• Peaking of T waves
• Increase in PR interval (AV conduction delay)
• Wide QRS complex
• Loss of P waves

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• ST elevation with concavity upward
• T inversion occurs after some days (once ST segment returns to baseline)
• No change in QRS complexes (decrease in QRS voltage may occur in massive pericardial effusions)
• PR segment depression (due to atrial involvement)
• Atrial premature beats, atrial fibrillation

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1. Winter bronchitis
2. Paroxysmal nocturnal dyspnoea
3. Pulmonary oedema
4. Pulmonary apoplexy
5. Pulmonary infarction
6. After anticoagulant therapy.

1. Radiological signs in mitral stenosis
2. AIIMS November 2011 – MCQ 14
3. Air bronchogram – Mechanism, Causes

• By inducing a stress response which increases the sympathetic tone
• Increased sympathetic tone can precipitate atrial fibrillation (AF)
• Hypoxia leading to increased pulmonary resistance
• This results in pulmonary hypertension and atrial dilatation
• Atrial dilatation can lead to AF
• Direct involvement of the atria

1. Mechanism of development of atrial fibrillation in valvular heart disease
2. Atrial fibrillation with bigeminal rhythm
3. Pharmacology – MCQ 122 – 60 year old man with atrial fibrillation

1. Radiology – MCQ 31 – Most preferred route for cerebral angiography
2. Anatomy – MCQ 57 – Branches of external carotid artery
3. Anatomy – MCQ 12 – Posterior communicating artery a branch of

1. Mechanism of wide fixed split in Atrial septal defect (ASD)
2. Mechanism of wide fixed split in severe right heart failure
3. Mechanism of physiological split in second heart sound

• First you can review the Mechanism of normal split in second heart sound
• In severe right heart failure, the right ventricle takes a longer time to eject the blood – hence the wide split
• Also since it cannot accomodate the increased blood flow during inspiration, there is no increase in the split during inspiration

If you couldn’t grasp the rationale behind it, here’s an example:

• Imagine the right ventricle to be a plane with 100 seats (seats referring to the capacity)
• Lets first take the case of a normal right ventricle
• Imagine that during the weekdays (expiration) about 50 people travel in it
• But during the weekends (inspiration) about 60 people travel in it (due to increased venous return)
• Its easy to understand that during the weekends, it takes a longer time for the people to get out of the plane
• But in the holiday season (right heart failure), the plane (right ventricle) is full during both weekdays and weekends
• Even though there is more demand for the plane during the weekends, (due to increased venous return) the plane (right ventricle) cannot accommodate any more people (blood)
• Hence there is no difference in time taken for people to exit from the plane (the time taken to eject the blood is the same)
• This explains the fixed split
• Hope I didn’t confuse you with the explanation! If you find any difficulty in understanding this concept, please leave a comment below.

1. Mechanism of wide fixed split in Atrial septal defect (ASD)
2. Mechanism of physiological split in second heart sound
3. Split of second heart sound in Ventricular Septal Defect (VSD)

So, why does it cause a wide fixed split instead of a wide variable split?

• During inspiration, the blood flow through the vena cava increases, whereas that from the left atrium decreases
• Whereas during expiration, blood flow through the vena cava decreases, and that from the left atrium increases
• During the respiratory cycle, the blood flow through the vena cava and left atrium vary reciprocally
• Hence the wide fixed split

You can also read about : Split of second heart sound in Ventricular Septal Defect (VSD)

1. Mechanism of wide fixed split in severe right heart failure
2. Split of second heart sound in Ventricular Septal Defect (VSD)
3. Mechanism of physiological split in second heart sound

• During inspiration, a negative intrathoracic pressure is created to inhale air into the lungs
• This creates a vaccum effect which results in increased venous return to the right side of the heart
• Hence the right ventricle takes a longer time to eject the blood into the pulmonary system
• Also since pulmonary vasculature expands in capacity, lower amount of blood flows into the left atrium
• Hence the left ventricle takes a shorter time to eject blood into the aorta
• Because of these 2 factors, the aortic valve closes before that of the pulmonary valve and we can appreciate the split during inspiration

1. Mechanism of wide fixed split in severe right heart failure
2. Mechanism of wide fixed split in Atrial septal defect (ASD)
3. Hangout interval – Mechanism, significance

Why does pulmonary valve remain open even after pressure equilisation?

• According to Newton’s first law of motion, every body continues to move at constant speed unless acted upon by an external force
• In this case, the blood continues to flow from the right ventricle even after the the pressure in the right ventricle and the pulmonary artery becomes equal
• Just like a rolling ball is stopped by the friction offered by the ground, the ejection of blood is stopped by the resistance offered by the pulmonary vasculature
• Since the pulmonary vascular resistance is low compared to the systemic vascular resistance, it takes some time for the blood flow from the right ventricle to stop
• This corresponds to the hangout interval

Significance of hangout interval

• Hangout interval is shortened in cases of increased pulmonary vascular resistance such as pulmonary vasospasm, obliteration of pulmonary vessels etc

Does the aortic valve have a hangout interval?

