Advanced Cardiac Nursing — GCC Nurse Guide

ECG Interpretation — Systematic Approach

Rate — large-square method (300/number of large squares between QRS) or 6-second strip count. Normal 60-100 bpm.
Rhythm — regular or irregular? Use calipers/paper-measure R-R interval.
P waves — present? Upright in I, II, aVF? One per QRS? Morphology normal?
PR interval — normal 120-200 ms (3-5 small squares). Prolonged = heart block.
QRS duration — narrow <120 ms (3 small squares) = supraventricular. Broad ≥120 ms = BBB or ventricular origin.
QT/QTc interval — measure QT, apply Bazett: QTc = QT / √RR. Normal QTc <440 ms men, <460 ms women. >500 ms = high TdP risk.
ST segment & T waves — elevation, depression, T inversion, peaked T waves? Identify territory.

Rate Calculation

Large Square Rule (300): 300 ÷ number of large squares between consecutive R waves.

1 large sq = 300 bpm • 2 = 150 • 3 = 100 • 4 = 75 • 5 = 60 • 6 = 50

6-second strip: Count QRS complexes × 10 = bpm. Best for irregular rhythms.

Paper speed: Standard 25 mm/s. 1 small sq = 40 ms. 1 large sq = 200 ms.

Rhythm Assessment

Measure at least 3 consecutive R-R intervals. If all equal → regular.

Regularly irregular: Pattern repeats (e.g., 2nd degree block, bigeminy).

Irregularly irregular: No pattern → suspect AF, multifocal AT.

Use a piece of paper to mark R peaks for comparison.

P Waves

Normal: upright I, II, aVF; inverted aVR
Absent: AF, junctional, ventricular rhythms
Inverted in II: retrograde conduction (junctional)
Saw-tooth flutter waves at 300 bpm: atrial flutter
Multiple morphologies: multifocal AT (≥3 shapes)
More P waves than QRS: heart block

PR Interval

Measured from start of P wave to start of QRS.

Normal: 120–200 ms (3–5 small squares)
Short <120 ms: WPW, junctional, LGL
Long >200 ms: 1st degree AV block
Progressive lengthening: Mobitz I (Wenckebach)
Constant then dropped: Mobitz II

QRS Duration

Narrow <120 ms: supraventricular origin (normal conduction)
Broad ≥120 ms: BBB, WPW, pacemaker, ventricular ectopic/VT
Delta wave + short PR = WPW (pre-excitation)
RSR' in V1 = RBBB; notched R in V5/V6 = LBBB

QT / QTc Interval

Bazett Formula: QTc = QT (sec) / √RR (sec)

Measure from start of Q to end of T wave in lead II or V5.

Normal QTc men: <440 ms; women: <460 ms
Borderline: 440–500 ms — monitor drug list
High risk >500 ms: Torsades de Pointes risk — review all QT-prolonging drugs immediately
Correct for heart rate — QT shortens with tachycardia

Axis Determination

Axis	Lead I	Lead aVF	Degrees	Causes
Normal	Positive	Positive	-30° to +90°	Normal
LAD	Positive	Negative	-30° to -90°	LBBB, inferior MI, LVH
RAD	Negative	Positive	+90° to +180°	RBBB, RVH, PE, lateral MI
Extreme	Negative	Negative	-90° to ±180°	Ventricular tachycardia, severe disease

ST Changes — STEMI Territories

Territory	Leads	Artery	Reciprocal Changes
Anterior	V1–V4	LAD	II, III, aVF
Inferior	II, III, aVF	RCA (80%) / LCx (20%)	I, aVL
Lateral	I, aVL, V5–V6	LCx	III, aVF
Posterior	V7–V9 (ST elevation)	RCA / LCx	V1–V3 ST depression
Septal	V1–V2	Septal LAD branches	—
RV	V3R–V4R	RCA proximal	—

Always perform right-sided and posterior leads when inferior STEMI suspected. Right ventricular MI contraindication to nitrates — risk of severe hypotension.

ECG Rhythm Identifier Tool

Select clinical features to identify the most likely rhythm and initial management guidance.

Rate:

Rhythm:

P Waves:

QRS:

ST Changes:

Common Arrhythmias — Classification & ECG Features

Sinus Rhythms

Sinus Bradycardia

Rate <60 bpm. Regular. Normal P morphology. PR/QRS normal.

Causes: vagal tone, athletes, hypothyroidism, beta-blockers, inferior MI, hypothermia.

Management: treat only if symptomatic (hypotension, syncope, HF).

Sinus Tachycardia

Rate 100–150 bpm. Regular. Normal P waves precede each QRS.

