CVS L3: CAD Flashcards
Coronary Perfusion in Right coronary dominant individuals
LAD artery supplies:
- Anterior free wall of LV
- Anterior & major part of septum
- Apex
LCX artery supplies:
- Most of lateral free wall of LV
RCA supplies:
- Right ventricle
- Large part of Inferior wall
- Posterior wall of LV
- Posterior & minor part of septum
- SA node, AV node
In Left coronary dominant individuals, coronary perfusion is
The LCX supplies:
- Major part of Inferior wall
- Posterior wall of LV
- Apex
The remaining perfusion is same as that in RCA dominance
Location of lesion (ischemia/MI) by observing changes in 12 lead ECG:
- Inferior (diaphragmatic) wall: Lead II, III & aVF
- Anterior wall/Anteroseptal: V1-V4
- Lateral wall: Lead I, aVL, V5, V6
- Right Ventricle: V1, V2 & sometimes V3
- Septal wall : V1, V2
Prinzmetal’s or Variant Angina: clues to diagnosis
- A form of acute coronary syndrome caused by coronary spasm
- Patients are usually younger, female, smokers, and without other significant risk factors for coronary artery disease
- Transient ST-segment elevation during chest pain
- Intermittent chest pain: often repetitive; usually at rest; typically in the early morning hours & rapidly relieved by nitroglycerine
- Patients often have manifestations of other vasospastic disorders such as migraine headaches and Raynaud’s phenomenon
- Most attacks resolve without progression to MI
- Angiography shows no obstructions in vessels at rest.
Clinical presentations of CAD include:
- Silent ischemia
- Angina pectoris
- Acute coronary syndromes –
- unstable angina and acute Mi
- Sudden cardiac death
Patient 01 DDx
A 64-year-old man is brought to ER with nausea, dyspnea and a crushing substernal chest pain. The pain has lasted for about 30 min, radiates to left arm and jaw, not
relieved by rest. Personal history reveals a sedentary lifestyle, moderate hypercholesterolemia, obesity, diabetes and smoking.
Physical Examination: BP 100/60 mmHg; rapid low volume pulse; diaphoresis; Bibasilar rales on chest auscultation. Laboratory findings:
EKG - shows elevation of ST segment with prominent
Q waves and inverted T waves
Blood biomarkers: Elevated CK-MB; elevated troponin T & I Blood count: Mild leukocytosis
Chest X ray: Bilateral mild pulm edema without pleural disease or widening of the mediastinum
Most likely diagnosis in patient 01: Acute Myocardial Infarction
Other differential diagnosis:
- Gastroesophageal reflux disease
- Myocarditis
- Pneumothorax
- Pulmonary embolism
- Acute pancreatitis
- Anxiety
Patient 02 DDx
54-year-old chronic smoker complains of pain in the calf muscles by an half mile walk associated with coldness and numbness in both the legs since a year. The symptoms are relieved by rest. Patient also gives history of sexual dysfunction. Patient has a strong family history of hypercholesterolemia.
PE: BP 160/100 mm Hg; Low volume peripheral pulses in both lower limbs; Loss of hair on dorsum of
feet; Atrophy of calf muscles; Bruits on femoral artery.
