ANGINA PECTORIS

Angina Pectoris is clinically syndrome usually characterized by episodes or paroxysms of pain or

pressure in the anterior chest.
The cause is insufficient coronary blood flow, resulting in a decreased oxygen supply when there
is increased myocardial demand for oxygen.
ASSESSMENT AND DIAGNOSTIC FINDINGS
ECG may show changes indicative of ischemia such as T-wave inversion
Nuclear scan or invasive procedure (eg, cardiac catherization, coronary angiography).
ST depression
MEDICAL MANAGEMENT
The objectives of the medical management of angina are to decrease the oxygen demand of
the myocardium and to increase the oxygen supply.
Percutaneous transluminal coronary angioplasty (PTCA)
*Balloon-tipped catheter is used to open blocked coronary vessels and resolve ischemia.
The purpose of PTCA is to improve blood flow within the coronary artery by compressing and
Cracking the atheroma.
Intracoronary stents
*A stents is a metal mesh that provides structural support to vessel at risk of acute
closure.

CABG (Coronary Artery Bypass Graft)

*surgical procedure in which a blood vessel is grafted to an occluded artery so that
blood can flow beyond the occlusion.

PHARMACOLOGIC MANAGEMENT
Nitroglycerine cause dilation of the veins the result is venous pooling of blood throughout the body. As
result, less blood retuns to the heart, decreasing the cardiac workload.
Facts about nitroglycerine
Can be given

Sublingual tablet
Stray
topical agent
intravenous IV administration
MEDICATIONS TO USED TO TREAT ANGINA
NITRATES
NITROGLYCERIN (NITROSTAT, NITROBID) SHORT TERM AND LONG TERM OF MYOCARDIAL OXYGEN
CONSUMPTION THROUGH SELECTIVE VOSODILATION
Beta adnergic blocking agent (bet blockers)
Notoprolol (Lopressor,toprol)
Reduction of myocardial oxygen consumption by blocking beta adrenergic
Atenolol (Tenormin) stimulation of the heart
Cacium Iron Antagonist (calcium channel blockers)
Amlodipine (Norvasc) negative inotropic effects indicated in patients not responsive to bet blockers.
Ditiazem (Cardizine. Tiaza) used as primary treatment for vasospasm
Felodipine (plendil)
ANTI PLATELET MEDICATIONS
Aspirin prevention of platelet aggregation
Clopidogrel (Plavix)
Glycoprotein ilb/lla agents
Abviximab (Reopro)
Tirofiban (aggrastat)
Eptifibapide (integrelin)
ANTICOAGLANTS
Heparin (unfractionated) prevention of thrombus formation
Low molecular weight heparins
Enoxaparin (lovenox)
Dalteparin (fragmin)
MYOCARDIAL INFARCTION
In an MI, a area of the myocardium is permanently destroyed, typically because plaque rupture and
subsequent thrombus formation result in complete occlusion of the artery.
The ECG usually identifies the tight and location of the MI, another ECG indicators such as a P wave in
patient history identify the timing. Regardless of the location, the goals of medical therapy are to
prevent or minimize myocardial tissue dead and prevent complications.

RISK FACTORS
NON MODIFIABLE RISK FACTOR
Age- average age of a person having a first heart attack is 65.8 years (male) and 70.4 years (female)
Family history
Ethnic background African Americans has higher risk for developing MI
MODIFIABLE RISK FACTOR
Hypertension
Smoking
Hyperlipidimia
Obesity
Impaired glucose tolerance (DM)
Physical inactivity
Stress
ASSESSEMENT
Substantial chest pain
The pain associated with an MI usually lasts longer than 30 minutes
Radiating to the left arm, back or jaw
Occurring without a cause usually in the morning
Relieved only by opioids assocated nausea, diaphoresis, dyspnea, fear and anxiety, palpitations, fatigue,
shortness of breath.
Decrease left ventricular function
Decrease cardiac output
Cardiovascular system compensate by increasing heart rate (frank sterling law)
ECG and cardiac enzymes assessments
T wave inversion
ST segment elevation
Abdominal P wave
Elevated CKMB assessed by mass assay is an indicator of acute MI
An increase in the level of troponin in the serum can be detected within a few hours during acute MI
Enzymes that indicate Myocardial infarction
ENZYME
TIME OF ELEVATION
MYOGLOBIN
First 1-3 hours
TROPONIN I

2-4 hours

AST (ASPARTETE AMINO

TRANSFERASE)
CK-MB

8 hours

DESCRIPTION
First enzyme to elevate due to
decreased oxygenation
Released at the mentioned time
frame
Is also used for liver damage

24 hours

Cardiac-specific isoenzyme; it is

LDH (LACTIC DEHYDOGENASE)

72 hours

found mainly in cardiac cells and

therefore increases only when
there has been damage to these
cells.
Reflects tissue breakdown and
hemolysis

MEDICAL MANAGEMENT
The goals of medical management are to minimize myocardial damage, preserve myocardial function,
and prevent complications this can be achieved by:
Reperfusing the area with the emergency use of thrombolytic medications
Reducing myocardial oxygen demand and increasing oxygen supply with medication, oxygen
administraton and bed rest.
PHARMACOLOGIC THERAPY
Analgesic of choice: Morphine I.V
(ACE) inhibitors decreases blood pressure thus decreasing the workload of the heart
Thrombolytics dissolved (ie, lyse) the thrombus in a coronary artery (thrombolysis) allowing
blood to flow through the coronary artery again.