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Electrolyte inbalance
Calcium
Hypercalcaemia and hypocalcaemia predominantly alter the action
potential (AP) duration. An increased extracellular Ca concentration
shortens the ventricular AP duration. In contrast, hypocalcaemia
prolongs the ventricular AP duration. These cellular chancges correlate
with abbreviation and prolongation of the QT interval (ST segment
portion)) with hypercalcaemia and hypocalcaemia, respectively.
Potassium
Hyperkalaemia is associated with a distinctive sequence of
electrocardiographic changes. The earliest effect is usually the narrowing
and peaking (tenting) of the T wave. The QT interval is shortened by this
stage, associated with decreased AP duration. The QRS begins to widen
and P wave amplitude decreases. PR interval prolongation can occur
followed by second/third degree AV block. Complete loss of P waves can
occur too. Moderate to severe hyperkalaemia occasionally induces ST
elevations in the righ precordial leads (V1 & V2). Severe hyperkalaemia
can also present with atypical finds. Very marked hyperkalaemia leads to
eventual asystole. The triad of (1) peaked T waves (from hyperkalaemia),
(2) QT prolongation (from hypocalcaemia) and (3) LVH (from
hypertension) is strongly suggestive of chronic renal failure.
Hypokalaemia, in contrast, include hyperpolarisation of myocardial cell
membranes and increased AP duration. The major manifestations are ST
depression with flattened T waves and increased I wave prominence.
Hypokalaemia also predisposes to tachyarrythymias.
Magnesium
Specific ECG findings of mild/moderate magnesium abnormalities are not
well characterised. Severe hypermagnesaemia can cause AV and
intraventricular conduction disturbances that may culminate in complete
heart block and cardiac arrest. Hypomagnesaemia can pontentiatre
certain digitalis toxic arrythymias.
Sodium and
other
Hypo/hypernatraemia does not produce consistent effects on ECG.
Systemic hypothermia may be associated with an appearance of a
distinctive convex elevation of (J point) of ST segment and QRS complex (J
wave or Osborne wave).
Basics of ECG pattern
Rate
Rhythym
Big square is 0.2s small square is 0.04s. To calculate rate, divide 300
divided by number of big squares
Use the ‘card method’ to confirm whether regular/irregular
Axis
The mean frontal axis is the sum of all ventricular forces during ventricular
depolarisation. The axis lies 90 degrees to the isoelectric complex.
Generally if the complexes in leads I and II are both positive the axis is
normal.
P wave
Absent P wave: AF, sinoatrial block. Dissociation between P and QRS
indicates complete heart block. Bifid P wave indicates left atrial
hypertrophy. Peaked P (P pulmonale) wave indicates right atrial
hypertrophy.
PR interval
Range is 0.12-0.2s. Prolonged PR interval indicates delayed Av conduction
(1st degree heart block). A short PR interval indicates unusual fast AV
conduction down an accessory pathway e.g. WPW syndrome.
QRS complex
Normal duration <0.12s. If prolonged suggests ventricular conduction
defect eg Bundle branch block. Large QRS complexes suggest ventricular
hypertrophy. Normal Q waves (0.04s wide and <2mm deep) are often seen
in leads V5 V6 aVL and I, and reflex normal septal depolarisation.
Pathological Q waves may occur within a few hours of a MI.
QT interval
Varies with rate, normal is 0.38-.042s. The corrected QT interval equals the
measured QT interval divided by the square root of the cycle length.
ST segment
Usually isoelectric. Planar elevation (<1mm) or depression (<0.5mm)
usually implies infarction or ischaemia, respectively.
T wave
Normally inverted in aVR, V1 and occasionally V2. Abnormal if inverted in I,
II, and V4-V6. Peaked in hyperkalaemia and flattened in hypokalaemia.
J wave
Seen in hypothermia, subarachnoid haemorrhage and hypercalcaemaia.
Cardiac arrest
Causes – two ways to remember
H’s & T’s
Hypovolaemia
Hypoxia
Hydrogen ions (acidosis)
Hyper/hypokalaemia
Hypothermia
Hyper/hypoglycaemia
Tablets/toxins
Tamponade (cardiac)
Tension pneumothorax
Thrombosis (MI)
Thromboembolism
Trauma
COLD PATCH
C
Cold (hypothermia)
O
Oxygen deficit
L
‘Lytes’ (potassium)
D
Drugs
P
Pulmonary Embolus
A
Acidosis
T
Tension Pneumothorax
C
Cardiac Tamponade
H
Hypovolemia.
Pathophysiology
In VT/VF, acute myocardial ischaemia results in changes in the concentration of many
components of the intracellular and extracellular milieu (e.g., pH, electrolytes, and ATP). In
turn, these changes form the basis for pathogenic impulse formation and propagation of
arrhythmia. In patients with areas of myocardial scarring, the mechanism for arrhythmia is
likely to be a re-entrant circuit generated by surviving myofibrils within areas of fibrosis.
Studies of non-ischaemic dilated cardiomyopathy have shown that the mechanism of
arrhythmia is not re-entry, but more likely the initiation of VT/VF from early or late afterdepolarisations in the setting of a prolonged action potential duration, which in turn is due
to the altered function of various ion channels.
Despite widespread and long-standing use, no drug has definitively been shown to increase
survival to hospital discharge in patients with cardiac arrest. In a patient with a peripheral IV
line, drug administration is followed by a fluid bolus.
Epinephrine is the main drug used in cardiac arrest although its benefit is increasingly
challenged. It is given 3 to 5 min. Epinephrine has combined α- and β-adrenergic effects. The
α-adrenergic effects may augment coronary diastolic pressure, thereby increasing
subendocardial perfusion during chest compressions. Epinephrine also increases the
likelihood of successful defibrillation. However, β-adrenergic effects may be detrimental
because they increase O2 requirements (especially of the heart) and cause vasodilation.
