Question 1. A. AIRWAY– Maintaining a clear airway is always considered a high priority because airway is essential for gas exchange (Ramkumar, 2011). However, the patient has a patent airway. Therefore, the nursing strategy is to conduct an airway assessment “look, listen and feel” continuously to detect any changes. This is to provide immediate respiratory care if the patient’s airway is compromised (Higginson, Jones & Davies, 2011). This is a low priority.
B. BREATHING – Respiration is altered due to left ventricular failure. The patient is tachypnoeic due to an increased pressure in the pulmonary veins that will lead to pulmonary congestion that lessens pulmonary compliance, which raises the respiratory rate. Also, increased blood flow in the lungs can cause shallow or less effective breathing and the oxygen uptake will be inadequate, therefore the patient’s breathing is in laboured (Barthel, Wensel, Bauer, Muller, Wolf, & Ulm et al., 2012).
Whereas, hypoxia is due to damaged alveolar capillary interface due to inhibition of oxygen and carbon dioxide exchange. The presences of bilateral crackles are due to pulmonary congestion and collapsed alveoli caused by fluid accumulation in the lungs (Gallagher & Driscoll, 2015). Therefore, the nursing strategy is to place the patient in a high fowlers position while continuously monitoring the patient’s respirations (rate, rhythm, depth, pattern, colour). This will promote chest expansion and reduced the workload of the heart. Early detection of respiratory distress will assist in emergency interventions and reduce the risk of complications (Jaffe & Cabrera, 2016). This is considered a high priority.
C. CIRCULATION – The contraction of heart muscle is less effective due to necrotic tissue in the myocardium. Therefore, cardiac contractility and cardiac output is impaired. There is a progressive ischaemia because the oxygenated blood is unable to impel in the myocardium due to the damaged ventricle (Wagner & Hardin-Pierce, 2014). The heart will compensate for decreased cardiac output from the failing ventricle.
Therefore, tachycardia will develop as an effect of sympathetic stimulation while hypotension is due to compromised coronary flow (Bucher, Johnson & Rolley, 2015). The increased SNS stimulation creates vasoconstriction, which will prolonged the capillary refill and the extremities will be cool, clammy and mottled due to reduced tissue perfusion (Bucher et al., 2015). The increased JVP indicates fluid overload due to left ventricle failure and pulmonary oedema. Peripheral pulses are rapid and faint because of the decreased circulation and tachycardia.
Bilateral ankle oedema is caused by accumulation of fluid and reduces blood flow out of the heart. The 3rd heart sounds indicates left ventricular dysfunction and the rapid filling of the ventricle. The temperature of 37.5°c is a systemic manifestation of the inflammatory process caused by myocardial cell death (Bucher et al., 2015). The nursing strategy is to assess the patient’s cardiac and hemodynamic status through monitoring the arterial line, ECG, and fluid status. Immediate detection of complications is essential to minimise the risk and maintain hemodynamic stability (Jones & Rushton, 2012). This is a medium priority.
D. DISABILITY – (Pain and anxiety) The pain score is 5/10, which is moderately strong. The pain causes anxiety and restlessness, which increases the stimulation of sympathetic nervous system and decreases the cerebral oxygenation (Doenges, Moorhouse & Murr, 2014). The GCS is normal and the patient is orientated to person, time and place. Staying with the patient and encourage verbalization of feelings will create reduction of anxiety or fear. Monitor the characteristics of pain to assess the effectiveness of the treatment (Doenges et al., 2014). This is a low priority.
E. EXPOSURE – Grace has no signs of bruising. However, monitor the patient for bruising due to the side effect of aspirin. Other than that, No further management is needed. This is a low priority.
F. FLUIDS – The heart is unable to pump the blood as there is too much fluid in the lungs and this will cause difficulty in breathing. Therefore, the nursing strategy is fluid restriction to 1.5-2L/day in order to improve their symptoms. This is to prevent complications related to fluid overload (Gallagher & Driscoll, 2015). This is a low priority.
G. GLUCOSE – Blood glucose level is normal. Provide continuous monitoring to control sudden increase of blood sugar. This is a low priority
Question 2. A. Chest X-ray: Heart normal size. Pulmonary vascular congestion and pulmonary oedema
There is a failure in the left atrium when ejecting blood into left ventricle therefore pressure in the left atrium increases. Pulmonary congestion occurs when the vessels are distended due to an increased backpressure in the pulmonary veins. Pulmonary oedema will occur when fluid accumulates in the lungs and later fluid will start to leak into the alveoli. High left ventricular (LV) filling pressure leading to pulmonary venous hypertension (increased PCWP) is the main underlying mechanism of pulmonary congestion.
Elevation of LV diastolic pressure (LVDP) results from fluid overload caused either by fluid retention or by fluid redistribution. On the other hand, a rapid increase in blood pressure (afterload), particularly in patients with diastolic dysfunction, may precipitate severe pulmonary congestion. Often, elevation of LVDP (hemodynamic congestion) precedes clinical congestion by days or even weeks (Pappas & Filippatos, 2011).
B. Arterial blood gas analysis
The pH is low, which indicates an increase of acidity in the blood, this is due to the build-up of lactic acid due to shortage of oxygen. The PaO2 is low because less oxygen is dissolving in the blood and reflected as hypoxemia. The PaCO2 is normal which means the amount of carbon dioxide gas dissolved in the blood is adequate and represents the effectiveness of ventilation. This is evident by increased respiratory rate of the patient. The HCO3 indicates acidosis in the metabolic component.
The patient is in metabolic acidosis, uncompensated because the PaCO2 is within normal. The Base excess is high outside the normal range, which suggests a metabolic cause. An elevated lactate indicates lactic acidosis as a result of tissue hypoxia as evidence by decreased in systemic blood flows. Metabolic acidosis in myocardial infarction is due to the build up of lactic acid (Gandhi, & Akholkar, 2015).
Question 3. Dobutamine is a direct-acting inotropic agent with synthetic catecholamine and it is commonly used in severe heart failure and management of cardiogenic shock. It has synthetic sympathomimetic amine that mimics the characteristic of the sympathetic nervous system and it stimulates the beta1-adrenergic receptors (Australian Medicine Handbook, 2016). It also has a chronotropic effect by controlling the nerves of the heart that changed the heart rate and likewise by affecting the rhythm produced by the sinoatrial node (Bryant & Knights, 2015).
Due to its cardiac stimulant action it increases myocardial contractility and stroke volume, which will increase the cardiac output that will improve cardiac performance (Lehne, Moore, Crosby & Hamilton, 2012). Dobutamine’s onset of action is between 1 to 2 minutes. Since, it has a minimal beta2 and alpha-adrenergic effect, the main therapeutic effect is it will strengthen the contractions of the heart and the blood flow will increase without increasing the heart rate.
Therefore, the result is it will increase myocardial oxygen consumption (Drugguide.com, 2016). In addition, further therapeutic uses are treating hypotension, arrhythmias and heart failure (Australian Medicine Handbook, 2016). In evaluating the therapeutic effect of the drug, cardiac function such as heart rate, electrocardiogram, blood pressure, and urine output should be monitored closely.
Plus, monitoring the central venous pressure and pulmonary wedge pressure is essential for safe infusion of dobutamine (Lehne et al., 2012). The major adverse effect of this drug is tachycardia. During administration of dobutamine constant physical assessment such as palpating the peripheral pulses should be routinely done. If pulse deteriorates or any significant changes in vital signs emerged, notify physician immediately (Drugguide.com, 2016).
