ANGINA PECTORIS

→ cranial syndrome usually characterized by episodes of

paroxysm of the pain or pressure in the anterior chest.
→ cause is insufficient coronary blood flow that results in low
oxygen supply.
Pathophysiology
→ most common cause of angina pectoris is
atherosclerotic disease.

→ associated with significant obstruction of a major

coronary artery.
Precipitating Factors
physical exertion
exposure to cold
eating heavy meal
stress or emotion provoking situation
Clinical Manifestations
Chest pain
→ poorly localized
→ may radiate to neck, jaw, shoulders & inner aspects of the
upper arms
→ retrosterna
Types
stable angina → predictable & consistent pain that occurs on exertion
& relieved by rest.
unstable angina/ preinfarction angina/ crescendo angina →
symptoms occurs frequently, last longer pin. The threshold for pain
is lower & pain occur at rest.
intractable/ refractory angina → severe incapacitating chest pain.
variant angina → pain at rest. ST segmentation elevation – caused of
vasospasm.
silent ischemia/ obstructive ischemia → no symptoms
Medical Management
objective:
• decrease oxygen demand & increase oxygen
supply
nitroglycerin → remain the mainstay for treatment of angina to
decrease myocardial oxygen consumption w/c decrease ischemia &
pain.

→ vasodilators (especially in high dose)

→ administered to decrease cardial oxygen consumption w/c decrease

ischemia & pain.

→ Decrease pre & afterload

sublingual/ spray → alleviates the pain after 3mins.

Reminders
Nitroglycerin effect → hypotension
If the symptoms is free, nitroglycerin is switched to topical preparation
Mouth should be moist
Saliva is not swallowed until the nitroglycerin is dissolved
If severe, patient crush the tablet between the teeth to
hasten the absorption
Topical
IV → given if there is recurring symptoms of ischemia
→ for unstable angina
Beta-adrenergic blocking agents
Propanolol, Metaprolol, Atenolol
→ blocks the beta-adrenergic sympathetic stimulation to the
heart.
→ this help to control chest pain & delays the onset of
ischemia during work exercise.
→ produce the cardiac mortality, recurrent angina,
infarction.
Side effects:
hypotension
bradycardia
advance atrioventricular block
decompensated failure
hyperlipidemia
decreased libido
hypoglycemia
→ if given intravenously for an acute
cardiac event
∙ ECG, BP ,HR monitored
Caution: not to stop abruptly
decrease gradual over several days
Mode of Action
→ ↓ conduction → ↓HR & ↓ heart contraction → ↓ workload
→ relax blood vessels → ↓ BP → ↑ coronary perfusion
→ dilating the coronary arteries
→ most commonly drug use are Amlodipine, verapamil, Diltiazem
use of Nifidepine was found poorly tolerated % to increase the risk of
MI in patient w/ hypertension & the risk of death in patient with ACS
first generation calcium channel blockers should take w/ caution
especially patient w/ HF → Amlodopine & Felodipine
Antiplatelet & Anticoagulant
Medications
Aspirin
→ prevents platelet activation & reduces the incidence of MI & death in
patients w/ CAD. 160-325mg Dose of aspirin should be given to the
patient w/ angina & then 81-325mg/day
→ causes intestinal upset & bleeding, treatment for helicobacter pylori
& use of H2-blockers (Cimetidine, Famotidine, Ranitidine,
Misoprostol) should be considered to allow continued aspirin.
Clopidogrel & Ticlodipine
→ given if the patient is allergic to aspirin
→ take few days to achieve their antiplatelet effect
→ given with aspirin in patient w/ high risk for MI &
GI upset, N&V, diarrhea & ↓ neutrophil level.
Heparin
→ prevents the blood clots
→ use alone in treating patients w/ unstable angina, reduces the
occurrence of angina
→ if cardiac event → patient is hospitalized & IV bolus of heparin &
continuous infusion / IV bolus every 4-6hrs
→ Heparin is given in base on result of activated partial thromboplastin
time (aPTT)
→ Heparin is therapeutic when the aPTT is 1.5-2 times the normal aPTT
→ SC- injection of LMWH Enoxoparin or Dalteparin to treat unstable
angina
Elevation MI
→ more stable & effective anticoagulation
→ because Heparin & LMWH ↑ the risk of bleeding
(IRE) so monitor the patient BP, ↑HR, ↓ serum
hemoglobin & hematocrit levels
→ Heparin-induced thrombocytopenia → an
antibody-mediated reaction to heparin that may
result to thrombosis
GPIIb/IIIa Agents
→ IV agents ABCIXIMAB, TIROFIBAN, EFTIFIBATIDE
→ prevent platelet aggregation by blocking GIIb/IIIa
receptor on the platelet
Oxygen Administration
→ initiated at the onset o chest pain in attempt to
increase the amount of oxygen delivered to the
myocardium & to ↓ pain.
MYOCARDIAL INFARCTION
→ necrosis
→ myocardial cells in the heart are permanently
destroyed
→ like angina, MI is usually caused by reduced blood
flow in coronary artery due to atherosclerosis &
occlusion of embolus/thrombus
→ acute coronay syndrome (ACS) term for the
diagnose
Causes:
Vasospasm
↓ Oxygen Supply
Pathophysiology
→The area of infarction takes time to develop as the cells
deprived of oxygen
 ↓
Ischemia Develops
↓
Cellular Injury
↓
Lack of Oxygen
↓
Infarction
Clinical Manifestations
Chest pain occurs and continues despite rest and
medication is presenting symptoms.
Shortness of breath ↓ 55 age.
Assessment and Diagnostic Findings
Patient’s History
2 parts
→ Presenting Symptoms
→ Previous illness and family history
Electrocardiogram
→ The classic ECG changes are T- wave inversion, ST
segment elevation and development of Q- wave.
→The first ECG signs of an acute M.I are from
myocardial injury & ischemia.
Injury
↓
→ Causes T-wave to become enlarge and Symmetric.
altered and delayed, causing
→ Causes also to ST-segment changes.
→ Injured Myocardial cells depolarize normal
but repolarization is more rapidly than normal cells,
causing the ST-segment rises to 1 mm above the isoelectric line.
→ If the Myocardial Injury is n the Endocardial tissue the ST-segment
is usually horizontal or downward slope.

