Cardiovascular Case Study Answers

Use this case study as an educational tool by answering the questions posed by the author, then reviewing the answers further down.

At 6:45 a.m., your unit is dispatched for a 50-year-old male with chest pain. You and your partner proceed to the scene, with a response time of approximately eight minutes. The closest hospital from the scene is 40 miles away.

You arrive at the scene, don appropriate BSI precautions and ensure that the area is safe, then knock on the door of the patient's residence. A middle-aged male answers the door and identifies himself as the patient. You note that he is diaphoretic and anxious, and is clenching his fist against the center of his chest.

1. What is the significance of the patients clenched fist in the center of his chest?

You sit the patient down and perform an initial assessment (Table I). Your partner attaches a pulse oximeter and prepares to administer oxygen to the patient.

Your partner administers 100% oxygen to the patient with a nonrebreathing mask while you perform a focused history and physical examination (Table II). The patient tells you that his doctor prescribed nitroglycerin for him; however, because he recently moved into the house, he thinks it's still packed in one of the boxes.


2. What are the physiologic effects of nitroglycerin?

After confirming no history of bleeding disorders or allergies, you administer 324 mg of aspirin to the patient. Your partner obtains baseline vital signs and a SAMPLE history (Table III). The patient remains conscious and alert, but is becoming increasingly restless. You attach the patient to a cardiac monitor and interpret his cardiac rhythm as sinus tachycardia at 110 beats per minute.

After administering 0.4 mg of nitroglycerin sublingually to the patient, you and your partner attach the remaining ECG leads and obtain a 12-lead tracing of the patient's cardiac rhythm. As your partner stands up to retrieve the stretcher from the ambulance, you tell him that it looks as though the patient may be having an anterior wall MI.

3. How could this patient's current blood pressure and heart rate affect his condition?

The patient's chest pressure is unrelieved following two more doses of sublingual nitroglycerin. You place him on the stretcher and load him into the ambulance. En route to the hospital, you continue oxygen therapy and successfully establish an IV of normal saline with an 18-gauge catheter. Reassessment of his blood pressure reveals a reading of 140/88 mmHg. Because three doses of nitroglycerin failed to relieve his pain, you administer 2 mg of morphine sulfate via IV push. Within 10 minutes, the patient tells you that the pressure in his chest has improved and is now a "3" on a 0--10 scale. With an estimated time of arrival at the ED of 20 minutes, you begin an IV infusion of nitroglycerin at 10 µg/min and perform an ongoing assessment (Table IV).

The patient's condition continues to improve en route to the hospital. You ask him if he has a history of ulcers, bleeding disorders, recent surgeries or stroke. He tells you that other than his high blood pressure and occasional chest pain, he has no other medical problems. You call your radio report to the receiving facility and continue to monitor the patient.

4. Why are you asking the patient these specific questions?

The patient tells you that he is still experiencing chest pressure; however, it is less severe. Since his blood pressure remains stable (130/84 mmHg), you administer another 2 mg dose of morphine via IV push. You continue to monitor the patient's vital signs and cardiac rhythm. Your estimated time of arrival at the hospital is 5--10 minutes.

5. Are there any special considerations for this patient?

Upon arriving at the emergency department, the patient states that he is pain-free. You give your verbal report and field-obtained 12-lead ECG to the attending physician. Following additional assessment in the emergency department, the patient is diagnosed with an acute anterior wall myocardial infarction. Following successful treatment with fibrinolytic therapy, he is admitted to the cardiac care unit and transferred to a cardiac rehabilitation facility 10 days later.

Cardiac Case Study: Answers and Summary

1. What is the clinical significance of the patient’s clenched fist in the center of his chest?

Ischemic cardiac chest pain is typically described as being crushing, tight, oppressive, pressuring or constricting in nature. Patients may describe their pain as though a vise were placed around their chest or the sensation that an elephant is sitting on their chest, while others may only report a vague or "strange" sensation in their chest. The pain associated with cardiac ischemia is usually substernal; however, it may be localized to the epigastrium and is commonly mistaken for indigestion.

A clenched fist in the center of the chest (the precordium) conveys the feeling of pressure or squeezing and is called Levine's sign (see the photo on page 50). The presence of Levine's sign is suggestive, but not conclusive, of cardiac-related chest pain and should increase your index of suspicion.

Chest pain or discomfort is the most common presenting symptom of an acute coronary syndrome (ACS), occurring in 70%--80% of patients. However, 20% or more of patients with acute myocardial infarction present with no pain or discomfort at all. Elderly patients and patients with diabetes may present without classic symptoms or with only vague, nonspecific symptoms, such as malaise, lightheadedness, syncope, changes in mentation or sudden diaphoresis.

Patients with cardiac ischemia may also present with referred pain to other areas of their body, such as the jaw, arm, shoulder or back. Less commonly, patients may present with atypical chest pain, which may be described as sharp or stabbing in nature.

During your general impression of the patient with chest pain or pressure, look for clues suggestive of cardiac compromise, such as diaphoresis, restlessness or apprehension. The absence of chest pain or the presence of atypical chest pain, however, does not rule out an ACS--especially if the patient has other signs and symptoms and a history of cardiac disease (e.g., prescribed nitroglycerin).

Acute coronary syndrome is a term used to describe many types of compromised circulation to the heart muscle, including unstable angina pectoris or acute myocardial infarction. Because the clinical presentations of the two are extremely similar, if not identical (i.e., unrelieved chest pain, ECG changes, diaphoresis), treatment should focus on the assumption that acute myocardial infarction is occurring.

