Introduction

Psychotropic drugs are medications and chemical formulations that cross the blood brain barrier to act on the central nervous system to stimulate the change of mood and behaviour of an individual. Schatzberg and Nemeroff (2009) underscore that it is important to note that these medications are not curative but rather palliative, and although they may improve symptoms associated with various mental disorders, they do not cure the primary cause of the disorders. According to Perry (2007), psychotropic medications include antidepressants, antipsychotic or neuroleptics, attention deficit hyperactivity disorder (ADHD) drugs, and antimanic or anxiolytics among others. This paper aims at discussing the physiological implications of using psychotropic medications in paediatric and adolescent populations with a bias on neuroleptic/antipsychotic, anxiolytic/antianxiety and ADHD drugs.

While there may be reservations regarding the use of psychotropic medication in children and the physiologic effect of these drugs on young people’s central nervous system development, leaving mental disorders untreated is not a viable option as evidently supported by medical literature. This is because untreated mental illness may cause paramount long-term morbidity and even irreversible deficits in socio-emotional and cognitive functioning. Regardless of ethical and legal reservations surrounding the use of psychotropic drugs among paediatric and adolescent patients, analyses of data on their use reveals fast changing trends pointing to increased use. According to Hsia and MacLennan (2009) there was a three-fold increase of the number of children/adolescents taking any psychotropic drug between 1987 and 1996. Adolescent visit to physicians significantly increased psychotropic prescriptions as evidenced by an increase to 8.3% of the prescriptions in 2001, up from 3.4% in 1994 (Hsia & MacLennan, 2009). In 2001, psychotropic prescriptions made up 8.8% of all psychopharmacological prescriptions among patients aged between 6 and 17 years (Hsia & MacLennan, 2009). In terms of gender, more male paediatrics and adolescents are on these medications compared to their female counterparts. Due to increased incidences of anxiety, depressive, manic, and other psychotropic disorders in paediatrics and adolescents, there has been an increased acceptance and need for use of neuroleptics, anxiolytics and antidepressant drugs in these patients.

Neuroleptics and their implications on paediatrics/adolescent

Neuroleptics, also known as major tranquilizers or antipsychotic drugs are used primarily to treat psychoses and symptoms. In paediatrics and adolescents, they are also indicated in the treatment of other non-psychotic psychiatric disorders. They are the drugs of first choice in treatment of autism and schizophrenia in children and adolescence. Kalyna and Virani (2007) explain that neuroleptics are used in treatment of paediatrics and adolescents with severely aggressive conduct disorders, Tourette’s disorder, and chronic motor or vocal tic disorder. Antipsychotic drugs are also used in the treatment of ADHD but their use has decreased due to increased use of stimulant medications which are more effective for this disorder. Examples of antipsychotic drugs include haloperidol, chlorpromazine, molindone and fluphenazine. Newer formulations include olanzepine, clozapine, quetiapine, risperidone and ziprasidone (Hamrin, McCarthy & Tyson, 2010).

The use of neuroleptics on paediatrics and adolescents has several implications. Side effects associated with long-term use of these medications in this population include akathesia, acute dystonic reactions, parkinsonian symptoms, tardive dyskinesia, anticholinergic symptoms and sedation. They also lower seizure threshold in susceptible subjects and drugs such as Chlorpromazine should not be used in such patients. Tardive dyskinesia is a grave concern and has been reported in about 1 to 20% of paediatrics and adolescents on long-term use of neuroleptics (Kalyna & Virani, 2007). It may occur as early as 5 months after commencement of treatment or may delay to up to 3 years. Since paediatrics and adolescents have more dopamine receptors than adults, they are more sensitive to side effects affecting the central nervous system. Long-term use of neuroleptics should be avoided in this population but ….contends that low doses may be recommended in selected difficult cases.

Other side effects associated with neuroleptics include weight gain, irregular menses and breast enlargement in adolescents. Doran (2013) documents that second-generation anti-psychotic (SGA’s) drugs can cause metabolic disturbances and weight gain in paediatrics and adolescents even during first-time treatment. For instance, in a trial of treatment of schizophrenia with olanzapine, 30% of the paediatric/adolescent subjects gained weight compared to 6% in adult subjects (Doran, 2013). Other SGAs such as risperidone, quetiapine and clozapine also posted similar results with the paediatric/adolescent subjects gaining between 0.9 to 16.2 kilograms (Doran, 2013).