• Due to high systemic vascular resistance, the aortic valve closes almost immediately
• Hence hangout interval is negligible

1. Mechanism of physiological split in second heart sound
2. Split of second heart sound in Ventricular Septal Defect (VSD)
3. Inspiratory decrease in systolic blood pressure and pulse volume – Mechanism

• Paroxysmal AF – Lasting upto 7 days. But usually it undergoes spontaneous resolution within 48 hours
• Persistent AF – Lasting more than 7 days upto 1 year
• Long standing persistent AF – If an AF lasts more than 1 year and we are planning to do rhythm control treatment (chemical cardioversion / electrical cardioversion / ablation of the excitation focus)
• Permanent AF – If AF lasts for more than 1 year and we are not planning to do any rhythm control treatment (due to any reason)

1. Atrial fibrillation with bigeminal rhythm
2. Planning commission of India
3. Mechanism of development of atrial fibrillation in chest infections

• Backward displacement of esophagus by enlarged left atrium (in lateral view X-ray)
• Enlarged left atrium in AP view X-ray (Blood pools in the left atrium as it is unable to pass into the left ventricle. This results in progressive dilatation.)
• Straightening of left heart border
• Double shadow due to enlarged left atrium
• Splaying of carina (The left main bronchus is lifted up by the enlarged left atrium)
• Prominent upper zone pulmonary veins (Inverted moustache sign /  Antler’s horn sign / Cephalisation pulmonary of blood flow)
• Enlarged pulmonary trunk (This occurs following the development of pulmonary hypertension)
• Kerley B lines (indicating fluid collection in the interlobular septa)
• Calcification of mitral valve

1. Causes of hemoptysis in Mitral Stenosis
2. Normal indentations on the esophagus in barium swallow – Right anterior oblique view chest X-ray
3. Mechanism of physiological split in second heart sound

Pattern of cardiac involvement in carcinoid syndrome

• Serotonin which is secreted in excess amounts in carcinoid syndrome is the cause of the cardiac manifestations
• It is metabolised in the lungs and liver
• So in most cases of carcinoid syndrome, there is no involvement of the heart
• But in cases of metastatic carcinoid syndrome involving liver and the lungs, the heart is directly exposed to huge quantities of serotonin
• Right heart lesions are seen in liver metastasis and left heart lesions are seen in lung metastasis
  • There is no involvement of the left heart in liver metastasis because serotonin is metabolised in the lungs before reaching the left heart
  • Similarly, the right heart is spared in lung metastasis because the blood passes through the liver before reaching the right heart

Pathology of the cardiac changes in carcinoid syndrome

• High concentration of serotonin causes fibrosis of the papillary muscles and valve leaflets resulting in valve defromity

1. Mechanism of physiological split in second heart sound
2. Mechanism of development of atrial fibrillation in valvular heart disease
3. Obstetrics & Gynaecology – MCQ 27 – Heart disease in pregnancy

Click on image for an enlarged view

• The normal indentations of the esophagus seen in a right anterior oblique view during barium swallow are made by (from above downwards):
  • Aortic arch – 22.5 cm from incisor teeth
  • Left bronchus – 27.5 cm from incisor teeth
  • Left atrium
• Clinical importance:
  • In olden days, when echocardiography was not available, this was used to detect left atrial enlargement in cases of mitral stenosis
  • When left atrium is enlarged, it may compress on the esophagus and cause dysphagia – known as cardio esophageal syndrome

1. Constrictions of oesophagus
2. Radiological signs in mitral stenosis
3. Normal chest X-ray

Causes:

• Constrictive pericarditis
• Restrictive cardiomyopathy

Mechanism:

• Normally there is inspiratory decrease in JVP (Read Mechanism of inspiratory decrease in JVP)
• In the conditions mentioned above, the pericardium / myocardium is stiff
• The negative intrathoracic pressure is not transmitted to the heart
• The heart cannot accommodate the increased blood flow that occurs during inspiration
• Hence the jugular venous pressure will be elevated

1. Mechanism of inspiratory decrease in JVP
2. Pulsus paradoxus
3. Inspiratory decrease in systolic blood pressure and pulse volume – Mechanism

1. Kussmaul’s sign – Causes, Mechanism
2. Inspiratory decrease in systolic blood pressure and pulse volume – Mechanism
3. Mechanism of physiological split in second heart sound

• Tall tented T waves
• Widening of PR interval and QRS complex
• Absence of P wave in extreme cases

1. Medicine – MCQ 133 – Features of hyperkalemia
2. Medicine – MCQ 15 – ECG findings are seen in Hypokalemia
3. Left bundle branch block

Advantages:

• The pulmonary valve that is transplanted can continue to grow
• Better longevity for the homograft valve as it is placed in the low pressure pulmonary circulation

1. Hangout interval – Mechanism, significance
2. Mechanism of physiological split in second heart sound
3. Aortic stenosis with coexistent aortic regurgitation – Causes

Reference:
Hypertension: a companion to Brenner and Rector’s the kidney By Suzanne Oparil, Michael A. Weber

1. Physiology – MCQ 22 – Cardiovascular changes in isometric exercise
2. Anaesthesia – MCQ 10 – Dissociative anaesthesia
3. Heart conditions in which pregnancy is contraindicated

How to assess distal runoff?

