Reflection:
Using
the Gibb’s Reflective Model I will reflect on the fourth Lab session we had for this
semester. It took place on the 30th of September.
Description: At the
start of this session, we worked through our advanced airway insertion
workbook. After we finished that we practiced preparing an i- gel supraglottic
airway and inserting it. First I lubricated the distal tip of the device,
making sure the pt. is unconscious. Then I positioned myself at the patient’s
head and opened his airway, using the head tilt-chin lift positioning. After
that I simply inserted the i-gel into the patient’s airway.
Feelings: After finishing the workbook I felt confident
about the device, it’s advantages and it’s method of insertion. When I actually
did it, I was sure of what I was doing and found it super easy. This made me
feel good.
Evaluation: It was really good to have the preparation,
through solving the workbook, before performing the skill. Also, it was great
to be able to perform the skill and experience how it’s done. There was nothing
bad about my experience of this skill.
Analysis: It is very important to make sure the pt. is
unconscious and does not have a gag reflex, to avoid any risk of aspiration.
Also, I stood at the patient’s head for better visualization of the pt.’s
airway and easier insertion of the i-gel.
Conclusion: This skill was very easy. Therefore, I believe
there was nothing more to do, than what I did.
Action Plan: I plan to go through the OSCE checklist and
make sure I know all the steps in the correct sequence. Moreover, I would like
to practice this skill again during the semester, so as this easy skill doesn’t
become hard for me.
Domain
Knowledge: This week we had one lecture. I will be writing my notes of this lecture, and what i learned.
The lecture covered ectopy first. Ectopic rhythms are defined as complexes that are in an abnormal place position. They could be from hypoxia, tissue damage, hyperkalemia or hypokalemia. Moreover, automaticity, which we learned about in week 3, is determined by the permeability of the cell membrane to sodium during phase 4. This movement occurs slowly until the threshold potential and then depolarization occurs.
Pacemaker cells such as the SA node, possess automaticity. On the other hand, in normal conditions, myocardial cells do not possess automaticity. When an ectopic beat happens it is caused by "enhanced automaticity".
This is when pacemaker cells increase their automaticity and increase their firing rate. This also happens when cardiac cells, that do not normally possess automaticity, develop automaticity. This occurs under abnormal conditions. This enhanced automaticity can cause an ectopic pacemaker to fire causing an ectopic beat on the ECG. Enhanced automaticity occurs due to different causes, including: increased catcholamines, hypoxia, hypercapnea, myocardial ischemia or infarction, administration of atropine, hypokalemia and hypocalcemia.
Premature ectopic complexes are caused by an irritable focus generating an action potential before the next depolarization of the normal pacemaker. It can be unifocal or multifocal and can be atrial, junctional, or ventricular. Ectopic complexes are not a rhythm in themselves, but are described as an addition to the underlying rhythm.
Premature atrial complexes(PAC) are extra complexes generated by an atrial focus outside the SA node or very high in the AV junction and they occur earlier than the next expected beat of the underlying rhythm, Their impulse may be conducted through the AV node or not. On the ECG, they will have a P' wave of varying morphology and a QRS complex of normal or abnormal morphology, and the PR interval will be <0.20 sec. It will cause an irregular pulse. It has a non compensatory pause.
Premature junctional complexes(PJC) are generated by an irritable focus within the AV junction and occurs earlier than the next expected beat of the underlying rhythm. May be conducted through the AV node or not, and its very difficult to distinguish between non-conducted PJC from non-conducted PAC.
May have a P' wave of varying morphology before, after or buried in QRS. That is if there is a P' wave. If QRS is present it can have normal or abnormal morphology. Same as PAC, it causes an irregular pulse. However, it causes a PR interval of <0.12 sec and has a compensatory pause.The lecture covered ectopy first. Ectopic rhythms are defined as complexes that are in an abnormal place position. They could be from hypoxia, tissue damage, hyperkalemia or hypokalemia. Moreover, automaticity, which we learned about in week 3, is determined by the permeability of the cell membrane to sodium during phase 4. This movement occurs slowly until the threshold potential and then depolarization occurs.
Pacemaker cells such as the SA node, possess automaticity. On the other hand, in normal conditions, myocardial cells do not possess automaticity. When an ectopic beat happens it is caused by "enhanced automaticity".