Intracardiac injection of epinephrine is not recommended because pneumothorax, coronary
artery laceration, and cardiac tamponade may occur.
Atropine sulfate is a parasympatholytic drug that increases heart rate and conduction
through the atrioventricular node. It is given for asystole (except in children),
bradyarrhythmias, and high-degree atrioventricular nodal block, although no survival
benefit has been demonstrated.
Amiodarone can be given once if defibrillation is unsuccessful following epinephrine
Mg sulfate has not been shown to improve outcome in randomized clinical studies.
However, it may be helpful in patients with torsades de pointes or known or suspected Mg
deficiency (ie, alcoholics, protracted diarrhea).
Prevention of cardiac arrest
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Early recognition of symptom and quick action – follow early warning scores
Treat risk factors for cardiac arrest in community
In hospital – recognition of at risk patients e.g. critically ill
Improve education of cardiac arrest prevention
Pulmonary embolism
Risk factors
Symptoms
Signs
Investigations
Treatment
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Surgery
Pregnancy
Reduced mobility
IV drug use
Dyspneoa
Pleuritic chest pain
Haemoptysis
Collapse
Tachycardia
Tachypnoeic
Pleural rub
Raised JVP
In major PE signs of shock
Baseline investigation for ill patient
CXR
Echo
Pulmonary angiogram
ECG
D-Dimer
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Oxygen
Morphine
Heparin
Aortic dissection
Aortic dissection starts with a tear in the intima of the aortic lining. The tear allows a column
of blood under pressure to enter the aortic wall forming a haematoma which separates the
intima from the adventitia and creates a false lumen. The false lumen extends for a variable
distance in either direction. Most common site is within 2-3cm of aortic valve. Risk factors
include hypertension, smoking, cholesterol, etc.
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90% of all patients with aortic dissection, present with a sudden severe pain of the chest or
back, classically described as "ripping/sharp".
In aortic dissection, pain is abrupt in onset and maximal at the time of onset. In contrast, the
pain associated with acute myocardial infarction starts slowly and gains in intensity with
time. It is usually more oppressive and dull.
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pain migrates as the dissection progresses.
Investigations – ECG, CXR, CT/MRI
Management – Morphine, manage hypertension, then placing of stents or grafts to the aorta.
MI
Risk factors
Symptoms
Signs
Investigations
Treatment
 Gender
 Smoking
 Diabetes
 Family history
 Hypertension
 Obesity
 Dull chest pain
 Dyspnoea
 Sweating, vomiting, nausea
 Low grade fever
 Pale clammy skin
 Pericardial rub
 Baseline investigation for ill patient
 ECG
 Cardiac enxymes (troponin)
 CXR
 Echo
MONA – acute care
 Morphine
 Oxygen
 Nitro-glycerine
 Aspirin
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Reperfusion
Fibrinolytic drugs
(streptokinase/alteplase)
Percutaneous coronary intervention
CABG
Aortic stenosis
Senile calcification commonest cause
Classic triad is angine, syncope and heart failure. Signs include slow rising pulse, aortic thrill,
ejection systolic murmur which radiates to carotids. In severa AS second heart sound be
inaudible. ECG and echo are used to diagnose AS. Treatment is valve replacement.
Cardiomyopathy
Is disease of the cardiac muscle. According to WHO 5 main Groups.
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Dilated cardiomyopathy: commonest form. The left or both ventricles are dilated
with impaired contraction. Causes include: ischaemia, alcoholic, toxic, thyroid
disorders, valvular, familial/genetic and idiopathic.
Hypertrophic obstructive cardiomyopathy: 2nd commonest; left and/or right
ventricular hypertrophy. Usually familial (autosomal dominant).
Restrictive cardiomyopathy: rare; with restrictive filling and reduced diastolic filling
of one/both ventricles and normal or near normal systolic function. Causes include:
amyloidosis, endomyocardial fibrosis, and idiopathic.
Arrhythmogenic right ventricular cardiomyopathy: with fibro-fatty replacement of
right ventricular myocardium. Cause is unknown; familial form is usually autosomal
dominant with incomplete penetrance but may be recessive.
Unclassified: with no typical features of the above. Causes include: fibroelastosis,
non-compacted myocardium, systolic dysfunction with minimal dilatation,
mitochondrial diseases.
Investigations – typical cardiac investigation i.e. bloods, ECG, echo, etc.
Management – symptomatic and mainly directed towards heart failure treatments
Ventricular tachycardia
>120 BPM. Monophormic (regular) or polymorphic (irregular).
Risk factors – coronary heart disease, electrolyte deficiencies, use of sympathomimetic
agents e.g. caffeine/cocaine
Presentation – symptoms of ischaemic heart disease/failure
ECG
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Rate greater than 100 bpm (usually 150-200).
Wide QRS complexes (>120 ms).
Presence of atrioventricular (AV) dissociation.
Fusion beats.
Other investigations – U/E’s, CXR, levels of therapeutic drugs
Management – see advanced life support protocol.
Digoxin toxicity
The therapeutic level for digoxin is 0.8-2.0 ng/mL. Hypokalaemia and renal failure increases
the risk of digoxin toxicity and cardiac dysrhythmias.
Symptoms
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Hyper salivation
nausea/vomiting
diarrhoea
heart arrhythmia (classically paroxysmal atrial tachycardia with block)
Digoxin should not be given if heart rate less than 60 BPM
Treatment - Digoxin Immune Fab