Basic Life Saving BLS

ECG Interpretation Rhythm

Normal SR: P wave upright lead II, inverted lead AVR, each p wave looks the same.
i. Rate, rhythm, axis
ii. P wave, PR interval
iii. QRS complex
iv. ST segment
v. T wave
vi. QT interval

Heart rate  300/RR interval (large square)

Or Number of QRS complexes in 10 sec x 6.
Axis
P wave
 Normal QRS normal ventricular conduction
Wide QRS abnormal ventricular conduction ie BBB, ventricular origin, accessory
pathyway.
Wide QRS complex will cause ST segment and T wave changes*.
Tall QRS complex ventricular hypertrophy.
Small QRS complexpericardial effusion.

Q waves: First downward deflection is Q wave.

Due to normal left to right depolarisation of septum.
Usually seen in left sided leads.

PR intervalatrial depolarization and contraction.

Normal range 120-200 msec (3-5 small squares)

Pathological if > 1 small square, 2 mm deep, >25% height of following QRS,

present in lead V1-3.

QRS complexventricular depolarization.

Look for width (narrow or wide), height and shape (Q wave, R wave progression).
Normal width less than 120 msec (3 small squares)
R wave progression
Ventricles depolarise down and towards the left.
Right sided leads V1 should be negative, left sided leads V6 should be positive.
Should be smooth transition.

Normal transition point in V3-V4.
Abnormal R wave progression in anterior MI, LVH, RVH or others.
ST segments no electrical activity, ventricles are depolarised.
Look for elevation, depression, shape (concave up, down, horizontal, etc).
T waveventricular repolarization.
Anything that disrupt depolarisation (QRS) usually affects repolarization.
Occasionally inverted in V1 and AVR. Occasionally inverted in V2 and inferior
leads.
QT intervalventricular depolarisation and repolarisation.
EXAMPLES
Myocardial Ischemia

- Persistent STE >1 mm in 2 limb leads

- Persistent STE >2 mm in 2 chest leads
- New or presumed new LBBB
Posterior STEMI
Why important not to miss?
- Susceptible to hypotension and nitrate can worsen this.
WELLEN SYNDROME
SGARBOSSA CRITERIA

Dance with discordance, cry with concordance.

Conduction Disease

If SA node does not fire, another area may take overescape rhythm
The more distal the origin of the escape rhythm, the slower the rate.
Identify the origin of a beat. Heart block
Use the P wave and QRS morphology to identify where a beat originated.
Conduction disease of AV node
1st degree: every P wave is conducted but slower than usual.
2nd degree: some P waves are conducted
3rd degree: none P waves are conducted

1st degree heart block

2nd degree heart block

 Left bundle branch block

3rd degree heart block

Right bundle branch block

Bundle branch block

Lead to abnormal ventricular conductionwide QRS

QRS>3 small squares, T waves may be abnormal or inverted, ST segments may be
abnormal.
Fascicular blocks (Hemiblocks)

Trifascicular block

Bifasciular block + heart block  incomplete trifascicular block.

RBBB plus LAD  RBBB + LAFB

RBBB plus RAD  RBBB + LPFB
These are bifascicular blocks.
Paced rhythm

Keep an eye out for pacing spikes.

Ventricular pacing will cause a wide QRS.

Sinus tachycardia

Tachyarrythmias

Heart rate >100.

Treatment depends on presence of hemodynamic compromise and type of
tachycardia.
Look for wide vs narrow QRS, regular vs irregular, p waves.
AVNRT

Atrial fibrillation

Atrial flutter
Wolff Parkinson White syndrome

AVNRT

Supraventricular tachycardia (SVT)

Technically, this refers to any tachycardia originating in the atria or AV node.

Every example so far has been a type of SVT.
Sometimes SVT is used to imply AVNRT.
 VT vs SVT with aberrancy.

Wide complex tachycardia

ventricular tachycardia until proven otherwise.
Differentials: SVT with aberrancy or preexcitation.

ECG features increasing the likelihood of VT.

i. absence of RBBB or LBBB morphology
ii. extreme axis deviation: QRS positive in AVR and negative in I and AVF.
iii. very broad complexes >160 ms
iv. AV dissociation- P and QRS at different rates, sometimes superimposed on QRS
complex and maybe difficult to discern.
v. positive concordance in precodial leadsentirely positive R complexes with no
RS complex seen
 RSR’ complexes with taller left rabbit ear.
vi. negative concordance troughout precordial leads.
 Ventricular fibrillation
shockable rhythm
Chaotic irregular baseline
no identifiable P, QRS or T wave.
Amplitude decrease with timecourse, fine, asystole.

