Additional information

Quick tips on infective endocarditis

• Most common cause of ABE: S.aureus, Group A streptococci (beta hemolytic streptococci), Brucella, Listeria
• SABE most common cause: S.viridans
• Prosthetic valve endocarditis most common cause: S.epidermidis
• Most common cause of infective endocarditis: S.viridans
• Most common cause of infective endocarditis in intravenous drug abusers: S.aureus
• Culture negative endocarditis: Coxiella burnetii, Bartonella, HACEK group of bacteria, anaerobic bacteria, Legionella, Mycoplasma, Abiotrophia
• S.bovis endocarditis: look for Ca colon
• Fungal endocarditis: Candida albicans and aspergillus most common; high mortality, previous surgery or intravenous drug use, prosthetic valves, parenteral nutrition, indwelling catheters, broad spectrum antibiotics

Constrictive pericarditis and cardiac tamponade

Constrictive pericarditis

• Thickened, fibrotic, calcified pericardium
• Elevated JVP
• Muffled heart sounds
• Pericardial knock
• Apical impulse may be impalpable
• Positive Kussmaul sign*
• Pulsus paradoxus present**
• Steep Y descent on JVP tracing
• Low voltage QRS complexes on ECG
• Ventricular septal motion defects may be seen on echo

Cardiac tamponade

• Bottle-shaped heart
• Positive Beck’s triad of elevated JVP, hypotension and muffled or distant heart sounds
• Positive Kussmaul sign
• Pulsus paradoxus present
• Abolished Y descent on JVP tracing
• Electrical alternans on ECG***
• Echo shows diastolic collapse of the right atria and ventricle

* Kussmaul sign is increased JVP during inspiration.

** Pulsus paradoxus is decrease in blood pressure of more than 10 mmHg during inspiration

*** Electrical alternans shows varying amplitudes of ECG complexes due to the heart swinging in the fluid filled pericardial sac in cardiac tamponade

Causes of sudden cardiac death

• CAD
• Aortic stenosis
• HOCM
• Mitral valve prolapse
• Disorders of conduction system of the heart, channelopathies
• Family history
• Long QT syndrome

Carotid sinus syndrome (CSS) and carotid sinus hypersensitivity (CSH): Carotid sinus syndrome is defined as syncope with reproduction of symptoms during carotid sinus massage (CSM) of 10s duration. It may be cardioinhibitory, vasodepressor or mixed. Cardioinhibitory CSS shows 3s asystole on CSM and vasodepressor CSS shows >50 mmHg fall in blood pressure. CSH is present when a patient has cardioinhibitory, mixed or vasodepressor findings on CSM, with or without symptoms but is asymptomatic otherwise. CSS presents more commonly in old men > 75 years of age. It is often associated with cardiovascular disease. Abnormal function of the baroreceptors and degeneration of the medulla are the causative factors. Tight collars and neck movements, neck tumours, neck surgery or irradiation may act as triggers. Patients present with syncope that has little or no prodrome. Treatment for CSS is dual chamber pacing.

Classically, cardiac output is decreased in heart failure, but in some cases there can be high-output cardiac failure, where the exceedingly high metabolic demands cannot be met even by increasing the cardiac output.

Causes of high output heart failure

• Severe anemia
• Hyperthyroidism
• Paget’s disease of bone
• AV fistulas e.g. from trauma
• Berberi
• Early septic shock

Aschoff nodules or bodies: It is the pathognomonic histopathological feature of rheumatic carditis. They are spheroidal or fusiform lesion and shows fibrinoid necrosis, inflammatory infiltrate of T cells, plasma cells and Anitschkow cells (modified cardiac histiocytes with caterpillar shaped or owl’s eye shaped nucleus) and multinucleate Aschoff cells (modified Anitschkow cells).

Innocent or functional or flow murmurs

• Common in infants and children
• No structural valvular lesion
• Intensity changes with changes in flow
• Increase in fever, anemia, exercise
• Grade 1 or 2
• Typically systolic

Complications of artificial valves

• Thromboembolism with stroke
• Prosthetic valve thrombosis
• Endocarditis (Staphylococci most common)
• Bleeding from drug adverse effect (warfarin)
• Structural dysfunctions of valve
• Paravalvular leaks
• Hemolytic anemia, acanthocytes
• Pannus formation (ingrowth of tissue)

Cor Pulmonale

• May be acute or chronic
• Right ventricular enlargement due to pulmonary artery hypertension from lung disease
• Elevated RV end-diastolic pressure
• Seen in COPD, massive PE, mechanical ventilation in ARDS, systemic sclerosis, ILD, obesity
• Dyspnea, fatigue, hepatomegaly, lower limb edema
• Left parasternal heave , loud P2, S3, S4
• Raised JVP, prominent “a” wave

Sick Sinus Syndrome

In this progressive disorder, the SA node fails to function properly. It is more common in old age, in those with age related SA node fibrosis, amyloidosis, sarcoidosis,cardiac surgery, muscular dystrophy, hypoxia, antiarrhythmics etc. Mutations in SCN5A, MYH6 and HCN4 may cause sick sinus syndrome. These genes encode ion channels or myosin and mutations may be inherited asAR or AD. Presentation is with dizziness, light-headedness, syncope, a sensation of fluttering or pounding in the chest , and confusion or memory problems. During exercise, many affected individuals experience chest pain, difficulty breathing or excessive tiredness. ECG shows brady or tachy-arrhythmias, sinoatrial block or arrest and missed beats, or it may even be normal.

Long QT syndrome

It is characterized by abnormally long QT interval which predisposes to life threatening arrhythmias. Congenital long QT syndrome is inherited as an AD or AR disease with mutations in genes KCNQ1, KCNH2, SCN5A etc. most of them coding for ion channels that play a role in cardiac action potential. Congenital long QT syndromes are Romano - Ward and Jervell and Lange-Nielson syndromes. The latter is associated with sensorineural deafness.

 A corrected QT interval or QTc > 450 milliseconds, notched or biphasic T waves along with history of syncopes is highly suggestive of long QT syndrome. There is a high risk of Torsades de pointes, ventricular fibrillation and sudden death. Exercise, emotional or auditory stimuli or even sleep may trigger arrhythmias in long QT syndrome. 


Acquired QT prolongation may be seen in AMI, seizures, antipsychotics like chlorpromazine, haloperidol etc, TCAs, antidepressants and electrolyte imbalances.