Withdrawal of neuroleptics or lowering of the dosage may lead to withdrawal emergent syndrome with resultant aggravation of psychotic symptoms. This has been reported in paediatrics and symptoms include ataxia, vomiting and nausea. In a study by Vitiello (2008) as high as 51% of the paediatric patients showed the withdrawal symptoms, usually occurring after few days to few weeks after drug withdrawal. Clozapine has been associated with deaths of two paediatric patients with the mechanism being linked to sudden cessation of treatment (Vitiello, 2008). Haloperidol has been demonstrated to interfere with the children and adolescent’s daily routine including social and school activities. Neuroleptics increase sedation, lethargy and somnolence in paediatrics and adolescents than in adults; for instance, this was demonstrated in 30% to 49% of paediatric patients being treated with Risperidone in contrast to 7% of adults taking the same drug for bipolar mania (Hamrin, McCarthy & Tyson, 2010).

Anxiolytics and their implications on paediatric/adolescents

Anxiolytics are psychopharmacologic drugs used to treat anxiety disorders in paediatrics and adolescents. Other conditions for which they may used include sleep disorder, aggressive behaviours and psychosis. They include selective serotonin-reuptake inhibitors (SSRIs) benzodiazepines, tricyclic antidepressants (TCAs) and busipirone. Anxiety disorders are greatly predominant in adolescence; between 6 and 20% of children have a type of anxiety disorder (Kalyna & Virani, 2007). Doran (2013) documents that use of benzodiazepines in paediatrics and adolescents has tripled over the last 10 years.

Anxiolytics are recommended to be used only after an aftermath of an event e.g. traumatic event and should be used for short periods (not more than two weeks) to avoid the risk of developing addiction or diminished efficacy. A recent review shows that SSRIs have become the preferred pharmacological intervention for paediatric anxiety disorders. They have very potent anxiolytic effects and their tolerance among paediatrics and adolescents is high. However, this class of psychotropic drugs has been associated with increased suicidal ideation.

A well-documented controversy in paediatric and adolescent psychopharmacology occurred in 2003 when FDA issued public alert warning prescribers of increased ideation and attempts of suicide among patients below 18 years on anxiolytics (Vitiello, 2008). This contributed to a substantial drop in rates of diagnosis and prescription of these drugs among paediatric and adolescent population. Later, after a meta-analysis of numerous clinical trials of nine drugs in this class, it was demonstrated that there was only a marginal increase (0.7%) increase in the suicidal ideation with no actual increase in completed suicides (Schatzberg & Nemeroff, 2009). However, this has led to adoption of a multidisciplinary approach towards management of paediatric and adolescent depression to encompass both pharmacological and non-pharmacological interventions.

Cardiovascular adverse effects are often reported with most anti-anxiety medications because these drugs act on the autonomic system. Such side effects include increase in heart rate and changes in blood pressure. Although these side effects are generally not of major clinical significance while taking psychotropic medications, tricyclic antidepressants (TCAs) such as desipramine have been inconclusively linked to sudden death among paediatric patients (Kalyna & Virani, 2007). Therefore, it is imperative for the prescribing physicians to take a comprehensive patient history, as well as monitor the electrocardiograms, heart rate and blood pressure changes of the paediatric and adolescent patients before and during treatment with psychotropic agents such as TCAs. Lamotrigine manifestly increases the risk for severe skin reactions and hives in paediatrics and adolescents (Dulcan, 2010).

Another critical consideration in anxiolytic use of drugs in these subjects is drug interactions. Drugs that inhibit the cytochrome P450 enzyme system could have adverse effects on the subjects if concomitantly administered with anxiolytics (Perry, 2007). Antifungal drugs and some antibiotics such as erythromycin when co-administered with SSRIs such as fluoxetine can cause cardiac arrhythmias (Perry, 2007). Others such as imipramine and Lamotrigine can cause toxic delirium (Hamrin, McCarthy & Tyson, 2010). The prescribers must document all medications that may have drug-drug interactions with psychotropics as well as those that have direct or indirect effect on the cytochrome P450 enzyme system.

ADHD drugs and their implications on paediatrics/adolescents

Stimulants used in management of ADHD are some of the most used psychotropic drugs among paediatrics and adolescents. However, trepidation persists due to concerns of the adverse effects of these drugs on the growth rate in paediatrics. Use of stimulant psychotropic drugs has been associated with stunted growth rates. The Multimodal Therapy of ADHD study demonstrated that stimulant psychotropic drugs, especially in high doses, reduce growth velocity and weight (Gelder et. al, 2009). This is due to appetite loss, a common adverse effect associated with these stimulant drugs. However, in most cases normal growth seems to rebound once the psychostimulant agents are withdrawn with no significant suppression of ultimate height attained. Nevertheless, some studies have revealed that pyschostimulants continue to suppress growth in early and late adolescence. Rosenberg and Gershon (2002) explain that pyschostimulants such as methylphenidate may permanently cause stunted growth by affecting epiphyseal closing of long bones if used between ages 17 and 21 years. However, Cheng and Myers (2010) outline that suppression of growth could be because of the underlying mental disorder, for instance, ADHD rather than the treatment.

