ECG and Arrhythmias:
ECG changes in MI:
Early acute phase:
ST segment elevation
Hyperacute tall T waves
Fully evolved phase:
Large Q waves
Elevated ST segment begins to resolve
Inversion of T waves
Old infarction:
Large Q waves
ECG in constrictive pericarditis:
Low voltage waves and flattening or inversion of T waves
Causes of ST segment elevation :
1) Acute Mi
2) Prinzmetal angina
3) Ventricular aneurysm
4) Acute pericarditis
5) Early repolarization
6) LVH/LBBB
7) Brugada syndrome
8) DC cardioversion
9) Hyperkalemia
10) Hypothermia
Prolonged QT interval:
Hypocalcemia
Myocarditis
Acute rheumatic carditis
CVA
Drugs like quinidine, procainamide, disopyramide
Short QT interval:
Hypercalcemia
Vagal nerve stimulation
Hyperthermia
Digitalis toxicity
Digitalis toxicity:
Sign and symptoms;
Earliest manifestation is nausea and vomiting
Cachexia, weight loss
Neuralgias, gynecomastia, yellow vision, delirium
Hypokalemia , hpercalcemia ,thyroid disease ,hypomagnesemiaprecipitates digitalis toxicity
ECG changes:
Non paroxysmal atrial tachycardia with variable block is characteristic
Ventricular bigeminy and VPCs
Ventricular tachycardia and VF
Short QT interval
Treatment:
Stop the drug
Potassium supplementation
Phenytoin, b-blockers and lidocaine
Cardioversion for VF
FAB antibodies
No role of hemodialysis
ECG changes in Hypokalemia:
Prolonged PR interval
Prominent U waves
ST depression and flattening or inversion of T waves
ECG changes in hyperkalemia:
Tall peaked T waves
Prolonged PR and QRS interval
Loss of P waves
Sine wave pattern
WPW syndrome:
Short PR interval
Slurred upstroke of QRS complex or Delta wave
Wide QRS complex
Friday, May 9, 2008
Hypertrophic Obstructive Cardiomyopathy
Hypertrophic obstructive cardiomyopathy:
Characterised by ;
1. Asymmetric hypertrophy of IVS
2. Systolic anterior motion of mitral valve
3. Dynamic obstruction of left ventricle
Patient usually present with dyspnoea,anginal pain,fatigue and syncope. Sometimes sudden death occurs.
Double or triple apical impulse may be seen and there occurs rapid carotid upstroke, S4 may be heard
Systolic crescendo decrescendo diamond shaped murmur heard at lower left sternal border
Diagnosis made by echocardiography
Valsalva maneuvre , nitrate inhalation , handgrip and standing increase the intensity of murmur.
Beta-blockers are helpful in treatment
Drugs contraindicated in HOCM:
Digitalis, beta-agonists, sympathomimetic amines, nitrates, diuretics
Causes of reversible dilated cardiomyopathies:
Alcohol abuse, Pregnancy, throid disease, cocaine use and chronic uncontrolled tachycardia
Holiday heart syndrome:
Usually occurs after a alcoholic binge, Characterised by atrial fibrillation, atrial flutter and VPCs.
Peripartum cardiomyopathy:
Seen in last trimester or first six months after delivery.
Drug induced cardiomyopathy:
Doxorubicin (adriamycin) induced CMP causes cardiomyopathy when given in dose of >550mg/m2
Other risk factors include irradiation, age>70 years, underlying heart disease, HT, treatment with cyclophosphamide
To reduce toxicity, either drug is given slowly or given with some iron chelator ( dexrazoxone)
Cyclophosphamide may cause cardiotoxicity and development of CHF , characterized by myocardial oedema and hemorrhagic necrosis
Characterised by ;
1. Asymmetric hypertrophy of IVS
2. Systolic anterior motion of mitral valve
3. Dynamic obstruction of left ventricle
Patient usually present with dyspnoea,anginal pain,fatigue and syncope. Sometimes sudden death occurs.
Double or triple apical impulse may be seen and there occurs rapid carotid upstroke, S4 may be heard
Systolic crescendo decrescendo diamond shaped murmur heard at lower left sternal border
Diagnosis made by echocardiography
Valsalva maneuvre , nitrate inhalation , handgrip and standing increase the intensity of murmur.
Beta-blockers are helpful in treatment
Drugs contraindicated in HOCM:
Digitalis, beta-agonists, sympathomimetic amines, nitrates, diuretics
Causes of reversible dilated cardiomyopathies:
Alcohol abuse, Pregnancy, throid disease, cocaine use and chronic uncontrolled tachycardia
Holiday heart syndrome:
Usually occurs after a alcoholic binge, Characterised by atrial fibrillation, atrial flutter and VPCs.