This is when pacemaker cells increase their automaticity and increase their firing rate. This also happens when cardiac cells, that do not normally possess automaticity, develop automaticity. This occurs under abnormal conditions. This enhanced automaticity can cause an ectopic pacemaker to fire causing an ectopic beat on the ECG. Enhanced automaticity occurs due to different causes, including: increased catcholamines, hypoxia, hypercapnea, myocardial ischemia or infarction, administration of atropine, hypokalemia and hypocalcemia.
Premature ectopic complexes are caused by an irritable focus generating an action potential before the next depolarization of the normal pacemaker. It can be unifocal or multifocal and can be atrial, junctional, or ventricular. Ectopic complexes are not a rhythm in themselves, but are described as an addition to the underlying rhythm.
Premature atrial complexes(PAC) are extra complexes generated by an atrial focus outside the SA node or very high in the AV junction and they occur earlier than the next expected beat of the underlying rhythm, Their impulse may be conducted through the AV node or not. On the ECG, they will have a P' wave of varying morphology and a QRS complex of normal or abnormal morphology, and the PR interval will be <0.20 sec. It will cause an irregular pulse. It has a non compensatory pause.
Premature junctional complexes(PJC) are generated by an irritable focus within the AV junction and occurs earlier than the next expected beat of the underlying rhythm. May be conducted through the AV node or not, and its very difficult to distinguish between non-conducted PJC from non-conducted PAC.
Any abnormal complex that's origin is in the ventricles will have a QRS complex >0.12 sec. Premature ventricular complexes(PVC) are generated in the ventricles, i.e. its name. It can be from the bundle branches, Purkinje fibers or the ventricular myocardium.It also occurs earlier than the next expected beat of the underlying rhythm. P waves, if present, will be unassociated with the ectopic complex, since they occur before the ectopic complex in the ventricles. Will cause an irregular pulse and a compensatory pause. PVCs can be unifocal, happening at the same point on the ECG everytime. Or it could be multifocal, which means it occurs at different locations on the ECG everytime. There is no pattern. Moreover, PVCs can occur in couplets, which is two PVCs happening consecutively. Also, they can occur as triplets or even more after each other. Once it reaches three or more, it is called ventricular tachycardia.
Ventricular tachycardia(VT) has a rate >100 bpm but it is normally within the range 150-250 bpm. It has a regular rhythm but its QRS complex is wide (>0.12 sec). If there are any P waves they will be dissociated with the QRS complexes. VT can be sustained or non-sustained. Sustained is when the rhythm stays for >30 sec.
If the rhthm is wide, fast, regular, and has no P waves, it is VT until proven otherwise.
Patients presenting with a VT can range from being conscious with a good BP to unconscious and pulseless.
The next rhythm was ventricular fibrillation (VF). It doesn't have a recognizable rate since multiple foci are firing at the same time. However, it can range from 300 to, sometimes, 700 bpm! It's rhythm is completely irregular, no P waves, and has disorganized, irregular and bizarre QRS complexes. VF can be coarse or fine.
Lastly, asystole. When this rhythm is seen on the screen the first thing to be done is to check the leads. If they are still on, start compressions!
Enquiry
and Research:
PAC appear upright if the ectopic sits is near the SA node. However, they appear inverted if the ectopic site is near the AV junction. This is because the impulse travels retrograde from near the AV junction to the atria. A P' wave followed by a QRS complex is said to be a conducted PAC.When complete AV block occurs, the P' wave is not followed by a QRS complex. This is called a nonconducted or blocked PAC. The PR intervals of PACs are normal, however, they differ from those of the underlying rhythm. Therefore, they will be abnormal for the underlying rhythm. PACs usually depolarize the SA node prematurely, the SA node is reset, causing the next cycle of the SA node to begin all over again. The next expected P wave of the underlying rhythm appears earlier than it would have if the SA node had not been reset.The resulting PP' interval is called a non-compensatory pause (Wesley, 2011).
During the lecture i didn't understand what compensatory and non-compensatory pauses are. However, the following helped me understand.