One disconcerting physiological implication of ADHD drugs especially in paediatrics being treated for hyperactivity or outbursts is the aggravation of the condition with the medication, a phenomenon referred to as paradoxical response. Doran (2013) explains that in a small number of paediatric/adolescent patients may severely increase nervousness and agitation instead of reducing it (disinhibition). These subjects may become giddier, act sillier or even manic. Similarly, some younger patients may be more depressed after being put on antidepressants. Studies have shown paediatrics and adolescents getting more moody and agitated after receiving mood treatment psychotropic drugs in ADHD treatment (Kalyna & Virani, 2007). Others on stimulants may become more hyperactive and fail even to respond to sleep-inducing drugs. Research by Hamrin, McCarthy and Tyson (2010) shows that if a paediatric or adolescent patient shows paradoxical effect to one class of psychotropic drugs, there is a 50% of similar reaction if he or she is given another drug of the same class.

Paediatrics and adolescents have a lower albumin binding capacity and reduced adipose compartment, leading to a higher percentage of unbound compound than adults. Similarly, their drug biotransformation rates are higher, and this could reduce the half-life of the drugs relatively increasing the risk for toxic metabolite levels. This may contribute to physiological rebound effect where the paediatric and adolescent patients present with exacerbation of symptoms than original symptomatology (Dulcan, 2010). This often occurs when drug plasma levels decrease due to increased hepatic elimination and subsequent renal excretion. The subjects show symptoms such as hyperactivity, irritability, insomnia, over talkativeness, excitability and non-compliance (Dulcan, 2010). Schatzberg and Nemeroff (2009) explain that this can be remedied by adding a small afternoon dose or using slow-release preparations. The physician may also opt to use short- and long acting medications.

Other implications of ADHD drugs on paediatrics and adolescents are the drug’s adverse effects. In a meta-analysis review, 32% of the doctors were concerned with decreased appetite and loss of weight association with these drugs. Half of them raised concerns about disturbed sleep while 22% were apprehensive of the increased anxiety. Other physicians indicated that they were concerned about possible diversion of ADHD drugs and felt burdened by prescribing these controlled drugs for paediatrics and adolescents. There is a high potential for abuse of controlled stimulant drugs used in ADHD treatment which can be achieved by crushing and snorting the medication. However, this abuse potential has been addressed through extended release formulations and introduction of skin patches which are less susceptible to abuse.

Conclusion

Psychopharmacological treatment in paediatrics and adolescents is an area of on-going ethical discussion, as these subjects affected by mental disorders are a vulnerable class of patients. The use of psychotropic drugs in children below 8 years is under-researched; this is because most of these drugs are developed and researched in adults. In addition, it could also be due to existing ethical and legal considerations that hamper access of research to such studies. Paediatrics and adolescents with psychotic disorders will classically be put on psychotropic drugs while those with other disorders will be put on non-pharmacological treatment. Sometimes, both approaches may be used simultaneously. Logically, the benefits of pharmacological intervention must outweigh potential risks associated with use of these drugs in these young people. An important consideration is the proof of the efficacy and safety of the drug for the age of the patient and the specific disorder. Psychopharmacotherapy in paediatrics and adolescents requires a holistic, multidisciplinary approach. Pharmacovigilance in use of psychotropic agents among these subjects as well as their long-term efficacy and adverse effects are indispensable. It is evident that paediatric and adolescent patients are, to say the least, more vulnerable to adverse effects of psychotropics than adults are. With the increasing adoption of psychopharmacological interventions in treatment of paediatrics and adolescents with mental disorders, novel research is vital to come up with clear evidence-based recommendations on use psychotropics in these subjects.

References

Cheng, K. & Myers, K. M. (2010).

Child and Adolescent Psychiatry: The Essentials

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Dulcan, M. K. (2010).

Dulcan’s Textbook of Child and Psychiatry

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Doran, C. M. (2013).

Prescribing Mental Health Medication: the Practitioner’s Guide

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Hamrin, V., McCarthy, E. M. & Tyson, V. (2010). Paediatric psychotropic medication initiation and adherence: a literature review based on social exchange theory.

