Constrictive pericarditis
Cardiac tamponade
* 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
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 is more common in older men (>75 years). 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 with little or no prodrome. Treatment for CSS is dual chamber pacing.
Classically, cardiac output is decreased in heart failure. However, in some cases there can be high-output cardiac failure, where exceedingly high metabolic demands can’t be met even by increasing the cardiac output.
Aschoff nodules or bodies: It is the pathognomonic histopathological feature of rheumatic carditis. They are spheroidal or fusiform lesions and show fibrinoid necrosis and an inflammatory infiltrate of T cells, plasma cells and Anitschkow cells (modified cardiac histiocytes with caterpillar shaped or owl’s eye shaped nucleus), along with multinucleate Aschoff cells (modified Anitschkow cells).
In this progressive disorder, the SA node fails to function properly. It is more common in old age, especially with age related SA node fibrosis. Other associations include amyloidosis, sarcoidosis, cardiac surgery, muscular dystrophy, hypoxia, and antiarrhythmics.
Mutations in SCN5A, MYH6 and HCN4 may cause sick sinus syndrome. These genes encode ion channels or myosin, and mutations may be inherited as AR or AD.
Presentation includes 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 may show brady- or tachy-arrhythmias, sinoatrial block or arrest and missed beats, or it may be normal.
It is characterized by an 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 the 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 a 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.