1. Blood group determination
2. Blood transfusion
3. Blood pressure measurement
4. ECG recording
5. Acute coronary syndrome and troponin test
6. Pulmonary edema
7. Cardiogenic shock
8. Iron-deficiency anemia
9. Vitamin B12 and folate-deficiency anemia
10. Congenital hemolytic anemia
11. Acquired hemolytic anemia
12. Acute leukemia
13. Chronic leukemia
14. Mitral stenosis
15. Mitral regurgitation
16. Aortic stenosis
17. Aortic regurgitation
18. Ulcerative colitis
19. Crohn disease

• 1-4: Basic clinical procedures
• 5-7: Acute cardiology
• 8-13: Hematology
• 14-17: Valvular heart diseases
• 18-19: Ulcerative colitis and Crohn disease

5. Acute Coronary Syndrome (ACS) and Troponin Test

Definition

• ACS is myocardial ischemia caused mainly by acute coronary thrombosis due to plaque rupture or erosion.
• Types:
  1. Unstable angina (UA): ischemic symptoms, no myocardial necrosis, troponin not elevated.
  2. NSTEMI: no persistent ST elevation, troponin rise/fall present.
  3. STEMI: persistent ST-segment elevation or equivalent, with myocardial necrosis.

Laboratory changes in ACS

• Cardiac troponin I or T: most sensitive and specific marker of myocardial injury.
• CK-MB: rises after myocardial necrosis; useful for detecting possible reinfarction because it normalizes earlier than troponin.
• Myoglobin: rises early but has poor cardiac specificity.
• Other supportive tests:
  • CBC: leukocytosis may occur.
  • Blood glucose and HbA1c.
  • Lipid profile.
  • Renal function and electrolytes.
  • Coagulation profile before anticoagulation/intervention.
  • BNP/NT-proBNP: may indicate heart failure and prognosis.

Troponin test

• Suspected ACS or acute myocardial infarction.
• Acute chest pain, dyspnea, syncope, or unexplained shock.
• Suspected myocarditis, pulmonary embolism, severe heart failure, or tachyarrhythmia with possible myocardial injury.
• Risk stratification and prognosis in ACS.

• Cardiac troponin I (cTnI).
• Cardiac troponin T (cTnT).
• High-sensitivity troponin I or T (hs-cTn): preferred assay.

• Venous blood sample is taken.
• Measured by immunoassay, usually automated high-sensitivity assay.
• Test at presentation and repeat serially, commonly at 1-3 hours depending on the local protocol.
• Interpretation requires symptoms, ECG, and a rise and/or fall in troponin values.

• Myocardial injury: troponin above the assay-specific 99th percentile upper reference limit.
• Acute myocardial injury: rise and/or fall of troponin values.
• Myocardial infarction: acute myocardial injury plus evidence of ischemia, such as:
  • Typical ischemic symptoms.
  • New ischemic ECG changes.
  • New pathological Q waves.
  • New regional wall-motion abnormality on imaging.
  • Coronary thrombus on angiography.
• Troponin elevation alone does not always mean MI. It can occur in myocarditis, heart failure, renal failure, pulmonary embolism, sepsis, and tachyarrhythmia.

6. Acute Pulmonary Edema

Definition

• Acute accumulation of fluid in lung interstitium and alveoli.
• Usually due to acute left ventricular failure causing raised pulmonary capillary hydrostatic pressure.

Causes

• Acute myocardial infarction/ACS.
• Hypertensive emergency.
• Acute decompensated left ventricular failure.
• Severe mitral regurgitation.
• Aortic stenosis or aortic regurgitation.
• Tachyarrhythmia or bradyarrhythmia.
• Cardiomyopathy.

• Acute respiratory distress syndrome.
• Renal failure/fluid overload.
• High-altitude pulmonary edema.
• Neurogenic pulmonary edema.
• Sepsis, aspiration, drugs/toxins.

Clinical features and diagnostic signs

• Sudden severe dyspnea, orthopnea, paroxysmal nocturnal dyspnea.
• Anxiety, sweating, cyanosis.
• Cough with pink frothy sputum.
• Tachypnea and tachycardia.
• Fine inspiratory basal crepitations that may spread throughout lungs.
• Hypoxemia and low oxygen saturation.
• S3 gallop may be present.
• Raised JVP and peripheral edema if congestive heart failure is present.
• Chest X-ray:
  • Cardiomegaly in cardiogenic edema.
  • Bilateral perihilar “bat-wing” alveolar shadows.
  • Kerley B lines.
  • Pleural effusions.
• ECG: may show ischemia, infarction, LV hypertrophy, or arrhythmia.
• Echocardiography: assesses LV function, regional wall-motion abnormalities, and valve disease.
• BNP/NT-proBNP may support a cardiac cause.

