MODULE VI: Cardiac Medications 4.
4. Pumping action of the heart
(Part 1)
Heart- muscular organ
Preload- volume of blood in ventricles at
the end of diastole.
Increased in: Hypervolemia,
Regulation of cardiac valve, Heart failure
Afterload- resistance left ventricle must
overcome to circulate blood.
Increased in: Hypertension,
Vasoconstriction
Increase afterload= increase cardiac
workload
Regulators of Blood Pressure
1. Renin-Angiotensin Aldosterone
System
 activated when circulating
blood volume is low.
 Increased BP by increasing Na
reabsorption (increased water
reabsorption)
2. Baroreceptors in the aorta and carotid
sinus
 Detects changes in BP.
 Sends signals to vasomotor
center in medulla, triggering
sympathetic/ parasympathetic
response.
3. Hormones
 Antidiuretic Hormone (ADH)-
released by posterior pituitary
gland due to hypotension to
increase water reabsorption of
kidneys.
 Atrial Natriuretic peptide
(ANP)- released by cardiac
muscle due to HPN to increase
renal Na excretion.
Factors that affect Blood Pressure
1. Blood volume
2. Blood viscosity
3. Peripheral vascular resistance
Note: Check apical pulse, heart rate  Nursing Action: take on empty
5. Elasticity of the vessel wall should be more than 60 before
administering a drug.
Normal Ejection Fraction- 50-70% is Drug Interactions: +K-wasting Diuretics,
pumped out during each contraction amiodarone, Ca, propafenone,
Note: Less than 50% pumped blood per omeprazole, cyclosporine, macrolides.
contraction causes left sided heart Side Effects/Adverse Effects:
failure. bradycardia, N/V, diarrhoea
Nursing Action: check apical pulse, serum
Heart Failure- inability of the heart to drug levels, electrolytes.
pump enough blood to meet the body’s
needs. This is due to any structural or 2. Beta Blockers
functional impairment of ventricular  Blocks beta 1 receptors on the
filing. heart which decreases
 Left Sided Heart Failure- myocardial contractility (HR,
afterload. BP) the results in decrease
 Right Sided Heart Failure- myocardial oxygen demand.
preload  Ends with OLOL
Side Effects: bradycardia, decrease BP,
4 Stages of Chronic Heart Failure N/V, bronchospasm, AV block
1. Breathlessness or tiredness Note: Do not give beta blockers to left
2. Heart races or breathlessness when sided heart failure patients.
walking or taking the stairs. Drug Interaction- +digoxin, CCB,
3. Palpitation or tiredness with simple cimetidine= increase effect and toxicity.
tasks like getting up from the sofa and +antacid, Ca salts, NSAIDS= decrease
walking over to the kitchen. effect.
4. Heart and breath go faster even at Nursing Action: taper. Abrupt D/C may
rest. Tiredness even while sitting. Anxiety cause rebound HPN.
and palpitations almost all the time.
3. Vasodilators
Drugs for Heart Failure- minimised  Dilate blood vessels which
adrenergic responses. decrease BP, improve
1. Inotropic (Cardiac Glycosides) symptoms, functional capacity
 Promote movement of Ca from and survival.
extracellular to intracellular  Anti-hypertensive
 Strengthens myocardial ACE inhibitor
contractility: Positive inotropic  (Angiotensin-converting (ACE)
action enzymes)
 Enhance vagal tone, slowing  Given as anti-hypertensive
contractility through SA and AV  Right sided heart failure.
node  Side effects: proteinuria, non-
 Ex. Digoxin productive cough,
 Antidote: Digifab angioedema, increase BUN and
creatinine
stomach. Monitor proteinuria.
 Right sided heart failure
ARBs (Angiotensin II Receptor Blockers)
 Blocks angiotensin II from its
receptors, preventing
vasoconstriction and
aldosterone-secreting effect of
angiotensin, thus, lowering BP.
 Left sided heart failure
 Ends with TAN.
 Side Effects; headache, fatigue
 Nursing Action: monitor BP and
maintain fluid intake.
Nitrates/Nitrites
 Vasodilator, decreases preload
and afterload, decrease
myocardial O2 consumption.
 Ex: isosorbide mononitrate,
isosorbide dinitrate,
nitrogylcerin.
 Side Effects: headaches,
dizziness, orthostatic
hypotension.
 Nursing Action: teach client on
proper use of sublingual
tablets. Inform client that
headache is common and will
subside. Avoid alcohol. Monitor
for tolerance.
4. Diuretics
Loop Diuretics- acts in the loop of
Henley.
 inhibits chloride and sodium
reabsorption in Loop of Henle
an distal tubule, increase
sodium and water excretion by
inhibiting sodium absorption in
o=proximal tubule
 Thiazide Diuretics- increase
water excretion by increasing
GFR or decrease sodium
reabsorption in the tubules
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,