Causes: pain, fever, anaemia, hypovolaemia, PE, anxiety, sepsis, thyrotoxicosis.

Management: treat underlying cause — not the rhythm.

Sinus Arrhythmia

Varies with respiration. Rate varies by >10% with breathing cycles. Normal morphology.

Physiological — reassure patient. Common in young patients and athletes.

Supraventricular Tachycardias (SVT)

AVNRT (AV Nodal Re-entry)

Most common SVT. Rate 150–250 bpm. Regular. Narrow QRS.

P waves buried in or just after QRS (retrograde). Pseudo-R' in V1, pseudo-S in II/III/aVF.

Management: vagal manoeuvres → adenosine 6 mg IV → 12 mg → 18 mg. If unstable: DC cardioversion.

AVRT (Accessory Pathway / WPW)

Rate 150–250 bpm. Regular. Narrow QRS (orthodromic) or broad (antidromic).

In sinus rhythm: short PR + delta wave + broad QRS = WPW.

AVOID adenosine, digoxin, verapamil in AF + WPW — risk of VF. Use procainamide or DC cardioversion.

Atrial Flutter

Atrial rate 300 bpm. Saw-tooth flutter waves (negative in II, III, aVF).

AV block ratio typically 2:1 (ventricular rate ~150 bpm), 3:1, or 4:1.

Regular or regularly irregular. Narrow QRS unless aberrant conduction.

Management: rate control, anticoagulation (same as AF), consider cardioversion or ablation.

Atrial Fibrillation (AF)

Irregularly irregular rhythm. No discernible P waves. Fibrillatory baseline.

Narrow QRS (unless BBB or aberrant). Ventricular rate variable 100–180 bpm if uncontrolled.

Classification: paroxysmal/persistent/permanent. CHA₂DS₂-VASc for stroke risk.

Junctional Rhythms

Junctional Escape

Rate 40–60 bpm. Regular. Absent or inverted P waves (before, during, or after QRS).

Narrow QRS. Escape mechanism when sinus node fails.

Accelerated Junctional

Rate 60–100 bpm. AV dissociation. Associated with digoxin toxicity, inferior MI, post-cardiac surgery.

Ventricular Arrhythmias

Monomorphic VT

Rate >100 bpm. Broad QRS ≥120 ms. Uniform morphology. AV dissociation (independent P waves).

Features supporting VT: fusion beats, capture beats, concordance V1–V6, northwest axis.

Treat as VT unless proven otherwise — haemodynamic assessment determines urgency.

Polymorphic VT / Torsades de Pointes

Varying QRS morphology, twisting around isoelectric line. Pause-dependent onset.

Associated with: prolonged QT, hypokalaemia, hypomagnesaemia, drugs.

Management: Magnesium sulphate 2g IV over 10 min. Correct electrolytes. Remove offending drugs. Overdrive pacing if recurrent.

Ventricular Fibrillation (VF)

Chaotic irregular waveforms. No organised QRS. Loss of cardiac output = pulseless.

Immediate defibrillation (200J biphasic). ALS algorithm. Adrenaline 1 mg IV after 3rd shock.

PVC / VEB

Broad bizarre QRS. No preceding P wave. Compensatory pause. T wave opposite to QRS.

Isolated PVCs benign if structurally normal heart. Frequent (>10/hr), runs, R-on-T in ACS = concerning.

Heart Blocks

Block	PR Interval	QRS Dropped?	Significance	Action
1st Degree	>200 ms, constant	No	Usually benign	Monitor, no pacing
2nd Degree Mobitz I (Wenckebach)	Progressive lengthening	Yes (periodic)	Often inferior MI, usually benign	Treat if symptomatic, atropine
2nd Degree Mobitz II	Constant, then dropped	Yes (sudden)	High risk of progression to 3rd degree	Pacing — urgent
2:1 Block	Constant PR with 2:1 ratio	Alternate	Cannot distinguish Mobitz I vs II from single strip	Treat as Mobitz II — pace
3rd Degree (Complete)	AV dissociation — no relationship	All P waves dissociated	Medical emergency	Pacing immediately, atropine as bridge

Bundle Branch Blocks

WiLLiaM pattern = LBBB: W in V1, M in V5/V6

LBBB

QRS ≥120 ms, broad notched R in V5/V6/I
Deep S or W pattern in V1–V2
No septal Q waves in I, V5, V6
New LBBB with chest pain = treat as STEMI equivalent
Causes: IHD, cardiomyopathy, hypertension, aortic stenosis

