CARDIOVASCULAR AGENTS

REVIEW OF ANATOMY AND PHYSIOLOGY Cardiovascular System:

Heart, Blood Vessels (arteries and veins) Blood
4 chambers: Atria – thin walled. Ventricle – thick- walled.
Right atrium → receives deoxygenated blood. Right ventricle → pumps blood to the pulmonary artery.
Left atrium → receives oxygenated blood. Left ventricle → pumps blood into aorta for systemic circulation.
Layers of the heart:
Pericardium → covering of heart Myocardium →middle heart muscle Endocardium → inner layer
4 valves:
2 atrio-ventricular (AV) valves: Tricuspid Mitral 2 semilunar valves: Pulmonic valve Aortic valve
Conduction of Electrical Impulses
SA NODE (the pacemaker) → AV NODE (functional pacemaker) → AV bundle (Bundle of His) → right and left
bundle branches → conduction myofibers (Purkinje fibers).
SA NODE- Regulates the heartbeat (firing of cardiac impulses)
AV NODE- 40-60 beats/min
Regulation of Heart Rate and Blood flow
Average heart beat Average blood pressure Mean arterial pressure = CO x total peripheral resistance (TPR)
Average cardiac output (CO) = 4-8 L/min CO = HR x SV
Factors affecting SV
preload (blood flow force that stretches the ventricle or Ventricular filling)
contractility (force of ventricular contraction)
afterload (resistance to ventricular ejection of blood or systematic vascular resistance)
Effects of drugs on heart
1. inotropic - affects the force of contraction
positive inotropic effect: ↑ myocardial contraction, which may ↓ heart size in client with cardiomyopathy
negative inotropic effect: ↓myocardial contraction
2. chronotropic - interferes with the rate of heart beat
negative chronotropic effect: ↓ heart rate positive chronotropic effect: ↑ heart rate
3. dromotropic - pertains to conduction
negative dromotropic effect: slows conduction through AV node
positive dromotropic effect: speeds up conduction

DRUGS FOR CARDIAC DISORDERS

A. Drugs for heart failure (CHF) Congestive Heart Failure)

Heart failure- Condition in which the heart is unable to pump sufficient blood for metabolizing tissues or can do so
only from an abnormally elevated filling pressure
Precipitating factors
Increased Na intake, Noncompliance with anti-CHF medications, Acute MI, Exacerbation of hypertension
Acute arrhythmias, Infections and/or fever
S/Sx: dyspnea, fatigue, orthopnea, paroxysmal nocturnal dyspnea (PND), peripheral edema, jugular venous
distention, signs of pulmonary congestion (rales), ascites, edema
Non-pharmacologic treatment
Restrict salt intake (<2gm/day or 1tsp/day), Avoid smoking
Obese clients should decrease fat, caloric intake and have mild exercise.

Pharmacologic Treatment

1. Cardiac Glycosides (Digitalis )

Rapid acting digitalis: digoxin (Lanoxin)
Long acting digitalis: digitoxin (Crystodigin)
MOA : inhibit Na-K ATPase pump à inc intracellular calciumàCardiac muscle fibers contract more efficiently
Effects:
positive inotropic effect (myocardial contraction) Negative chronotropic effect (lower heart rate)
Indications: CHF , Atrial fibrillation ,Atrial flutter ,(SVT) Supraventricular tachycardia
Dosage: 0.5-1.0 mg initially in 2 divided doses (digitalization) then maintained at 0.125-0.5 mg/day.
Adverse reactions: digitalis toxicity Overdose or accumulation of digoxin
S/S of digitalis toxicity: Anorexia nausea, vomiting, headache, blurred vision (yellow-green halos)
Antidote: digixin immune fab (Digibind)
Nursing responsibilities
Monitor blood levels for toxicity
Monitor factors associated with toxicity (hypokalemia, hypercalcemia, hypomagnesemia)
Assesses heart rate (hold for HR < 60 beats/min; >120/min
2. Vasodilators
MOA: venous blood return to heart in cardiac filling, ventricular stretching (preload) and O2 demand on heart
Prototype drugs : nitroprusside, Used especially if heart failure is caused by an increased afterload
3. Angiotensin-converting enzyme (ACE) inhibitor
reduce aldosterone secretion, salt and water retention, and vascular resistance
first line drugs for heart failure, along with diuretics and digitalis
4. Diuretics
reduce intravascular volume leading to reabsorption of fluid into the interstitium
dec. peripheral pooling of blood, dec. Right , Left ventricular filling pressures
prototype drugs: furosemide, spironolactone
5. Beta blockers: prototype drugs: carvedilol (Dilatrend)
not recommended for patient with class IV heart failure

