Week 6

Reflection

Using the Gibb’s Reflective model, I will be reflecting on the lab session we had on the 7^th and 8^th of October, 2015.

Description: This week we learned about the different needle gauges, syringes, and drug containers through working through the workbook, then applying and practicing. We also learned the correct method to aseptically prepare the equipment and administer drugs by working through the OSCE workbook. Moreover, we practiced drug calculation, where our lecturer gave us examples of doses of different drugs. We calculated the right volume for the dose and drew up that volume. We also practiced documenting the drugs, dose, and route of administration on a PCR. Furthermore, every time we drew up a drug we would check the drug’s indications and effects from the JRCALC.  Later in the afternoon, we practiced our clinical approach to a cardiac patient. 

Feelings: I felt very interested when we were learning about the different needles and drug containers. I enjoyed opening the drug vials and learning about the different types. I felt confident when we were doing drug calculations and got it right almost every time. Moreover, it was easy documenting information about the medication I drew up. However, I felt that I lacked in knowledge of the different drugs and their effects.  Moreover, I was not very confident in my approach to the cardiac patient.

Evaluation: It was very good to have different dosage questions and have to calculate, draw up the drug and document that. It made the experience of drawing drugs more realistic. However, it was bad when we were practicing approaching a cardiac patient. I got lost and did not have a systematic approach to questioning the patient’s chief complaint and history.

Analysis: It is very important to be quick and careful with calculations and drawing up drugs. Moreover, I believe I forgot my clinical approach because I had not practiced it previosly. However, it annoyed me that I did not perform well in the history taking, since it’s one of the most important components of the PCI. My main problem was that I would ask for the patient’s history in a very random order. This lead to me forgetting major components.

Conclusion: I should have reviewed the OSCE assessment worksheet, in order to refresh my memory on the steps in approaching a cardiac patient. Moreover, I should have followed the DOLOR+S and AMPLE in order to avoid any confusion and forgetting to ask about important information.

Action Plan: If this happened again, I will stick to the order of DOLOR+S and AMPLE.

Picture 1: Drugs, needles and syringes used for practice

Picture 2: Sodium Bicarbonate and Nitroglycerin

Picture 3: Documentation of a couple of drugs drawn up on a PCR

Picture 4: Information about GTN from the JRCALC. Adopted from ( JRCALC, 2013).

Furthermore, we watched videos demonstrating the skill of drug administration, aseptic technique, different routes of administration and everything else associated with this skill. These videos can be found on this link: http://expertinmypocket.com.au/category/medication/
Reference:

Joint Royal Colleges Ambulance Liaison Committee. (2013). UK ambulance services: Clinical practice guidelines 2013. Bridgwater, England: Class Professional Publishing.

University of the Sunshine Coast. (2014). Expert in my pocket: Medications. Retrieved from http://expertinmypocket.com.au/category/medication/

Domain Knowledge: 

Ventricular standstill is when there is a complete absence of ventricular electrical activity. P or P' waves are present indicating atrial electrical activity. This is a cardiac arrest rhythm requiring CPR. Supraventricular tachycardias (SVT) are tachycardias originating from above the ventricles or the Bundle of His. These can be divided as follows:

Picture 5: Types of supraventricular tachycardias

Three were covered in this week's lecture: Atrial fibrillation, atrial flutter, and SVT specifically the AVNRT one.

Atrial fibrillation is irregularly irregular. It is caused by multiple ectopic sites in the atria firing. There are no P waves. Instead, there are fibrillatory waves present between the QRS complexes. Since the atria are fibrillating, conduction through the AV node to the ventricles is random. The ventricular rate can reach up to  200 bpm. It is controlled if it is <100 bpm and uncontrolled if >100 bpm. The QRS complexes may be normal or wide. The HR on the monitor may not match the pulse rate. A good way to check the regularity of a rhythm is to draw a line at each QRS complex on the edge of a plain paper. Then move the paper along the rhythm and see if the QRS complexes land on the same lines drawn earlier. If not, the rhythm is irregular. AF can be caused by HT, IHD, CCF, and valve disease. It is very common as the first rhythm post resuscitation from cardiac arrest.

