• Start with a crisp definition
• Use standard exam headings and subheadings
• Give classifications in tables or flowcharts where useful
• Include etiopathogenesis, clinical features, investigations, complications, and management in sequence
• Mention important diagnostic criteria, drug doses, and emergency steps when relevant
• Add differentiating points, viva pearls, and common examiner-favourite facts
• Write in a format suitable for 5-mark, 10-mark, or long-answer questions
• Include mnemonics only when they genuinely help recall
• Keep terminology aligned with standard undergraduate medicine texts and current guidance where applicable

1. Definition and universal diagnostic criteria
2. Etiology, risk factors, and pathogenesis
3. STEMI versus NSTEMI
4. Clinical features and examination
5. ECG localization and evolution
6. Cardiac biomarkers and other investigations
7. Immediate treatment and reperfusion strategy
8. Complications with time course and management
9. Secondary prevention and discharge advice

• Start with a crisp definition
• Use standard exam headings and subheadings
• Give classifications in tables or flowcharts where useful
• Include etiopathogenesis, clinical features, investigations, complications, and management in sequence
• Mention important diagnostic criteria, drug doses, and emergency steps when relevant
• Add differentiating points, viva pearls, and common examiner-favourite facts
• Write in a format suitable for 5-mark, 10-mark, or long-answer questions
• Include mnemonics only when they genuinely help recall
• Keep terminology aligned with standard undergraduate medicine texts and current guidance where applicable

1. Definition and universal diagnostic criteria
2. Etiology, risk factors, and pathogenesis
3. STEMI versus NSTEMI
4. Clinical features and examination
5. ECG localization and evolution
6. Cardiac biomarkers and other investigations
7. Immediate treatment and reperfusion strategy
8. Complications with time course and management
9. Secondary prevention and discharge advice

Definition

• Ischemic symptoms
• New ischemic ECG changes
• Development of pathological Q waves
• New regional wall-motion abnormality or loss of viable myocardium on imaging
• Coronary thrombus on angiography/autopsy

Classification

1. According to ECG

2. Universal definition of MI

Etiology and Risk Factors

Usual mechanism

1. Platelet adhesion and activation
2. Platelet aggregation
3. Activation of coagulation cascade
4. Formation of occlusive coronary thrombus
5. Myocardial ischemia and necrosis

Non-modifiable risk factors

• Increasing age
• Male sex, or postmenopausal woman
• Family history of premature CAD
• Genetic predisposition

Modifiable risk factors

• Smoking
• Diabetes mellitus
• Hypertension
• Dyslipidemia
• Obesity and sedentary lifestyle
• Unhealthy diet
• Psychosocial stress
• Cocaine/amphetamine use

Less common causes

• Coronary vasospasm, for example cocaine-induced
• Coronary embolism
• Spontaneous coronary artery dissection
• Coronary arteritis/vasculitis
• Severe anemia, shock, hypoxemia, sepsis, tachyarrhythmia: Type 2 MI

Pathogenesis

Sequence

• ATP depletion begins within seconds.
• Loss of contractility occurs within about 1 minute.
• Irreversible myocyte injury begins after approximately 20-30 minutes of severe ischemia.
• Necrosis progresses from subendocardium to subepicardium over several hours: the wavefront phenomenon.
• Early reperfusion salvages ischemic but viable myocardium: “Time is muscle.”

Coronary artery commonly involved

Clinical Features

Symptoms

Typical presentation

• Severe central/retrosternal constricting or crushing chest pain
• Lasts >20 minutes
• May radiate to left shoulder, left arm, neck, jaw, epigastrium, interscapular area
• Not completely relieved by rest or sublingual nitrate
• Sweating, anxiety, restlessness, sense of impending doom
• Dyspnea
• Palpitations
• Nausea and vomiting, especially in inferior-wall MI
• Syncope, especially with arrhythmia or cardiogenic shock

Atypical or silent MI

• Elderly patients
• Women
• Diabetes mellitus
• Chronic kidney disease

• Dyspnea
• Syncope
• Acute pulmonary edema
• Unexplained weakness
• Epigastric discomfort
• Confusion
• Sudden collapse

Signs

• Pallor, sweating, cold clammy extremities
• Tachycardia or bradycardia
• Hypotension
• Raised JVP in right ventricular infarction
• S4 gallop: reduced LV compliance
• S3 gallop: LV failure
• Basal crepitations/pulmonary edema
• New pansystolic murmur:
  • Acute MR due to papillary muscle rupture
  • VSD due to interventricular septal rupture
• Pericardial rub in acute pericarditis

Diagnosis

1. ECG - obtain within 10 minutes of first medical contact

STEMI criteria

• Generally ≥1 mm in all leads other than V2-V3
• In V2-V3, higher cutoffs apply:
  • Men ≥40 years: ≥2 mm
  • Men <40 years: ≥2.5 mm
  • Women: ≥1.5 mm

ECG localization

Evolution of ECG changes

1. Hyperacute tall T waves
2. ST elevation
3. Development of pathological Q waves
4. T-wave inversion
5. ST segment returns to baseline over days
6. Q waves may persist permanently

2. Cardiac biomarkers

Important point

3. Other investigations

• Serial ECGs
• CBC: anemia, leukocytosis
• Blood glucose and HbA1c
• Renal function and electrolytes
• Lipid profile, preferably within 24 hours
• Coagulation profile
• Chest X-ray: pulmonary edema, exclude other causes
• Echocardiography:
  • Regional wall-motion abnormality
  • LV function/ejection fraction
  • Mechanical complications
  • LV thrombus
• Coronary angiography: defines culprit vessel and permits PCI

Management

Initial emergency management

Immediate steps

1. Admit to coronary care unit.
2. ABC approach.
3. Cardiac monitor and defibrillator readiness.
4. Two IV lines.
5. Obtain 12-lead ECG within 10 minutes.
6. Measure troponin, but do not delay reperfusion in clear STEMI.
7. Assess hemodynamic status and complications.

Immediate medications

Avoid/withhold nitrates if

• Systolic BP <90 mmHg
• Suspected right ventricular infarction
• Severe aortic stenosis
• Recent phosphodiesterase-5 inhibitor use:
  • Sildenafil/vardenafil within 24 h
  • Tadalafil within 48 h

Reperfusion Therapy in STEMI

Primary PCI - preferred reperfusion method

Indications

• STEMI within 12 hours of symptom onset
• Ongoing ischemia, shock, severe heart failure, or life-threatening arrhythmia even if presentation is late
• Contraindication to fibrinolysis

Advantages

• Higher rate of patency of infarct artery
• Lower risk of intracranial hemorrhage
• Can identify anatomy and treat culprit lesion
• Useful in cardiogenic shock and after failed thrombolysis

Fibrinolysis

• STEMI within 12 hours of onset, and
• Primary PCI cannot be performed within 120 minutes, and
• No contraindication exists.

Drugs

• Tenecteplase
• Alteplase
• Reteplase
• Streptokinase, where other agents are unavailable

Absolute contraindications to fibrinolysis

• Previous intracranial hemorrhage
• Known intracranial vascular lesion
• Known malignant intracranial tumor
• Ischemic stroke within previous 3 months
• Suspected aortic dissection
• Active bleeding/bleeding diathesis
• Significant closed head/facial trauma within 3 months
• Recent intracranial/intraspinal surgery

Signs of successful thrombolysis

• Relief of chest pain

• 50% reduction in ST elevation at 60-90 minutes

• Reperfusion arrhythmias, especially accelerated idioventricular rhythm
• Early peak of cardiac enzymes

Failed fibrinolysis

NSTEMI Management

• Aspirin + P2Y12 inhibitor
• Anticoagulation
• High-intensity statin
• Anti-ischemic treatment
• Risk stratification using GRACE score
• Early invasive coronary angiography in high-risk patients

Immediate invasive strategy

• Hemodynamic instability/cardiogenic shock
• Recurrent or refractory chest pain
• Life-threatening arrhythmia or cardiac arrest
• Acute heart failure due to ongoing ischemia
• Mechanical complication
• Recurrent dynamic ST/T changes

Early invasive strategy

Complications of AMI

1. Electrical complications

2. Pump failure

3. Mechanical complications

4. Inflammatory complications

• Early fibrinous pericarditis: 1-3 days; pleuritic chest pain and pericardial rub
• Dressler syndrome: weeks to months later; autoimmune fever, pericarditis, pleuropericardial effusion

5. Thromboembolic complications

• LV mural thrombus, particularly with large anterior MI
• Systemic embolism: stroke, limb ischemia, renal infarction

Secondary Prevention After MI

Drug therapy

• Aspirin indefinitely
• P2Y12 inhibitor usually for 12 months after ACS, adjusted for bleeding risk
• High-intensity statin
• Beta-blocker, especially with LV dysfunction, angina, arrhythmias
• ACE inhibitor/ARB, especially with LVEF ≤40%, diabetes, hypertension, CKD, or heart failure
• Mineralocorticoid receptor antagonist if LVEF ≤40% with heart failure or diabetes, provided renal function and potassium permit

Lifestyle and risk-factor control

• Complete smoking cessation
• Cardiac rehabilitation
• Regular graded exercise
• Weight reduction if overweight
• Diabetes and BP control
• Mediterranean-style heart-healthy diet
• Limit alcohol and avoid cocaine/amphetamines
• Influenza vaccination where appropriate
• Education regarding adherence and recurrent symptoms

One-Minute Proff Viva Summary

Acute MI is myocardial necrosis caused by acute ischemia, most commonly due to rupture or erosion of an atherosclerotic plaque followed by coronary thrombosis. Diagnosis requires a rise/fall of cardiac troponin with evidence of ischemia. STEMI requires urgent reperfusion, preferably primary PCI within 120 minutes of first medical contact; otherwise, fibrinolysis is used if no contraindication exists. Initial treatment includes aspirin, a P2Y12 inhibitor, anticoagulation, statin, nitrates where appropriate, oxygen only for hypoxemia, and management of pain and complications. Major complications are arrhythmias, LV failure, cardiogenic shock, papillary muscle rupture, VSD, free-wall rupture, pericarditis, mural thrombus, and ventricular aneurysm.

Acute Coronary Syndrome (ACS)

Definition

1. ST-elevation myocardial infarction (STEMI)
2. Non-ST-elevation myocardial infarction (NSTEMI)
3. Unstable angina (UA)

Classification

Key distinction: NSTEMI and unstable angina together are called NSTE-ACS. Troponin elevation differentiates NSTEMI from unstable angina.