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Delirium in children is relatively common (between 4.5-28% in critically ill children) but not widely understood by medical professionals. The manifestation of the symptoms and the progression of the disease are well known in adults. It presents with acute onset altered sleep-wake cycle, disorientation, perceptual disturbances and altered mood and affect. Features specifically reported in pediatric delirium include developmental regression, purposeless behaviors, altered or labile affect, inconsolability, and autonomic instability. Delirium can be categorized into subtypes according the motor activation level including hyperactive (agitation and restlessness), hypoactive (apathy, decrease responsiveness) and mixed (includes both hyperactive and hypoactive symptoms). The etiologies of delirium are multifactorial and often present as physiological consequences of an acute medical condition, medical complication or substance intoxication/withdrawal.  The most common cause of severe delirium is a critical illness Other most common reasons include infections, drug withdrawals or intoxications. Deliriogenic medications include but not limited to anticholinergics, opioids, sedatives, toxins and steroids. Medications are most common cause of reversible delirium.

The primary aim of the treatment of delirium is identifying and treating the underlying cause as well as avoiding possible precipitant factors effectively. The best approach for identifying delirium is diagnosis by a child and adolescent psychiatrist according the Diagnostic and Statistical Manual of Mental Disorders (Fifth Edition) criteria but it could be challenging to assess someone preverbal/nonverbal and developmentally delayed in the clinical setting. There are also reliable, validated and clinically suitable rating scales are available for pediatric population (1).

Treatment of Pediatric Delirium

Treatment of delirium may be pharmacological or non-pharmacological basis.

Non-pharmacological treatments include identifying and addressing the underlying etiology, minimizing iatrogenic factors such as deliriogenic medications including benzodiazepines, opioids and other sedative agents. Supportive care in delirium include adequate nutrition, early mobilization and deep venous thrombosis prophylaxis. Behavioral modifications can include presence of constant caregiver, having familiar environment, normalizing sleep-wake cycle. Health care providers can reduce too much noise by adjusting alarm volumes on medical equipment, as well as limiting conversation around the room. Strategies to orient the older child include using calendars, clocks, family photos, favorite objects (e.g., stuffed animals) and talking to the child. Multicomponent interventions are more effective rather than single intervention.

Pharmacologic strategies may be necessary to control agitation, sleep-wake cycle abnormality, and establish safety environment if the child continues to display behaviors after nonpharmacologic interventions. Currently, there is no Federal Drug Agency (FDA) approved medication to treat delirium. Antipsychotic agents have been regarded as the primary treatment and should be administered at the lowest dosages possible. In clinical practice, atypical antipsychotics prefer to typical ones due to side effects profile even studies show that both typical and atypical antipsychotics decreases delirium scores effectively. Haloperidol can be used as intravenously form which helps for rapid symptom control, but it also can cause significant QT prolongation. Atypical antipsychotics, such as risperidone, olanzapine, quetiapine, among others, can be equally useful in the treatment with fewer side effects. Melatonin may also use to combat sleep disturbance related to delirium.

NON PHARMACOLOGICAL INTERVENTIONS
Removing/minimizing precipitant factors	-Reduce, substitute or taper deliriogenic medications such as opiates, benzodiazepines -Remove unnecessary invasive devices/tubes/catherization -Promote mobility and avoid physical restraints. -Prevent electrolyte disturbance, hypoxia, hemodynamic instability or infection -Optimize of analgesia and sedation -Avoid overstimulating the patient
Support and orientation	– Use frequent orientation cues through visible and verbal reminders. – Provide familiar objects and reassuring companionship. – Provide frequent reassurance through tactile and verbal reorientation – Avoid frequent staff changes
Minimize sleep deprivation	– Promote natural circadian rhythm – Optimize noise and light exposure – Use ear plug and eye mask
PHARMACOLOGICAL INTERVENTION
MEDICATION	Dose Range	Administration	Comments
Haloperidol	(IV) Loading dose3 0.05 mg in 30 minutes (Age 0-1) (3.5-10 kg) 0.15 mg in 30 minutes (Age 1-3) (10-15 kg) 0.3-0.5 mg in 30 minutes (Age 3-18) (>15kg) (IV) Maintenance dose (divided into 2-4 times daily) 0.01-0.05 mg/kg/day (Age 0-1) (3.5-10 kg) 0.025 mg/kg/day (Age 1-3) (10-15 kg) 0.05 mg/kg/day (Age 3-18) (>15kg) PO (Loading dose) 0.02 mg/kg (<45kg) 0.5-1 mg/kg (>45 kg) (PO) Maintenance dose (divided into 2-4 times daily) 0.01-0.08 mg/kg/day PO Maximum dosage: 4 mg/day(<45 kg) 6 mg/day (>45 kg)	PO/IV/IM/ Oral solution	-IV form is advantage for quick response – higher risk of EPS – In 2007, FDA issued a black box warning for IV haloperidol due the risk of QT prolongation
Risperidone	PO (Initial dose)4 0.1-0.2 mg once at bedtime ( 0.2-0.5 mg once at bedtime (>age5) (PO) Maintenance dose (divided into 2-4 times daily) 0.2-2.5 mg/day (>age5) PO Maximum dose: 1mg/day (<20 kg) 2.5 mg/day(<20-45 kg) 3mg/day (>45 kg )	PO/ODT/Oral solution	– Lack of anticholinergic effects is advantage
Olanzapine	PO Usual dose: 2.5-20 mg mg per day (age 13-17) maximum dosage: 20 mg/day	PO/IM/ODT	Comes in orally disintegrated tablet and IM form
Quetiapine	PO Usual dose: 25-100 mg per day Maximum dosage: 175 mg/day	PO	lower risk for EPS and safe for delirium in critically ill patient
Melatonin	0.5 mg to 10 mg per day	PO
PO: Per Oral ; IV: Intravenous ; IM: Intramuscular ; ODT: Oral disintegrating tablet

