Test: Arrhythmias and Emergency Medicine- 2 - NEET PG MCQ

For the management of symptomatic bradycardia, the following medications are advised:

• Atropine 0.5 mg (maximum of 3 mg)
• Epinephrine 2-10 µg/kg/min
• Dopamine 2-10 µg/kg/min

In cases of symptomatic bradycardia accompanied by indications of inadequate perfusion, transcutaneous pacing is advised according to the ACLS 2015 guidelines.
​

• Transcutaneous pacing (TCP) should be considered.
• If TCP is unavailable, the administration of two medications, dopamine and epinephrine, is recommended.
• Should the patient still be unstable, transvenous pacing is performed.

The initial and most important action in the treatment of symptomatic bradycardia is the provision of atropine.

The ECG indicates a heart rate of 40 beats per minute, featuring a P wave of normal duration preceding each normal qRS complex. The PR interval remains consistent, and there are no dropped beats in the observed rhythm. The patient is experiencing sinus bradycardia.

• The five Hs and five Ts associated with pulseless electrical activity (PEA) are outlined below.
• PEA indicates that while electrical activity is observed on an ECG, there is no detectable pulse.
• The primary cause of PEA is hypoxia due to respiratory failure, which accounts for approximately 40-50% of cases, followed by hypovolemia.

In PEA, the treatment protocol to follow is for asystole. Always administer epinephrine and assess for reversible causes.

CPR Duality

• Push hard (at least 2 inches (5cm) and fast (100-120/min) and allow complete chest recoil Minimize interruptions in compressions Avoid excessive ventilation
• Rotate compressor every 2 minutes, or sooner if fatigued
• If no advanced airway, 30:2 compression-ventilation ratio
• Quantitative waveform capnography
  • If PETCO, <10 mm Hg, attempt to improve CPR quality
• Intra-arterial pressure
  • If relaxation phase (diastolic) pressure <20 mm Hg, attempt to improve CPR quality

Shock energy for defibrillation

• Biphasic: Manufacturer recommendation (e g. initial dose of 120- 200 J); if unknown, use maximum available. Second and subsequent doses should be equivalent, and higher doses may be considered.
• Monophasic: 360 J

Drug therapy

• Epinephrine IV/IO dose: 1 mg every 3-5 minutes
• Amiodarone IV/IO dose: First dose: 300 mg bolus. Second dose: 150 mg

Advanced airway

• Endotracheal intubation or supraglottic advanced airway
• Waveform capnography or capnometry to confirm and monitor ET tube placement
• Once advanced airway in place, give 1 breath every 6 seconds (10 breaths/mln) with continuous chest compressions

Return of spontaneous circulation (ROSC)

• Pulse and blood pressure
• Abrupt sustained increase In PETCO₂ (typically 240 mm Hg)
• Spontaneous arterial pressure waves wth intra-arterial monitoring

Reversible causes

• Hypovolemia - Tension pneumothorax
• Hypoxia - Tam ponade, cardiac
• Hydrogen ion (acidosis) - Toxins
• Hypo-/hyperkaiemia - Thrombosis, pulm onary
• Hypothermia - Thrombosis coronary

Non-penetrating blunt trauma to the chest can induce ventricular fibrillation, potentially resulting in sudden cardiac death. This phenomenon is known as commotio cordis and is frequently observed in sports-related injuries.
When trauma occurs to the chest at the peak of the T wave, a time often referred to as the vulnerable period of the heart, it can trigger ventricular fibrillation.

According to the AHA 2015 BLS guidelines, as the patient is already noted as unresponsive, the rescuer should promptly check the carotid pulse and breathing for no longer than a 10-second interval.

• Call for assistance to activate the emergency response system.
• If the unresponsive patient is not breathing and has no carotid pulse, the C-A-B sequence is used, and chest compressions commence at a rate of 30:2 for all age groups.
• If the unresponsive patient is not breathing but has a detectable carotid pulse, administer rescue breaths once every 6 seconds to reach a minimum of 10 breaths per minute.

The ratio of chest compressions to ventilations is 30:2 across all age groups, except for neonatal resuscitation, where it is 3:1. This 30:2 ratio also applies to infants and children. For adults, regardless of the number of rescuers, the ratio remains 30:2. In the case of children with one rescuer, the ratio is 30:2, while with two or more rescuers, it adjusts to 15:2.

• Table: Summary of High-Quality CPR Components for BLS Providers.
  

Atropine is indicated solely for the treatment of bradycardia, and its routine use during resuscitation is discouraged.

• The heart rate is consistently irregular because of rhythm variations.
• The estimated heart rate is 60 beats per minute (6 QRS complexes in 6 seconds in lead II [30 large squares]).
• The axis remains normal.
• There is a progressive lengthening of the PR interval that is followed by a dropped beat.
• The PR interval prior to the dropped beat is longer than the PR interval in the subsequent beats.
• The diagnosis is Mobitz I heart block.

The ECG displays a broad complex QRS tachycardia, which is indicative of ventricular tachycardia. Given that the patient's blood pressure is rapidly declining, a DC shock must be administered without delay.

• AVNRT occurs without the presence of structural heart disease and is typically well tolerated.
• Neck pulsations are often perceived due to the simultaneous contraction of the atria and ventricles.
• A 'frog sign' may be observed during a physical examination when the arrhythmia is present.

• The fast pathway, located in the upper section of the node, has a longer refractory period.
• Conversely, the pathway situated lower in the AV node area conducts at a slower rate but has a shorter refractory period.

The ECG displays a fluctuating heart rate with the RR interval in lead II (refer to the lowest lead) ranging from 150 to 300 bpm. The axis remains normal.

• The P wave is absent, accompanied by a shortened RR interval and narrow complex qRS.
• Hyper-acute T waves are observed in leads V₂ to V₅, indicating an anterior wall myocardial infarction (MI).
• Hypertension serves as a risk factor for both subendocardial ischaemia and atrial fibrillation.

Ventricular tachycardia presents with a wide complex qRS, thereby eliminating choices A and B.

The ECG indicates a variable heart rate resulting from an irregularly irregular RR interval. The P waves are absent in the ECG, while the QRS complex has a normal duration. These findings suggest the presence of atrial fibrillation.


Atrial Fibrillation (AF)

The presystolic accentuation of the mid-diastolic murmur associated with atrial fibrillation arises from atrial contraction against a closed mitral valve. As atrial fibrillation begins, the atria will twitch, causing the presystolic accentuation to vanish. Other alterations in the findings of mitral stenosis with the initiation of atrial fibrillation include:

• The first heart sound shows variability in intensity due to the irregularly irregular heart rhythm.
• The opening snap persists as long as the valves remain pliable and non-calcified.
• The A₂-O snap interval is generally less affected by atrial fibrillation, as it is primarily influenced by the mean left atrial pressure at the start of diastole, which exhibits minimal variation from beat to beat.
• The duration of the diastolic murmur fluctuates.

Treatment focuses on modifying conduction within the AV node. Vagal stimulation, such as that produced by the Valsalva manoeuvre or carotid sinus massage, can sufficiently slow conduction in the AV node to successfully terminate AVNRT. In cases where physical maneuvers fail to resolve the tachyarrhythmia:

• The administration of adenosine, typically 6-12 mg IV, often proves effective.
• Intravenous beta blockade or calcium channel therapy should be contemplated as a secondary treatment option.

If there is a presence of haemodynamic compromise, R wave synchronous DC cardioversion at 100-200 J can effectively terminate the tachyarrhythmia.