Etiopathogenesis

Usual mechanism

Pathological sequence

1. Atherosclerotic plaque becomes unstable due to inflammation and a thin fibrous cap.
2. Plaque rupture or superficial erosion exposes collagen and tissue factor.
3. Platelets adhere, activate, and aggregate.
4. Thrombin is generated and fibrin-rich thrombus forms.
5. Coronary vasoconstriction worsens obstruction.
6. Myocardial ischemia develops.
7. Persistent severe ischemia causes irreversible myocyte necrosis, that is, MI.

Other causes

• Coronary artery vasospasm, including cocaine-induced
• Coronary embolism
• Spontaneous coronary artery dissection
• Coronary vasculitis
• Severe anemia, hypoxemia, sepsis, tachyarrhythmia, or shock causing supply-demand mismatch, that is, Type 2 MI

Risk Factors

Non-modifiable

• Increasing age
• Male sex or postmenopausal women
• Family history of premature coronary artery disease
• Genetic predisposition

Modifiable

• Smoking
• Diabetes mellitus
• Hypertension
• Dyslipidemia
• Obesity
• Sedentary lifestyle
• Unhealthy diet
• Psychosocial stress
• Chronic kidney disease
• Cocaine or amphetamine use

Clinical Features

Symptoms

Typical symptoms

• Severe central or retrosternal constricting chest pain
• Pain lasting more than 20 minutes
• Occurs at rest or with minimal exertion
• Radiation to left arm, shoulder, neck, jaw, back, or epigastrium
• Pain not completely relieved by rest or sublingual nitrate
• Sweating, nausea, vomiting
• Dyspnea
• Palpitations
• Giddiness or syncope
• Anxiety and sense of impending doom

Atypical presentation

• Isolated dyspnea
• Fatigue
• Epigastric discomfort
• Syncope
• Acute confusion
• Acute pulmonary edema
• Silent MI

Signs

• Pallor, sweating, cold clammy extremities
• Tachycardia or bradycardia
• Hypotension
• S4 gallop due to stiff ischemic ventricle
• S3 gallop in LV dysfunction
• Basal crepitations in LV failure
• Raised JVP in right ventricular infarction
• New murmur:
  • Acute mitral regurgitation due to papillary muscle rupture
  • Ventricular septal rupture
• Pericardial rub in post-MI pericarditis

Diagnosis

1. ECG

STEMI

ECG localization

ECG findings in NSTE-ACS

• ST-segment depression
• Transient ST elevation
• T-wave inversion
• Non-specific ST-T changes
• ECG may be normal

2. Cardiac Biomarkers

High-sensitivity cardiac troponin I or T

• Preferred biomarker for ACS
• Elevated in NSTEMI and STEMI
• Normal in unstable angina
• Diagnosis of MI requires a rise and/or fall in troponin with at least one value above the 99th-percentile upper reference limit, plus clinical evidence of ischemia.

3. Other Investigations

• CBC
• Blood glucose and HbA1c
• Renal function, electrolytes
• Lipid profile
• Coagulation profile
• Chest X-ray
• Echocardiography:
  • Regional wall-motion abnormality
  • LV ejection fraction
  • Mechanical complications
  • LV thrombus
• Coronary angiography:
  • Defines coronary anatomy
  • Identifies culprit artery
  • Enables PCI

Management of ACS

A. Initial Management for All Patients

Immediate measures

1. Admit to coronary care unit.
2. ABC assessment.
3. Cardiac monitoring and defibrillator availability.
4. Two IV access lines.
5. Obtain ECG within 10 minutes.
6. Send cardiac biomarkers, but do not delay STEMI reperfusion while waiting for troponin.
7. Assess for heart failure, shock, arrhythmia, or mechanical complication.

Initial drugs

Common initial doses for proff exams

• Aspirin: 162-325 mg chewed immediately, then 75-150 mg/day lifelong.
• Clopidogrel: 300-600 mg loading dose, then 75 mg/day, or use ticagrelor/prasugrel where suitable.
• Atorvastatin: 80 mg orally as early as possible.
• GTN: 0.4 mg sublingual, repeated every 5 minutes up to 3 doses if blood pressure permits.

Do not give nitrates in

• Hypotension
• Right ventricular infarction
• Severe aortic stenosis
• Recent PDE-5 inhibitor use, for example sildenafil within 24 hours or tadalafil within 48 hours

B. STEMI Management

Principle: Immediate reperfusion

Primary PCI

• STEMI within 12 hours of symptom onset
• Persistent ischemic symptoms
• Cardiogenic shock
• Acute heart failure
• Life-threatening arrhythmias
• Failed fibrinolysis

Fibrinolysis

• STEMI is diagnosed within 12 hours of symptom onset
• PCI cannot be done within the recommended time
• There is no contraindication

Fibrinolytic drugs

• Tenecteplase
• Alteplase
• Reteplase
• Streptokinase

Absolute contraindications

• Previous intracranial hemorrhage
• Ischemic stroke within previous 3 months
• Known intracranial neoplasm or AV malformation
• Suspected aortic dissection
• Active bleeding
• Significant head injury within 3 months
• Recent intracranial or spinal surgery

Indicators of successful fibrinolysis

• Relief of chest pain
• More than 50% resolution of ST elevation at 60-90 minutes
• Reperfusion arrhythmias, especially accelerated idioventricular rhythm
• Early enzyme peak

C. NSTEMI and Unstable Angina Management

Medical treatment

• Aspirin plus P2Y12 inhibitor
• Anticoagulation
• High-intensity statin
• Nitrates for pain, if appropriate
• Beta-blocker if no contraindication
• ACE inhibitor/ARB in LV dysfunction, diabetes, hypertension, or CKD
• Risk stratification using GRACE score

Indications for immediate angiography, usually within 2 hours

• Hemodynamic instability or cardiogenic shock
• Recurrent or refractory chest pain
• Life-threatening arrhythmias or cardiac arrest
• Acute heart failure due to ongoing ischemia
• Mechanical complication
• Recurrent dynamic ST-T changes

Indications for early angiography, usually within 24 hours

• Confirmed NSTEMI
• Dynamic ST-T changes
• GRACE score >140
• Transient ST elevation

Complications of ACS

1. Electrical complications

• Ventricular tachycardia
• Ventricular fibrillation
• Sinus bradycardia
• AV block
• Atrial fibrillation
• Bundle branch block

2. Pump failure

• Acute LV failure
• Pulmonary edema
• Cardiogenic shock

3. Mechanical complications

4. Inflammatory complications

• Early post-infarction pericarditis: 1-3 days
• Dressler syndrome: weeks to months later

Secondary Prevention

1. Aspirin lifelong.
2. Dual antiplatelet therapy, commonly for 12 months after ACS, depending on bleeding and ischemic risk.
3. High-intensity statin.
4. Beta-blocker where indicated.
5. ACE inhibitor/ARB, especially in LV dysfunction, diabetes, hypertension, CKD, or heart failure.
6. Mineralocorticoid receptor antagonist when LVEF ≤40% with heart failure or diabetes, if potassium and renal function permit.
7. Smoking cessation.
8. Diabetes, BP, and lipid control.
9. Exercise-based cardiac rehabilitation.
10. Healthy diet, weight reduction, and regular follow-up.

Short Conclusion for Exams

Acute coronary syndrome includes STEMI, NSTEMI, and unstable angina. It most commonly results from atherosclerotic plaque rupture with superimposed coronary thrombosis. ECG and serial high-sensitivity troponin are central to diagnosis. STEMI requires immediate reperfusion by primary PCI or fibrinolysis where PCI is delayed, whereas NSTE-ACS requires antithrombotic therapy and risk-guided early invasive management. Early diagnosis, timely reperfusion, and aggressive secondary prevention reduce mortality and recurrent cardiovascular events.

Meningitis

Definition

Classification

Based on etiology

1. Acute pyogenic/bacterial meningitis
2. Viral (aseptic) meningitis
3. Tuberculous meningitis (TBM)
4. Fungal meningitis, especially cryptococcal meningitis
5. Spirochetal, parasitic, autoimmune, drug-induced, or neoplastic meningitis

Based on duration

Acute Bacterial Meningitis

Etiology

Common organisms by age and setting

Predisposing Factors

• Otitis media, sinusitis, mastoiditis
• Pneumonia
• Head injury with CSF rhinorrhea or otorrhea
• Neurosurgery, ventricular shunt
• Immunosuppression, HIV, malignancy
• Diabetes mellitus, alcoholism
• Splenectomy/asplenia
• Extremes of age
• Lack of vaccination
• Close living conditions, for example hostels and military barracks, in meningococcal disease

Pathogenesis

Clinical Features

Symptoms

1. Fever
2. Headache
3. Neck stiffness

• Vomiting
• Photophobia
• Altered sensorium, confusion, drowsiness, or coma
• Seizures
• Myalgia and malaise
• Cranial nerve palsies
• Focal neurological deficit

Signs

• Fever, tachycardia, hypotension
• Nuchal rigidity
• Positive Kernig sign
• Positive Brudzinski sign
• Photophobia
• Altered level of consciousness
• Papilledema, suggesting raised ICP
• Cranial nerve palsies
• Focal neurologic deficits
• Seizures
• Petechial or purpuric rash in meningococcal meningitis
• Features of shock or disseminated intravascular coagulation in meningococcemia

Kernig sign

Brudzinski sign

Investigations

1. Blood investigations

• CBC with differential count
• Blood culture, preferably before antibiotics
• Blood glucose, taken at the time of lumbar puncture
• Renal and liver function tests
• Serum electrolytes
• Coagulation profile
• HIV testing where appropriate
• ABG/lactate in sepsis or shock

2. Lumbar puncture and CSF examination

• Opening pressure
• Appearance
• Cell count and differential count
• Protein
• CSF glucose with simultaneous blood glucose
• Gram stain
• Bacterial culture and sensitivity
• PCR, if available
• AFB smear, CBNAAT/NAAT, and culture if TB is suspected
• Cryptococcal antigen/India ink in immunocompromised patients

CSF patterns in meningitis

Exam pearl: Neutrophilic pleocytosis with high protein and low glucose strongly suggests pyogenic meningitis. Lymphocytic pleocytosis with very high protein and low glucose suggests TBM.

