Drop the Beat! – Adenosine in SVT

Drop the Beat! – Adenosine in SVT

Supraventricular tachycardia (SVT) is defined as a dysrhythmia that originates proximal to (or ‘above’) the atrioventricular (AV) node of the heart. It commonly manifests as a regular, narrow complex (QRS interval < 120ms) tachycardia in affected patients. It is most frequently attributable to re-entrant electrical conduction through accessory pathways in the heart, with typical Electrocardiogram (ECG) findings depicting ventricular rates of 150 to 250 beats/min without the preceding P wave usually seen in sinus tachycardias. [1,2]

In the stable adult patient presenting with SVT, where no ‘red flags’ such as shock, altered mental state, ischemic chest pain or hypotension are present, management typically begins with an attempt to convert the rhythm back to its baseline sinus state using vagal manoeuvres.[3] Vagal manoeuvres such as the carotid sinus massage and the Valsalva manoeuvre are effective first-line therapies, terminating approximately 25% of spontaneous SVTs,[4] with the newer, modified Valsalva manoeuvre showing even greater efficacy of 43% conversion.[5] When these fail or are otherwise not feasible to use in patients, management involves the administration of a drug called Adenosine.

The Evolution of Adenosine Use for SVT

In 1927, studies found that the injection of extracts from cardiac tissue into animals appeared to decrease heart rates and that this effect was attributable to an ‘adenine compound’.[6] This compound was later identified as Adenosine, comprised of the purine-based nucleobase Adenine attached to a ribose sugar. Fifty years after its initial discovery, Adenosine began to emerge as a treatment for stabilizing SVTs and has remained a mainstay in its management ever since.[7]

Current guidelines recommend Adenosine for the management of SVT, usually administered through a peripheral intravenous (IV) access initially as a 6 mg bolus. Adenosine has an extremely short half-life (less than 10 seconds) and is therefore rapidly metabolized soon after it enters the body.[8] Therefore, IV dosage is commonly followed by a 20 mL rapid saline flush to facilitate the drug’s transport to cardiac tissue where it can act before being broken down into inactive metabolites. If the 6mg dose does not convert the SVT back to sinus rhythm, subsequent doses are given at 12 mg, also followed by 20-mL saline for rapid infusion.

Pro-Tip: Single syringe technique

Before we dive into the concept of the single syringe method of administering Adenosine, take a look at the segment above. How would you give 6 mg of Adenosine through an IV site, making sure a total of 20 mL saline follows right after, in enough time to make sure you don’t waste that precious 10-second half-life of Adenosine? In many places, one of the two methods are used to make this happen:

  1. Use an IV line to push Adenosine > remove syringe > push 10 mL saline using a pre-filled syringe > remove syringe > push 10mL saline using a second pre-filled syringe.
  2. Fancier places use what’s known as a stopcock, a device usually with 3 ports attached to the IV site. Adenosine syringe is attached to one port and a 10 mL saline flush is attached at a separate port. The process looks something like this: Push adenosine through stopcock port > turn stopcock to open saline port’s access to IV site > push 10 mL saline flush > push an additional 10 mL saline using second syringe or remainder of a 20 mL prefilled syringe.

Now we all know that nurses are indistinguishable from ninjas at times when handling IV medication. However, even the most experienced practitioner is not immune to the occasional stumble when switching between the various syringes and swivels required in the methods above. In fact, a study in 2018 found that, in pediatric patients, adenosine given using the stopcock method delivered suboptimal doses.[9]

In an attempt to improve administration time, a potential work-around was proposed where adenosine could be combined with the flush solution in one 20 mL syringe and pushed altogether.[10] This potentially eliminates any time wasted changing syringes and manipulating stopcocks, but does it still work the same? Fortunately, a few studies have demonstrated the feasibility of the single syringe method, with non-inferior efficacy compared to standard methods of drug administration.[11,12]

Caveats: Coffee Conundrums

Let’s talk a bit about dosage. We mentioned above that guidelines recommend starting at 6 mg and moving to 12 mg for subsequent dosages. These dosages assume uninhibited action of adenosine at its receptors which, unfortunately, may not always be the case in patients. What would inhibit adenosine’s activity, I hear you ask? You’ll want to put down that Caramel Macchiato because the answer (pause for dramatic effect) … is coffee – caffeine to be exact.

