Clinical reasoning Cycle is the process by which nurses collect cues, process the information, come to an understanding of a patient problem or situation, plan and implement interventions, evaluate outcomes, and reflect on and learn from the process. A nurse’s clinical reasoning ability is a key factor in the provision of quality care and the prevention of adverse patient outcomes.

Consider The Patient:

• Describe or list facts, context, objects or people 

Collect Cues: 

• Review current information (eg patient Hx

• Gather new information (eg patient Ax)

• Recall knowledge (eg physiology, pathophysiology and medications): References needed here

Process Information :

• Interpret the information.  Ask yourself WHY…why am I seeing these signs and symptoms?  Why are these blood results and vital signs abnormal?  Why are these medical orders requested? Reference here to support your work

References :
Inclusive of in text referencing also include your APA style 7th ed. references here
 

Clinical Reasoning Cycle Example - Scenario (highlighting information to be interpreted):

Carlos Ricci is a 54-year-old male who travels frequently.
NKDA.
Nil relevant past history.
Wife is NOK.
Height: 175cm Weight: 110kg

He was seen in the Emergency Department at 12:30 hours for complaints of chest pain 9/10, diaphoresis, and shortness of breath. He has a past history of hypertension and elevated cholesterol.

His vitals on admission were: HR132, BP 155/90, RR22, SpO2 91% Room Air.

He was treated in the Emergency Department with aspirin and two doses of sublingual glyceryl trinitrate.

Chest pain improved with glyceryl trinitrate administration. IV infusion of normal saline was started in the Emergency Department and is running at 5 mL/hour. Ordered pathology (Cardiac Enzymes, FBE, UEC, LFT, Coagulation) results are pending. The medical officer wants to be called as soon as the results are available.

The 12-lead ECG shows anterior ST elevation consistent with myocardial infarction. He is for admission to the coronary care ward, pain is now settled.

Medical Orders:

IVT NaCl TKVO
SpO2>92%
Continuous Cardiac & SpO2 Monitoring Bed rest with bathroom privileges
Low salt, low fat cardiac diet
Morphine 2mg IV bolus PRN for chest pain 10/60, max 3 doses every 2 hours
CXR, UECr, FBE, Cardiac enzymes 6/24 x 3 (two sets to collect)

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Consider The Patient :

Carl Ricci
54-year-old male
Travels frequently (more information required)
Emergency Department (ED)
Day 0
Nil Known Drug Allergies (NKDA)
Height: 175 cm
Weight: 110kg (increased Body Mass Index: BMI)
Married, wife Next Of Kin (NOK)
Admission Diagnosis: Acute Myocardial Infarction (AMI)

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Collect Cues:

Nil relevant past history

Seen in ED at 1230 hours for complaints of chest pain (CP), diaphoresis, and shortness of breath (SOB). HR132, BP 180/90, RR22, SpO2 91% Room Air (RA). He was treated in the ED with aspirin and two doses of sublingual glyceryl trinitrate (GTN).

Intravenous (IV) infusion of normal saline (NaCl) was started in ED and is running at 5 mL/hour: to keep vein open (TKVO). Ordered pathology results are pending. The medical officer (MO) wants to be called as soon as the results are available.

The 12-lead Electrocardiograph (ECG) shows anterior ST elevation consistent with AMI

VITAL SIGNS:

Medical Orders:

IV Therapy (IVT) NaCl TKVO at 5mls/hour
SpO2>92%
Continuous Cardiac & SpO2 monitoring Bed rest with bathroom privileges
Low salt, low fat cardiac diet
Morphine 2mg IV bolus PRN for chest pain 10/60, max 3 doses every 2 hours
CXR, UECr, FBE, Cardiac enzymes 6/24 x 3 (two sets to collect)

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AMI Pathophysiology

In an AMI, an area of the myocardium is permanently destroyed, typically because plaque rupture and subsequent thrombus formation results in occlusion of the artery. Vasospasm (sudden constriction or narrowing) of a coronary artery; decreased oxygen supply (e.g. from acute blood loss, anaemia or low blood pressure); and increased demand for oxygen (e.g. from a rapid heart rate, thyrotoxicosis or ingestion of cocaine) are other causes of AMI (insert reference here). In each case, a profound imbalance exists between myocardial oxygen supply and demand .

As the cells are deprived of oxygen, ischaemia develops, cellular injury occurs and over time, the lack of oxygen results in infarction, or the death of cells (insert reference here). The expression ‘time is muscle’ reflects the urgency of appropriate treatment to improve patient outcomes .

Various descriptions are used to further identify an AMI: the type (Non ST elevation infarction [NSTEMI], ST Elevation infarction [STEMI]), the location of the injury to the ventricular wall (anterior, inferior, posterior or lateral wall) and the point in time within the process of infarction (acute, evolving or old) (insert reference here). The differences between NSTEMI and STEMI are diagnostic (insert reference here).

The 12 lead ECG usually identifies the type and location of the AMI, and other ECG indicators such as a Q wave and patient history identify the timing (insert reference here). Regardless of the location, the goals of medical therapy are to prevent or minimise myocardial tissue death and prevent complications .