The risks associated with AF include the loss of the atrial kick, blood pooling creating clots in the atria which can detach and cause an embolic stroke. Patients with AF are placed on anticoagulants for life. Examples include Aspirin and Clopidogrel. 

The treatment of AF is only for a rapidly deteriorating patient and it is synchronized cardioversion. However, the underlying causes could be treated, and they include: chest pain, SOB, nausea. 

Atrial flutter is defined by macro-reentry circuit activity within the atria, often in the right atrium. This affects the return of blood from the superior and inferior vena cavae. AF originates in atrial ectopic sites outside the SA node. Most commonly they originate in the AV node. Atrial rate can range from 240-360 bpm, but usually its around 300 bpm. P waves are absent.Instead there are F waves that have a characteristic sawtooth pattern. Ventricles fire at a rate relative to the atrial rate. This is called the conduction ratio and is shown as A:V (A: Atrial firing rate, V: Ventricular firing rate). Most common conduction ratio is 2:1, with a ventricular rate of around 150 bpm. However, it can be 3:1, 4:1, 5:1, or very rarely 1:1. When the conduction ratio changes in the same rhythm this is variable conduction. AF is caused by HT, IHDm CCF, emphysema, rheumatic heart disease, damage to SA node or atria.

AVNRT is the most common SVT. It involves a reentry circuit within the AV node. SVT is a regular rhythm with normal T waves. P waves may be before, after or buried in the QRS complex. SVT may require vagal maneuvers, adenosine, or synchronized cardioversion to be treated. 

In the AV node there are fast and slow pathways. The normal conduction is through the fast pathway, where the fast pathway has a longer refractory period and the slow path has a short refractory period. If a PAC fires while the fast path is still in refractory period, the action potential will travel down the slow pathway. By the time the action potential reaches the end of the slow pathway, the fast pathway will no longer be in the refractory period. Therefore, the action potential will now travel in a retrograde direction back up the fast pathway. Then back down the slow path and back up the fast one. This is how reentry occurs.

Causes of SVT are:

• PAC
• Emotion
• Catecholamines
• Tobacco, cocaine (stimulants)
• Hypoxia
• Ischemia
• AMI
• Sepsis
• Hypomagnesaemia
• Hypokalemia

Stable SVT	Unstable SVT
HR > 100 bpm Patient asymptomatic Patient has underlying cardiac electrical abnormality generating the arrhythmia	Patient exhibits compromise due to tachycardia: Chest pain, SOB, altered LOC, hypoxia

Table 1: Difference between stable and unstable SVT

One treatment is abdominal valsalva manoeuvre. It includes supine posturing, 15 sec of strain, intrathoracic/intraoral pressure of 40mmHg, and then getting the patient to blow into a 10 mL syringe.

Enquiry and Research:

I read the readings from Huszar's book and the following is information i found that was not present in the lecture, but supplemented it.

Atrial flutter is uncontrolled when the ventricular rate is about 150 bpm, and is controlled when the ventricular rate is about 60-75 bpm. Also, atrial fibrillation can occur during atrial flutter and vice versa. This is called atrial fib-flutter.  The loss of the atrial kick in atrial fibrillation and atrial flutter can reduce the CO by as much as 25%. In atrial fibrillation, the ventricular rate is about 160-180 bpm in uncontrolled atrial fibrillation, and <100 bpm in controlled atrial fibrillation (Wesley, 2011).

The onset and termination of Paroxysmal supraventricular tachycardia (PSVT) are typically abrupt, with the onset initiated by a PAC. Following the termination of the dysrhythmia, a brief period of asystole may follow. When the reentry mechanism involves only the AV node, the dysrhythmia is called AV nodal reentry tachycardia. PSVT is characterized by repeated episodes of tachycardia that last from a few seconds to days, and can recur for many years. Vagal maneuvers usually terminate PSVT.Syncope may occur after the termination of PSVT because of the asystole that may follow its termination (Wesley, 2011).

