Cardiology 2
Cardiology--ECG--
Electrocardiography is a transthoracic interpretation of the electrical activity of the heart over time captured and externally recorded by skin electrodes.It is a noninvasive recording produced by an electrocardiographic device.The ECG works mostly by detecting and amplifying the tiny electrical changes on the skin that are caused when the heart muscle “depolarises” during each heart beat. At rest, each heart muscle cell has a charge across its outer wall, or cell membrane. Reducing this charge towards zero is called de-polarisation, which activates the mechanisms in the cell that cause it to contract. During each heartbeat a healthy heart will have an orderly progression of a wave of depolarisation that is triggered by the cells in the sinoatrial node, spreads out through the atrium, passes through “intrinsic conduction pathways” and then spreads all over the ventricles. This is detected as tiny rises and falls in the voltage between two electrodes placed either side of the heart which is displayed as a wavy line either on a screen or on paper. This display indicates the overall rhythm of the heart and weaknesses in different parts of the heart muscle.
Normal P waves
Height less than 2.5 mm in lead II
Width less than 0.11 s in lead II
Abnormal P waves see in right atrial hypertrophy, left atrial hypertrophy, atrial premature beat, hyperkalaemia
Normal PR interval
0.12 to 0.20 s (3 – 5 small squares)
Short PR segment consider Wolff-Parkinson-White syndrome or Lown-Ganong-Levine syndrome (other causes – Duchenne muscular dystrophy, type II glycogen storage disease (Pompe’s), HOCM)
Long PR interval see first degree heart block and ‘trifasicular’ block
Normal QRS complex
Less than 0.12 s duration (3 small squares)
for abnormally wide QRS consider right or left bundle branch block, ventricular rhythm, hyperkalaemia, etc.
no pathological Q waves
Normal QT interval
Calculate the corrected QT interval (QTc) by dividing the QT interval by the square root of the preceeding R – R interval. Normal = 0.42 s.
Causes of long QT interval
Myocardial infarction, myocarditis, diffuse myocardial disease
Hypocalcaemia, hypothyrodism
Subarachnoid haemorrhage, intracerebral haemorrhage
Drugs (e.g. sotalol, amiodarone)
Hereditary – Romano Ward syndrome (autosomal dominant) ,Jervill + Lange Nielson syndrome (autosomal recessive) associated with sensorineural deafness
Normal ST segment – no elevation or depression
Causes of elevation include acute MI (e.g. anterior, inferior), left bundle branch block, normal variants (e.g. athletic heart, Edeiken pattern, high-take off), acute pericarditis
cCauses of depression include myocardial ischaemia, digoxin effect, ventricular hypertrophy, acute posterior MI, pulmonary embolus, left bundle branch block
Normal T wave
Causes of tall T waves include hyperkalaemia, hyperacute myocardial infarction and left bundle branch block
Causes of small, flattened or inverted T waves are numerous and include ischaemia, age, race, hyperventilation, anxiety, drinking iced water, LVH, drugs (e.g. digoxin), pericarditis, PE, intraventricular conduction delay (e.g. RBBB)and electrolyte disturbance.
Congenital heart disease is a type of defect in one or more structures of the heart or blood vessels that occur before birth.
* Congenital valve defects* Atrial and ventricular septal defects* Patent Foramen Ovale* Anomalous Pulmonary Veins* Coarctation of the Aorta (CoA)* Ebstein Anomaly* Pulmonary Artery Stenosis* Tetralogy of Fallot (TOF)* Transposition of the Great Arteries (TGA)* Patent Ductus Arteriosus (PDA)* Pulmonary Hypertension
Rheumatic fever is an inflammatory disease that occurs following a Group A streptococcal infection.Believed to be caused by antibody cross-reactivity that can involve the heart, joints, skin, and brain, the illness typically develops two to three weeks after a streptococcal infection.This cross-reactivity is a Type II hypersensitivity reaction and is termed molecular mimicry. Acute rheumatic fever commonly appears in children between the ages of 5 and 15.According to revised Jones criteria, the diagnosis of rheumatic fever can be made when two of the major criteria, or one major criterion plus two minor criteria, are present along with evidence of streptococcal infection.
- In the preimplantation period, two variables are predicted to predispose to the syndrome. First is low sinus rate, and second is a higher programmed lower rate limit.
- Patients with intact VA conduction are at greater risk for developing pacemaker syndrome.
- Patients with noncompliant ventricles and diastolic dysfunction_such as hypertensive cardiomyopathy, hypertrophic cardiomyopathy,restrictive cardiomyopathy, and aging, can result in loss of atrial contraction and significantly reduces cardiac output.
Mitral valve prolapse (MVP) is a valvular heart disease characterized by the displacement of an abnormally thickened mitral valve leaflet into the left atrium during systole. Prolapsed mitral valves are classified into several subtypes, based on leaflet thickness, concavity, and type of connection to the mitral annulus. Subtypes can be described as classic, nonclassic, symmetric, asymmetric, flail, or non-flail.In its nonclassic form, MVP carries a low risk of complications. In severe cases of classic MVP, complications include mitral regurgitation, infective endocarditis, congestive heart failure, and in rare circumstances cardiac arrest, usually resulting in sudden death.MVP may occur with greater frequency in individuals with Ehlers-Danlos Syndrome and Marfan syndrome.Upon auscultation of an individual with mitral valve prolapse, a mid-systolic click, followed by a late systolic murmur heard best at the apex is common.
- First degree heart block, which manifests as PR prolongation
- Second degree heart block
- Type 1 Second degree heart block, also known as Mobitz I or Wenckebach
- Type 2 Second degree heart block, also known as Mobitz II
- Third degree heart block, also known as complete heart block