Caffeine is known to work by antagonizing adenosine receptors, thereby decreasing adenosine’s biologic effect.[13] A component in many frequently consumed beverages, such as coffee, tea, energy drinks and sodas, and with a half-life of approximately 4-5 hours, caffeine is very likely to be present in the bloodstreams of many Emergency Department patients (and doctors). A 2010 multi-centre study in Australia found that recent ingestion of caffeine less than 4 hours prior to a 6 mg adenosine bolus significantly reduced its effectiveness in treating SVT. [14]

This makes it all the more important to not only include information on any known recent beverage consumption during history taking for patients presenting with SVT, but also to potentially increase dosage for patients with a confirmed or suspected recent ingestion of caffeine. In such cases, it would be reasonable to start at 12 mg adenosine as the first dose, followed by 18 mg subsequent dosages to manage SVT.[15]

A 2010 multi-centre study in Australia found that recent ingestion of caffeine less than 4 hours prior to a 6 mg adenosine bolus significantly reduced its effectiveness in treating SVT.

References and Further Reading

  1. Bibas, L., Levi, M., & Essebag, V. (2016). Diagnosis and management of supraventricular tachycardias. CMAJ : Canadian Medical Association journal = journal de l’Association medicale canadienne, 188(17-18), E466–E473. https://doi.org/10.1503/cmaj.160079
  2. Mahtani, A. U., & Nair, D. G. (2019). Supraventricular Tachycardia. The Medical clinics of North America, 103(5), 863–879. https://doi.org/10.1016/j.mcna.2019.05.007
  3. Advanced Cardiac Life Support Provider Manual, American Heart Association, Mesquite 2016
  4. Lim, S. H., Anantharaman, V., Teo, W. S., Goh, P. P., & Tan, A. (1998). Comparison of Treatment of Supraventricular Tachycardia by Valsalva Maneuver and Carotid Sinus Massage. Annals of emergency medicine, 31(1), 30–35.
  5. Appelboam, A., Reuben, A., Mann, C., Gagg, J., Ewings, P., Barton, A., Lobban, T., Dayer, M., Vickery, J., Benger, J., & REVERT trial collaborators (2015). Postural modification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): a randomised controlled trial. Lancet (London, England), 386(10005), 1747–1753. https://doi.org/10.1016/S0140-6736(15)61485-4
  6. Drury, A. N., & Szent-Györgyi, A. (1929). The physiological activity of adenine compounds with especial reference to their action upon the mammalian heart. The Journal of physiology, 68(3), 213–237. https://doi.org/10.1113/jphysiol.1929.sp002608
  7. Delacrétaz E. (2006). Clinical practice. Supraventricular tachycardia. The New England journal of medicine, 354(10), 1039–1051. https://doi.org/10.1056/NEJMcp051145
  8. Kazemzadeh-Narbat, M., Annabi, N., Tamayol, A., Oklu, R., Ghanem, A., & Khademhosseini, A. (2015). Adenosine-associated delivery systems. Journal of drug targeting, 23(7-8), 580–596. https://doi.org/10.3109/1061186X.2015.1058803
  9. Weberding, N. T., Saladino, R. A., Minnigh, M. B., Oberly, P. J., Tudorascu, D. L., Poloyac, S. M., & Manole, M. D. (2018). Adenosine Administration With a Stopcock Technique Delivers Lower-Than-Intended Drug Doses. Annals of emergency medicine, 71(2), 220–224. https://doi.org/10.1016/j.annemergmed.2017.09.002
  10. Hayes, B.D. (2019). ‘Trick of the Trade: Combine Adenosine with the Flush’. Academic Life in Emergency Medicine Blog Post https://www.aliem.com/trick-of-trade-combine-adenosine-single-syringe/
  11. Choi, S.C., Yoon, S.K., Kim, G.W., Hur, J.M., Baek, K.W., & Jung, Y.S. (2003). A Convenient Method of Adenosine Administration for Paroxysmal Supraventricular Tachycardia. Journal of the Korean society of emergency medicine, 14, 224-227.
  12. McDowell, M., Mokszycki, R., Greenberg, A., Hormese, M., Lomotan, N., & Lyons, N. (2020). Single-syringe Administration of Diluted Adenosine. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine, 27(1), 61–63. https://doi.org/10.1111/acem.13879
  13. Ribeiro, J. A., & Sebastião, A. M. (2010). Caffeine and adenosine. Journal of Alzheimer’s disease : JAD, 20 Suppl 1, S3–S15. https://doi.org/10.3233/JAD-2010-1379
  14. Cabalag, M. S., Taylor, D. M., Knott, J. C., Buntine, P., Smit, D., & Meyer, A. (2010). Recent caffeine ingestion reduces adenosine efficacy in the treatment of paroxysmal supraventricular tachycardia. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine, 17(1), 44–49. https://doi.org/10.1111/j.1553-2712.2009.00616.x
  15. Hayes, B.D. (2012). ‘Is the 6-12-12 adenosine approach always correct?’ Academic Life in Emergency Medicine Blog Post https://www.aliem.com/is-6-12-12-adenosine-approach-always/
Cite this article as: Mohammad Anzal Rehman, UAE, "Drop the Beat! – Adenosine in SVT," in International Emergency Medicine Education Project, September 14, 2020, https://iem-student.org/2020/09/14/adenosine-in-svt/, date accessed: October 23, 2020