Torsade de Pointes
 Pericarditis

Pulmonary embolism

Most common ECG finding:

Sinus tachycardia, RAD, RBBB, Right ventricular strain pattern (T inversion and ST
depression in V1-V4), S1Q3T3, Atrial tachycardia, normal in 18% of patients.
Left ventricular hypertrophy

Hypokalemia

Hyperkalemia
Digoxin effect

Long QT syndrome

Reverse tick appearance, T wave changes can be flattened, inverted or biphasic,

short QT interval
Not necessarily indicate digoxin toxicity.

Digoxin toxicity
Brugada syndrome
due to mutation in cardiac sodium channel gene, referred to as sodium
channelopathy.
Type 1 coved ST segment elevation >2mm in >1 of V1-V3 followed by negative
T wave.
Must be accompanies with one of the following clinical criteria to make the
diagnosis:
Documented VF/polymorphic VT, family history of sudden cardiac death <45 year
old, coved type ECG in family member, inducibility of VT with programmed
electrical stimulation, syncope, nocturnal agonal respiration.

Type 2 >2mm saddleback shaped ST elevation.

Type 3either type 1 or type 2 morphology but with <2mm ST segment elevation
Management of Heart Failure (CPG Malaysia 2019)

Clinical syndrome due to structural or physiological abnormality of the heart

resulting in its inability to meet the metabolic demands of the body or its ability
to do so only at higher-than-normal filling pressures.

LVEF <40%-->HFrEF
- Due to depressed myocardial contractility irrespective of aetiology.
LVEF >50%-->HFpEF
- Predominantly diastolic dysfunctionimpaired LV filling due to decreased
relaxation (during early diastole) and/or reduced compliance (early to late
diastole) leading to elevated filling pressurespulmonary and/or venous
congestion and occasionally systemic hypoperfusion.
- Limited therapies to improve survival.
LVEF 41-49%-->HFmrEF
- Clinical profile closer to HFpEF, poorly studied category.

Differential diagnosis

Coronary artery disease, hypertension, dilated cardiomyopathy (idiopathic or

familial), valvular heart disease, diabetic cardiomyopathy.
Congenital heart disease, cor pulmonale, pericardial disease (constrictive
pericarditis, cardiac tamponade), hypertrophic cardiomyopathy, viral myocarditis,
acute rheumatic fever.
Toxicalcohol, cardiotoxic chemotherapy ie doxorubicin, cyclophosphamide
Endocrinethyroid disease, acromegaly, pheochromocytoma.
CTDSLE, polymyositis, polyarteritis nodosa.
Tachycardia induced cardiomyopathy
Infiltrative cardiac diseaseamyloidosis, hyper-eosinophilic syndrome
Peripartum cardiomyopathy, Takotsubo cardiomyopathy
 Hypoperfusion cold peripheries, CRT>2 seconds, diaphoresis, oliguria, dizziness,
Exacerbating factor: confusion, narrow pulse pressure, hypotension.
Acute MI, arrythmia, hypertensive emergencies, infection, non-compliance to Congestion peripheral edema, orthopnea, PND, lung crepitation, jugular venous
medication, excessive fluid and salt intake, anaemia, renal impairment, NSAIDS. dilatation, hepatojugular reflux, congested hepatomegaly, gut congestion, ascites.

Investigations:
ECG, CXR, ECHO
BNP <100 or proBNP <300HF unlikely.
BNP levels affected by atrial fibrillation, age, renal function, obesity (reduced),
medication like ARNI.

TFT, GGT, Viral studies, iron studies.

Treadmill exercise test, stress echocardiography, radionuclide studies, cardiac
MRITest for myocardial ischemia and viability.
COROS, endomyocardial biopsyinvasive test.