Immediate treatment

• Sit patient upright with legs dependent.
• ABC approach: monitor BP, pulse, respiratory rate, oxygen saturation, ECG.
• Give oxygen only if hypoxemic; use CPAP/BiPAP if significant respiratory distress and no contraindication.
• IV loop diuretic, for example furosemide, especially with fluid overload.
• IV nitrates if BP is adequate or elevated.
• Treat precipitating cause: ACS, arrhythmia, hypertension, infection, valve lesion, etc.
• If hypotensive/hypoperfused: avoid vasodilators and assess for cardiogenic shock; consider ICU, inotrope/vasopressor support and urgent reperfusion when indicated.

7. Cardiogenic Shock

Definition

• A state of inadequate tissue perfusion due to severe cardiac pump failure.
• Usually presents with hypotension, low cardiac output, and signs of end-organ hypoperfusion.

Common causes

• Acute MI, especially extensive LV infarction: most common cause.
• Mechanical complications of MI:
  • Ventricular septal rupture.
  • Papillary muscle rupture causing acute severe MR.
  • Free-wall rupture with tamponade.
• Severe acute or chronic heart failure/cardiomyopathy.
• Acute myocarditis.
• Severe valvular disease.
• Acute severe arrhythmias.
• Right ventricular infarction.
• Massive pulmonary embolism may cause obstructive shock and can resemble cardiogenic shock.

Diagnostic signs

• Altered mental state, restlessness, confusion.
• Cold, clammy, mottled extremities.
• Oliguria: urine output less than 0.5 mL/kg/hour.
• Weak pulse, narrow pulse pressure.
• Tachycardia, although bradyarrhythmia can occur.
• Hypotension, often systolic BP below 90 mmHg or need for vasopressors.
• Raised JVP, pulmonary edema, basal crackles.
• Cyanosis.

• Raised serum lactate and metabolic acidosis.
• Rising creatinine due to acute kidney injury.
• Elevated liver enzymes due to hypoperfusion.
• Elevated troponin if MI is the cause.

• ECG: identifies MI/ischemia or arrhythmia.
• Echocardiography: urgent test to assess LV/RV function, valve lesion, tamponade, VSD, and papillary muscle rupture.
• Chest X-ray: pulmonary edema.
• Coronary angiography: if ACS is suspected.

Management

• ABC resuscitation and transfer to coronary care/ICU.
• Continuous ECG, oxygen saturation, BP, urine output, and lactate monitoring.
• Oxygen and ventilatory support if needed.
• Careful fluid challenge only if hypovolemia or RV infarction is suspected. Avoid excess fluids in LV failure.
• Norepinephrine is commonly used for severe hypotension.
• Dobutamine may be added when low cardiac output persists with adequate BP.
• Urgent reperfusion with PCI for MI-related shock.
• Urgent surgical/interventional correction for mechanical complications.
• Consider mechanical circulatory support in selected refractory cases.

Valvular Heart Disease Viva

14. Mitral Stenosis (MS)

Definition

• Narrowing of the mitral valve orifice, obstructing blood flow from left atrium to left ventricle during diastole.

Common cause

• Rheumatic heart disease is the commonest cause worldwide.
• Less common: mitral annular calcification, congenital MS, left atrial myxoma mimicking MS.

Auscultatory signs

• Loud S1 in early mobile valve disease. It becomes soft when valve is calcified/immobile.
• Opening snap (OS) shortly after A2.
  • Shorter A2-OS interval suggests more severe stenosis.
• Low-pitched mid-diastolic rumbling murmur at apex.
  • Best heard with bell of stethoscope.
  • Patient in left lateral position.
  • Heard better at end-expiration.
• Presystolic accentuation occurs in sinus rhythm due to atrial contraction.
  • Absent in atrial fibrillation.
• Loud P2 may occur with pulmonary hypertension.

Echocardiographic/ultrasound signs

• Thickened mitral leaflets with commissural fusion.
• Diastolic “doming” of anterior mitral leaflet: hockey-stick appearance.
• Reduced mitral valve area.
  • Severe MS: valve area generally ≤1.5 cm².
• Increased transmitral diastolic pressure gradient on Doppler.
• Left atrial enlargement.
• Spontaneous echo contrast or LA thrombus, especially in atrial fibrillation.
• Pulmonary hypertension and right-sided chamber enlargement in advanced disease.
• Assess coexisting mitral regurgitation and valve morphology before balloon valvotomy.

15. Mitral Regurgitation (MR) / Mitral Insufficiency

Definition

• Backflow of blood from LV to LA during systole due to incomplete mitral valve closure.