Anaphylaxis in a Nutshell

anaphylaxis in a nutshell

Anaphylaxis can be broadly defined as a severe, life-threatening, generalized or systemic hypersensitivity reaction. Literature suggests that anaphylaxis is not always easily recognized in the Emergency Department (ED). One study indicates around 50% of cases being misdiagnosed and up to 80% do not receive appropriate first-line treatment.

Triggers

The most commonly identified triggers of anaphylaxis include food, drugs and venom, but it is important to note that 30% of the cases can be idiopathic. Among drugs, muscle relaxants, antibiotics, NSAIDs and aspirin are the most commonly implicated.

Which patients are at an increased risk of anaphylaxis severity and mortality?

Extremes of age

Co-morbid conditions (asthma, COPD, cardiovascular disease)

Concurrent use of beta-blockers and ACE inhibitors

While the overall prognosis of anaphylaxis is good, the key to avoiding adverse outcomes is by prompt recognition and initiation of appropriate interventions. Below are key points to guide your management of anaphylaxis in the ED.

Recognizing Anaphylaxis in the ED

Anaphylaxis reactions vary significantly in duration and severity and a single set of criteria will not identify all anaphylactic reactions. The World Allergy Organization (WAO) has suggested the following criteria to help ED physicians be more consistent in their recognition of anaphylaxis.

Anaphylaxis is highly likely when any one of the following three criteria is fulfilled

1. Acute onset of an illness (minutes to several hours) with involvement of the skin, mucosal tissue, or both (eg, generalized urticaria, itching or flushing, swollen lips-tongue-uvula) AND AT LEAST ONE OF THE FOLLOWING

  • Respiratory compromise (eg, dyspnea, wheeze-bronchospasm, stridor, reduced PEF, hypoxemia)
  • Reduced blood pressure or associated symptoms of end-organ dysfunction (eg. hypotonia [collapse], syncope, incontinence) OR

2. Two or more of the following that occur rapidly after exposure to a likely allergen for that patient (minutes to several hours)