MaRRoW pattern = RBBB: M in V1, W in V5/V6

RBBB

QRS ≥120 ms, RSR' (M-pattern) in V1–V2
Wide slurred S wave in I, V5, V6
May be normal variant (incomplete RBBB)
New RBBB: consider PE, ACS, myocarditis
Brugada pattern: RBBB + ST elevation V1–V2 (coved type)

Pacemaker Rhythms

Mode	Full Name	ECG Feature	Use
AAI	Atrial paced/sensed, inhibited	Atrial spike before P wave	Sick sinus syndrome, intact AV node
VVI	Ventricular paced/sensed, inhibited	Ventricular spike + broad QRS (LBBB morphology if RV)	AF + bradycardia
DDD	Dual paced, dual sensed, dual response	Atrial &/or ventricular spikes; tracks atrial rate	Complete heart block, sick sinus

Pacemaker malfunction: failure to pace (no spike), failure to capture (spike without QRS), failure to sense (competition with native rhythm).

Emergency Arrhythmia Management — ALS 2021 Algorithm

Adverse Features (any one = unstable): Shock (SBP <90 mmHg, pallor, sweating) | Syncope | Myocardial ischaemia (chest pain, ischaemic ECG changes) | Heart Failure (pulmonary oedema, raised JVP, elevated BNP)

Tachycardia Algorithm

Step 1: Assess & Stabilise

Airway, Breathing, Circulation, Disability, Exposure (ABCDE)
12-lead ECG, IV access, O₂ if SpO₂ <94%, monitoring
Identify and correct reversible causes (4Hs/4Ts)

Step 2: Adverse Features Present?

YES — Haemodynamically Unstable: Synchronised DC Cardioversion up to 3 attempts. Sedate conscious patients (midazolam/ketamine). Start at 120–150J biphasic for AF; 70–120J for flutter/SVT; 200J for VT. Seek expert help. After failed cardioversion: amiodarone 300 mg IV over 10–20 min, then repeat shock.

NO — Haemodynamically Stable: Proceed by QRS morphology.

Narrow QRS Tachycardia (Stable)

Vagal manoeuvres (Valsalva 40 mmHg for 15 s; carotid sinus massage if no bruits/TIA history)
Adenosine 6 mg rapid IV bolus + 20 mL flush (warn patient — chest tightness, flushing, transient asystole)
Adenosine 12 mg if no response
Adenosine 18 mg if no response
If still no response: verapamil 2.5–5 mg IV (if not on beta-blocker), or seek expert opinion

Broad QRS Tachycardia (Stable)

Assume VT until proven otherwise
Amiodarone 300 mg IV over 20–60 min, then 900 mg over 24 h
If known SVT with aberrancy: adenosine may be considered
Do NOT use verapamil for broad complex tachycardia

Bradycardia Algorithm (ALS 2021)

ABCDE assessment. Identify adverse features.
Correct reversible causes: hypoxia, hypothermia, electrolytes, drug overdose (e.g., beta-blocker, digoxin)
Atropine 500 mcg IV; repeat up to total 3 mg if adverse features present
If inadequate response: interim measures — atropine repeat, isoprenaline 5 mcg/min IV, adrenaline 2–10 mcg/min IV, transcutaneous pacing
Seek expert help — transvenous pacing for Mobitz II, complete heart block, or symptomatic bradycardia unresponsive to atropine

Atropine is less effective or potentially harmful in: transplanted hearts, Mobitz II, 3rd degree block, wide-QRS bradycardia. Use pacing early in these cases.

AF Management

Rate vs Rhythm Control

Rate Control (first-line for most):

Target resting HR <110 bpm (lenient) or <80 bpm (strict if symptomatic)
Beta-blocker (bisoprolol 2.5–10 mg OD) or rate-limiting CCB (diltiazem)
Digoxin (adjunct, especially in sedentary/HF with reduced EF)
Avoid CCB in HFrEF

Rhythm Control:

Electrical cardioversion (DC cardioversion) or pharmacological (flecainide pill-in-pocket for paroxysmal AF without structural disease)
Amiodarone for structural heart disease

Cardioversion Timing & Anticoagulation

AF <48 h duration: can cardiovert after LMWH/heparin + anticoagulate 4 weeks post-cardioversion
AF >48 h or unknown duration: anticoagulate for ≥3 weeks before cardioversion (or TOE to exclude LAA thrombus)
Continue anticoagulation ≥4 weeks post-cardioversion regardless of CHA₂DS₂-VASc
Long-term anticoagulation based on CHA₂DS₂-VASc score: NOAC preferred over warfarin

VT Management

Haemodynamically Unstable VT

Pulseless VT: defibrillation (unsynchronised 200J biphasic), ALS algorithm
Pulse present but shocked: synchronised DC cardioversion — sedate first
Adrenaline 1 mg IV if pulseless (every alternate cycle)
Amiodarone 300 mg IV after 3rd shock if VT/VF persists