Management

CADAntiplatelet, B blocker, ACE inhibitor, statins, chronic revascularisation if

indicated.
Target BP <140/90.
Significant valve disease (moderate and above) should be assessed for Oxygenif SPO2 <95 or PO2 <60, titrate to achieve >95.
progression and timely intervention if indicated. - Routine use in non-hypoxic patient not recommended as may cause
ACE, ARB, B blocker, Statin vasoconstriction and reduction in cardiac output.
SGLT2 inhibitor in patients with diabetes. - CPAP or BIPAP should be considered in patients with respiratory distress
(RR>25 or SPO2<90% despite high flow oxygen), no difference when
Acute heart failure comparing CPAP and BIPAP.
- Consider intubation if any signs of exhaustion or respiratory muscle
May present as: fatigue.
- Pulmonary and/or peripheral edema (wet-volume overload) -
- Low output (dry-usually due to pump failure) IV Lasix 40-100 mg, if already on diuretics or have chronic renal disease may
- Combination of pulmonary edema and low output state. require higher dose. Target 0.5-1 kg decrease in body weight/day. No difference
between continuous infusion or bolus dosing of Lasix.
Nitrates can confer symptomatic relief and improvement in hemodynamic, most
useful if there is concomitant MI, severe hypertension or aortic or mitral
regurgitation. Considered if SBP >100. Combination of IV nitrate and low dose
Lasix was shown to be more efficacious than high dose diuretic treatment alone.
Contraindicated in severe valvular stenosis.

Dopamine infusionlow dose <2-3 mcg/kg/min to improve renal flow and

promote diuresis.
Dobutamine infusion 2-5 mcg/kg/min and titrated 1-2 mcg/kg/min at 30 minutes
interval until desired clinical and hemodynamic response is attained.
Noradrenaline is as efficacious as dopamine in term of 28 day mortality but safer
in cardiogenic shock.

In absence of LV failure, fluid challenge with normal saline 100-200ml may be

given tapered to clinical response and sign of fluid overload.

IV morphine 1-3 mg boles repeated as necessary up to 10 mg, reduce pulmonary

venous congestion, reduce anxiety and dyspnea. Side effect includes nausea,
hypotension, bradycardia and respiratory depression.
 Fluid restriction, salt restriction
Weight reduction, stop alcohol and smoking.

Workout for OSA or central sleep apnea or combination of both called sleep
disordered breathing (SDB). Polysomnography is the gold standard.
CPAP may improve QOL, LVEF function and HF symptoms.

If creatinine >250 should start ACE/ARB at lower dose, avoid excessive diuresis
before treatment. Start low and increase gradually to achieve maximum tolerated
dose. Stop if GFR>30% from baseline at 7-14 days.

Discharge medication:
Oral diuretics aim to achieve dry weight. If there is consistent increase more than
2kg in 3 days, patient should be educated to self adjust diuretic dose together
with restriction of fluid intake until dry weight is regained.
Combination of thiazide and loop diuretic may be used as these drugs work
synergistically to improve diuresis but associate4d with hypokalemia,
hyponatremia and worsening renal function.
Metolazone is given in combination with loop diuretic in severe HF and refractory
edema.
If SBP >120ACE/ARB, titrate depends on BP and renal function.
B blockers if BP is adequate and no longer congested.
MRA can be commenced at admission and to monitor renal function and
potassium.
ARNI ARNI should not be administered within 36 hours of the last dose of ACEcan
cause angioedema.
Ivabradine is indicated if patient already on optimal medical therapy with
diuretics, ACE, MRA, B blocker and still symptomatic, LVEF <35% and resting HR
>70 bpm.
Should achieve maximal tolerated dose of B blocker before initiation of
ivabradine.

Digoxin has no proven survival benefit but it relieves symptoms and reduce
hospitalisation, has narrow therapeutic range and thus require close RP
monitoring. It can be added to OMT and diuretic for patients with HFrEF and in
sinus rhythm who continue to have moderate to severe symptoms.
Combination of B blocker and digoxin is superior to either agent alone in AF.
Therefore, may be considered in AF patients with HF if rate control inadequate on
B blocker alone, B blocker contraindicated, rapid control of ventricular rate with
parenteral drugs is needed. No loading dose is required for chronic AF.
Regular TDM not required to guide dose adjustment.
Device therapy in heart failure
Patient who remains symptomatic despite optimal OMT. CRT improves
symptoms, hospitalisation and mortality. Can be considered in:
Sinus rhythm, LVEF <35%, LBBB, QRS >150 ms.
Heart failure with preserved left ventricular systolic function (HFpEF)
Clinical features:
Sign and symptoms of HF
Elevated BNP
Preserved or normal LVEF >50% within 72 hours of event and LV end diastolic
volume index < 97 ml/m2
LVH (increased LV wall thickness or LV mass index >115 g/m2 and >95 g/m2 for
women or left atrial enlargement (LA volume index >34 ml/m2).
Diastolic dysfunction if E/e’ >13 and mean e’ septal and lateral wall <9 cm/s or
tricuspid valve regurgitation velocity >2.8 m/s.
Invasive hemodynamic criteriaPCWP >15 mmhg or LV end diastolic pressure
>16 mmhg indicates elevated LV filling pressure.
Etiology:

ICD can be implanted as secondary prevention in patients with previous sudden

cardiac arrest or documented sustained ventricular arrhythmias.
Heart failure in diabetic patients
Heart failure in pregnancy

Chemotherapy induced heart failure

Cardiorenal syndrome
Management of Acute STEMI

STEMI is diagnosed when there is ST elevation >1mm in 2 contagious leads or new

onset LBBB in the resting ECG, in ischemic type of chest pain >30 minutes,
accompanied by rise and fall in cardiac biomarker.
Non interpretable resting ECG like paced rhythm, RBBB may be having NSTEMI, if
pain persist, these high-risk patients may be considered for early PCI if facilities
available, fibrinolysis not advisable.

Initial management directed at pain relief, establishing early reperfusion and

treatment of complications.
Troponin and CKMB can be used to determine reinfarction if >20% increase from
baseline between 2 samples 3-6 hours apart.
Chest pain post STEMI may be due to reinfarction/recurrent MI, post infarct
angina, pericarditis, non-cardiac causes like gastritis.
High risk patientsprimary PCI is the preferred strategy in contraindicated
patient and those with high risk patients.

Fibrinolytic therapy
Streptokinase 1.5 mega unit in 100 ml NS or D5 within 1 hour.
Anticoagulant doses
Complications post MI
Arrythmia, LV dysfunction, Others ie pericarditis, RV infarction, Mechanical
complications.
Target control
BP <140/90

Management of NSTEMI (CPG 2021)

Diagnosed when there is significant rise and fall in troponin with at least one
value above 99th percentile upper reference limit and accompanied with at leas
one of the following:
- Clinical history of ischemic chest pain 30 minutes
- ECG changes of ischemia or pathological Q wave
- Identification of intracoronary thrombus by angiography or autopsy

Triage
- Very low likelihoodmay have alternative diagnosis and can be
discharged from ED
- Definiterisk stratified using clinical feature, TIMI or GRACE risk score
- Possible or suspected NSTEMIuse rule out protocol, risk stratified using
HEART or TIMI risk score

Management
Stop smoking
Management of stable coronary artery disease (CPG Malaysia 2018)
Functional test
- Exercise stress ECG : must be able to perform moderate physical activity
and without disabling comorbidities like frailty, marked obesity,
peripheral arterial disease, COPD or orthopedic limitation. Must have
interpretable baseline ECG.
 - Stress test in combination with echo, myocardial perfusion imaging via
SPECT or PET or cardiac magnetic resonance imaging with stressor agent
like exercise treadmill or pharmacologic agent like dobutamine or
vasodilator like adenosine and dipyridamole for MI and CMR imaging.
These modalities are used in individuals who have intermediate PTP and
unable to exercise adequately or have uninterpretable ECG.
Anatomical testing
- Coronary calcium score

- CT Angiography
Management of Infective Endocarditis (CPG Malaysia 2017)
Surgical intervention
Management of Atrial Fibrillation (ESC Guidelines 2020)
 ABC pathway: Anticoagulation/avoid stroke. Better symptoms management.
Cardiovascular and comorbidity optimization.

Managements
High bleeding risk score should not lead to withholding OAC, however formal
assessment of bleeding risk informs management of patients taking OAC focusing
on modifiable bleeding risk factors that should be managed and reassessed at
every patient contact.

Absolute contraindication to OAC include active serious bleeding, severe

thrombocytopenia (platelet <50), severe anemia under investigation, recent
serous high risk bleeding event like ICB.
Diabetes Mellitus
Cardiomyopathies
Cardiac amyloidosis
Pregnancy management
Management of Pulmonary Hypertension (ESC 2022)

Definition: Mean pulmonary artery pressure >20 at rest.

PAH are hemodynamically characterized by pre capillary PH in the absence of

other causes of pre-capillary PH like CTEPH and PH associated lung disease.
Pulmonary arterial hypertension (PAH) Group 1

Symptoms non specific and mainly related to progressive RV dysfunction as

consequence of progressive pulmonary vasculopathy.

Severity depends on WHO-FC.

Pulmonary hypertension associated with left heart disease (group 2)
Pulmonary hypertension associated with lung diseases (Group 3)
Pulmonary hypertension with unclear mechanism (Group 5)