3. CT/MRI brain

CT brain before lumbar puncture is indicated if there is:

• Immunocompromised state
• New focal neurologic deficit
• Papilledema
• New-onset seizure
• Moderate-severe altered consciousness, for example GCS <10
• Known CNS mass lesion
• Previous CNS disease

Important emergency rule

Take blood cultures and start empirical antibiotics immediately.
Do not delay antibiotics for CT scan or lumbar puncture if meningitis is strongly suspected.

Treatment of Acute Bacterial Meningitis

Initial management

1. Admit to ICU/high-dependency area if unstable.
2. ABC resuscitation.
3. Oxygen if hypoxemic.
4. Two IV lines and cardiac monitoring.
5. Blood culture and baseline tests.
6. Start IV empirical antibiotics immediately.
7. Give IV dexamethasone before or with the first dose of antibiotic when indicated.
8. Control seizures.
9. Manage shock, raised ICP, fluid and electrolyte disturbances.
10. Isolate suspected meningococcal meningitis with droplet precautions.

Empirical Antibiotic Therapy in Adults

Common adult doses

• Ceftriaxone: 2 g IV every 12 hours
• Cefotaxime: 2 g IV every 4-6 hours
• Vancomycin: 15-20 mg/kg IV every 8-12 hours, adjusted for renal function and serum levels
• Ampicillin: 2 g IV every 4 hours
• Meropenem: 2 g IV every 8 hours

Organism-specific Therapy

Role of Dexamethasone

• Dexamethasone 10 mg IV every 6 hours for 4 days in adults.
• Give before or with the first antibiotic dose.
• It reduces inflammatory complications, especially in pneumococcal meningitis.
• Do not start dexamethasone after antibiotics have already been given.

Supportive Treatment

• Antipyretics
• IV fluids, avoiding both dehydration and fluid overload
• Vasopressors for septic shock
• Anticonvulsants for seizures
• Mannitol or hypertonic saline only when clinically indicated for raised ICP
• Mechanical ventilation if airway is compromised
• Treat SIADH and electrolyte imbalance
• Monitor GCS, pupils, BP, urine output, and neurologic status

Meningococcal Meningitis

Clinical clue

Chemoprophylaxis for close contacts

Tuberculous Meningitis (TBM)

Clinical Features

• Low-grade fever
• Persistent headache
• Vomiting
• Behavioral change, confusion
• Cranial nerve palsies, especially VI nerve
• Neck stiffness
• Focal deficits
• Seizures
• Features of raised ICP
• Hydrocephalus

CSF in TBM

• Raised opening pressure
• Lymphocytic pleocytosis
• High protein
• Low glucose
• AFB smear often negative due to low sensitivity
• CSF NAAT/CBNAAT, culture, and imaging aid diagnosis

Treatment

• Start anti-tubercular treatment promptly.
• Common regimen: 2 months HRZE followed by 10 months HR for TBM, in line with local/national protocols.
  • H: Isoniazid
  • R: Rifampicin
  • Z: Pyrazinamide
  • E: Ethambutol
• Add corticosteroid, for example dexamethasone or prednisolone, tapered over 6-8 weeks.
• Manage hydrocephalus with neurosurgical opinion, ventriculoperitoneal shunt, or endoscopic third ventriculostomy where required.

Complications

• Septic shock
• Disseminated intravascular coagulation
• Raised intracranial pressure
• Cerebral edema
• Hydrocephalus
• Seizures and status epilepticus
• Ischemic stroke due to vasculitis
• Cranial nerve palsies
• Sensorineural hearing loss
• Cognitive impairment
• Motor deficits
• Death

Prevention

• Hib vaccine
• Pneumococcal vaccination
• Meningococcal vaccination in indicated groups
• Prompt treatment of otitis, sinusitis, and CSF leaks
• Chemoprophylaxis of close contacts in meningococcal disease
• Infection-control precautions in hospital

5-Mark Short Note: Acute Bacterial Meningitis

Acute bacterial meningitis is an emergency characterized by infection and inflammation of the leptomeninges and CSF. It commonly presents with fever, headache, neck stiffness, vomiting, photophobia, altered sensorium, seizures, and focal deficits. The commonest adult pathogens are Streptococcus pneumoniae and Neisseria meningitidis; Listeria must be considered in patients older than 50 years and immunocompromised persons. Diagnosis is by blood culture and CSF analysis, which shows raised opening pressure, neutrophilic pleocytosis, high protein, and low glucose. Start empirical IV ceftriaxone or cefotaxime with vancomycin immediately; add ampicillin if Listeria is possible. Dexamethasone should be administered before or with the first antibiotic dose. Complications include shock, raised ICP, seizures, stroke, deafness, hydrocephalus, and death.

Heart Failure

Definition

Classification

1. Based on left-ventricular ejection fraction (LVEF)

2. Based on side involved

• Left-sided heart failure
• Right-sided heart failure
• Biventricular failure

3. Based on time course

• Acute heart failure
• Chronic heart failure
• Acute decompensated heart failure

4. Based on cardiac output

• Low-output failure: most common
• High-output failure: anemia, thyrotoxicosis, AV fistula, beriberi, Paget disease, sepsis

5. Functional classification: NYHA

Etiology

Causes of left-sided HF

Common causes

1. Ischemic heart disease and myocardial infarction
2. Hypertension
3. Valvular heart disease: MR, AR, AS
4. Dilated cardiomyopathy
5. Myocarditis
6. Arrhythmias, especially atrial fibrillation with rapid ventricular rate
7. Congenital heart disease

Causes of HFpEF

• Long-standing hypertension with LV hypertrophy
• Ischemic heart disease
• Diabetes mellitus
• Obesity
• Aging
• Hypertrophic cardiomyopathy
• Restrictive cardiomyopathy
• Constrictive pericarditis

Causes of right-sided HF

• Most commonly secondary to left-sided HF
• Cor pulmonale due to chronic lung disease or pulmonary hypertension
• Right ventricular infarction
• Tricuspid or pulmonary valve disease
• Congenital left-to-right shunts

Pathophysiology

Basic mechanism

Sequence

1. Primary cardiac insult
   MI, hypertension, valvular disease, cardiomyopathy, etc.
2. Reduced stroke volume/cardiac output
3. Compensatory mechanisms
   • Sympathetic nervous system activation
   • Renin-angiotensin-aldosterone system activation
   • ADH release
   • Natriuretic peptide release
4. Effects
   • Tachycardia
   • Peripheral vasoconstriction
   • Sodium and water retention
   • Increased preload and afterload
   • Ventricular hypertrophy and dilatation
5. Initially, compensation maintains perfusion. Later, it produces:
   • Pulmonary and systemic congestion
   • Increased myocardial oxygen demand
   • Myocyte apoptosis/fibrosis
   • Adverse ventricular remodeling
   • Progressive fall in cardiac output

Role of Frank-Starling mechanism

Clinical Features

Symptoms of left-sided HF

Due to pulmonary venous congestion

• Exertional dyspnea
• Orthopnea
• Paroxysmal nocturnal dyspnea
• Nocturnal cough
• Wheeze, termed cardiac asthma
• Pink frothy sputum in acute pulmonary edema

Due to low cardiac output

• Fatigue
• Weakness
• Reduced exercise tolerance
• Cold extremities
• Dizziness
• Oliguria
• Confusion in severe HF

Symptoms of right-sided HF

• Pedal edema
• Abdominal distension due to ascites
• Right upper quadrant discomfort due to congestive hepatomegaly
• Early satiety
• Weight gain
• Nocturia

Signs

General signs

• Tachycardia
• Tachypnea
• Hypotension in severe failure
• Cold clammy extremities in low-output state
• Cyanosis
• Cachexia in chronic advanced HF

Left-sided HF

• Displaced, diffuse apex beat
• S3 gallop rhythm: suggests LV volume overload and systolic dysfunction
• S4: reduced ventricular compliance
• Basal fine crepitations
• Pleural effusion
• Pulsus alternans in severe LV dysfunction

Right-sided HF

• Raised JVP
• Positive hepatojugular reflux
• Dependent pitting edema
• Tender hepatomegaly
• Ascites
• Pleural effusion, often right-sided

Investigations

1. ECG

• LVH
• Previous MI/Q waves
• Ischemic ST-T changes
• Atrial fibrillation
• Bundle branch block
• Tachyarrhythmias or bradyarrhythmias

2. Chest X-ray

1. Upper-lobe venous diversion
2. Kerley B lines
3. Perihilar “bat-wing” alveolar edema
4. Pleural effusions
5. Cardiomegaly, especially in chronic HF

3. Echocardiography - key investigation

• LVEF
• Regional wall-motion abnormalities
• LV hypertrophy/dilatation
• Diastolic dysfunction
• Valve lesions
• Pulmonary artery pressure
• RV function
• Pericardial disease
• Intracardiac thrombus

4. Natriuretic peptides

• BNP and NT-proBNP help in diagnosis and prognosis.
• Low levels make HF less likely.
• Levels may be high in renal failure, pulmonary embolism, AF, sepsis, and elderly patients.
• Levels may be falsely low in obesity.

5. Laboratory tests

• CBC: anemia/infection
• Renal function, urea, creatinine
• Serum electrolytes, especially sodium and potassium
• LFT
• Blood glucose and HbA1c
• Thyroid function tests
• Lipid profile
• Urinalysis
• Troponin if ACS suspected
• Iron studies where relevant

Management

A. General Measures

1. Explain disease and educate patient/family.
2. Salt restriction, usually less than 2 g sodium/day in congested patients.
3. Fluid restriction in severe congestion or hyponatremia.
4. Daily weight monitoring.
5. Stop smoking and avoid alcohol excess.
6. Regular supervised exercise/cardiac rehabilitation when stable.
7. Vaccination: influenza and pneumococcal vaccines.
8. Identify and treat precipitating factors.
9. Avoid NSAIDs, unnecessary calcium-channel blockers such as verapamil/diltiazem in HFrEF, and cardiotoxic drugs.

B. Treatment of Chronic HFrEF

Four pillars of guideline-directed medical therapy

Important points

• Start all four classes early in stable euvolemic HFrEF, then titrate toward tolerated target doses.
• Monitor BP, pulse, creatinine, eGFR, and potassium.
• Continue therapy even when EF improves in HFimpEF.