Haemodynamically Stable VT

Amiodarone 300 mg IV over 20–60 min (first-line)
Correct electrolytes: K⁺ target 4.0–5.0 mmol/L; Mg²⁺ target 0.8–1.2 mmol/L
Lidocaine 1–1.5 mg/kg IV (alternative, especially if amiodarone unavailable)
If TdP: magnesium sulphate 2 g IV over 10 min; overdrive pacing
Seek electrophysiology input for recurrent VT

Pre-Procedure Checklist

Confirm indication and consultant order. Obtain informed consent (if possible).
Confirm anticoagulation status (AF >48 h: 3 weeks NOAC/warfarin or TOE exclusion of thrombus)
NBM status: elective = 4–6 h fasting; emergency = proceed regardless
IV access (large bore, running IV fluid)
Continuous ECG, SpO₂, NIBP monitoring; crash trolley and defibrillator checked
Sedation prepared (midazolam 1–2 mg IV titrated; etomidate/propofol per anaesthesia)
Resuscitation team on standby; airway equipment at bedside
Remove glyceryl trinitrate patch — fire risk
Defibrillator pads: anteroposterior or anterolateral position
Select SYNCHRONISED mode — verify sync marker on R wave peak

Energy Selection

AF: 120–200J biphasic (escalate if unsuccessful)
Atrial flutter / SVT: 70–120J biphasic
Monomorphic VT (pulse): 120–200J biphasic

Post-Procedure Care

Record post-cardioversion ECG immediately — confirm sinus rhythm
Monitor ECG continuously for minimum 1 h post-procedure
Vital signs every 15 min for 1 h, then per unit protocol
Assess level of consciousness — recovery from sedation
Maintain anticoagulation for ≥4 weeks post-cardioversion (AF)
Document: time, energy delivered, number of shocks, pre/post rhythm, patient response
Skin care at pad sites — inspect for erythema/burns

Cardiac Monitoring & Devices

Continuous ECG Monitoring — Lead Selection

Lead II

Best P wave visualisation. Inferior territory monitoring. Standard monitoring lead for most patients. Tall upright P wave.

Lead V1

P wave morphology (flutter, ectopics). Best lead to distinguish RBBB vs LBBB. Atrial activity analysis.

Lead V5

Lateral territory ST monitoring. Best sensitivity for anterior and lateral ischaemia. Used in perioperative monitoring.

Telemetry Nursing Responsibilities

Ensure alarm limits are set appropriately (HR high/low, ST deviation, pause duration)
Check electrode placement daily; replace every 24–48 h or when signal quality poor
Document rhythm strips with nursing notes per unit protocol (minimum QID or with any change)
Respond to alarms promptly — assess patient clinically before silence alarm
Educate patient: activity restrictions, shower technique, reporting symptoms
Perform artefact troubleshooting: check leads, patient movement, skin preparation (abrade, dry, clean)
Maintain telemetry log; ensure coverage handover

12-Lead ECG Technique

Electrode Placement

Lead	Placement
RA (Red)	Right arm / just below right clavicle
LA (Yellow)	Left arm / just below left clavicle
RL (Black/Green)	Right leg / right lower abdomen
LL (Green/Red)	Left leg / left lower abdomen
V1	4th intercostal space, right sternal border
V2	4th intercostal space, left sternal border
V3	Between V2 and V4
V4	5th intercostal space, mid-clavicular line
V5	Anterior axillary line, same level as V4
V6	Mid-axillary line, same level as V4

Artefact Reduction

Prepare skin: shave if necessary, clean with alcohol wipe, lightly abrade
Ensure electrodes are not expired or dried out
Ask patient to breathe normally and remain still during recording
Minimise electrical interference: turn off unnecessary equipment nearby
For women: do not place precordial leads on breast tissue — displace laterally/under

Holter Monitoring — Patient Education

Duration: 24–48 h standard; extended 7–14 days for paroxysmal arrhythmia detection
Keep a symptom diary: note time and description of all symptoms (palpitations, dizziness, chest pain, syncope)
Avoid bathing/showering unless waterproof monitor provided
Continue normal activities as instructed by clinician
Avoid strong magnetic fields, electric blankets, metal detectors
Return device and diary at specified time — do not remove electrodes early