References

1-       Schieveld JNM, Ista E, Knoester H, Molag ML. Pediatric delirium: A practical approach. In Rey JM (ed), IACAPAP e-Textbook of Child and Adolescent Mental Health. Geneva: International Association for Child and Adolescent Psychiatry and Allied Professions 2015

2-       Lexicomp. Wolters Kluwer health, Inc. Hudson, OH. Accessed May 25, 2019.

3-       Turkel SB, et al. J Child Adolesc Psychopharmacol. 2012;22(2):126-30

4-       Tahir, T. A., Eeles, E., Karapareddy, V., Muthuvelu, P., Chapple, S., Phillips, B., … & Bisson, J. I. (2010). A randomized controlled trial of quetiapine versus placebo in the treatment of delirium.

Journal of psychosomatic research

,

69

(5), 485-490.

Nurses are required to continue education and upgrading of skills to ensure their patients receive the best possible nursing care. Cardiac nursing is a dedicated nursing practice that gives focused and precise nursing interventions, that are governed by the best practice nursing standards using latest research based facts. Nurses need to have good technique and skill when performing health history and physical assessments to enable them to look after the person as a whole. When nursing patients, nurses need to understand the care they give and reasoning of why they deliver the cares in a certain way. A sound knowledge of assessment and observations help nurses plan, initiate and deliver health care. Without knowledge and rationales the nurse may not deliver cares in the correct manner or have the ability to know when to initiate them. Myocardial infarction is a common cause for admission into the Coronary Care Unit and this case study follows cares, rationales and outcomes in this setting.

Mr Smith (synonym for confidentiality) is a retired 58 year old man that was admitted to a Coronary Care Unit (CCU) via the Emergency Department (ED) of the Atherton Hospital. His admission diagnosis was an Anterior ST Elevated Myocardial Infarction (STEMI), which had already been treated with thrombolytic therapy. On the morning of his admission, he drove himself to the ED with chest pain. He presented with left sided chest pain that radiated to his left jaw and left arm which he scored 10/10 and described as “crushing”. He was diaphoretic and hypertensive with nausea and vomiting. An ECG showed sinus bradycardia, rate of 60 bpm with hyperacute T waves in V2-V4, that progressed to ST Elevation. Thrombolytic therapy was administered 1 hour of his presenting to ED and within 2 hours of the initial chest pain that commenced at home. His ST segment was elevated approximately 8mm and continued to increase until 70 minutes post thrombolytic when he had 50% resolution of the ST elevation.

When he presented to the ED he was given oxygen, morphine, anginine, aspirin, clopidigrel and enoxaparin as first line pharmaceutical treatments. He was transferred that afternoon to Townsville. Mr Smith was not managed in Atherton due to the lack of cardiac catheter services and was transferred for a Percutaneous Coronary Intervention (PCI) the next day where he had a stent placed in his proximal area of his Left Anterior Descending Coronary Artery (LAD). Anterior MI’s affect a large surface of the heart, thrombolytic therapy and PCI are the most effective way to treat them (Evans-Murray, 2008 ).