Peripartum cardiomyopathy:
Seen in last trimester or first six months after delivery.
Drug induced cardiomyopathy:
Doxorubicin (adriamycin) induced CMP causes cardiomyopathy when given in dose of >550mg/m2
Other risk factors include irradiation, age>70 years, underlying heart disease, HT, treatment with cyclophosphamide
To reduce toxicity, either drug is given slowly or given with some iron chelator ( dexrazoxone)
Cyclophosphamide may cause cardiotoxicity and development of CHF , characterized by myocardial oedema and hemorrhagic necrosis
Cardiac Murmurs and Heart Sounds
Heart Sounds:
Loud S1 : 1) Tachycardia
2) High output states
3) Mitral stenosis
4) Short PR interval
Soft S1 :
1) Obesity
2) Long PR interval
3) Mitral regurgitation
4) Mitral valve calcification
Widening of S1 : Complete right bundle branch block
Reversed splitting of S1
1)Severe MS
2) Left atrial myxoma
3) Left Bundle Branch Block
Wide Fixed splitting of S2
1) ASD
Reversed Splitting of S2:
1)LBBB
2) Severe aortic outflow obstrucion
3) Large aorta to pulmonary artery shunt
4) Systolic hypertension
5) IHD
6) ICMP with LVF
Heart Murmurs :
Pansystolic murmur
1) MR
2) TR
3) PDA
4) VSD
Midsystolic murmurs :
Often crescendo -decrescendo in shape
1) Functional murmurs
2) AS
3) HOCM
Early Systolic murmur:
1)Large VSD with pulmonary hypertension
2) Small VSD
3) TR
4) Acute MR
Late Systolic murmurs
1) MI leading to papillary muscle dysfunction
2) MVP
Early diastolic murmurs
1) Aortic and pulmonary regurgitation
Murmur of AR increases with handgrip exercise and decreases with amyl nitrate inhalation
Middiastolic murmurs :
1) Mitral stenosis
2) Tricuspid stenosis
3) Acute rheumatic fever ( Carey coomb murmur)
4) Aortic regurgitation ( Austin flint murmur)
Late diastolic murmurs:
Right or left atrial myxoma
Continuous murmurs:
1) PDA
2) Congenital or acquired AV fistula
3) Coronary AV fistula
4) Anomalous origin of coronary from pulmonary artery
5) Communication between sinus of valsalva and right side of heart
6) Coarctation of aorta
Source: www.pgexam.com
Loud S1 : 1) Tachycardia
2) High output states
3) Mitral stenosis
4) Short PR interval
Soft S1 :
1) Obesity
2) Long PR interval
3) Mitral regurgitation
4) Mitral valve calcification
Widening of S1 : Complete right bundle branch block
Reversed splitting of S1
1)Severe MS
2) Left atrial myxoma
3) Left Bundle Branch Block
Wide Fixed splitting of S2
1) ASD
Reversed Splitting of S2:
1)LBBB
2) Severe aortic outflow obstrucion
3) Large aorta to pulmonary artery shunt
4) Systolic hypertension
5) IHD
6) ICMP with LVF
Heart Murmurs :
Pansystolic murmur
1) MR
2) TR
3) PDA
4) VSD
Midsystolic murmurs :
Often crescendo -decrescendo in shape
1) Functional murmurs
2) AS
3) HOCM
Early Systolic murmur:
1)Large VSD with pulmonary hypertension
2) Small VSD
3) TR
4) Acute MR
Late Systolic murmurs
1) MI leading to papillary muscle dysfunction
2) MVP
Early diastolic murmurs
1) Aortic and pulmonary regurgitation
Murmur of AR increases with handgrip exercise and decreases with amyl nitrate inhalation
Middiastolic murmurs :
1) Mitral stenosis
2) Tricuspid stenosis
3) Acute rheumatic fever ( Carey coomb murmur)
4) Aortic regurgitation ( Austin flint murmur)
Late diastolic murmurs:
Right or left atrial myxoma
Continuous murmurs:
1) PDA
2) Congenital or acquired AV fistula
3) Coronary AV fistula
4) Anomalous origin of coronary from pulmonary artery
5) Communication between sinus of valsalva and right side of heart
6) Coarctation of aorta
Source: www.pgexam.com
Subscribe to:
Comments (Atom)