Temporary Pacing — Nursing Management

External (Transcutaneous) Pacing

Emergency bridge only — painful, consider sedation/analgesia
Pad placement: anterior-posterior preferred (right infraclavicular — left posterior scapular)
Set rate 60–80 bpm; increase output (mA) until capture observed (QRS after each spike with pulse)
Confirm mechanical capture: palpate pulse, check SpO₂ waveform
Do NOT confuse pacing spikes with QRS — ECG artifact during pacing is expected
Check pads every 2 h; skin inspection; patient comfort

Transvenous Temporary Pacing

Monitor ECG continuously for pacing spikes and capture
Check pacemaker settings QID: rate, output (mA), sensitivity (mV), mode
Sensing threshold: typically <1/2 spontaneous R wave amplitude
Capture threshold: usually <2 mA — set output 2–3x above threshold
Immobilise insertion limb (subclavian/femoral/internal jugular); assess for lead displacement (loss of capture, ECG morphology change)
Daily CXR to check lead position. Strict aseptic technique at insertion site
Emergency: if pacemaker fails — check connections, replace battery, call physician immediately

Permanent Pacemaker — Post-Implant Care

Arm restriction on implant side for 6 weeks (no lifting >5 kg, no overhead movements) — prevent lead displacement
Wound inspection: redness, swelling, warmth, dehiscence, pocket haematoma daily
Monitor for: pacemaker pocket infection (fever, erythema, erosion), pocket haematoma
Patient education: MRI restrictions (unless MRI-conditional device confirmed), metal detector avoidance, no heavy machinery near chest, device card always carry
ICD patients: restrict driving per national regulations (DVLA equivalent — typically 6 months no driving after appropriate shock)

ICD — Implantable Cardioverter Defibrillator

ICD Shock Therapy & Nursing Response

Appropriate shock: VT/VF detected and treated — check patient clinically, obtain 12-lead ECG, contact EP team
Inappropriate shock: SVT, T-wave oversensing, lead fracture — distressing for patient, urgent device interrogation
Magnet use: places device in asynchronous mode (pacing) and inhibits tachytherapy — use in end-of-life or inappropriate shocks under physician supervision ONLY
Multiple shocks (electrical storm): sedation, antiarrhythmic therapy (amiodarone), urgent EP review

CIED Infection Prevention

Pre-operative antibiotic prophylaxis (cefazolin 1–2 g IV or vancomycin if penicillin allergy)
Strict aseptic technique throughout implant procedure
Post-implant: wound care per protocol, monitor for pocket infection signs, educate on dental antibiotic prophylaxis (not routinely required but patient awareness)
MRSA screening and decolonisation in high-risk patients pre-implant

Cardiac Medications

Vaughan Williams Classification — Antiarrhythmics

Class	Mechanism	Drugs	Key Indications	Cautions
Ia	Na⁺ channel block (moderate) + K⁺ block	Quinidine, Procainamide, Disopyramide	VT, AF (limited use)	Prolongs QT; lupus (procainamide)
Ib	Na⁺ channel block (fast)	Lidocaine, Mexiletine	VT (acute), post-MI ectopics	CNS toxicity (lidocaine); avoid in supraventricular arrhythmias
Ic	Na⁺ channel block (slow)	Flecainide, Propafenone	AF (paroxysmal, no structural disease), SVT	AVOID in structural heart disease (post-MI, HFrEF) — pro-arrhythmic
II	β-adrenergic blockade	Metoprolol, Bisoprolol, Atenolol, Esmolol	AF rate control, SVT, VT, post-MI	Bradycardia, bronchospasm, hypoglycaemia masking
III	K⁺ channel block (prolongs AP)	Amiodarone, Sotalol, Dronedarone	VT, VF, AF maintenance	See amiodarone toxicity below; sotalol prolongs QT
IV	L-type Ca²⁺ channel block	Verapamil, Diltiazem	SVT termination, AF rate control	AVOID in HFrEF, WPW, broad complex tachycardia

Amiodarone has a very long half-life (40–55 days). Toxicity can occur months–years after starting. Annual monitoring required.

Pulmonary Toxicity

Incidence: 1–5% per year. Life-threatening.
Symptoms: progressive dyspnoea, dry cough, fever
Monitoring: CXR at baseline and annually; HRCT if symptoms; DLCO (pulmonary function)
Management: stop amiodarone, prednisolone 40–60 mg/day

Thyroid Toxicity

Hypothyroidism (more common in iodine-replete areas): fatigue, cold intolerance, weight gain — treat with levothyroxine, continue amiodarone if necessary
Hyperthyroidism (AIT): weight loss, palpitations, tremor — requires specialist management, consider stopping amiodarone
Monitoring: TFT (TSH, free T4) at baseline, 3 months, then every 6 months

Hepatic Toxicity

Elevated transaminases (common, may be asymptomatic)
Hepatitis and cirrhosis (rare, long-term)
Monitoring: LFTs at baseline, 6 months, annually

