Week 12

Description: This week we performed the IV OSCE, and I passed. After that we practiced approaching a cardiac patient again. I followed the systematic approach and did very well. After that, suddenly, when we were done my teachers changed the rhythm on the mannequin to be a VF and asked us what we will do. Aya started CPR and Asma was attaching the pads of the AED. In that moment, my teacher told me to insert an advanced airway. I quickly ran to the store and got an i-gel. I lubricated it and inserted it in the patient’s airway and started ventilating at a rate of 8-10 breaths/min. Then my teacher told Asma to administer Morphine so she went to prepare the IV set. I took over defibrillating the patient while providing breaths. Aya and I kept alternating, her doing CPR and me on the defibrillator and airway then her on the airway and defibrillator and me on the chest. This scenario kept going for around 15 minutes. The rhythm kept changing from VF to NSR. But when we would check the pulse, there was none. It was PEA. So we would continue CPR. The last rhythm was PEA, and my colleague shocked the patient, putting me, as I was doing compressions, into arrest in the process. This ended the epic scenario.

Feelings: I passed the OSCE so I felt REALLY good! After that I felt confident of my approach to the cardiac patient. In the epic scenario I felt a thrill and was so excited. At first I was confused but that subsided as we went through the scenario. I had so much fun and felt it was the best lab session of the whole semester, in my opinion. However, at the end of the session I felt so tired, but still it felt so good!

Evaluation: This whole session was so good and there was nothing bad about it. I learned so much!

Analysis: After this session, I realized how much I’ve learned this semester, and this made me so happy. It surprised me but it was certainly a great surprise.

Conclusion: The only thing is that I could have communicated with my partner in a better way. This could have helped avoid shocking a PEA, since I knew we had to continue CPR without shocking the patient.

Action Plan: I plan to communicate better with my partner and when placed in such a situation, to act fast and not pause in confusion. Also, I plan to exercise more to increase my stamina, so that I can perform CPR for longer periods without getting tired.

Domain Knowledge:

In neonates congenital heart defect (CHDs) are the most common and there are 35 types. Risk fators include maternal infections (Rubella, Herpes, inta-uterine infection) ,metabolic disorders (diabetes, hypercalcaemia), drugs (alcohol, lithium, warfarin), chromosomal abnormalities, where up to 50% of Down syndrome babies have a CHD! Other risk factors include increased maternal age, prematurity, and family history. 

Patent ductus arteriosus: Aorta and Pulmonary artery connected. Not obvious at birth and if left untreated causes shunting from left to right. Can lead to pulmonary overload and eventual HF.

Atrial septal defect: Interatrial septum open. Causes shunting of blood from left to right side of heart. Mostly asymptomatic. Causes increased pulmonary blood flow but rarely pulmonary HT. Found by routine heart auscultation and repair is carried out to prevent HF, AF and embolic events.

Patent foramen ovale: form of atrial septal defect. Normally closes soon after birth but, abnormally, it stays patent.

Ventricular septal defect: there is an opening between the ventricles. Most common type of CHD. Shunt from left to right and may not be apparent at birth.

Tetralogy of Fallot: Includes 4 things: Pulmonary stenosis, thickened RV wall, ventricular septal defect, and aorta overrides septal defect. Results in right to left shunt and cyanosis. Can be surgically repaired. 

Coarctation of Aorta (COA): narrowing of the aorta mostly around the junction of ductus arteriosus. Depends on timing of closing of ductus arteriosus and location of COA.

Aortic stenosis: Diseased aortic valve. Asymptomatic but can develop exercise intolerance. Depends on severity. Tends to be progressive and can lead to sudden cardiac death, left ventricular hypertrophy and heat failure. 

HF in children presents as: poor feeding, dyspnea, tachypnea, retractive respirations, grunting, nasal flaring, pallor or mottling. Usually discovered after baby goes home.

Sudden death: Can occur at any age secondary to undiagnosed cardiac disease.

Pediatric cardiac diseases are dysrhythmias, Kawasaki disease, systemic HT, childhood obesity, cardiomyopathy, and valvular dysfunction.

Rheumatic fever: Streptococcal infection common in children. If untreated can lead to rheumatic heart disease (RHD). Develops as a sequel to pharyngeal streptococcal infection. Risks include: poor hygiene, overcrowding, underprivileged populations.

In younger adults some diseases include: Obesity related heart disorders, HIV complications, dysrhythmias, and drug use leading to dysrhythmias and cardiomyopathy.

Adult cardiac diseases include: IHD, Prinzmetal angina, ACS, Pericarditis, pericardial effusion, complications from HIV.

Cardiomyopathy is due to ventricular dilatation.  Mostly unknown cause but some known causes include: Ischemic heart disease, diabetes, renal failure, alcohol abuse, drug toxicity, and nutritional  deficiency. 

Hypertrophic Cardiomyopathy/ Hypertrophic Obstructive Cardiomyopathy: thickening of septal wall restricting ventricular outflow. Genetic. Decreased ventricular compliance and exercise intolerance. S&S: SOB, angina, syncope, palpitations, and sudden death. Two types: Hypertensive and restrictive. First one due to HT or valvular stenosis and second one because of rigid, non-compliant myocardium leading to reduced ventricular filling (common symptom RHF).  

Elderly cardiac diseases include CCF, LVF, RVF, intractable angina.

There are some cultural issues that most be dealt with with caution and they involve commencement and stopping resuscitation, agressive or palliative care, and family needs.

Heart Transplant patients have specific complications that result from the body's immune system attacking the transplanted heart. Can be hyperacute, acute orr chronic. Patient is more prone to infections due to immunosuppressants.

Enquiry and Research:

Sudden Cardiac Death is greater in athletes compared with their nonathletic people. This is due to the  strenuous exercise of an athlete that poses an increased risk in undiagnosed cardiac abnormalities. Typically this occurs as a ventricular arrhythmia, due to exerciseinduced catecholamine release acting on an arrythmia inducing substrate (Chandra et al. 2013).

Syncope that occurs during exercise is strongly associated with cardiac syncope. Moreover, if a patient has transient loss of consciousness while lying down this is a sign of the possibility of cardiac syncope. Patients with cardiac syncope eaxperience a rapid reassuring sense of wellbeing on regaining consciousness, due to endogenous sympathetic activity arising in response to the underlying cardiac condition. Auscultation, peripheral edema, raised jugular venous pressure can imply CAD and provide evidence for possible structural heart disease. Cardiac syncope with the presence of structural heart disease are both associated with increased risks of future sudden death (Anderson & O'Callaghan, 2012).

References

Anderson, J., & O'Callaghan, P. (2012). Cardiac syncope. Epilepsia, 53(7), 34-41. doi: 10.1111/j.1528-1167.2012.03713.x

Chandra, N., Bastiaenen, R., Papadakis, M., & Sharma, S. (2013). Sudden cardiac death in young athletes: Practical challenges and diagnostic dilemmas. Journal of the American College of Cardiology, 61(10), 1027-1040. doi: 10.1016/j.jacc.2012.08.1032