His medical history includes a previous STEMI and PCI in 1997, hypercholesterolemia, depression, a ruptured bowel and neck injury from a Motor Vehicle Accident in 1977. Upon further questioning Mr Smith admitted to recently becoming “very short of breath” whilst mowing the lawn. His risk factors include ex-smoker ceasing in 1993, hypercholesteremia, and stress of brother dying 3 weeks previous. His current medications were aspirin 100mg daily, atorvastatin 20 mg daily and zoloft 200mg daily.

Upon arrival to a Townsville Coronary Care Unit (CCU), Mr Smith was pain free. He was connected to continuous cardiac monitoring and admission workup was attended, this includes admission paperwork, ECG, vital signs, mobile Chest x-ray and pathology tests. He was ordered and given stat doses of aspirin, clopidigrel and IV lasix. Mr Smith had an IVT running in his Left hand and an IVC in his Right hand.

During the next few days Mr Smith remained febrile 37.6° with only a small elevation in white cell count (Huszar, 2007). Four days post infarction, Mr Smith became short of breath (SOB) in the shower and felt light headed; he was monitored in Sinus Rhythm with SaO2 of 95% on 3lpm via nasal cannula. On auscultation, crackles were heard in his lower bases. He was commenced on lasix 20mg daily. This was an indication that his Left Ventricle may not have been functioning adequately. An Echocardiogram was performed to see if the heart wall motion and valves were performing to their best ability (Kern, 2003). The report showed extensive akinesis of the septal, anterior and apex left ventricle wall. His Left Ventricle Ejection Fraction (LEVF) was 35%. Normal values for (LVEF) are 60-65% (Moser & Riegel, 2008). He was commenced on a Beta Blocker – Cavedilol 6.25mg and Ramipril, which was commenced post PCI and decreased from 2.5mg to 1.25 mg. Use of these medications follow the criteria of the Reducing Risk in Heart Disease (Heart Foundation, 2007). He was sent to the cardiothoracic unit on day 5 with telemetry, to monitor for any changes in his cardiac condition (Jayasekara, 2009) and discharged two days later.

A systematic approach should be taken when attending to health history and physical assessment. Throughout the assessment, skin temperature, body odour, mood and appearance are observed. Patients need to feel comfortable with nurses so Mr Smith had the physical assessment explained to him and the reasons for performing it. (Brown, 2007)

Mr Smith’s physical assessment was completed in the morning prior to his PCI. He seemed relaxed with a jovial manner but at times did appear nervous. He was of a clean well kept appearance and looked younger than his 58 years.

Neuro – intact. Orientated to time, person and place, GCS – 15 and PEARLA. He had a good memory of the event.

Cardiovascular – monitored in sinus rhythm with frequent PVC’s and runs of bigeminy. ECG attached. Febrile- low grade 37.4 °, Pulse – 70 bpm, blood pressure 102/69, no peripheral oedema. Jugular venous pressure was approximately 4 cm’s. Initially I could not palpate the apical pulse but when patient positioned onto his left side it was felt 5th ICS MCL. The reason it is felt is due to the apex of the heart comes into contact with the chest wall (Marieb & Hoehn, 2010) No thrills or heaves heard. Mr Smith was warm to touch but not diaphoretic. Upon auscultation of the carotid arteries no bruits were heard. Normal S1 and S2 heart sounds were heard upon auscultation. Good radial, carotid and femoral pulses, Normal 2+ – according to pulse volume scale (Lewis, 2007). Mr Smith did look pale and his haemoglobin was 121g/L.

Respiratory – rate of 18 per minute. Sao2 – 94% on 2lpm via Nasal cannula. Inspection of the thorax area revealed equal shape, size and symmetry of chest with nil use of accessory muscles. Trachea was midline. Lips and nail beds showed no signs of cyanosis. Diaphragmatic excursion was equal at 4 cms. Anterior, lateral and posterior areas revealed equal air entry, bilaterally in high and mid thoracic zones. Basal zones of thorax areas were bilaterally dull. No adventious sounds heard. Chest X-ray noted that some consolidation in bilateral bases which corresponds to the decreased air entry heard in the bases (Wang, Baumann, Slutsky, Gruber, & Jean, 2010).

Gastrointestinal – revealed an old scar midline under the umbilicus from previous MVA. Bowel sounds heard in all 4 quadrants. Abdomen was soft with no distension.

Mr Smith’s upper and lower limbs and nail beds showed no signs of cyanosis or clubbing, ulceration or varicose veins. Capillary refill was normal – less than 3 seconds in all limbs. Range of motions and strength were bilaterally equal and normal in all 4 limbs. Dorsalis pedis and posterior tibial veins were felt on palpation and scored 2+ bilaterally (Lewis, 2007).