Ischemia
↓
Myocardial repolarization is altered & delayed
causing T-wave to invert
 M.I is classified as Q-wave or Non Q-wave
Infarction
Q-wave
↓
Develops 1-3 days
→ Because there is no Deporalization
Current conducted from necrotic tissue.
→ Abnormal Q-wave is 0.04c op longer 25% of R-wave.
Non Q-wave Infarction
↓
Do not develop a Q-wave on the ECG after ST-Segment and
T-wave changes.

→ During Recovery to M.I, ST- segment is the first to

return normal (1-6 weeks) T-wave become large
symmetric for 24 hours, and it then inverts within
1-3 days for 1-2 weeks.
→ Q-wave alteration
Echocardiogram
→ Can detect hypokinetic and akinetic wall motion
and can determine the ejection fraction.
Laboratory Test
Creatinine kinase and its isoenzymes
3 CKI
CK-MM (Skeletal Muscle)
CK-BB (Brain Tissue)
CK-MB (Heart Muscle)
Specific Cardial specimen Isoenzymes
Found mainly in Cardiac cells and therefore rises only when
there is damage cells.
→ The level starts to ↑ 4-8 hours, peaks 24-36 hours that will
last for 1-3 days.
Myoglobin
→ It is a Heme protein that helps transport Oxygen.
→ Found in Cardiac and Skeletal Muscle starts to ↑ 1-
3 and peaks within 12 hours.
After Onset of Surgery
→ ↑ in myoglobin; not specific acute Cardiac event.
→ ↓ (-) ruling out M.I

Troponin, a found in the myocardium, regulates the

myocardial contractile process.
→ 3 Isomers ( C, I and T)
→ Use more frequently
→ 3-4 peaks 4-24 last from 1-3 weeks
Medical Management
Goal:
Minimize myocardial damage
Preserve myocardial function
Prevent complications
Pharmacological Therapy
Thrombolytics
→ IV given
→ To dissolve and lyse the thrombus in a coronary artery
allowing reperfusion.
→ Administration
20 minutes unrelieved by Nitroglycerin
→ Administer after the onset of symptom
→ Not given to unstable Angina
→ Door-to-needle time → administer within 30 minutes from
the time the patients arrive in the emergency department.

Streptokinase
→ Increase the amount of plasminogen Activator,
which then increase the amount of circulating and
clot- bound plasmin.
→ Vasculitis occurred up to 9 days after
administration.
Alteplase
→ Tissue Plasminogen avtivator, ( t- PA)
→ Activates the plasminogen on the clot more.
→ Heparin with ( t- PA)