Ocular Toxicity

Corneal microdeposits: nearly universal — usually asymptomatic, reversible
Optic neuropathy (rare, serious): blurred vision, visual field loss — stop amiodarone
Monitoring: annual ophthalmology review; patient education on visual symptoms

Other Side Effects

Photosensitivity: advise high-factor sunscreen, protective clothing
Skin discolouration (slate-grey): cosmetically unacceptable, persistent
Peripheral neuropathy; tremor; ataxia
Bradycardia, QT prolongation (monitor ECG)
Drug interactions: warfarin (increases INR — halve warfarin dose), digoxin (increase digoxin toxicity), statins

Anticoagulation in AF

NOAC vs Warfarin

	NOAC	Warfarin
Monitoring	None routine	Regular INR (target 2.0–3.0)
Onset	Rapid (<2 h)	2–5 days
Reversal	Idarucizumab (dabigatran); andexanet alfa (Xa)	Vitamin K, PCC, FFP
Interactions	Fewer	Many (food, drugs)
Preferred in	Non-valvular AF, CrCl>30	Mechanical valve, mitral stenosis, CrCl<30

INR Monitoring Points

Target INR 2.0–3.0 for AF; 2.5–3.5 for mechanical mitral valve
Sub-therapeutic INR (<2.0): increased stroke risk — review compliance, interactions
Supra-therapeutic INR (>4.0): bleeding risk — hold dose, assess for bleeding, FFP/Vit K if active bleeding
Bridging: LMWH used peri-procedurally when warfarin held
GCC note: dietary variations during Ramadan affect INR — increase monitoring frequency

Rate Control Drugs

Drug	Route/Dose	Mechanism	Key Nursing Points
Bisoprolol	PO 1.25–10 mg OD	β1-blocker	Monitor HR and BP; hold if HR <50 or SBP <90; avoid abrupt cessation
Metoprolol	PO 25–200 mg BD; IV 5 mg slowly	β1-blocker	As above; IV very slowly over 5 min; monitor ECG
Diltiazem	PO 60–360 mg/day; IV 5–15 mg/h infusion	CCB (non-DHP)	AVOID in HFrEF; monitor BP; constipation counselling
Digoxin	PO/IV 125–250 mcg OD	Na/K ATPase inhibitor; vagotonic	Narrow therapeutic index (0.5–2.0 ng/mL); toxicity: nausea, yellow-green halos, bradycardia, AV block; check K⁺ before administration (hypokalaemia increases toxicity)

Inotropes & Vasopressors (ICU Context)

Dobutamine

Beta-1 agonist. Dose: 2.5–20 mcg/kg/min IV infusion. Positive inotrope; mild vasodilation.

Used in cardiogenic shock, acute decompensated HF. Monitor: HR, BP, lactate, urine output, arrhythmias. May increase HR/cause tachycardia — use caution in AF.

Milrinone

PDE-III inhibitor. Dose: 0.375–0.75 mcg/kg/min. Inotrope + vasodilator ("inodilator").

Useful in HF not responding to dobutamine. Risk of hypotension. Renally cleared — reduce dose in AKI.

Noradrenaline (Norepinephrine)

Alpha-1 + Beta-1 agonist. Dose: 0.01–3 mcg/kg/min. Primary vasopressor.

Used in distributive shock (septic) when CO maintained. Requires central line. Monitor for peripheral ischaemia, hypertension overshoot, arrhythmias.

Adrenaline (Epinephrine)

Alpha + Beta agonist. Cardiac arrest: 1 mg IV every 3–5 min. Refractory cardiogenic shock: 0.05–0.5 mcg/kg/min.

High arrhythmogenic potential. Causes hyperglycaemia and hyperlactataemia (not indicative of poor perfusion when on adrenaline).

QTc >500 ms or increase >60 ms from baseline: consider stopping offending drug, correct electrolytes (K⁺, Mg²⁺), and continuous monitoring.

Cardiac Drugs

Amiodarone
Sotalol
Quinidine
Procainamide
Disopyramide
Dofetilide
Ibutilide

Antibiotics & Antifungals

Azithromycin
Clarithromycin
Erythromycin
Ciprofloxacin
Levofloxacin
Moxifloxacin
Fluconazole
Voriconazole

Psychiatric / Other

Haloperidol
Droperidol
Quetiapine
Chlorpromazine
Methadone
Ondansetron (high dose)
Hydroxychloroquine
Cisapride
Domperidone

Resource: CredibleMeds / AzCERT database for comprehensive and updated QT risk stratification.