Also, i read the guidelines in the JRCALC for cardiac rhythm disturbance. The principles of treatment include:

• Manage pt using ABCDE approach
• Administer oxygen to achieve a saturation with the range 94-98%
• Gain venous access
• Always take a defibrillator to any patient with suspected cardiac rhythm disturbance
• Establish cardiac rhythm monitoring ASAP
• Document the arrhythmia, using a 12-lead ECG preferably
• Record ECG rhythm during any interventions

Picture 6: Steps to the assessment and management of patients with tachycardia, broad and narrow complex tachycardias. Adopted from (JRCALC, 2013).

Also, i searched the JRCALC for information about Aspirin and Clopidogrel.

Aspirin dose is 300mg in tablet form and it is an anti-platelet which reduces clot formation. It also acts as an analgesic, anti-pyretic and anti-inflammatory. It is indicated for adults with clinical or ECG evidence of myocardial infarction or ischemia.

Clopidogrel comes in tablets with dosages of 75 mg and 300 mg. It is indicated in patients with ST elevation MI. It inhibits platelet aggregation. Usually given in conjunction with Aspirin, unless there is a known allergy to Aspirin (JRCALC, 2013).

I read an article about the valsalva maneuver(VM) and found that baroreceptors located within the carotid bodies are stimulated by increased pressure created as a result of impeded circulation. This impedecnce of circulation occurs during this period of increased intrathoracic pressure. The baroreceptors trigger an increase in vagal tone, stimulating a bradycardia response at the level of the AV node. This prolongs the refractoriness of the nodal tissue and disrupts the re-entry circuit.

Also, supine positioning is advised since sitting or standing were associated with syncope and other side-effects. The supine position, although widely used, has not been universally adopted. As a result, examples of syncope and hypotension resulting from VM performance in prehospital emergency care continue to occur. Moreover, a 10 mL syringe demonstrated recently to be effective in producing the 40 mmHg optimum pressure (Smith, 2011).

Another similar management of SVT is the human dive reflex, which as initially observed in aquatic animals. It is effective in inducing bradycardia through the stimulation of thermoregulatory sensors in the skin. This is accomplished by the immersion of just the head of the patient in cold water. Also, it was found that after deep inhalation and breath holding further increased the vagal tone and resulted in mild bradycardia. As useful as this method is, further research must be conducted to determine its appropriateness in the prehospital setting (Smith et al., 2012). 

I found a video demonstrating the valsalva maneouver. However, the video was a trial testing a modification in the posture of the patient during the maneouver. I benefited from this video because it showed the maneouver exactly how it was described in the lecture, except for the positioning. The video's link is https://www.youtube.com/watch?v=8DIRiOA_OsA

The video intrigued me so i read the article for this trial. The tested positioning in this trial was from semi-recumbent with supine repositioning and passive leg raise immediately after the Valsalva strain. It was found that 17% of participants assigned to the standard Valsava maneuver achieved sinus rhythm. Compared with 43% in the modified valsava maneuver group (Appelboam et al., 2015). 

References

Appelboam, A., Reuben, A., Mann, C., Gagg, J., Ewings, P.Barton, A.,...,& Benger, J. (2015). Postural modification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): a randomised controlled trial. Lancet, 386, 1747-1753. doi: 10.1016/S0140-6736(15)61485-4

Defacto Films. (2015). Modified Valsalva manoeuvre for supraventricular tachycardia [Video]. England: TheLancetTV. 

Joint Royal Colleges Ambulance Liaison Committee. (2013). UK ambulance services: Clinical practice guidelines 2013. Bridgwater, England: Class Professional Publishing.

Smith, G. (2011). Management of supraventricular tachycardia using the Valsalva manoeuvre: a historical review and summary of published evidence. European Journal of Emergency Medicine, 19, 346-352.  doi: 10.1097/MEJ.0b013e32834ec7ad

Smith, G.,  Morgans, A., Taylor, D.M.D., & Cameron, P. (2012). Use of the human dive reflex for the management of supraventricular tachycardia: a review of the literature. Emergency Medicine Journal, 29, 611-616. doi: 10.1136/emermed-2011-200877

Wesley, K. (2011). Huszar's basic dysrythmias and acute coronary syndromes: Interpretation and management (4th ed.). St Louis, MO: Elsevier.