Drugs for symptomatic relief

Diuretics

• Furosemide is used for fluid overload, pulmonary edema, and peripheral edema.
• It improves symptoms and reduces congestion but does not independently confer the mortality benefit of the four foundational classes.
• Monitor daily weight, urine output, renal function, sodium, and potassium.

Other drugs in selected HFrEF patients

• Ivabradine: sinus rhythm, LVEF ≤35%, resting heart rate ≥70/min despite maximally tolerated beta-blocker.
• Hydralazine plus isosorbide dinitrate: if ACEi/ARB/ARNI cannot be used, or in selected persistently symptomatic patients.
• Digoxin: may reduce hospitalization and helps rate control in AF. It does not improve survival.
• IV iron: consider if iron deficiency is confirmed.
• Anticoagulation only for AF, LV thrombus, venous thromboembolism, or another clear indication.

C. Management of HFpEF

1. Diuretics for congestion.
2. SGLT2 inhibitor, unless contraindicated.
3. Strict control of hypertension.
4. Control AF: rate/rhythm control and anticoagulation when indicated.
5. Treat ischemic heart disease.
6. Treat obesity, diabetes, CKD, sleep apnea, and valvular disease.
7. Exercise training and weight management.

D. Acute Decompensated Heart Failure and Acute Pulmonary Edema

Clinical picture

• Severe breathlessness
• Orthopnea
• Tachypnea
• Hypoxemia
• Widespread crepitations
• Pink frothy sputum
• Sweating and anxiety
• S3 gallop
• May present with hypertension or cardiogenic shock

Immediate Management: LMNOP

Practical acute management

1. Sit patient upright.
2. ABC approach and cardiac monitoring.
3. Oxygen if SpO₂ <90% or respiratory distress.
4. Non-invasive ventilation, CPAP/BiPAP, if severe pulmonary edema.
5. IV furosemide for congestion.
6. IV nitrates in hypertensive acute pulmonary edema.
7. Identify and treat trigger: ACS, arrhythmia, infection, hypertensive crisis, anemia, renal failure, drug/dietary non-adherence.
8. In hypotension/hypoperfusion or cardiogenic shock, use ICU care and consider inotrope/vasopressor support and urgent revascularization if ACS is the cause.

Do not use routine oxygen in a normoxemic patient.

Devices and Advanced Therapy

ICD

• Symptomatic HFrEF despite optimal therapy
• LVEF ≤35%
• Expected survival >1 year

CRT

• LVEF ≤35%
• Sinus rhythm
• LBBB with broad QRS, particularly ≥150 ms
• Persistent symptoms despite optimal medical therapy

Advanced HF

• LV assist device
• Heart transplantation
• Palliative-care referral when appropriate

Precipitating Factors of Acute Decompensation

• F: Failure of drug/dietary compliance
• A: Arrhythmia, especially AF
• I: Ischemia/infarction
• L: Lifestyle excess, salt, fluid, alcohol
• U: Up-titration failure or use of harmful drugs, especially NSAIDs
• R: Renal failure
• E: Embolism, infection, endocrine causes such as thyrotoxicosis

Complications

• Acute pulmonary edema
• Cardiogenic shock
• Atrial fibrillation and ventricular arrhythmias
• Sudden cardiac death
• Cardiorenal syndrome
• Hyponatremia
• Hepatic congestion/cardiac cirrhosis
• Pleural effusion and ascites
• Thromboembolism
• Progressive multiorgan dysfunction

Exam Conclusion

Heart failure is a clinical syndrome resulting from impaired cardiac pump function or impaired ventricular filling. It is classified by ejection fraction into HFrEF, HFmrEF, HFpEF, and HFimpEF. Diagnosis is based on clinical features, natriuretic peptides, chest X-ray, and echocardiography. HFrEF should receive early foundational therapy with ARNI/ACEi/ARB, evidence-based beta-blocker, MRA, and SGLT2 inhibitor, while diuretics relieve congestion. Acute pulmonary edema requires urgent positioning, oxygen only if hypoxemic, IV loop diuretic, nitrates when suitable, ventilatory support, and prompt treatment of the precipitating cause.

Ischemic Heart Disease (IHD)

Definition

Clinical Spectrum of IHD

1. Chronic coronary syndrome
   • Stable angina pectoris
   • Silent myocardial ischemia
   • Ischemic cardiomyopathy/heart failure
2. Acute coronary syndrome
   • Unstable angina
   • NSTEMI
   • STEMI
3. Sudden cardiac death due to ischemia-induced fatal arrhythmia

Etiology and Risk Factors

Major cause

• Coronary vasospasm, for example Prinzmetal angina
• Coronary embolism
• Spontaneous coronary artery dissection
• Coronary arteritis, for example Kawasaki disease
• Congenital coronary anomalies
• Severe anemia, hypoxemia, or tachyarrhythmia causing supply-demand mismatch

Non-modifiable risk factors

• Increasing age
• Male sex and postmenopausal women
• Family history of premature CAD
• Genetic predisposition

Modifiable risk factors

• Cigarette smoking
• Hypertension
• Diabetes mellitus
• Dyslipidemia, especially raised LDL cholesterol
• Obesity and sedentary lifestyle
• Unhealthy diet
• Psychosocial stress
• Chronic kidney disease
• Cocaine/amphetamine use

Pathogenesis

Atherosclerotic IHD

Steps

1. Endothelial dysfunction occurs due to hypertension, smoking, diabetes, and dyslipidemia.
2. LDL enters and accumulates in the intima, then undergoes oxidation.
3. Monocytes enter the vessel wall and become macrophages.
4. Macrophages ingest lipid, becoming foam cells.
5. Atherosclerotic plaque develops with a lipid core and fibrous cap.
6. The plaque may produce:
   • Fixed narrowing causing exertional stable angina
   • Rupture or erosion causing platelet activation and thrombus, leading to ACS

Important concept

• A fixed coronary stenosis of approximately 70% or more often causes stable angina during exertion.
• Acute MI may occur after rupture of a previously non-critical but vulnerable plaque.

Types of Angina

Stable Angina Pectoris

Definition

Classical anginal pain

1. Constricting discomfort in chest, neck, jaw, shoulder, or arm
2. Provoked by exertion or emotional stress
3. Relieved by rest or nitrates within a few minutes

Clinical features

• Retrosternal constricting, tightness, heaviness, or pressure
• Radiation to left arm, both arms, jaw, neck, back, or epigastrium
• Provoked by walking, climbing stairs, cold weather, emotional stress, or heavy meals
• Relieved by rest or sublingual GTN
• Dyspnea may be an anginal equivalent, especially in elderly patients and people with diabetes

Diagnosis of IHD

1. ECG

• Normal ECG at rest
• Previous MI with pathological Q waves
• LVH
• ST depression and T-wave inversion during ischemia
• Arrhythmias or conduction defects

2. Exercise stress test

• Horizontal or downsloping ST depression ≥1 mm
• Reproduction of angina during exercise
• Exercise-induced arrhythmia or hypotension

3. Echocardiography

• Regional wall-motion abnormality
• LV ejection fraction
• Valve disease
• Stress echocardiography can identify inducible ischemia

4. Coronary CT angiography

5. Coronary angiography

• Persistent angina despite optimal medical treatment
• High-risk findings on non-invasive tests
• Suspected left-main or severe multivessel disease
• Acute coronary syndrome
• Consideration for PCI or CABG

6. Laboratory evaluation

• Lipid profile
• Blood glucose and HbA1c
• Renal function
• CBC for anemia
• Thyroid function if clinically indicated
• Troponin only if ACS is suspected

Management of Chronic IHD/Stable Angina

A. Lifestyle and risk-factor modification

1. Stop smoking completely.
2. Regular aerobic exercise/cardiac rehabilitation as tolerated.
3. Weight reduction if overweight.
4. Heart-healthy diet: reduced saturated/trans fats, salt, and refined carbohydrates.
5. Control hypertension.
6. Optimize diabetes management.
7. Treat dyslipidemia.
8. Avoid cocaine and amphetamines.
9. Annual influenza vaccination where appropriate.

B. Drugs that improve prognosis

Statins

• Atorvastatin 40-80 mg/day
• Rosuvastatin 20-40 mg/day

C. Anti-anginal Drugs

1. Beta-blockers - first line

• Severe bradycardia
• High-grade AV block
• Acute decompensated HF
• Severe bronchospasm/asthma

2. Calcium-channel blockers

• Non-dihydropyridines: verapamil, diltiazem
  Reduce heart rate and contractility. Avoid in HFrEF and AV block.
• Dihydropyridines: amlodipine
  Useful for BP control and in combination with beta-blocker.

3. Nitrates

• Sublingual GTN for acute angina attack.
• Long-acting nitrates for symptom prevention.

• Headache
• Flushing
• Postural hypotension
• Reflex tachycardia
• Tolerance, so provide a daily nitrate-free interval

4. Other drugs

• Ivabradine: lowers sinus rate
• Ranolazine: useful if symptoms persist despite conventional drugs
• Nicorandil: nitrate-like and potassium-channel opening action
• Trimetazidine: metabolic anti-anginal drug used in some settings

Revascularization

Percutaneous coronary intervention (PCI)

Indications

• Persistent limiting angina despite optimal medical therapy
• High-risk anatomy or ischemia
• Acute coronary syndrome
• Suitable focal coronary lesions

Coronary artery bypass grafting (CABG)

• Left-main coronary artery disease
• Complex multivessel CAD, especially with diabetes
• Severe LV dysfunction with suitable viable myocardium
• Anatomy unsuitable for PCI
• Failed PCI

Acute Coronary Syndrome: Red Flags

• Occurs at rest
• Is new-onset and severe
• Is increasing in frequency, severity, or duration
• Lasts >20 minutes
• Is associated with sweating, vomiting, syncope, breathlessness, or hypotension

Complications of IHD

• Acute myocardial infarction
• Arrhythmias, especially VT/VF and atrial fibrillation
• Sudden cardiac death
• Ischemic cardiomyopathy
• Chronic heart failure
• Papillary muscle dysfunction causing MR
• Ventricular aneurysm
• LV mural thrombus and systemic embolism

Exam Conclusion

Ischemic heart disease is most commonly caused by coronary atherosclerosis. It ranges from stable angina due to fixed coronary stenosis to acute coronary syndrome caused by plaque rupture and thrombosis. Management rests on lifestyle modification, aggressive control of risk factors, antiplatelet therapy, statins, anti-anginal drugs, and revascularization by PCI or CABG in suitable patients.