Drug	Indication	IV Dose (Acute)	Monitoring
Adenosine	SVT termination, diagnosis	6 mg rapid IV; repeat 12 mg, then 18 mg	ECG; warn patient — chest tightness; AVOID in asthma, 2nd/3rd block; reduce dose in heart transplant
Amiodarone	VT, VF, AF rhythm control	300 mg in 5% dextrose 20–60 min; 900 mg/24 h	ECG, BP, LFTs, TFTs, CXR, eyes annually; phlebitis risk — central line preferred for infusions
Atropine	Symptomatic bradycardia	500 mcg IV; repeat to max 3 mg	HR, rhythm, anticholinergic effects (urinary retention, dry mouth, confusion in elderly)
Lidocaine	VT (alternative), cardiac arrest	1–1.5 mg/kg IV bolus; infusion 1–4 mg/min	CNS toxicity: drowsiness, tremors, convulsions; reduce dose in hepatic failure/low CO
Magnesium sulphate	TdP, hypomagnesaemia	2 g (8 mmol) IV over 10 min	Serum Mg²⁺; respiratory depression (antidote: calcium gluconate 10 mL 10% IV); deep tendon reflexes
Metoprolol IV	Rate control, SVT	5 mg IV over 5 min; repeat up to 15 mg	HR, BP, PR interval; bronchospasm
Digoxin	AF rate control, SVT	500 mcg in 50 mL over 30 min (loading)	Level 0.5–2.0 ng/mL (check 6 h post-dose); K⁺; arrhythmia; nausea; visual disturbance

GCC Context & Exam Preparation

GCC-Specific Cardiac Considerations

High IHD Burden in GCC

Gulf countries have among the highest age-standardised IHD mortality rates globally
Smoking prevalence among Gulf males: up to 35–40% in some populations — primary risk factor for premature IHD and arrhythmia
High prevalence of type 2 diabetes mellitus (Qatar, UAE, Saudi Arabia: 15–20% adult prevalence) — silent ischaemia common
Metabolic syndrome and central obesity: contributes to AF risk in younger populations
Expat construction and labour workers: heat-related illness, dehydration, electrolyte disturbance — arrhythmia precipitants

Ramadan Fasting — Cardiac Medication Considerations

Amiodarone: Once-daily dosing — administer at Iftar (break-fast meal). No dose change required but monitor adherence. Maintain sun avoidance.
Warfarin: Dietary change (dates, traditional foods, altered vitamin K intake) — increase INR monitoring to weekly during Ramadan. Watch for sub-therapeutic INR.
Digoxin: Once daily — administer at Iftar. Dehydration during fasting increases risk of digoxin toxicity — monitor levels, renal function, electrolytes.
Beta-blockers: Bisoprolol (once daily) — ideal for Ramadan. Twice-daily metoprolol: consider switching to once-daily extended-release form.
NOACs: Twice-daily dosing: give at Suhoor and Iftar. Once-daily: at Iftar. No pharmacokinetic impact of fasting itself.
Electrolytes: Monitor K⁺ and Mg²⁺ — diuretic timing adjustments needed to prevent nocturnal polyuria and dehydration.

Heat & Electrolyte Disturbance — Arrhythmia Risk

Extreme summer heat (45–50°C in GCC) + high humidity = significant sweat losses
Hypokalaemia from sweat/vomiting/diuretics: risk of VT, TdP, AF, U waves on ECG
Hypomagnesaemia: refractory hypokalaemia, TdP, muscle cramps
Hypernatraemia/dehydration: sinus tachycardia, decreased perfusion
Heat stroke: direct myocardial injury, arrhythmias, QT prolongation
Nursing action: electrolyte monitoring protocol for at-risk patients during summer months and heat waves

AF in GCC Expat Elderly Workers

Increasing prevalence of AF in expatriate elderly population (>65 years)
Cultural and language barriers may delay symptom reporting and medical help-seeking
Often inadequately anticoagulated prior to GCC employment medical — screen proactively
CHADS₂-VASc assessment and anticoagulation initiation per DHA/DOH/MOH guidelines
NOAC preferred — no dietary interactions relevant to varied GCC diet patterns

Regulatory Standards

DHA (Dubai Health Authority)

DHA-licensed nurses must demonstrate cardiac monitoring competency
CCU nurses: mandatory arrhythmia recognition and defibrillation competency
BLS + ACLS/ALS certification required for critical care and emergency settings
Annual competency verification through DHA-approved education providers

DOH (Department of Health — Abu Dhabi)

Cardiac care standards aligned with international guidelines (AHA/ESC)
STEMI network protocols: door-to-balloon time targets <90 min
Telestroke/telecardiology services expanding in remote areas
PPM (Performance & Patient Management) framework includes cardiac nursing KPIs