  • Involvement of the skin-mucosal tissue (eg, generalized urticaria, itch-flush, swollen lips-tongue-uvula)
  • Respiratory compromise (eg, dyspnea, wheeze-bronchospasm, stridor, reduced PEF, hypoxemia)
  • Reduced blood pressure or associated symptoms (eg, hypotonia [collapse], syncope, incontinence)
  • Persistent gastrointestinal symptoms (eg, crampy abdominal pain, vomiting) OR

3. Reduced blood pressure after exposure to known allergen for that patient (minutes to several hours)

  • Infants and children: low systolic blood pressure (age-specific) or greater than 30% decrease in systolic blood pressure
  • Adults: systolic blood pressure of less than 90 mm Hg or greater than 30% decrease from that person’s baseline

Management Algorithm of Anaphylaxis in the ED

Anaphylaxis algorithm
Anaphyaxis algorithm 2

Key Points in Management

References and Further Reading

Cite this article as: Neha Hudlikar, UAE, "Anaphylaxis in a Nutshell," in International Emergency Medicine Education Project, January 31, 2020, https://iem-student.org/2020/01/31/anaphylaxis-in-a-nutshell/, date accessed: October 23, 2020

Clinical examination of the hemodynamically unstable patient

Clinical examination of the hemodynamically unstable patient

Authors: Job Rodríguez Guillén. Chief of Emergency Department. Hospital H+ Querétaro. México and Paola Rivero Castañeda. Medical Intern, Anahuac Querétaro University, Mexico. 

Introduction

Clinical examination accounts as a fundamental part in the management of most critical scenarios. Although there are few publications and it remains controversial, its value considered as limited by 50% of medical practicioners (1). None of the well-known semiology books include any section about the physical examination in the critically ill patient (2). Nonetheless, an adequate clinical evaluation at the patient’s bedside may save lives in the context of a serious situation.

Clinical Examination Objectives

The main objectives are identifying and discerning from types of shock, emphasizing in the identification of life-threatening conditions, clinical signs of organic hypoperfusion, as well as to evaluate treatment response regarding therapies employed, and risk stratifying.

Identify hemodynamic instability

  • Life-threatening conditions (Tension pneumothorax, Cardiac tamponade, Pulmonary thromboembolism, Active hemorrhage, etc.)
  • Organ hypoperfusion
    (Altered mental state, decreased uresis, mottled skin, prolonged CFT, etc.)

Evaluate treatment response

  • Vital signs and normalization of the clinical state
    (Mental state improvement, diminished skin mottling, improved uresis, normalization of prolonged capillary filling time, etc.)

Risk stratifying

  • Scale and prognostic scores calculation. Prognostic scores use a combination of clinical and/or laboratoy variables (SOFA: Squential Organ Failure Assessment; APACHE: Acute Physiology and Chronic Health Evaluation; SAPS: Simplified Acute Physiology Score; MPM: Mortality Probability Models, etc.)

Clinical Exam Systematization

The clinician must be able to do a quick and efficient clinical examination to recognize different states of shock as early as possible, or even situations that may compromise organic perfusion. At a given time, it’s suggested to check out the clinical history, re-interrogate the patient and his/her family members, as well as patient’s family/regular physician (or even look for their previous medical notes), in order to help clinical integration, and so for decision making.

Systematization of the evaluating process, based on the previously proposed objectives, can be identified with the following mnemonic: PROA.

PROA - Summary

P - Probabilistic thinking

  • Think about any probability.
  • Look for intentionally.
  • Analyze clinical context and individualize.

R - Risk of dying

Identify life-threatening causes: Cardiac tamponade, Tensionpneumothorax, Pulmonary thromboembolism, Active hemorrhage, etc.

O - Organic hypoperfusion

Cutaneous perfusion signs: examine mottled skin and capillary filling time.

A - Approach of the clinical examination

Clinical exam by regions. Some components may not be relevant for all patients, even requiring other physical maneuvers. Even though laboratory and imaging are not part of the clinical exam, their interpretation must be integrated with the examination findings.