Acute coronary syndrome is a common cause of death. Myocardial infarction can have a good mortality rate if treated early. Treatment can be as basic as oxygen, ECG, observations, nitroglycerine through to thrombolytic therapy or a rescue angiogram/angioplasty (Overbaugh, 2009). One is not more important than the other and the patient’s prognosis is the main concern.

Patient’s complain of chest pain due to myocardial oxygen demand and supply mismatching. The coronary arteries supply the myocardium with blood supply, if the supply is interrupted by a clot, spasm or atherosclerotic plaque the myocardial oxygen requirement (demand) is not met which causes myocardial cells to “starve” for oxygen supply. This causes the depolarization of the cells to be interrupted and changes will occur on the ECG. (Woods, 1995)

Ischemia is shown on the ECG by ST segment elevation. This is primarily an emergency situation as the first 6 hours post infarction is when myocardial damage becomes irreversible (Thelan, 1994). In this time many interventions can be attended to resupply the myocardium with oxygen enriched blood supply. Oxygen is administered for at least the first 48 hours post MI so that tissue hypoxia does not become evident. At times chest pain can be relieved by applying oxygen.(Swearingen & Keen, 2001)

Vital signs are attended to frequently in CCU, usually hourly, which enables nurses to see any changes in hemodynamic monitoring. Complications of infarctions are heart failure and arrhythmias, due to the large area of heart wall damaged. When Mr Smith suddenly became SOB and adventious breath sounds were heard on auscultation, it alerted medical staff that his left side of the heart was congested and not efficiently pumping. Early indications of Left ventricular failure are shortness of breath (SOB) and intolerance of beta blockers, nitrates, or ACE inhibitors. Mr Smith showed signs of SOB and lightheadedness, which may be due to Ramipril ( ACE inhibitor) that was then decreased in dose (Schell & Puntillo, 2006).

Continuous cardiac monitoring enables nurses to keep constant checks on heart rates and rhythms, it gives nurses the ability to act on any life threatening rhythms immediately or enables them with the knowledge of impending problems that could arise (Drew, 2004). Premature Ventricular Contractions (PVC), Ventricular Tachycardia (VT) or Ventricular Fibrillation(VF) are the most likely rythyms to be noted due to the scarring or necrotic myocardial tissue (Aehlert & eInstruction Corp., 2011). Mr Smith was noted to have occasional PVC’s that became more frequent until he was monitored in bigeminy, which can lead to runs of VT (Huszar, 2007). Monitored patient’s can be observed in pulseless VT/ VF via the central monitor at the nurses’ station and can be immediately defibrillated, whereas if a ward patient collapses a monitor needs to be attached before the heart rhythm can be established and treatment given (McDonough, 2009).

ST Segment monitoring shows significant changes in monitoring that can indicate ischemia or infarction. Central monitors should have regular nurse surveillance, will alarm if there is a significant change to the ST segment. Changes occur with or without complaints of chest pain or shortness of breath, indicating myocardial oxygen mismatch (Smith, 2008). Patient’s need to advised to tell staff of chest pain whilst being monitored. Some patients assume nursing staff know from the monitor when they are experiencing chest pain. (Swearingen & Keen, 2001)

An ECG can be performed to show any significant changes of the heart. Mr Smith showed ST segment changes in his anterior /septal (V3 &V4 position) aspect of his left ventricle. This area is supplied by the Left Anterior Descending Coronary Artery. Treatment does not differ depending on which area of the heart is affected. All areas require oxygen supply. While in hospital Mr Smith was ordered serial ECG’s, these are taken daily to show any changes. Expected changes expected post MI are the development of a pathological Q wave. Q waves indicate the necrosis of myocardial tissue and specifically in V1 to V4 indicates anteroseptal infarction (Dubin, 2000)

Mr Smith was initially given morphine, an opioid that relieves pain by decreasing myocardial oxygen demand by decreasing the Autonomic Nervous System and decreasing anxiety (Lewis, 2007). Nitro-glycerine, was ordered as a smooth muscle relaxant that vasodilates the vessels to restore blood supply if the mismatch is due to a coronary spasm(Yassin, 2007). Aspirin is given daily indefinitely as it is a antiplatelet aggregation inhibitor that Hung, 2008 states is ”proven for secondary prevention of myocardial infarction, stroke and cardiovascular death in both men and women”. He also discusses the combined use of clopidigrel and aspirin to reduce subacute stent thrombosis after PCI’s (Hung, 2008).

