milrinone is a phosphodiesterase III inhibitor.

n It potentiates the effect of cyclic AMP, increases Ca+ uptake & L ventricular relaxation.

n It has positive inotropic & vasodilating and minimal chronotropic effects.

n Used for heart failure only when conventional treatment with vasodilators and diuretics is insufficient, due to the potentially fatal adverse effects, including ventricular arrythmias.

Anti-Dysrhythmics

Atropine

is an ACh antagonist and therefore suppresses parasympathetic nervous stimulation.

n Uses: bradyarrythmias, asystole, 1^st degree heart block, Type 1 - 2^nd degree heart block & 3^rd degree heart block.

n Contraindicated in ischaemia-induced conduction block, because it increases oxygen demand of the AV nodal tissue,  aggravating ischaemia and the resulting heart block.

Amiodarone – class III antidysrhythmic

n Mechanism of action is unknown.

n ? involves prolonging the action potential duration, prolonging the refractory period, or interacting with K⁺ channels.

n Uses: ventricular and supraventricular tachydysryhthmias.

Lignocaine is a class IB antidysrhythmic.

n Stabilises neuronal membrane & prevents the initiation & transmission of nerve impulses

Antiarrhythmic effect by increasing the electrical stimulation threshold of the ventricle during diastole.

n Depresses slow spontaneous depolarisation ie decreases automaticity.

n Increases effective refractory period. Potent suppressor of abnormal cardiac activity.

Blocks both activated & inactivated sodium channels

n Suppresses activity of depolarised, arrhythmogenic tissues while minimally interfering with the electrical activity of normal tissues: therefore is effective in suppressing arrhythmias associated with depolarisation [eg ischaemia, digitalis toxicity] but is relatively ineffective against arrhythmias occurring in normally polarised cells.

Contraindications:

n Heart blocks.

n Rarely effective in supra-ventricular arrhythmias except WPW syndromes.

n Severe heart failure.

Caution :

may make myocardium resistant to depolarization (defib) in emergency situations.