Due to the non-compensatory pause, the interval between the P waves of the underlying rhythm before and after the PAC is less than twice the PP interval of the underlying rhythm. On the other hand, when the SA node is not depolarized by the PAC its timing is not reset, This allows the next P wave of the underlying rhythm to appear at the time expected. Such a P'P interval is called a compensatory pause. However, the compensatory pause is more likely to occur due to a PVC (Wesley, 2011).
The QRS complex of the PAC resembles that of the underlying rhythm because the electrical conduction through the bundle branches is usually unchanged. However, the QRS complec may be absent due to a temporary complete AV block/ nonconducted PAC. Some causes of PACs include:
In PJCs absent P' waves indicate one of two things. Either retrograde atrial depolarizations occurred during the QRS complexes or atrial depolarizations did not occur because of a retrograde AV block between the ectopic pacemaker site in the AV junction and the atria.
In PJCs, a compensatory pause follows the PJC because the SA node is not depolarized by the PJC. Therefore, the SA node does not restart and fires when it should. The main cause of PJC is digitalis toxicity (Wesley, 2011).
PAC appear upright if the ectopic sits is near the SA node. However, they appear inverted if the ectopic site is near the AV junction. This is because the impulse travels retrograde from near the AV junction to the atria. A P' wave followed by a QRS complex is said to be a conducted PAC.When complete AV block occurs, the P' wave is not followed by a QRS complex. This is called a nonconducted or blocked PAC. The PR intervals of PACs are normal, however, they differ from those of the underlying rhythm. Therefore, they will be abnormal for the underlying rhythm. PACs usually depolarize the SA node prematurely, the SA node is reset, causing the next cycle of the SA node to begin all over again. The next expected P wave of the underlying rhythm appears earlier than it would have if the SA node had not been reset.The resulting PP' interval is called a non-compensatory pause (Wesley, 2011).
During the lecture i didn't understand what compensatory and non-compensatory pauses are. However, the following helped me understand.
Due to the non-compensatory pause, the interval between the P waves of the underlying rhythm before and after the PAC is less than twice the PP interval of the underlying rhythm. On the other hand, when the SA node is not depolarized by the PAC its timing is not reset, This allows the next P wave of the underlying rhythm to appear at the time expected. Such a P'P interval is called a compensatory pause. However, the compensatory pause is more likely to occur due to a PVC (Wesley, 2011).
The QRS complex of the PAC resembles that of the underlying rhythm because the electrical conduction through the bundle branches is usually unchanged. However, the QRS complec may be absent due to a temporary complete AV block/ nonconducted PAC. Some causes of PACs include:
- Increase in sympathetic tone
- infections
- emotional stress
- stimulants
- sympathomimetic drugs
- digitalis toxicity
- CVD
In PJCs absent P' waves indicate one of two things. Either retrograde atrial depolarizations occurred during the QRS complexes or atrial depolarizations did not occur because of a retrograde AV block between the ectopic pacemaker site in the AV junction and the atria.
 |
| Picture 1: Table showing the relation between the site of origin of P' wave and its location on the ECG. Adopted from (Wesley, 2011). |
This cause has been recurrent and has attracted my attention, so i conducted a search about it and this is what i found: Digitalis is a medication given to some cardiac patients. Toxicity occurs when a person takes too much of this drug or has low tolerance to it. Also, patients with heart failure are given digitalis and diuretics, where the diuretics cause potassium loss. This increases the chances of digitalis toxicity happening. Treatment of it includes activated charcoal. This toxicity can lead to enhanced automaticity, arrythmias and even heart failure (Dugdale, 2013).
To identify PVCs there are some factors that can help. These factors are a combination of a compensatory pause, and upright P wave of the underlying rhythm superimposed on a premature ectopic beat, and a wide and bizarre QRS complex. Also, it is interesting to note that the QRS complex of a PVC from the left ventricle resembles that of a right bundle branch block and the QRS complex of a PVC from the right ventricle resembles that of a left bundle branch block (Wesley, 2011).