Probabilistic Thinking

Medicine is a science of uncertainty and an art of probability.

— William Osler

Clinical decision making in the emergency department begins with the estimation of the probability of a determined patient to have or do not have specific conditions (Bayesian reasoning or pretest probability).

Example; the probability of septic shock in a young patient after having a car crash is very low compared to the high probability of presenting with hemorrhagic or obstructive shock.

Proposed decisions related to initial probabilistic thinking vary in clinical relevance depending on the patient’s condition. It should always be re-evaluated through available additional data (posttest probability) (Figure 1).

Relationship between probability thresholds and decision‐making zones
Figure 1: Relationship between probability thresholds and decision‐making zones (3).

Risk of Dying

Shock is a momentary pause in the act of death.

— John Collins Warren

Currently, there are four types of shock, all with a common pathophysiological pathway: acute circulatory insufficiency associated with cell oxygen utilization dysfunction (altered-balance between oxygen input and consumption: DO2/VO2 dysfunction), a central situation that takes part in the development of multiorgan dysfunction (4-5).

Initial physical examination should be directed to the identification of immediate life-threating pathologies such as obstructive shock (Tension pneumothorax, cardiac tamponade, pulmonary thromboembolism), hemorrhagic shock etc.

These pathologies require immediate action. Otherwise, early multi-organ dysfunction and death may occur. The Point of Care Ultrasound (PoCUS), is a fundamental tool used for the evaluation of patients with hemodynamic instability of unknown origin.

Organ Hypoperfusion

When assessing the damage an earthquake or fire has caused inside a building, one looks through the windows. Using this analogy, it would be useful to be able to see inside the body to view the damage caused by the shock process.

— Jean-Louis Vincent

The initial approach to clinical examination begins with the skin. It is essential to remember that microcirculation cannot be globally defined through its dependency with macrocirculation, autoregulation mechanisms and organ interactions. Moreover, the availability of devices to evaluate it remains limited. Therefore, the evaluation is done from clinical, biochemical and hemodynamic data integration (6) (Figure 2)

Figure 2: three windows of shock

The correct way of measuring capillary filling time

Approach of The Clinical Examination

Clinical exam is not an art, is an essential ability.

— Leonel Martínez-Ramírez

During the initial evaluation, multiple situations can affect the accomplishment of a detailed physical examination. Therefore, it is recommended to follow a structured exploration method, looking at every main organ system and region. Documenting its results would allow avoiding the inclusion of essential data, and would permit to identify tendencies or any change in the patient’s clinical status.

Clinical examination approach in the critically-ill patient.

7Clinical examination approach emphasized in the critically-ill patient. This examination is realized based on every region in the body. Some components may not be relevant for all patients, or even some other maneuvers shall be executed in the physical examination. The verification list should be modified to be adapted to each patient’s circumstances. Laboratory and other studies analysis does not conform part of the clinical examination, although, their interpretation should be added to exploration findings (7).

  • General appearance

    Introduce yourself to the patient. Evaluate general appearance, physical state, complexity or the presence of particular face patterns, etc.

  • Head

    Inspect pupils' symmetry and reactiveness to light. Look for facial asymmetry and signs of bleeding in nostrils and oropharynx. Inspect lips, mouth and tongue, searching for lesions or signs of ulceration.

  • Neck

    Evaluate neck symmetry, venous distension and tracheal positioning. Palpate searching for adenopathies, subcutaneous emphysema, etc.

  • Thorax

    Expose the thorax, inspect the use of accessory respiratory muscles, diaphragmatic movement, and type of respiration. Also, look for ecchymosis or hematomas. Palpate searching for subcutaneous emphysema or bone crepitations. Auscultate respiratory sounds bilaterally, as well as heart sounds, noting the physiological splitting of the second heart sound, murmurs, friction and gallop rhythm or third heart sound.

  • Upper extremities

    Evaluate upper extremities symmetry. Inspect all arterial and venous line catheters. Evaluate for presence of mottled skin, peripheral pulses and perfusion through capillary filling time.

