MODULE VI: Cardiac Medications

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MODULE VI: Cardiac Medications 4.

4. Pumping action of the heart Note: Check apical pulse, heart rate  Nursing Action: take on empty
(Part 1) 5. Elasticity of the vessel wall should be more than 60 before stomach. Monitor proteinuria.
administering a drug.  Right sided heart failure
Heart- muscular organ Normal Ejection Fraction- 50-70% is Drug Interactions: +K-wasting Diuretics, ARBs (Angiotensin II Receptor Blockers)
Preload- volume of blood in ventricles at pumped out during each contraction amiodarone, Ca, propafenone,  Blocks angiotensin II from its
the end of diastole. Note: Less than 50% pumped blood per omeprazole, cyclosporine, macrolides. receptors, preventing
Increased in: Hypervolemia, contraction causes left sided heart Side Effects/Adverse Effects: vasoconstriction and
Regulation of cardiac valve, Heart failure failure. bradycardia, N/V, diarrhoea aldosterone-secreting effect of
Afterload- resistance left ventricle must Nursing Action: check apical pulse, serum angiotensin, thus, lowering BP.
overcome to circulate blood. Heart Failure- inability of the heart to drug levels, electrolytes.  Left sided heart failure
Increased in: Hypertension, pump enough blood to meet the body’s  Ends with TAN.
Vasoconstriction needs. This is due to any structural or 2. Beta Blockers  Side Effects; headache, fatigue
Increase afterload= increase cardiac functional impairment of ventricular  Blocks beta 1 receptors on the  Nursing Action: monitor BP and
workload filing. heart which decreases maintain fluid intake.
 Left Sided Heart Failure- myocardial contractility (HR, Nitrates/Nitrites
Regulators of Blood Pressure afterload. BP) the results in decrease  Vasodilator, decreases preload
1. Renin-Angiotensin Aldosterone  Right Sided Heart Failure- myocardial oxygen demand. and afterload, decrease
System preload  Ends with OLOL myocardial O2 consumption.
 activated when circulating Side Effects: bradycardia, decrease BP,  Ex: isosorbide mononitrate,
blood volume is low. 4 Stages of Chronic Heart Failure N/V, bronchospasm, AV block isosorbide dinitrate,
 Increased BP by increasing Na 1. Breathlessness or tiredness Note: Do not give beta blockers to left nitrogylcerin.
reabsorption (increased water 2. Heart races or breathlessness when sided heart failure patients.  Side Effects: headaches,
reabsorption) walking or taking the stairs. Drug Interaction- +digoxin, CCB, dizziness, orthostatic
2. Baroreceptors in the aorta and carotid 3. Palpitation or tiredness with simple cimetidine= increase effect and toxicity. hypotension.
sinus tasks like getting up from the sofa and +antacid, Ca salts, NSAIDS= decrease  Nursing Action: teach client on
 Detects changes in BP. walking over to the kitchen. effect. proper use of sublingual
 Sends signals to vasomotor 4. Heart and breath go faster even at Nursing Action: taper. Abrupt D/C may tablets. Inform client that
center in medulla, triggering rest. Tiredness even while sitting. Anxiety cause rebound HPN. headache is common and will
sympathetic/ parasympathetic and palpitations almost all the time. subside. Avoid alcohol. Monitor
response. 3. Vasodilators for tolerance.
3. Hormones Drugs for Heart Failure- minimised  Dilate blood vessels which
 Antidiuretic Hormone (ADH)- adrenergic responses. decrease BP, improve 4. Diuretics
released by posterior pituitary 1. Inotropic (Cardiac Glycosides) symptoms, functional capacity Loop Diuretics- acts in the loop of
gland due to hypotension to  Promote movement of Ca from and survival. Henley.
increase water reabsorption of extracellular to intracellular  Anti-hypertensive  inhibits chloride and sodium
kidneys.  Strengthens myocardial ACE inhibitor reabsorption in Loop of Henle
 Atrial Natriuretic peptide contractility: Positive inotropic  (Angiotensin-converting (ACE) an distal tubule, increase
(ANP)- released by cardiac action enzymes) sodium and water excretion by
muscle due to HPN to increase  Enhance vagal tone, slowing  Given as anti-hypertensive inhibiting sodium absorption in
renal Na excretion. contractility through SA and AV  Right sided heart failure. o=proximal tubule
node  Side effects: proteinuria, non-  Thiazide Diuretics- increase
Factors that affect Blood Pressure  Ex. Digoxin productive cough, water excretion by increasing
1. Blood volume  Antidote: Digifab angioedema, increase BUN and GFR or decrease sodium
2. Blood viscosity creatinine reabsorption in the tubules
3. Peripheral vascular resistance
Upright position reducing myocardial oxygen Potassium Sparing Diuretics-act on distal
Nitrates demand. tubule to excrete Na, bicarbonate, and Ca
Lasix  Very Nice Drugs but conserve potassium.
Oxygen  Side Effects: hypotension,
ACE inhibitors palpitations, tachycardia or Potassium Deficit:
Digoxin bradycardia, constipation Alkalosis
 Nursing Action: monitor VS. Shallow Respi
Fluids decrease 4. Diuretics Irritability
Afterload decrease  Accelerate the rate of urine Confusion and drowsiness
Sodium restriction formation.
Test (digoxin level, AGBs, Potassium  Side Effects: metabolic Weakness, Fatigue
Level) alkalosis, hypovolemia, Arrythmias= tachycardia, Irregular
dehydration, hyponatremia, Rhythm and/or bradycardia
B. Anti-Anginas hypokalemia.
Angina Pectoris- chest pain is due to  Contraindications: when less Lethargy
insufficient O2 in the blood to meet potent diuretics are sufficien, Thready Pulse
myocardial demand. hypersensitivity, anuria, hepatic
Ischemia- lack of blood flow and oxygen coma, severe uncorrected Decrease intestinal motility
to the heart muscles. It causes angina electrolyte depletion, sulfa Nausea
pectoris. energy. Vomiting
Infarct- obstruction of the blood supply Carbonic Anhydrase Inhibitors (CAI)- Ileus
to the heart causing tissue death. block the action of carbonic anhydrase
thus preventing the exchange of H+ ions
Types of Angina with sodium and water.
1. Chronic Stable- aka classic or effort Osmotic Diuretics- mannitol is given IM
angina. Caused by stress. Relieved by or IVF. Inhibits proximal tubule
stress and NTG. reabsorption of water and solutes
2. Unstable Angina- aka pre-infarction or producing and osmotic effect: rapid
crescendo angina. Occurs at rest, many diuresis.
progress to MI.  Indication: cerebral edema, to
3. Vasospastic Angina- aka prinzmetal’s decrease ICP.
or variant angina. Occurs at rest, relieves Loop Diuretics- inhibit Cl and Na
bt NGT and Ca blockers. reabsorption in Loop of Henle and distal
tubule. Increase Na and water excretion
Anti-Angina Drugs by inhibiting sodium absorption in
1. Nitrates/Nitrites’ proximal tubule.
 vasodilation  Indications: edema in HF,
2. Beta Blockers- blocks beta 1 hepatic cirrhosis, HPN, renal
disease, cerebral edema
3. Calcium Channel Blockers  Left sided heart failure
 blocks Ca from entering the Thiazide Diuretics- increase water
cell, which case coronary artery excretion by increase GFR or decrease
vasodilation decreasing Na.
systemic vascular resistance,

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