Acute Pulmonary Edema

Definition

Classification

Etiology of Cardiogenic Acute Pulmonary Edema

Cardiac causes

• Acute myocardial infarction or ongoing ischemia
• Acute decompensated chronic heart failure
• Hypertensive emergency
• Severe mitral regurgitation, including papillary muscle rupture
• Acute aortic regurgitation
• Severe aortic stenosis
• Arrhythmias:
  • Rapid atrial fibrillation
  • Ventricular tachycardia
  • Severe bradycardia/complete heart block
• Myocarditis
• Cardiomyopathy

Precipitating factors in a patient with chronic heart failure

• Drug or dietary non-adherence, particularly salt excess
• Stopping diuretics
• Infection, especially pneumonia
• Anemia
• Renal failure
• Pulmonary embolism
• Thyrotoxicosis
• Drugs: NSAIDs, some calcium-channel blockers, excess IV fluids

Pathophysiology

Stages

1. Interstitial edema
   • Peribronchial cuffing
   • Kerley B lines
   • Reduced lung compliance
2. Alveolar edema
   • Flooding of alveoli
   • Severe V/Q mismatch and shunt
   • Hypoxemia
   • Pink frothy sputum in severe cases

Clinical Features

Symptoms

• Sudden severe breathlessness
• Orthopnea
• Paroxysmal nocturnal dyspnea
• Cough with pink frothy sputum
• Wheeze, called cardiac asthma
• Chest pain if ACS is the cause
• Palpitations
• Sweating, fear, and sense of impending doom

Signs

• Patient sits upright, distressed, unable to lie flat
• Tachypnea and use of accessory muscles
• Tachycardia
• Hypoxemia and central cyanosis
• Cold clammy extremities
• Hypertension is common initially, though hypotension suggests cardiogenic shock
• Fine inspiratory crepitations, initially basal then diffuse
• Wheeze
• S3 gallop
• Raised JVP, peripheral edema, or hepatomegaly if there is pre-existing congestive HF
• New murmur may suggest acute MR, VSD, or another valvular lesion

Investigations

Bedside and laboratory tests

• Pulse oximetry and arterial blood gas
  • Hypoxemia
  • Often respiratory alkalosis initially
  • Hypercapnia/acidosis in severe, exhausting respiratory failure
• ECG: ischemia/infarction, LVH, arrhythmia
• CBC: anemia, infection
• Renal function, electrolytes, blood glucose
• Troponin if ACS is suspected
• BNP/NT-proBNP, helpful if diagnosis is uncertain
• Blood cultures if sepsis is suspected

Chest X-ray

• Cardiomegaly in chronic cardiac failure
• Upper-lobe venous diversion
• Kerley B lines
• Peribronchial cuffing
• Bilateral perihilar fluffy alveolar opacities, the “bat-wing” or butterfly pattern
• Pleural effusions

Echocardiography

• LV systolic function and regional wall-motion abnormality
• Acute MR/AR
• Aortic stenosis
• RV function
• Pericardial tamponade
• Mechanical complication of MI

Management

Principle

Treat respiratory failure, relieve pulmonary congestion, reduce preload/afterload where appropriate, and identify and correct the precipitating cause.

Immediate management: ABCDE

1. Position

• Sit patient upright with legs dependent, if BP permits.
• This reduces venous return and improves ventilation.

2. Airway and breathing

• Give oxygen only if hypoxemic, typically SpO₂ <90%, or if there is respiratory distress/shock.
• Target SpO₂ approximately 94-98%, or 88-92% in those at risk of hypercapnic respiratory failure.
• Use CPAP/BiPAP (NIV) early in severe respiratory distress, hypoxemia, hypercapnia, or acidaemia, provided BP is adequate and the patient is cooperative.
• Intubate and mechanically ventilate if there is worsening respiratory failure, reduced consciousness, exhaustion, or inability to protect airway.

3. Circulation and monitoring

• Cardiac monitor, frequent BP measurement, pulse oximetry
• Two IV lines
• Urine output monitoring, often with catheter in severe cases
• Obtain ECG within 10 minutes if ACS is possible
• Look actively for MI, hypertensive crisis, tachyarrhythmia, valvular catastrophe, or infection

Drug Management

IV loop diuretic

• Typical initial dose: furosemide 20-40 mg IV, then reassess urine output and clinical response.
• If the patient already takes loop diuretics, a higher IV dose may be necessary.
• Monitor potassium, sodium, renal function, urine output, and BP.

IV nitrates

• Hypotension
• Right ventricular infarction
• Severe aortic stenosis
• Recent PDE-5 inhibitor use
• Marked hypovolemia

Management According to Hemodynamic Profile

Treat the Cause

Complications

• Acute hypoxemic respiratory failure
• Hypercapnic respiratory failure
• Cardiogenic shock
• Cardiac arrest
• Acute kidney injury
• Arrhythmias
• Myocardial ischemia/infarction
• Death

Differentiate Cardiogenic from Non-cardiogenic Pulmonary Edema

5-Mark Exam Answer

Acute pulmonary edema is rapid accumulation of fluid in lung interstitium and alveoli, most commonly due to acute left ventricular failure causing raised pulmonary venous pressure. It presents with sudden severe dyspnea, orthopnea, cough with pink frothy sputum, tachypnea, hypoxemia, diffuse crepitations, wheeze, tachycardia, and often hypertension. Chest X-ray shows pulmonary venous congestion, Kerley B lines, bilateral perihilar bat-wing opacities, and frequently cardiomegaly. Management consists of upright positioning, monitoring, oxygen only for hypoxemia, early CPAP/BiPAP when severe, IV furosemide for congestion, IV nitrates in hypertensive/ischemic patients with adequate BP, and urgent treatment of the precipitating cause such as ACS, arrhythmia, hypertensive emergency, or acute valvular dysfunction.

Infective Endocarditis (IE)

Definition

Classification

1. By clinical course

2. By site

• Native-valve endocarditis
• Prosthetic-valve endocarditis
• Device-related IE: pacemaker, ICD leads
• Right-sided IE, usually tricuspid, often in injection-drug use
• Left-sided IE, usually mitral or aortic valve

3. By source

• Community-acquired
• Healthcare-associated
• Injection-drug-use associated

Etiology

Common microorganisms

Predisposing Factors

• Previous infective endocarditis
• Rheumatic or degenerative valvular heart disease
• Congenital heart disease
• Prosthetic heart valve or valve repair material
• Intracardiac devices: pacemaker/ICD
• Intravenous drug use
• Long-term IV cannula, central venous catheter
• Hemodialysis
• Diabetes mellitus
• Immunosuppression
• Poor oral hygiene or dental infection
• Recent invasive procedure, especially in high-risk cardiac patients

Pathogenesis

Sequence

1. Turbulent blood flow, valvular disease, prosthetic material, or devices damage the endocardium.
2. Platelets and fibrin deposit on the damaged surface, forming sterile non-bacterial thrombotic vegetation.
3. Transient bacteremia follows dental, skin, gastrointestinal, genitourinary, or catheter-related infection.
4. Organisms adhere to the vegetation and multiply.
5. Vegetations enlarge because they are relatively avascular, making antibiotic penetration difficult.
6. Complications follow:
   • Local valve destruction and regurgitation
   • Perivalvular abscess
   • Emboli
   • Metastatic infection
   • Immune-complex injury

Clinical Features

Constitutional features

• Fever, often prolonged
• Chills and rigors
• Malaise, fatigue, anorexia
• Weight loss
• Night sweats
• Arthralgia/myalgia

Cardiac features

• New regurgitant murmur or change in previous murmur
• Features of heart failure due to valvular destruction
• Conduction abnormalities, especially new AV block, suggesting aortic root abscess
• Palpitations/arrhythmias

Peripheral stigmata

Viva point: Osler nodes are painful, whereas Janeway lesions are painless.

Embolic manifestations

• Stroke or transient ischemic attack
• Splenic infarct/abscess: left upper abdominal pain
• Renal infarct: hematuria/flank pain
• Coronary embolism: MI
• Limb ischemia
• Pulmonary emboli, lung infarcts, or septic pulmonary abscesses in right-sided IE

Diagnosis

1. Blood cultures

• Collect three sets of blood cultures from separate venepuncture sites.
• Ideally take them before starting antibiotics.
• In a critically ill/septic patient, obtain cultures promptly, but do not delay antibiotics unnecessarily.
• Persistent bacteremia supports IE.
• Repeat cultures every 24-48 hours until they are negative.

2. Echocardiography

• TTE is negative/inconclusive but clinical suspicion remains high
• Prosthetic valve is present
• Cardiac device is present
• There is suspected abscess or complication
• Pre-operative assessment is needed

3. Other investigations

• CBC: normocytic anemia, leukocytosis/leukopenia
• ESR and CRP: elevated
• Renal function, electrolytes, LFT
• Urine routine/microscopy: microscopic hematuria, proteinuria, RBC casts due to glomerulonephritis
• ECG: PR prolongation/new AV block may suggest abscess
• Chest X-ray: pulmonary edema in HF, septic pulmonary emboli in right-sided IE
• CT/MRI brain, chest, abdomen: embolic infarcts/abscesses
• Cardiac CT, FDG-PET/CT or WBC-SPECT/CT: useful particularly in prosthetic-valve/device-related IE when echo is inconclusive

Modified Duke Criteria

Major criteria

1. Positive blood culture for IE

• Typical organism from two separate blood cultures:
  • Viridans streptococci
  • Streptococcus gallolyticus
  • HACEK organisms
  • Staphylococcus aureus
  • Community-acquired enterococci without primary focus

• Persistently positive cultures:
  • Two positive cultures taken >12 hours apart, or
  • Three of three or majority of four separate cultures positive

2. Evidence of endocardial involvement

• Echocardiographic vegetation
• Abscess
• New partial dehiscence of prosthetic valve
• New valvular regurgitation

Minor criteria

1. Predisposition: cardiac lesion or injection-drug use
2. Fever ≥38°C
3. Vascular phenomena: arterial emboli, septic pulmonary infarcts, Janeway lesions, intracranial hemorrhage, mycotic aneurysm
4. Immunological phenomena: glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor
5. Microbiological evidence not fulfilling a major criterion

Interpretation

Management

Principles

1. Admit and manage under a multidisciplinary Endocarditis Team.
2. Obtain blood cultures before antibiotics whenever possible.
3. Give prolonged, high-dose, bactericidal IV antibiotics.
4. Modify therapy according to culture and sensitivity.
5. Monitor for heart failure, embolism, renal dysfunction, abscess, and arrhythmia.
6. Evaluate early for cardiac surgery where indicated.