SCFHS (Saudi Commission for Health Specialties)

CCU nursing competency framework: Domains — Assessment, Monitoring, Pharmacology, Emergency Response
Exam: Saudi Nursing Licensing Exam (SNLE) includes cardiac dysrhythmia identification and management questions
Mandatory continuing education units (CEUs) including cardiovascular topics
Saudi Heart Association guidelines used in clinical practice standards

DHA / DOH / SCFHS Exam Preparation

Must-Know Rhythms for GCC Exams

Sinus tachycardia vs SVT: rate >150 with regular narrow complex — think SVT; P waves in SVT often not visible
AF: irregularly irregular, no P waves, narrow QRS — the most commonly tested arrhythmia
2nd degree Mobitz II vs Wenckebach: Mobitz II has constant PR then sudden dropped QRS — urgent pacing indication
3rd degree (complete) heart block: P waves and QRS at independent rates, never related
VT vs SVT with aberrancy: Brugada criteria, AV dissociation, concordance — treat as VT if uncertain
Torsades de Pointes: twisting, polymorphic VT preceded by long QT interval
WPW: short PR + delta wave + broad QRS — avoid adenosine/digoxin/verapamil in AF with WPW

ECG Exam Questions — Common Patterns

"Patient with palpitations, rate 160, narrow QRS, no visible P waves" = SVT — adenosine first-line
"Irregular rhythm, no P waves, rate 80–120" = AF — anticoagulate, rate control
"PR interval increases until QRS dropped, then resets" = Wenckebach/Mobitz I — usually inferior MI, often benign
"Broad complex tachycardia, AV dissociation" = VT — amiodarone or cardioversion
"QTc 520 ms on azithromycin" = drug-induced QT prolongation — stop drug, monitor, correct electrolytes
"Spiked waveform before each QRS, LBBB morphology" = ventricular pacemaker (VVI/DDD)

Question Stem	Answer
First-line drug for SVT termination	Adenosine 6 mg IV rapid bolus
Drug for rate control in AF + HFrEF	Digoxin or beta-blocker (bisoprolol); NOT verapamil/diltiazem
Antiarrhythmic for VT in haemodynamically stable patient	Amiodarone 300 mg IV
Drug for Torsades de Pointes	Magnesium sulphate 2 g IV over 10 min
Drug class AVOIDED in WPW + AF	Adenosine, digoxin, verapamil (risk of VF)
Vaughan Williams Class III drug with multi-organ toxicity	Amiodarone (lungs, thyroid, liver, eyes)
Antidote for digoxin toxicity	Digibind (digoxin-specific antibody fragments)
Reversal agent for dabigatran (NOAC)	Idarucizumab (Praxbind)
Why avoid flecainide in post-MI patient with AF?	Pro-arrhythmic in structural heart disease (CAST trial)
First-line vasopressor in septic shock	Noradrenaline (norepinephrine)

Tachycardia Algorithm Summary

Adverse features? YES → Synchronised DC cardioversion (sedate if conscious)
Narrow QRS + stable → Vagal manoeuvres → Adenosine
Broad QRS + stable → Assume VT → Amiodarone
Adenosine CONTRAINDICATED: asthma, 2nd/3rd AV block, WPW with AF
Pulseless VT/VF → Defibrillation (unsynchronised)

Adverse Features (Mnemonic: SHIP)

Shock (hypotension, pallor, sweating)
Heart failure (pulmonary oedema)
Ischaemia (chest pain, ECG changes)
Pre-syncope / Syncope

Bradycardia Algorithm Summary

Reversible causes: hypoxia, hypothermia, drugs, electrolytes
Atropine 500 mcg IV (max 3 mg total)
No response → Transcutaneous pacing or isoprenaline/adrenaline infusion
Expert help → Transvenous pacing
Atropine less effective in: transplanted heart, Mobitz II, complete block

DC Cardioversion — Synchronised vs Unsynchronised

Synchronised: AF, atrial flutter, SVT, haemodynamically stable VT (pulse present)
Unsynchronised (defibrillation): pulseless VT, VF, polymorphic VT
Key: synchronised avoids delivering shock on T wave (R-on-T phenomenon → VF)

Study Tip for GCC Nurses: DHA/DOH/SCFHS exams commonly test: (1) drug contraindications in specific arrhythmias (especially WPW), (2) antiarrhythmic class mechanisms, (3) identifying 2nd vs 3rd degree block on a rhythm strip description, (4) management priority — synchronised vs unsynchronised cardioversion. Master these 4 areas for high exam performance.