B. Drugs for Angina

ANGINA PECTORIS:
Results from an imbalance of myocardial O2 supply and demand
most commonly resulting from atherosclerotic coronary artery obstruction
S/sx: chest tightness, pain may radiate to left arm, lasting for a few minutes
Types of angina pectoris
1. Classic (stable) Occurs with stress or Exertion, Due to build up of Plaque (atherosclerosis)
2. Unstable (preinfarction) Occurs frequently over the course of a day with progressive severity
3. Variant (prinzmetal vasopastic)= Occurs during rest , Caused by vasopasm of coronary arteries
Nonpharmacologic Measures:
AVOID heavy meals, smoking, extremes in weather changes, strenuous exercise, and emotional upset
Proper nutrition, moderate exercise, adequate rest, relaxation techniques

Antianginal Drugs:
1. Nitrates MOA: release nitric oxide (NO) in smooth muscle →stimulates Guanylyl cyclase → inc. of cGMP → smooth
muscle Relaxation →Vasodilation
Reduction in peripheral arterial resistance à↓ afterload Dilate veins , reduce venous return à ↓ preload
End result: ↓ demand for oxygen
Classification:(Nitrates)
a. Rapidly acting agents: nitroglycerin (Nitrostat) Usually given sublingually, Used in acute attack of angina
b. Long term agents: . isosorbide dinitrate (Isoket, Isordil), Isosorbide mononitrate (Imdur)
Used to prevent attacks of angina, Usually administered orally
Routes of administration: NITRATES
a. Sublingual= Effective for the treatment of acute attacks
b. Oral= Used to provide convenient and prolonged prophylaxis against attacks of angina
c. Intravenous = Used in the treatment of coronary vasospasm and unstable angina pectoris
d. Topical (patches ointment)= to provide gradual absorption& for prolonged prophylactic purposes
Adverse reactions : Throbbing headache flushing of face, dizziness, postural hypotension
Tolerance = Repeated administration leads to tolerance (need to administered higher doses same effects
Nursing responsibilities: Assess the frequency and nature of angina, Know how to administer the available forms
Monitor BP before any dose, Advise patients to lie or sit down while taking NTG

2. Calcium channel blockers

MOA- block calcium channels in cardiac and smooth muscles→ ↓ calcium influx→ dec intracellular Ca → ↓muscle
Contractility (thereby decreases oxygen demand)
Also causes peripheral vasodilation w/c further reduces cardiac work load
Indications: Acute and long term prevention of angina attacks, Hypertension
Prototype drugs: verapamil (Isoptin) diltiazem (Dilzem)
nifedipine (Calcibloc, Adalat) –LONG-ACTING
amlodipine (Norvasc), nicadarpine (Cardipine)felodipine (Plendil)
Side effects: headaches, hypotension, dizziness, flushing of the skin, reflex tachycardia (as a result of hypotension), can cause
changes in liver and kidney function (check regularly), edema
Nursing responsibilities; Monitor vital signs, Monitor ECG pattern, Monitor renal and liver status

3. Beta adrenergic blockers:MOA: blocks beta 1- receptors in the heart→ ↓ force of the contraction → ↓ heart rate and
myocardial contractility → reduce need for myocardial oxygen demand
Indications/ uses:
Long –term prevention of angina (esp. for classic angina), Hypertension, Myocardial infarction
Non-selective: propanolol (Inderal, Duranol) nadolol pindolol (Visken)
Selective : atenolol (Tenormin, Therabloc, Durabeta) metoprolol (Neobloc, Betabloc, Cardiostat)
Side effects: Hypotension, bradycardia, heart blocks
Nursing responsibilities: Monitor vital signs,Use with caution in patients with chronic airway limitations, asthma, CHF, Heart
blocks