• Angiography can be used to assess distal runoff – TIMI (Thrombolysis In Myocardial Infarction) flow grading
• Based on the amount of contrast material that reaches the distal segment and the rate of clearance of contrast in distal segment, there are 4 TIMI flow grades
  • Grade 3 – Good opacification of distal segment with rapid clearance of contrast material as in the proximal segment
  • Grade 2 – Good opacification of distal segment with slow clearance of contrast material
  • Grade 1 – Poor opacification of distal segment
  • Grade 0 – Contrast material does not reach distal segment

1. Physiology – MCQ 39 – Factors determining coronary blood flow
2. Physiology – MCQ 17 – Cerebral blood flow regulation
3. Physiology – MCQ 35 – Factors influencing turbulence in blood flow

Aortic stenosis – rheumatic
Click on image for an enlarged view

In the following conditions, aortic stenosis can coexist with aortic regurgitation (aortic incompetence).

• Rheumatic
• Congenital bicuspid aortic valve
• Calcific degeneration of aortic valve
• Atherosclerotic degeneration of aortic valve
• Infective endocarditis in a case of aortic stenosis

H0w aortic stenosis and regurgitation can coexist?

• It can be explained by the following analogy
• Consider a normal aortic valve to be a door
• It closes and opens completely during each cardiac cycle
• Now consider the door to be stuck in the mid position
• It neither closes completely nor opens completely
• Similarly, when the aortic valve is deformed, both stenosis and regurgitation can coexist

1. Medicine – MCQ 53 – Water hammer pulse
2. Medicine – MCQ 151 – 59 year old man with severe myxomatous mitral regurgitation
3. Ross procedure (aortopulmonary translocation)

The reason for the decrease in systolic blood pressure during inspiration is explained in this article : Inspiratory decrease in systolic blood pressure and pulse volume – Mechanism

Mechanism of pulsus paradoxus:

1. In cardiac tamponade
   • Tense fluid in the pericardial sac impairs ventricular filling
   • Also, the negative intrathoracic pressure is not well transmitted to the pericardial sac
   • Fall in pulmonary venous pressure is more than the fall in left atrial pressure
   • Hence filling of the left atrium and in turn the left ventricle is decreased resulting in decrease in stroke volume more than normal
2. In obstructive pulmonary disease
   • There is exaggeration of the inspiratory decrease in intrathoracic pressure
   • Hence the fall in stroke volume and blood pressure is more

What is the paradox?
Pulsus paradoxus is an exaggeration of the normal variation in the systolic blood pressure and hence it is not truly paradoxical.

1. Inspiratory decrease in systolic blood pressure and pulse volume – Mechanism
2. Kussmaul’s sign – Causes, Mechanism
3. Frusemide in left ventricular failure

Mechanism

• During inspiration there is increased venous return (due to negative intrathoracic pressure)
• right ventricles expands more
• interventricular septum is pushed to the left side (Reverse  Bernheim effect)
• This decreases the left ventricular volume
• Also the pooling of blood in the pulmonary circulation occurs, decreasing amount of blood reaching left ventricle

This causes decrease in stroke volume of left ventricle, thus decreasing the systolic blood pressure. The maximum decrease in blood pressure that is considered normal is 10 mm Hg. If the decrease is more than 10 mm Hg, it is called pulsus paradoxus.

1. Pulsus paradoxus
2. Mechanism of inspiratory decrease in JVP
3. Physiology – MCQ 18 – Blood pressure measurement

Can occur due to

• Physiologically during inspiration due to increased filling of the right ventricle (because of increased venous return)
• pulmonary embolism

1. Bernheim effect
2. Mechanism of physiological split in second heart sound
3. Inspiratory decrease in systolic blood pressure and pulse volume – Mechanism

1. Reverse Bernheim effect
2. Paediatrics – MCQ 44 – Tetralogy of Fallot
3. Pathology – MCQ 54 – Subendocardial infarction

Straw coloured pericardial fluid

Straw coloured pericardial fluid aspirated into a syringe. Straw coloured fluid indicates an exudative effusion and tuberculosis is an important cause.

1. Pleural effusion – left
2. Multiple air-fluid levels in intestinal obstruction
3. Minimal pleural effusion

CI = CO/BSA

1. Ankle brachial index
2. Aedes aegypti Index
3. Physiology – MCQ 81 – Absence of edema in acute cardiac failure – mechanism

1. Physiology – MCQ 82 – Valvular events in cardiac cycle
2. Physiology – MCQ 29 – Special features of Pulmonary circulation
3. Physiology – MCQ 81 – Absence of edema in acute cardiac failure – mechanism

1. CO – Acronym
2. CI – Acronym
3. ICD – Acronym

abbreviation, expansion

1. Most common site of aortic aneurysm
2. ICD – Acronym
3. Aortic stenosis with coexistent aortic regurgitation – Causes