Lab: Elevated LDL and decreased HDL; elevated total serum cholesterol
Angiogram: Narrowing of arterial lumens at multiple sites in the aortoiliac region
Plain X ray: Irregular arterial calcifications in abdominal aorta and iliac arteries
- Atherosclerosis
- Diabetic neuropathy
- Vasculitis
- Collagen vascular disease
The most likely diagnosis:
Atherosclerosis
Arterial biopsy: Fibrofatty plaque formation with dystrophic calcification, atheroma. Fibrous cap by smooth muscles and collagen with necrotic lipid core and fibrous plaque
Sites of severe atherosclerosis in order of frequency:
- Abdominal aorta & iliac arteries
- Proximal coronary arteries
- Thoracic aorta, femoral and popliteal arteries
- Internal carotid arteries
- Vertebral, basilar and middle cerebral arteries
Pathogenesis of atherosclerosis
2 forms of foam cells:
- macrophage-induced foam cell formation
- Cytokines released by macrophages activate smooth cells -> release foam cells
- The plaques with defective or broken caps are most prone to rupture
- The lesions alone may distort vessels & obstruct the flow
- Ulceration and rupture of plaques trigger the formation of thrombi that obstruct flow
Pathways for metabolism of ingested lipids
- Dietary cholesterol and triglycerides (TGs) enter circulation in the form of chylomicrons
- Under the influence of lipoprotein lipase, chylomicrons release TGs to fat depots and muscles, and the resulting chylomicron remnants are taken up by the liver
- The liver synthesizes cholesterol and packages it (along with TGs) with specific proteins to form very low-density lipoproteins (VLDL)
- VLDL enter the circulation and donate TGs to tissues under the influence of lipoprotein lipase
- VLDL become cholesterol-rich intermediate-density lipoproteins (IDL) and low-density lipoproteins (LDL) when it loses TGs in tissues
- The LDL supply cholesterol to the tissues for production of cell membranes and the cholesterol as precursor for all steroid hormones
- LDL are taken up by peripheral tissues as well as liver
- The oxidized LDL are taken up by macrophages and smooth muscle cells in atherosclerotic lesions
- Liver releases high density lipoproteins (at this stage called, nascent HDL) into circulation
- HDL takes up cholesterol from peripheral cells and transport it to the liver where it is metabolized, keeping plasma and tissue cholesterol low
Coronary Perfusion during different phases of the cardiac cycle
Coronary blood flow is maximum during ventricular diastole and least during isovolumetric contraction
- 2 & 3: Ventricular systole
- 1 & 4: Ventricular diastole
- 2: Isovolumetric vent. contraction 3: Ventricular ejection
- 4: Isovolumetric vent. relaxation 1: Ventricular filling
Pathophys of CAD
- Atherosclerosis of large coronary arteries is the predominant cause of angina and myocardial infarction
- Most common sites: In areas exposed to increased shear stresses such as bending points and bifurcations
- Fissuring of the atherosclerotic plaque can lead to platelet accumulation and transient episodes of thrombotic occlusion, usually lasting 10–20 min (in unstable angina)
- Platelet release of vasoconstrictor factors such as thromboxane A2 or serotonin can cause vasoconstriction and contribute to decreased flow
Within 60 sec after coronary artery occlusion
↓
Myocardial oxygen tension in the affected cells falls to zero
↓
Rapid shift to anaerobic metabolism in myocytes
↓
Lactic acid production
↓
Dysfunction in myocardial contraction and relaxation.
If perfusion is not restored within 40–60 min, an irreversible stage of injury occurs
Irreversible stage of CAD-induced injury
Possible causes:
- Severe ATP depletion
- Increased extracellular calcium concentrations -Lactic acidosis
- Free radicals
Cellular features:
- Diffuse mitochondrial swelling
- Damage to the cell membrane
- Marked depletion of glycogen
Clinical Manifestations of CAD:
- Chest Pain
- Shortness of breath
- S4
- Shock
- Tachycardia or Bradycardia
- Nausea and Vomiting
Chest Pain:
- Angina pectoris
- Acute coronary syndrome
- Chest pain is mediated by sympathetic afferent fibers – T1-T5
- In the spinal cord, the pain impulses probably converge with impulses from other somatic structures and hence radiated to the chest wall, back, and arm
- The actual trigger for nerve stimulation is adenosine. Blocking adenosine receptor (P1) with aminophylline leads to reduced anginal pain
Ischemia without pain may be due to:
i) Autonomic dysfunction of afferent nerves Examples: Patients with peripheral neuropathy or transplanted heart
ii) Transient reduced perfusion
iii) Differing pain thresholds
ECG in angina:
ECG changes during an attack:
- T wave discordant to the QRS complex
- ST-segment depression
- Decreased R-wave height
The ECG between attacks:
- At rest is normal (30%)
- In the remaining 70%, the ECG shows evidence of previous infarction, or hypertrophy
- Depression of ST segment; T wave inversion
ECG changes in STEMI
- Elevation of ST segment; pathologic Q wave
- B. During acute stage of MI: Marked ST elevation
- C. After a few hours of MI: Pathologic Q waves, less ST elevation and inverted T wave
- D. After many days of MI: Pathologic Q wave alone persists indicating old infarct
- Acute lateral wall infarction (tracing obtained within a few hours of onset of illness)
- striking hyperacute ST-segment elevation in leads I, aVL, V5, and V6 and reciprocal depression in other leads.
- Artery most likely affected is : LCX artery
- Acute Septal wall Infarction
- Note the striking ECG changes in V2
- The artery most likely affected is: LAD artery
- Acute Anteroseptal Infarction
- ECG changes in V1, V2, V3 & V4
- Arteries involved: RCA and LAD artery
Diagnosis of underlying disorders or complications following Acute MI by certain physical findings