  • Abdomen

    Take into consideration the diaphragmatic movement during ventilation. Evaluate distension and tympanic sounds during the percussion of the abdomen. Palpate for any rigidity or involuntary guarding. Evaluate abnormal growth of spleen and liver, palpable masses, murmurs or other intestinal sounds.

  • Lower extremities

    Evaluate all sites of vascular accesses and palpate pulses. Evaluate mottled skin, peripheral perfusion and edema.

  • Central Nervous System and Mental State

    Evaluate if the patient is able to follow orders and if his/her four extremities can move equally. Evaluate plantar response as well as withdrawal to pain stimuli. Check pupils and facial symmetry if they were not previously evaluated.

  • Devices and Incisions

    Every possible surgical site should be evaluated, as well as the entrance of every device, including endotracheal tubes, vascular accesses, thoracic tubes, enteral probes and urinary catheters. It should be taken into consideration the characteristics and quantity of urine in the Foley bag.

  • Monitors and waveforms

    The mode, pressures, ventilation per minute and waveforms, hemodynamic monitor (venous pressure, arterial pressure), telemetry and vital signs, as well as any other type of bedside monitor, should be inspected in order to detect any qualitative or quantitative alteration/abnormality.

  • Posterior region

    Exam executed when the patient is in a prone position. Inspect looking for lesions or penetrating wounds. Pressure ulcer appearance should be evaluated.

  • Environment

    Family’s or visitors' moods should be taken into consideration. Light quality, ambient temperature, etc. should be evaluated.

Conclusions

Clinical integration of initial clinical history and the physical examination should be added to the biochemical complementation as well as advanced hemodynamic monitoring parameters, when these are available. Even so, if clinical examination answers raised questions during the initial evaluating process, the clinician must act according to physiological principles. There is no ideal hemodynamic monitoring, meaning that all parameters have to be individualized for each patient and his/her clinical context. Therefore, clinical examination systematization results are an excellent aid for the clinician regarding his/her clinical practice.  

References and Further Reading

  1. Vazquez R, Vazquez Guillamet C, Adeel Rishi M, Florindez J, Dhawan PS, Allen SE, Manthous CA, Lighthall G.  Physical examination in the intensive care unit: opinions of physicians at three teaching hospitals. Southwest J Pulm Crit Care. 2015;10(1):34-43. DOI: http://dx.doi.org/10.13175/swjpcc165-14
  2. Cook CJ, Smith GB. Do textbooks of clinical examination contain information regarding the assessment of critically ill patients?Resuscitation. 2004;60:129–136.
  3. Zehtabchi S, Kline J.A. The Art and Science of Probabilistic Decision‐making in Emergency Medicine. Academic Emergency Medicine, 17:521-523. DOI: http://doi.org/10.1111/j.1553-2712.2010.00739.x
  4. Weil MH, Shubin H. Proposed reclassification of shock states with special reference to distributive defects. Adv Exp Med Biol.1971 Oct;23(0):13-23.
  5. Ince C. The microcirculation is the motor of sepsis. Crit Care. 2005;9 Suppl 4:S13-9. DOI: 1186/cc3753
  6. Vincent JL, Ince C, Bakker J. Clinical review: Circulatory shock–an update: a tribute to Professor Max Harry Weil.Crit Care. 2012 Nov 20;16(6):239. DOI: 10.1186/cc11510.
  7. Metkus TS, Kim BS. Bedside Diagnosis in the Intensive Care Unit. Is Looking Overlooked?. Ann Am Thorac Soc.2015 Oct;12(10):1447-50. DOI: 10.1513/AnnalsATS.201505-271OI.
Cite this article as: Job Guillen, Mexico, "Clinical examination of the hemodynamically unstable patient," in International Emergency Medicine Education Project, December 6, 2019, https://iem-student.org/2019/12/06/clinical-examination-of-the-hemodynamically-unstable-patient/, date accessed: October 23, 2020