Antibiotic choice and doses must be individualized according to organism, susceptibility, renal function, native versus prosthetic valve, and local antimicrobial policy.

Empirical Antibiotic Therapy

• Vancomycin-based regimen, often with ceftriaxone or cefepime depending on local policy and clinical setting.

Organism-Specific Treatment: Exam Outline

Important point

• Do not give aminoglycosides casually. They may cause nephrotoxicity and their use depends on the organism and regimen.
• Monitor renal function, serum drug levels where required, CRP, temperature, and serial blood cultures.

Indications for Surgery

H - Heart failure

• Acute severe aortic or mitral regurgitation causing pulmonary edema/HF
• Prosthetic-valve dysfunction causing HF
• Obstruction due to large vegetation

U - Uncontrolled infection

• Abscess, pseudoaneurysm, fistula, or enlarging vegetation
• Persistent positive blood cultures despite appropriate antibiotics
• Infection with fungi or highly resistant organism
• Prosthetic-valve endocarditis with destructive complications
• New conduction block suggesting periannular extension

I - Implant/device infection

• Infected pacemaker/ICD lead or pocket infection generally requires complete device removal plus antibiotics.

E - Embolic prevention

• Recurrent embolization despite treatment
• Large mobile left-sided vegetation, especially after embolic event
• Large vegetation with other surgical indications

Complications

Cardiac

• Acute valvular regurgitation
• Congestive heart failure
• Perivalvular abscess
• Conduction block
• Myocarditis
• Pericarditis
• Prosthetic-valve dehiscence

Embolic/infective

• Ischemic or hemorrhagic stroke
• Cerebral abscess
• Mycotic aneurysm
• Splenic infarct/abscess
• Renal infarct
• Septic pulmonary emboli in tricuspid IE
• Vertebral osteomyelitis/discitis

Immunological

• Immune-complex glomerulonephritis
• Vasculitis
• Rheumatoid-factor positivity

Other

• Sepsis and septic shock
• Acute kidney injury
• Death

Prevention

General measures

• Good dental and skin hygiene
• Early treatment of skin, dental, and bloodstream infections
• Avoid unnecessary intravascular catheters
• Strict asepsis during invasive procedures
• Avoid injection drug use

Antibiotic prophylaxis

• Prosthetic heart valve or prosthetic material used for valve repair
• Previous IE
• Selected congenital heart disease
• Cardiac transplant recipients with valvular disease

5-Mark Short Note

Infective endocarditis is microbial infection of the endocardium, usually the cardiac valves, leading to platelet-fibrin vegetations containing organisms. It commonly presents with prolonged fever, new or changing murmur, anemia, splenomegaly, petechiae, splinter hemorrhages, Osler nodes, Janeway lesions, embolic events, and heart failure. Diagnosis is based on serial blood cultures and echocardiography, interpreted using modified Duke criteria. Treatment consists of prolonged culture-directed bactericidal IV antibiotics, with surgery for acute heart failure due to valve destruction, uncontrolled infection/abscess or persistent bacteremia, prosthetic/device infection, fungi, and high embolic risk.

Valvular Heart Disease: Proff Topic Map

1. General approach
   • Definition, classification into stenosis and regurgitation
   • Rheumatic versus degenerative versus infective causes
   • Symptoms, murmurs, echocardiography, and principles of management
2. Mitral stenosis
   • Rheumatic etiology, clinical features, auscultation, ECG/CXR/echo
   • Complications: AF, embolism, pulmonary hypertension
   • Medical therapy and balloon mitral valvotomy
3. Mitral regurgitation
   • Acute versus chronic MR
   • Causes, murmur, investigations, complications, and surgery
4. Aortic stenosis
   • Degenerative/calcific versus bicuspid valve versus rheumatic AS
   • Classical triad: angina, syncope, dyspnea
   • Echo severity and valve replacement/TAVI
5. Aortic regurgitation
   • Acute versus chronic AR
   • Peripheral signs, murmur, investigations, and surgical indications
6. Tricuspid and pulmonary valve disease
   • TR, TS, PR, PS, and their classical murmurs
7. Infective endocarditis and rheumatic heart disease
   • Important etiologies and complications relevant to valvular lesions
8. Pregnancy and valvular lesions
   • High-yield lesion-specific maternal risks and management

High-level overview

Definition → etiology → pathophysiology → symptoms → signs and murmur → investigations, especially echocardiography → complications → medical and definitive management.

• “Describe mitral stenosis and its management.”
• “Discuss aortic stenosis/aortic regurgitation with clinical signs and treatment.”

Rheumatic Heart Disease (RHD)

Definition

Etiopathogenesis

Basic sequence

Group A streptococcal pharyngitis → acute rheumatic fever → recurrent valvulitis → fibrosis and scarring of valve → chronic stenosis and/or regurgitation.

Mechanism: molecular mimicry

• Streptococcal M protein shares antigenic similarity with cardiac myosin and valvular tissue.
• Antibodies and T-cells generated against streptococcal antigens cross-react with the host heart.
• This is an immune-mediated disease, not direct bacterial infection of the valve.
• Recurrent ARF causes cumulative valvular damage.

Pathology

Acute rheumatic carditis

• Pancarditis: endocarditis, myocarditis, and pericarditis.
• Characteristic lesion: Aschoff body.
• Aschoff bodies contain Anitschkow cells, also called caterpillar cells.

Chronic rheumatic valvular disease

• Leaflet thickening and calcification
• Commissural fusion
• Chordae tendineae thickening, fusion, and shortening
• Valve stenosis and/or regurgitation

Classical mitral-valve appearance

Valves Affected

Common combinations

• Mitral stenosis with mitral regurgitation
• Mitral stenosis with aortic regurgitation
• Mitral stenosis with aortic stenosis/regurgitation

Clinical Features

General symptoms

• Fatigue
• Reduced exercise tolerance
• Palpitations
• Dyspnea
• Orthopnea and paroxysmal nocturnal dyspnea
• Chest discomfort
• Hemoptysis
• Pedal edema and abdominal distension in right-heart failure
• Fever or constitutional symptoms if recurrent rheumatic activity or infective endocarditis occurs

Rheumatic Mitral Stenosis

Pathophysiology

Mitral obstruction → raised left atrial pressure → pulmonary venous hypertension → pulmonary arterial hypertension → right ventricular hypertrophy/failure → systemic venous congestion.

• Left atrial enlargement
• Atrial fibrillation
• Left atrial thrombus
• Systemic embolism, especially stroke

Symptoms

• Exertional dyspnea
• Orthopnea/PND
• Palpitations due to AF
• Hemoptysis
• Fatigue
• Recurrent bronchitis
• Hoarseness of voice due to left atrial enlargement compressing left recurrent laryngeal nerve: Ortner syndrome
• Thromboembolic stroke

Signs

• Malar flush
• Tapping, localized apex beat
• Loud S1
• Opening snap after A2
• Low-pitched, rumbling mid-diastolic murmur at apex
• Murmur is best heard with bell in left lateral position
• Presystolic accentuation if sinus rhythm is present
• Loud P2 if pulmonary hypertension
• Raised JVP, hepatomegaly, edema in right-heart failure

Rheumatic Mitral Regurgitation

Pathophysiology

MR → LV volume overload + LA volume overload → LA dilatation + LV dilatation → AF, pulmonary congestion, and heart failure.

Clinical features

• Fatigue and exertional dyspnea
• Palpitations
• Orthopnea/PND in severe disease
• Displaced, hyperdynamic apex beat
• Soft S1
• High-pitched, blowing pansystolic murmur at apex radiating to left axilla
• S3 gallop in severe MR

Rheumatic Aortic Stenosis

Clinical features

• Exertional angina
• Exertional syncope
• Exertional dyspnea/heart failure
• Slow-rising low-volume pulse: pulsus parvus et tardus
• Harsh ejection systolic murmur in aortic area radiating to carotids
• Soft/absent A2 in severe AS

Rheumatic Aortic Regurgitation

Clinical features

• Palpitations due to increased stroke volume
• Exertional dyspnea, orthopnea, PND
• Wide pulse pressure
• Collapsing or water-hammer pulse
• Displaced hyperdynamic apex
• High-pitched, early diastolic decrescendo murmur at left sternal edge, best heard with patient sitting forward in end-expiration
• Austin Flint murmur at apex in severe AR

Investigations

1. ECG

• Left atrial enlargement: P mitrale
• Atrial fibrillation
• Right ventricular hypertrophy in pulmonary hypertension
• LVH in MR, AR, or AS
• Conduction abnormalities

2. Chest X-ray

• Cardiomegaly depending on lesion
• Left atrial enlargement, double-density shadow
• Straightening of left heart border in MS
• Pulmonary venous congestion
• Kerley B lines
• Pulmonary edema in severe failure
• Prominent pulmonary arteries in pulmonary hypertension

3. Echocardiography with Doppler - investigation of choice

• Valve morphology and thickening
• Commissural fusion
• Severity of stenosis/regurgitation
• Valve area and transvalvular gradients
• LA/LV/RV size and function
• Pulmonary artery pressure
• Presence of LA thrombus
• Associated valvular lesions

4. Transesophageal echocardiography

• Left atrial appendage thrombus before cardioversion or balloon mitral valvotomy
• Prosthetic-valve dysfunction
• Infective endocarditis vegetation

5. Cardiac catheterization/coronary angiography

• Discrepancy between clinical and echo data
• Assessment before valve intervention in selected older patients or those at risk of CAD

Complications of RHD

1. Atrial fibrillation
2. Left atrial thrombus and systemic embolism
   • Ischemic stroke
   • Peripheral arterial embolism
3. Pulmonary hypertension
4. Right-heart failure
5. Congestive cardiac failure
6. Infective endocarditis
7. Hemoptysis
8. Pregnancy-related decompensation
9. Sudden deterioration due to tachyarrhythmia, infection, anemia, or embolism

