Question

A 58 y/o female visits the Health center due to palpitations.

Medical background:

• H/O myocardial infarction in the past and with left ventricular failure, on the following medication:

o Valsartan 80 mg OD

o Furosemide 40 mg OD

o Spironolactone 25 mg OD

o Isosorbide dinitrate PRN

• History of Dyslipidemia since 10 yrs, on

o Atorvastatin 10 mg OD

• Non- Diabetic

History of present illness:

Present condition started few weeks now with palpitations associated with some giddiness, no associated chest pains, cold sweating nor malaise/fever.

Pertinent On Examination:

BP 105/70mmhg​PR 96/min​RR 21/min​Temp: 36.7 C

No anemia

Cardiac: mild tachycardia, irregular rhythm, no murmur

Lungs: Bibasilar crepitation

No edema

ECHO done Ejection fraction 45% with LA and LV, no clots seen

ECG: atrial fibrillation

IMPRESSION:

IHD (ischemic heart disease), CHF(congestive heart failure) , atrial fibrillation w/ normal ventricular respond

INVESTIGATIONS:

a. CBC/LFT/RFT/TFT/CRP/Lipids/Trop I/CKMB if needed

b. Chest XRAY

c. Echo after 6 months to 1 year

Discharge with additional meds:

1. Digoxin 0.25 mg,1 tab OD

2. Aspirin 81 OD

QUESTIONS

1. Explain the pathophysiology process of Myocardial Infraction?

2. Explain how the signs and symptoms of Myocardial Infraction develops.

3. What is the clinical significance of doing cardiac enzymes for the patient with MI?

4. List at least two complications of MI and explain how they develop?

Answer 1

1.PATHOPHYSIOLOGY OF MYOCARDIAL INFARCTION

Myocardial infarction or heart attack is defined as the irreversible damage of the myocaridal tissue,mainly due prolonged ischemia and hypoxia.It can occur during the following conditions:

• Gradual obstruction of a blood vessel due to atherosclerosis
• Sudden reversible obstruction due to a coronary artery spasm
• Occlusion due to rupture of an atherosclerotc plaque and consequent thrombus formation

The end result is the imbalnce of myocardial oxygen supply and demand,leading to ischemia and hypoxia.If this imbalance persists for long,a cascade of cellular,inflammatory and biochemical events will be initiated.It initially presents as angina or chest pain and then progresses to mycardial tissue necrosis.Death of the tissue occurs due to the inability to produce ATP.Damaged tissues will be composed of a necrotic core which is surrounded by a border zone that can either become reversibly damaged or recovered.

The size of the infarction depends mainly on:

1. duration of coronary obstruction
2. magnitude of residual collateral blood flow which can restore the ischemic area
3. size of the ischemic area at risk

2.SIGNS AND SYMPTOMS OF MYOCARDIAL INFARCTION AND ITS MECHANISM

i)CHEST PAIN

• It is the most common symptom
• Described as a sensation of pressure,tightness,burning and squeezing in the chest.
• Radiating pain:spreads to left arm,lower jaw,neck ,back,right arm and upper abdomen
• Pain lasts for more than 20 minutes

HOW IT DEVELOPS:Decrease or cessation of blood flow leads to excitation of chemosensitive and mechanosensitive receptors in heart,leading to release of chemicals like adenosine,bradykinin and others.The action of these agents on the sensory ends of sympathetic and vagal afferent nerves causes pain sensation.

ii)ASSOCIATED SYMPTOMS

• Nausea or vomiting

HOW IT DEVELOPS:as a reflex from severe pain, release of lactic acid and other metabolites from the cardiomyocytes in the area of ischemia initiate vasovagal reflexes to cause vomiting

• Light-headedness and loss of consiousness

HOW IT DEVELOPS:due to inadequate blood supply to brain and cardiogenic shock.

• Dypnoea (or shortness of breath)

HOW IT DEVELOPS:due to pulmonary edema caused by limitation of the output of left ventrilcle and the resuting left ventricular failure.

• Diaphoresis(or excessive sweating)
• Weakness and fatigue
• Palpitations
• Abnormalities in heart rate and rythm

HOW IT DEVELOPS:due to massive release of catecholamines,which activate the sympathetic nervous system