Thrombolytic therapy is given within the first 6 hours of chest pain.(Levin, 2008) Tenecteplase 90mg was given. Thrombolytic Therapy is given to dispel the clot and allow blood flow to the affected area. It can take up to 90 minutes for full resolution to occur (Goldberger,2010). There are certain considerations that medical staff must ensure prior to administration of this therapy, these include an absence of CVA/TIA’s or surgery in the last 12 weeks (Gibson, 2009). Once administered ECG’s are taken in 15-30 min intervals to see changes of ST segment, showing that myocardial blood supply and depolarization being restored.

Cardiac markers are Pathology tests that also give evidence of myocardial damage. When cardiac cells are damaged the membrane walls leak these substances into the blood stream (Aehlert & eInstruction Corp., 2011). Myoglobin, Creatine kinase (CK), Troponin T and Troponin I are myocardial specific and along with ST elevation can be evident of a STEMI. Ëarly in ischaemia the ST segment may lose the ST-T wave slope and appear straight. Then as the T wave broadens and the ST segment rises, the segment loses it’s concave form and becomes upwardly convex with elevations” (Moser & Riegel, 2008). Non STEMI do not have a significant change on the ECG only cardiac markers alter. These markers usually peak between 15-24 hours post infarction and remain elevated for 2-3days (Huszar, 2007) Creatine Kinase has normal value of 45-250 U/L and Mr Smiths on admission was 4290 U/L decreasing to 800 U/L, 2 days post. Troponin T normal values are ≤0.03ug/L but Mr Smiths ranged from 14.20ug/L at 2200hours on the day of MI, to 4.39ug/L 2 days later. Serial pathology tests are taken usually every 6 hours for the first 24 hours.

Mr Smith was taken for a PCI the day after his MI. He had a stent put in his proximal area of his Left anterior descending coronary artery (LAD) in the Cardiac Catheter Lab. Mr Smiths had a PCI even though his blood supply looked like it had been reinstated, the stent will prevent clot formation again and reocclussion (Cannon, 2010). He was then transferred back to CCU and remained RIB overnight. He had a femoseal deployed into his groin to occlude the opening of the femoral vessel used for this procedure. Nurses need to do regular neurovascular and pedal pulse observations to check for bleeding or vessel occlusion (Shoulders-Odom, 2008).

Mr Smith needed to be educated on his procedure pre and post operative. He has previously been for this procedure but needed re-education. It must be a daunting experience to be given twilight sedation whist having the PCI. Mr Smith’s last procedure was 13 years ago which would see many new techniques being practiced that he was not familiar with. His post op education included the importance of keeping his affected leg still and care of his affected groin.(Moser & Riegel, 2008) Myocardial Infarction education can be given to him at the same time but this is information that needs to be reiterated continually during his hospitalization(Lewis, 2007). He and his family need to be aware of the risk of reinfarction especially in the next 2 weeks post MI as the heart muscle is still weak and irritable and increase in activity can cause another MI. This is the time that patients start to resume their normal daily activities after hospitalization and are at the most risk. (Douglas, 2010)

Documentation is very important and needs to be filled out correctly as it is a legal document (Lewis, 2007). The CCU’s clinical pathway for infarction indicated strict rest in bed with commode privileges for the first 48 hours, this decreases the need for myocardial oxygen. This is difficult for active patients but it needs to be strictly followed. Due to immobility other medical complications can arise, pneumonia and decreased gas exchange, deep vein thrombosis or emboli are common. To prevent these patients are encouraged to attend to hourly Deep Breathing Exercises (DBE), leg exercises and triflow. Patients can also be sat in an upright position which increases venous return (Thelan, 1994). Anticoagulants prevent clot formation therefore Mr Smith was administered daily Clexane 90mg post PCI until discharge and administered Abciximab (Reopro) for 12 hours post PCI. To test the adequacy of anticoagulants, INR and APPT are taken to check patient’s dose is therapeutic. Problems with administering the anticoagulant after thrombolytic therapy is bleeding (Yassin, 2007). Mr Smith was noted to have large traces of blood in his urinalysis and was sent for a Pelvic Ultrasound to be sure there was no other complications, the ultrasound was NAD.

Prior to discharge Mr Smith was educated on his new regime of medications and the importance of medication compliance to decrease his risks of further cardiac complications (Albert, 2008).

Nurses if experienced and up to date with current research and practices can work alongside medical staff and initiate nursing cares that are in the best interest of patients. Coronary Care Units must have confident and competent nurses to run the ward as most times they make significant decisions on implementation of nursing care. When Doctors have confidence in the nurse looking after their patients they will respect and listen to nurses opinions because they know they are educated and empowered with knowledge.