PVCs are considered frequent if the occur five or more times per minute. When PVCs alternate with the QRS complex of the underlying rhythm this is called a ventricular bigeminy. If one PVC occurs for every 2 QRS complexes of the underlying rhythm, or 2 PVCs for every QRS complex, this is called ventricular trigeminy. Also, when there is one PVC for every three QRS complexes of the underlying rhythm, this is called quadrigeminy. Sometimes PVCs can be generated at the relative refractory period. When this occurs its called R-on-T phenomenon. However, when this happens stimulation of the ventricles occurs and this can result in nonuniform conduction of the electrical impulse through the muscle fibers. This can lead to a reentry mechanism that may precipitate repetitive ventricular complexes resulting in VT or VF (Wesley,2011).
A PVC occurring between two normally conducted QRS complexes without disturbing the underlying rhythm is called an interpolated PVC (Wesley,2011).
Symptoms during VT depend on the ventricular rate, duration of tachycardia, and presence and extent of the underlying heart and peripheral vascular disease. In some patients with nonsustained VT initially, sustained episodes or VF develop later. VT may cause or aggravate existing angina pectoris, AMI, produce HT or shock, or terminate in VF pr asystole. Also, in VT the CO can get so low, the heart cannot produce a BP or palpable pulse, this is called pulseless VT (Wesley, 2011).
VF represent abnormal, chaotic and incomplete ventricular depolarizations caused by the depolarization of small individual groups of muscle fibers. The most common causes of VF are CAD, cardiomyopathy, mitral valve prolapse, hypoxia, acidosis, electrolyte imbalance, and following synchronized cardioversion. If VF is not immediately treated it causes death! However, before initiating treatment it is important to check the electrodes on the patient since artifacts can resemble VF. The treatment of VF is defibrillation, which stops all electric activity in the heart so that a normal pacemaker can awaken and produce a rhythm that results in a pulse (Wesley, 2011).
To identify PVCs there are some factors that can help. These factors are a combination of a compensatory pause, and upright P wave of the underlying rhythm superimposed on a premature ectopic beat, and a wide and bizarre QRS complex. Also, it is interesting to note that the QRS complex of a PVC from the left ventricle resembles that of a right bundle branch block and the QRS complex of a PVC from the right ventricle resembles that of a left bundle branch block (Wesley, 2011).
PVCs are considered frequent if the occur five or more times per minute. When PVCs alternate with the QRS complex of the underlying rhythm this is called a ventricular bigeminy. If one PVC occurs for every 2 QRS complexes of the underlying rhythm, or 2 PVCs for every QRS complex, this is called ventricular trigeminy. Also, when there is one PVC for every three QRS complexes of the underlying rhythm, this is called quadrigeminy. Sometimes PVCs can be generated at the relative refractory period. When this occurs its called R-on-T phenomenon. However, when this happens stimulation of the ventricles occurs and this can result in nonuniform conduction of the electrical impulse through the muscle fibers. This can lead to a reentry mechanism that may precipitate repetitive ventricular complexes resulting in VT or VF (Wesley,2011).
A PVC occurring between two normally conducted QRS complexes without disturbing the underlying rhythm is called an interpolated PVC (Wesley,2011).
Symptoms during VT depend on the ventricular rate, duration of tachycardia, and presence and extent of the underlying heart and peripheral vascular disease. In some patients with nonsustained VT initially, sustained episodes or VF develop later. VT may cause or aggravate existing angina pectoris, AMI, produce HT or shock, or terminate in VF pr asystole. Also, in VT the CO can get so low, the heart cannot produce a BP or palpable pulse, this is called pulseless VT (Wesley, 2011).
VF represent abnormal, chaotic and incomplete ventricular depolarizations caused by the depolarization of small individual groups of muscle fibers. The most common causes of VF are CAD, cardiomyopathy, mitral valve prolapse, hypoxia, acidosis, electrolyte imbalance, and following synchronized cardioversion. If VF is not immediately treated it causes death! However, before initiating treatment it is important to check the electrodes on the patient since artifacts can resemble VF. The treatment of VF is defibrillation, which stops all electric activity in the heart so that a normal pacemaker can awaken and produce a rhythm that results in a pulse (Wesley, 2011).
References
Dugdale, D.C. (2013). Digitalis
toxicity. Retrieved from https://www.nlm.nih.gov/medlineplus/ency/article/000165.htm
Wesley, K. (2011). Huszar's basic
dysrythmias and acute coronary syndromes: Interpretation and management (4th
ed.). St Louis, MO: Elsevier.
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