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Clinical manifestations of an AMI

Chest pain that occurs suddenly and continues despite rest and medication is the presenting symptom in most patients with AMI .Patients may present with a combination of symptoms, including chest pain, shortness of breath, indigestion, nausea and anxiety (insert reference here). They may have cool, pale and moist skin, their heart rate and respiratory rate may be faster than normal (insert reference here). These signs and symptoms, which are caused by stimulation of the sympathetic nervous system, may be present for only a short time or may persist (insert reference here) as seen with Mr Ricci’s presentation.

MORPHINE (paraphrased drug information obtained from McKenna & Mirkov, 2019):

Action: opioid antagonist that binds with the opioid receptors in the central nervous system to cause analgesia, sedation or euphoria

Indications: Relief of moderate to severe chronic and acute pain

Adverse Reactions: Respiratory depression, nausea & vomiting, hypotension, dizziness, urinary retention, sedation, constipation

Nursing Considerations: falls risk assessment, monitor vital signs, full respiratory assessment, naloxone and resuscitation equipment available, may need to administer antiemetic, may require stool softeners

Interactions/Contraindications of relevance: none to note with this patient
Dose relevant to patient & order: IV onset within 5 minutes, peaks at 20 minutes and half life is 1.7 hours. For direct injection, 2.5–15 mg may be diluted in 4–5 mL of sterile water for injection and given over 4–5 min. Dr has prescribed 2mg bolus as per drug order

GTN (paraphrased drug information obtained from McKenna & Mirkov, 2019):
Action: ………….
Indications: ………….
Adverse Reactions: ………….
Nursing considerations: ………….
Interactions/Contraindications of relevance: ………….
ASPIRIN (paraphrased drug information obtained from McKenna & Mirkov, 2019): Action: ………….
Indications: ………….
Adverse Reactions: ………….
Nursing considerations: ………….
Interactions/Contraindications of relevance: ………….


Cultural/Legal Considerations:
A statement regarding this should be here…….
 

Process Information:

Vital Signs (all normal values obtained from Tollefson, 2019).

HR132 (60-100) related to (R/T) pain, activation of Sympathetic Nervous System (SNS)

BP 180/90 (100-140/60-80) Elevated? ?what is patient’s normal? R/T ?pain, ?HPT history, activation of SNS as per Konstantinou et. Al, 2019

RR22 (12-20) R/T ?pain, ?anxiety (Maziar Zafari et al, 2019) , ?pulmonary congestion because when the ventricles is not able to pump efficiently as can occur in an AMI, blood can back up into the veins that take blood through the lungs therefore the pressure in these blood vessels increases and fluid is pushed into the alveoli (Iqbal and Gupta, 2021)

SpO2 91% (>95%) Room Air R/T ?pulmonary congestion (Maziar Zafari et al, 2019)

Chest pain R/T reduced blood flow through the coronary arteries therefore oxygen rich blood does not reach the cardiac muscle and cardiac ischemia occurs (Aroesty & Kannam, 2020)
Diaphoresis R/T stimulation of the SNS in response to pain (Gokhroo et al 2015)

Shortness of breath R/T ?acute pulmonary oedema, ?pain, ?anxiety (Maziar Zafari et al, 2019)

Medical Orders:

IV Therapy (IVT) NaCl TKVO at 5mls/hour to keep IV access patent (Doyle & McCutcheon, 2015). SpO2>92% to increase oxygen supply to the myocardium (Smeltzer & Bare, 2017).

Continuous Cardiac & SpO2 Monitoring to monitor any changes and act accordingly (Smeltzer & Bare, 2017).

Bed rest with bathroom privileges to reduce myocardial oxygen consumption (Smeltzer & Bare, 2017).

Low salt, low fat cardiac diet to reduce risk of cardiovascular disease (Heart Foundation, n.d) Morphine 2mg IV bolus PRN for chest pain 10/60, max 3 doses every 2 hours

CXR, UECr to determine kidney function and electrolyte levels which can , FBE, Cholesterol, Troponin 6/24 x 3 (two sets to collect) to confirm AMI diagnosis (RCPA, 2021).

Anterior ST elevation consistent with AMI: occurs when anterior myocardial tissue usually supplied by the left anterior descending coronary artery suffers injury due to lack of blood supply . The ST Segment on the ECG represents the interval between ventricular depolarization and repolarization with the most important cause of ST segment elevation being myocardial infarction which is seen in Mr Ricci’s ECG

Contributing factors to AMI: increased BMI, HPT, high cholesterol, age (Smeltzer & Bare, 2017).Is also a frequent traveller…more information to be obtained on recent flight history as could also have been a pulmonary embolism (Smeltzer & Bare, 2017).

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References:

Follow APA 7th ed referencing
Referencing guides available at:
https://www.vu.edu.au/library/get-help/referencing/referencing-guides OR
https://www.vu.edu.au/library/get-help/workshops-drop-in-sessions