Management

A. General Measures

• Regular cardiology follow-up with periodic echocardiography
• Counsel on adherence to secondary prophylaxis
• Avoid smoking and excess salt in heart failure
• Treat anemia, infection, hypertension, thyroid disease, and arrhythmias
• Pregnancy counselling before conception in women with significant valve lesions
• Maintain good oral and dental hygiene
• Screen and treat household streptococcal infections as appropriate

B. Secondary Prevention of Rheumatic Fever

Preferred regimen

• Benzathine benzylpenicillin G 1.2 million units IM every 3-4 weeks
• Children <27 kg: 600,000 units IM every 3-4 weeks

• Penicillin V orally
• Sulfadiazine orally
• Macrolide in true penicillin allergy

Duration of secondary prophylaxis

C. Treatment According to Valvular Lesion

1. Mitral stenosis

Medical treatment

• Diuretics for pulmonary congestion
• Beta-blocker, verapamil, or diltiazem for rate control in sinus tachycardia/AF if appropriate
• Anticoagulation for:
  • AF
  • Previous systemic embolism
  • Left atrial thrombus
• Digoxin may be used in AF with heart failure

Definitive treatment

• Symptomatic severe rheumatic MS
• Favorable valve morphology
• No left atrial thrombus
• No more than mild MR

• Valve anatomy is unsuitable for PBMV
• Significant associated MR/other valve disease
• Failed PBMV
• Need for concomitant cardiac surgery

2. Mitral regurgitation

• Diuretics for congestion
• Treat AF and anticoagulate when indicated
• Valve repair or replacement for severe symptomatic MR, LV dysfunction/dilatation, or pulmonary hypertension

3. Aortic stenosis

• Definitive therapy is aortic-valve replacement:
  • Surgical AVR
  • TAVI in selected patients
• Diuretics should be used cautiously if congested
• Avoid excessive vasodilation or dehydration in severe AS

4. Aortic regurgitation

• Diuretics for heart failure
• Control hypertension
• Aortic-valve surgery for severe symptomatic AR or progressive LV dilatation/dysfunction

Anticoagulation in Rheumatic Mitral Stenosis

• Atrial fibrillation
• Previous embolic event
• Left atrial thrombus

Exam pearl: In moderate-severe rheumatic MS with AF, warfarin is preferred. Direct oral anticoagulants are generally not used as a substitute in this setting.

Prevention

1. Primordial prevention

• Reduce overcrowding and poverty
• Improve sanitation, nutrition, healthcare access, and health education

2. Primary prevention

• Early diagnosis and adequate treatment of Group A streptococcal pharyngitis with penicillin

3. Secondary prevention

• Long-term benzathine penicillin to prevent recurrent ARF and progression of RHD

High-Yield Viva Points

• Most commonly affected valve: Mitral valve
• Most common chronic lesion: Mitral stenosis
• Most common cause of MS in young adults in endemic settings: Rheumatic heart disease
• Fish-mouth deformity: Rheumatic mitral stenosis
• Most important complication of MS: Atrial fibrillation with systemic embolism
• Investigation of choice: Echocardiography with Doppler
• Most important long-term preventive measure: Secondary benzathine penicillin prophylaxis
• Definitive intervention for suitable severe rheumatic MS: Percutaneous balloon mitral valvotomy

Short Exam Conclusion

Rheumatic heart disease is chronic valvular damage following acute rheumatic fever caused by an autoimmune response to Group A streptococcal infection. It predominantly affects the mitral valve and commonly causes mitral stenosis, mitral regurgitation, or mixed valvular disease. Diagnosis is clinical and echocardiographic. Management includes secondary penicillin prophylaxis, treatment of heart failure and atrial fibrillation, anticoagulation where indicated, and timely valvotomy, valve repair, or valve replacement.

Acute Rheumatic Fever (ARF)

Definition

Epidemiology

• Commonly affects children aged 5-15 years.
• Rare before 3 years of age.
• More prevalent in settings of overcrowding, poverty, poor sanitation, and poor access to treatment of streptococcal pharyngitis.
• Recurrent attacks produce cumulative valvular damage.

Etiopathogenesis

Causative event

GAS pharyngitis → molecular mimicry → autoimmune inflammation in heart, joints, brain, and skin.

Molecular mimicry

Organ-specific immune injury

Pathology

Acute rheumatic carditis

1. Endocarditis/valvulitis: most clinically important
   • Mitral valve most commonly involved
   • Aortic valve next most common
   • Acute inflammation causes valvular regurgitation.
2. Myocarditis
   • May cause tachycardia, cardiomegaly, heart failure.
3. Pericarditis
   • Fibrinous pericarditis with pericardial rub and chest pain.

Characteristic lesion: Aschoff body

• Central fibrinoid necrosis
• Surrounding lymphocytes and plasma cells
• Activated macrophages called Anitschkow cells or caterpillar cells, because of their wavy chromatin.

Clinical Features

Major manifestations: JONES

1. Migratory polyarthritis

• Most common major manifestation.
• Involves large joints: knees, ankles, elbows, wrists.
• Classically migratory: inflammation subsides in one joint and appears in another.
• Pain is often severe and disproportionate to physical signs.
• Responds dramatically to aspirin or NSAIDs.
• Joint disease is non-destructive and resolves without permanent deformity.

Failure of arthritis to respond to NSAIDs should prompt consideration of an alternative diagnosis.

2. Carditis

Features

• Tachycardia disproportionate to fever
• New murmur:
  • Apical pansystolic murmur of mitral regurgitation
  • Early diastolic murmur of aortic regurgitation
• Cardiomegaly
• S3 gallop
• Pericardial friction rub
• Heart failure
• ECG: PR prolongation

Important point

3. Sydenham chorea

• Delayed manifestation, often appearing weeks to months after GAS infection.
• Involuntary, irregular, purposeless, non-rhythmic movements involving face, limbs, and trunk.
• May be unilateral.
• Disappears during sleep.
• Associated with emotional lability, hypotonia, clumsiness, poor handwriting, and deteriorating school performance.

4. Erythema marginatum

• Rare but highly specific.
• Pink, non-pruritic, blanching macules or papules.
• Spread centrifugally with central clearing, giving a serpiginous or annular appearance.
• Mainly affects trunk and proximal limbs.
• Usually spares the face.
• Becomes more visible after warmth, such as a hot bath.

5. Subcutaneous nodules

• Firm, painless, freely mobile nodules.
• Usually 0.5-2 cm.
• Occur over extensor surfaces and bony prominences:
  • Elbows
  • Knees
  • Wrists
  • Ankles
  • Spine
  • Occiput
• Often associated with severe carditis.

Minor Jones Criteria

Diagnosis: Revised Jones Criteria

For an initial episode of ARF

• Two major criteria, OR
• One major + two minor criteria

Plus evidence of preceding GAS infection

• Positive throat culture for GAS
• Positive rapid streptococcal antigen test
• Elevated or rising ASO titre
• Elevated anti-DNase B titre
• Recent scarlet fever

For recurrent ARF

• Two major, OR
• One major + two minor, OR
• Three minor criteria
  with supporting evidence of preceding streptococcal infection.

Investigations

To support GAS infection

• Throat culture
• Rapid antigen detection test
• Antistreptolysin O titre: elevated or rising titre
• Anti-DNase B titre

A throat swab may be negative when ARF appears because the pharyngitis occurred several weeks earlier.

To assess inflammation

• CBC: leukocytosis, mild normocytic normochromic anemia
• ESR: raised
• CRP: raised

Cardiac assessment

• ECG:
  • Sinus tachycardia
  • PR interval prolongation
  • Arrhythmia in severe carditis
• Chest X-ray:
  • Cardiomegaly
  • Pulmonary edema in heart failure
• Echocardiography with Doppler:
  • Recommended in suspected or confirmed ARF
  • Detects clinical or subclinical carditis
  • Shows MR, AR, chamber enlargement, ventricular dysfunction, pericardial effusion

Differential Diagnosis

• Septic arthritis
• Viral arthritis
• Juvenile idiopathic arthritis
• Systemic lupus erythematosus
• Post-streptococcal reactive arthritis
• Infective endocarditis
• Kawasaki disease
• Lyme arthritis
• Viral myocarditis
• Functional chorea, Wilson disease, SLE, drug-induced chorea

Treatment

Principles

1. Eradicate residual streptococcal infection.
2. Suppress inflammation and relieve symptoms.
3. Treat carditis and heart failure.
4. Control chorea.
5. Start long-term secondary prophylaxis.
6. Ensure rest and follow-up.

1. Eradication of GAS

Preferred regimen

• Benzathine benzylpenicillin G IM single dose
  • ≥27 kg: 1.2 million units
  • <27 kg: 600,000 units

Alternatives

• Penicillin V orally for 10 days
• Amoxicillin orally for 10 days
• Macrolide, for example azithromycin, in true penicillin allergy

2. Anti-inflammatory treatment

Arthritis without severe carditis

• Aspirin or an NSAID, for example naproxen.
• Aspirin has traditionally been used and produces a rapid response in rheumatic polyarthritis.
• Provide gastroprotection where appropriate and monitor for adverse effects.

Moderate/severe carditis or heart failure

• Corticosteroids, typically prednisolone, may be used in significant carditis.
• Treat heart failure conventionally:
  • Rest
  • Salt restriction
  • Diuretics
  • ACE inhibitor where suitable
  • Digoxin selectively, especially for AF, but use cautiously in acute carditis

Activity restriction

• Bed rest during active carditis/heart failure.
• Gradual return to activity after clinical and inflammatory improvement.

3. Treatment of Sydenham chorea

General measures

• Rest in a quiet environment.
• Reassurance and psychological support.
• Protect patient from injury.

For troublesome chorea

• Sodium valproate
• Carbamazepine
• Haloperidol in selected severe cases

Secondary Prophylaxis

Preferred regimen

• 1.2 million units IM every 3-4 weeks in adults/larger children
• 600,000 units IM every 3-4 weeks in children <27 kg

Duration

Prevention

1. Primordial prevention

• Reduce overcrowding and poverty.
• Improve nutrition, sanitation, healthcare access, and awareness.

2. Primary prevention

• Diagnose and fully treat GAS pharyngitis promptly with appropriate antibiotics.