Causes

• Mitral valve prolapse/myxomatous degeneration.
• Rheumatic heart disease.
• Infective endocarditis.
• Chordae tendineae rupture.
• Papillary muscle rupture after MI.

• LV dilatation due to dilated cardiomyopathy.
• Ischemic LV remodeling after MI.
• Mitral annular dilatation, including due to atrial fibrillation.

Auscultatory signs

• High-pitched, blowing, pansystolic murmur.
• Best heard at apex with diaphragm.
• Classically radiates to left axilla.
• S1 is soft.
• S3 may occur in severe chronic MR due to LV volume overload.
• Murmur increases with handgrip due to increased afterload.
• Acute severe MR may have a short, soft murmur and severe pulmonary edema.

Echocardiographic/ultrasound signs

• Color Doppler: systolic regurgitant jet from LV to LA.
• Identify mechanism: prolapse, flail leaflet, vegetations, restricted leaflet motion, annular dilation.
• Enlarged LA and LV in chronic significant MR.
• LV systolic function and dimensions must be assessed.
• Quantify severity using integrated Doppler measures:
  • Vena contracta.
  • Effective regurgitant orifice area.
  • Regurgitant volume/fraction.
  • Pulmonary vein systolic flow reversal suggests severe MR.
• TEE is useful when valve anatomy is unclear or repair/intervention is planned.

16. Aortic Stenosis (AS)

Definition

• Obstruction to LV outflow due to narrowing of the aortic valve.

Causes

• Degenerative calcific AS: common in older adults.
• Bicuspid aortic valve: common in younger adults.
• Rheumatic heart disease.

Classical symptoms

• Angina
• Syncope on exertion
• Dyspnea/heart failure
• Mnemonic: SAD - Syncope, Angina, Dyspnea.

Auscultatory signs

• Harsh, ejection systolic crescendo-decrescendo murmur.
• Best heard in right second intercostal space, aortic area.
• Radiates to carotid arteries.
• Slow-rising, low-volume carotid pulse: pulsus parvus et tardus.
• Narrow pulse pressure.
• Soft or absent A2 in severe AS.
• Ejection click may occur in bicuspid valve disease.
• Sustained/heaving apical impulse due to LV hypertrophy.
• Murmur increases after a long diastolic filling interval and decreases with Valsalva.

Echocardiographic/ultrasound signs

• Calcified, thickened aortic valve with restricted leaflet opening.
• Doppler demonstrates increased transaortic velocity and pressure gradient.
• Severe AS generally:
  • Peak aortic jet velocity ≥4 m/s.
  • Mean transvalvular gradient ≥40 mmHg.
  • Aortic valve area ≤1.0 cm².
• Concentric LV hypertrophy.
• Assess LVEF and stroke volume.
• Low-flow, low-gradient AS may require dobutamine stress echo or CT calcium scoring for assessment.

17. Aortic Regurgitation (AR) / Aortic Insufficiency

Definition

• Backflow of blood from aorta to LV during diastole due to inadequate aortic valve closure.

Causes

• Bicuspid aortic valve.
• Rheumatic heart disease.
• Infective endocarditis.
• Trauma.

• Aortic root dilatation due to hypertension.
• Marfan syndrome and other connective-tissue disorders.
• Aortic dissection.
• Syphilitic aortitis.
• Ankylosing spondylitis.

Auscultatory signs

• High-pitched, blowing, early diastolic decrescendo murmur.
• Best heard at left sternal border, usually third or fourth intercostal space.
• Patient should sit forward, fully expire, and hold breath.
• Murmur may be louder with handgrip.
• Wide pulse pressure.
• Bounding/collapsing pulse: water-hammer pulse.
• Hyperdynamic, displaced apical impulse in chronic severe AR.
• Austin Flint murmur: low-pitched mid-diastolic apical murmur in severe AR, caused by regurgitant jet interfering with mitral inflow.

Echocardiographic/ultrasound signs

• Color Doppler: diastolic regurgitant jet from aorta into LV.
• Assess aortic valve leaflet morphology and aortic root/ascending aorta.
• Severe AR features include:
  • Large vena contracta.
  • Holodiastolic flow reversal in descending aorta.
  • Large regurgitant volume/fraction.
• Chronic severe AR causes LV dilatation and eccentric hypertrophy.
• Assess LV systolic function and serial LV dimensions.
• Acute severe AR may show normal-sized LV with severe pulmonary edema and early mitral valve closure.

One-line murmur comparison

• MS: diastolic rumble + opening snap at apex.
• MR: pansystolic blowing murmur at apex radiating to axilla.
• AS: ejection systolic murmur at aortic area radiating to carotids.
• AR: early diastolic blowing decrescendo murmur at left sternal border.