3. Secondary prevention

• Long-term benzathine penicillin prophylaxis after ARF to prevent recurrence and RHD.

Complications

• Chronic rheumatic heart disease
• Mitral regurgitation in acute carditis
• Mitral stenosis in chronic RHD
• Aortic regurgitation or mixed valvular disease
• Atrial fibrillation
• Heart failure
• Pulmonary hypertension
• Left atrial thrombus and systemic embolism
• Infective endocarditis

High-Yield Viva Points

• Cause: Autoimmune response following GAS pharyngitis.
• Usual age: 5-15 years.
• Latency: 2-4 weeks after pharyngitis.
• Most common major manifestation: Migratory polyarthritis.
• Most dangerous manifestation: Carditis.
• Most commonly involved valve: Mitral valve.
• Pathognomonic lesion: Aschoff body.
• Characteristic cell: Anitschkow or caterpillar cell.
• Painful arthritis with dramatic salicylate response: ARF.
• Chorea disappears during: Sleep.
• Most effective secondary prophylaxis: Benzathine benzylpenicillin G IM every 3-4 weeks.

5-Mark Short Note

Acute rheumatic fever is an immune-mediated, multisystem inflammatory disease occurring 2-4 weeks after Group A beta-hemolytic streptococcal pharyngitis, mainly in children aged 5-15 years. It is diagnosed by revised Jones criteria: two major or one major plus two minor criteria, together with evidence of previous GAS infection. Major manifestations are carditis, migratory polyarthritis, Sydenham chorea, erythema marginatum, and subcutaneous nodules. Management includes eradication of streptococci with penicillin, anti-inflammatory treatment for arthritis/carditis, management of heart failure or chorea, and long-term benzathine penicillin prophylaxis to prevent recurrent ARF and rheumatic heart disease.

Hypertension

Definition

Classification of Blood Pressure in Adults

Exam point: Diagnose hypertension only after repeated measurements on separate visits, except in very high BP with acute target-organ damage.

Types of Hypertension

1. Primary or essential hypertension

• Accounts for about 90-95% of cases.
• No single identifiable cause.
• Caused by interaction of genetic predisposition and environmental factors.

2. Secondary hypertension

Causes of secondary hypertension: “CRAP-D”

When should secondary hypertension be suspected?

• Hypertension before age 30 years without family history or risk factors
• Abrupt onset or rapidly worsening hypertension
• Resistant hypertension
• Severe hypertension or hypertensive emergency
• Hypokalemia, especially without diuretic use
• Episodic headache, palpitations, sweating
• Renal bruit
• Rise in creatinine after ACE inhibitor/ARB
• Features of endocrine disease
• Unequal upper and lower limb BP or weak femoral pulse

Risk Factors for Essential Hypertension

Non-modifiable

• Family history
• Increasing age
• Male sex before menopause
• Ethnicity/genetic predisposition

Modifiable

• High dietary salt intake
• Obesity and central obesity
• Sedentary lifestyle
• Excess alcohol
• Smoking
• Stress
• Diabetes mellitus
• Dyslipidemia
• Obstructive sleep apnea
• Unhealthy diet, low fruit and vegetable intake

Pathogenesis of Essential Hypertension

Important mechanisms

1. Increased sympathetic nervous system activity
2. Increased renin-angiotensin-aldosterone system activity
3. Renal sodium and water retention
4. Increased peripheral vascular resistance
5. Endothelial dysfunction with reduced nitric oxide
6. Vascular remodeling and arterial stiffness
7. Obesity, insulin resistance, and inflammation

Simple flowchart

Genetic susceptibility + environmental factors
→ sympathetic and RAAS activation
→ vasoconstriction + sodium/water retention
→ increased cardiac output and systemic vascular resistance
→ sustained hypertension
→ target-organ damage

Clinical Features

Symptoms, if present

• Occipital headache, especially in morning
• Giddiness
• Palpitations
• Tinnitus
• Blurring of vision
• Fatigue
• Epistaxis
• Dyspnea or angina due to cardiac involvement
• Neurologic deficits due to stroke/TIA

Examination

General examination

• Measure BP correctly in both arms initially.
• Check pulse rate and rhythm.
• Measure BMI and waist circumference.
• Look for features of Cushing syndrome, acromegaly, thyroid disease, or renal disease.
• Examine for peripheral edema.

Cardiovascular examination

• Displaced/heaving apex: LV hypertrophy
• S4 gallop
• Signs of heart failure
• Carotid, renal, abdominal, and peripheral bruits
• Weak/delayed femoral pulses in coarctation

Fundus examination: hypertensive retinopathy

Grade IV retinopathy with papilledema suggests malignant hypertension.

Renal and neurologic examination

• Renal bruit suggests renal artery stenosis.
• Assess for focal neurological deficit, encephalopathy, or stroke.
• Look for CKD and fluid overload.

Diagnosis and Correct Measurement of BP

Correct office BP measurement

1. Avoid smoking, caffeine, and exercise for at least 30 minutes before measurement.
2. Patient should sit quietly for 5 minutes.
3. Back supported, feet flat on the floor, legs uncrossed.
4. Use an appropriate cuff size.
5. Arm should be at heart level.
6. Take at least two readings, 1-2 minutes apart.
7. Use the average of readings.
8. Measure in both arms at first visit and use the arm with the higher reading thereafter.

Out-of-office confirmation

White-coat hypertension

• Office BP high
• Home/ambulatory BP normal

Masked hypertension

• Office BP normal
• Home/ambulatory BP high

Investigations

Routine investigations in all patients

Additional tests when indicated

• Echocardiography: LVH, LV dysfunction
• Renal ultrasound: renal parenchymal disease
• Renal artery Doppler/CT angiography: renal artery stenosis
• Aldosterone-renin ratio: primary hyperaldosteronism
• Plasma-free metanephrines or urinary fractionated metanephrines: pheochromocytoma
• TSH: thyroid disorder
• Sleep study: obstructive sleep apnea
• CT/MRI abdomen: adrenal lesion
• CT angiography/MR angiography: coarctation or renovascular disease

Target-Organ Damage

Heart

• Left ventricular hypertrophy
• Ischemic heart disease/MI
• Heart failure
• Atrial fibrillation
• Sudden cardiac death

Brain

• TIA
• Ischemic stroke
• Intracerebral hemorrhage
• Hypertensive encephalopathy
• Vascular dementia

Kidney

• Albuminuria/proteinuria
• Nephrosclerosis
• Chronic kidney disease
• Renal failure

Eye

• Hypertensive retinopathy
• Retinal hemorrhages/exudates
• Papilledema

Blood vessels

• Aortic aneurysm/dissection
• Peripheral arterial disease
• Accelerated atherosclerosis

Management

Treatment Goals

A. Non-pharmacological Management

B. Drug Treatment

First-line antihypertensive drugs

1. ACE inhibitors
   • Enalapril, ramipril, lisinopril
2. ARBs
   • Losartan, telmisartan, valsartan
3. Calcium-channel blockers
   • Amlodipine, nifedipine
4. Thiazide/thiazide-like diuretics
   • Hydrochlorothiazide, chlorthalidone, indapamide

Preferred combinations

ACE inhibitor or ARB + CCB
OR
ACE inhibitor or ARB + thiazide/thiazide-like diuretic

ACEi/ARB + CCB + thiazide-like diuretic

Do not combine an ACE inhibitor with an ARB because of increased risk of renal impairment and hyperkalemia.

C. Drug Choice in Specific Conditions

Contraindications and adverse effects

Resistant Hypertension

Definition

Approach

1. Confirm correct BP measurement.
2. Check adherence.
3. Exclude white-coat effect with home/ambulatory BP.
4. Review drugs that raise BP, especially NSAIDs and steroids.
5. Assess excess salt, alcohol, and obesity.
6. Investigate secondary causes.
7. Add spironolactone if appropriate.

Hypertensive Crisis

Definition

Hypertensive urgency versus emergency

High BP alone is not a hypertensive emergency. An emergency requires acute target-organ damage.

Features of hypertensive emergency

• Hypertensive encephalopathy: headache, confusion, seizures, visual disturbance
• Acute ischemic stroke or intracranial hemorrhage
• Acute pulmonary edema/LV failure
• Acute coronary syndrome
• Aortic dissection
• Acute kidney injury
• Eclampsia
• Grade III/IV hypertensive retinopathy

General principles of treatment

1. Admit to ICU/high-dependency unit.
2. Continuous BP monitoring.
3. Use titratable IV drug appropriate to the specific condition.
4. Usually lower mean arterial pressure by no more than 20-25% in the first hour.
5. Then lower toward about 160/100-110 mmHg over the next 2-6 hours, unless a special situation applies.
6. Avoid rapid uncontrolled BP reduction, which can cause cerebral, renal, or coronary ischemia.

Drugs in hypertensive emergency

High-Yield Viva Points

• Most common type: Essential hypertension
• Most common secondary cause in adults: Renal parenchymal disease
• Best test to assess BP outside clinic: Ambulatory BP monitoring
• Investigation of choice for LVH: Echocardiography
• Most important end-organ systems: Heart, brain, kidneys, retina, blood vessels
• First-line drug classes: ACEi/ARB, CCB, thiazide-like diuretic
• Drug of choice in pregnancy: Labetalol, nifedipine, or methyldopa
• Drug contraindicated in pregnancy: ACE inhibitor/ARB
• Best add-on in resistant hypertension: Spironolactone, if suitable
• Hypertensive emergency: Severe BP elevation with acute target-organ damage
• Do not rapidly lower BP in most hypertensive emergencies: Risk of ischemia

5-Mark Short Note

Hypertension is sustained elevation of systemic arterial BP, conventionally diagnosed at persistent office BP of at least 140/90 mmHg. Most cases are essential hypertension, while secondary causes include renal disease, renovascular disease, endocrine disorders, coarctation of aorta, and drugs. It is usually asymptomatic but produces target-organ damage involving the heart, brain, kidneys, retina, and blood vessels. Evaluation includes repeated BP measurement, urine examination, renal function, electrolytes, glucose, lipid profile, ECG, and fundoscopy. Management includes salt restriction, weight control, exercise, smoking cessation, and drug therapy with ACEi/ARB, calcium-channel blocker, or thiazide-like diuretic. Hypertensive emergency requires urgent controlled IV BP reduction because acute target-organ damage is present.