2. What are the physiologic effects of nitroglycerin?

Before discussing the physiologic effects of nitroglycerin, a brief review of coronary atherosclerosis, myocardial ischemia and angina pectoris is in order.

Coronary atherosclerosis is a progressive disease characterized by the buildup of lipid-laden plaque within the lumen (channel) of the coronary artery. Atherosclerosis causes narrowing of the artery (decreasing coronary blood flow) and hardening of the artery (limiting the ability of the artery to dilate). These negative consequences of atherosclerosis reduce the ability of the heart to accommodate increases in myocardial oxygen demand, such as that caused by stress or exertion.

When the scale of myocardial oxygen supply and demand is unbalanced, the patient develops ischemic chest pain or pressure (angina pectoris). Ischemia, which is defined as a relative deprivation of oxygen, occurs when oxygen demand exceeds supply, and is a reversible condition with prompt treatment.

Angina is described as being stable or unstable. Stable angina is characterized by a relatively predictable sequence of events. Patients are often aware of the extent of exertion that precipitates their chest pain (e.g., walking one block); therefore, they limit their activities in order to avoid symptoms. Additionally, patients are also aware of what they need to do to resolve their symptoms (e.g., a specific period of rest, nitroglycerin). Following resolution of their chest discomfort, many patients with stable angina never call EMS.

Unstable angina occurs when the patient experiences a change in his typical anginal pattern, indicating advanced coronary atherosclerosis and an oxygen supply-demand mismatch that is not so easily balanced with rest and nitroglycerin. Relative to stable angina, the patient with unstable angina experiences "off-pattern" chest pain, such as when exertion is minimal or when myocardial oxygen demand is otherwise low (e.g., during sleep). Additionally, the usual treatment modalities of rest and/or nitroglycerin afford them minimal or no relief from their symptoms. This change may prompt a call to EMS.

Nitroglycerin (NTG) causes relaxation of vascular smooth muscle (vasodilation), promoting systemic pooling of venous blood. This decreases the volume of blood that is returned to the heart (preload), as well as the amount of resistance that the heart must pump against (afterload). The combined effects of decreased preload and afterload cause an overall decrease in myocardial oxygen demand and consumption.

Additionally, nitroglycerin may dilate the coronary arteries and promote collateral circulation, thus improving oxygen supply to the ischemic myocardium. Collateral circulation, also referred to as "arteriogenesis," is a process in which smaller arteries that are normally closed become patent (open up) and connect two larger arteries or different parts of the same artery. Over time, myocardial ischemia can promote collateral vessels to grow, forming a "detour" for blood flow around the blocked coronary artery.

Because nitroglycerin dilates the systemic blood vessels, it can result in hypotension. Therefore, its use is generally contraindicated in patients with a systolic BP of less than 90 mmHg, as well as in patients who have taken Viagra (sildenafil), Levitra (vardenafil) or Cialis (tadalafil) within the past 24--36 hours. These drugs, which are used to treat sexual dysfunction, also cause vasodilation and, when used concomitantly with nitroglycerin, can result in potentially life-threatening hypotension. EMS providers should follow local protocol or contact medical control as needed regarding the use of nitroglycerin.

3. How could this patient's current blood pressure and heart rate affect his condition?

This patient's history, physical examination and 12--lead ECG findings suggest acute myocardial infarction (AMI) involving the anterior (front) wall. The patient's hyperdynamic vital signs--hypertension and tachycardia--indicate a discharge of epinephrine and norepinephrine from the sympathetic nervous system, most likely caused by a combination of pain, anxiety/fear and myocardial ischemia and injury. Epinephrine increases the rate (chronotropy) and strength (inotropy) of cardiac contractions and norepinephrine increases systemic blood pressure by constricting the blood vessels.

This patient's vital signs represent a classic case of "more is not better!" In order for the heart to beat stronger and faster, it requires and uses more oxygen. Additionally, an elevated blood pressure increases afterload (ventricular resistance), further increasing myocardial oxygen demand.

Unfortunately, in this patient, an occluded coronary artery is blocking the flow of oxygenated blood to the area of the myocardium that needs it most--the injured area. This increase in myocardial oxygen demand and consumption and decrease in myocardial oxygen supply can enlarge the area of injury, resulting in greater myocardial damage.

The anterior wall is the largest part of the heart and tends to sustain significant damage as the result of an MI. As the area of injury increases, lethal cardiac dysrhythmias, such as ventricular fibrillation (v--fib) or ventricular tachycardia (v--tach), can occur. Additionally, if an extensive area of the anterior wall is damaged, the patient can develop acute CHF and, in more severe cases, cardiogenic shock. Cardiogenic shock, which has a very high mortality rate, occurs when the heart is severely damaged and is no longer able to adequately perfuse the body.

4. Why are you asking the patient these specific questions?

This patient is a potential candidate for fibrinolytic (clot-buster) therapy; therefore, you should conduct a field screening to determine if he is eligible for this treatment. Although fibrinolytic therapy is not commonly initiated in the prehospital setting, the information you obtain regarding the patient's eligibility or ineligibility, in addition to the 12-lead ECG obtained in the field, will be valuable to the physician and can decrease the "door-to-drug" time when the patient arrives in the emergency department.

Fibrinolytic agents (Table V) work by a chemical process that converts plasminogen to plasmin, the central enzyme of the physiologic plasminogen system. Plasmin in turn digests fibrin, the active component of the clot matrix, through a process called fibrino­lysis. Fibrinolysis dissolves the clot that is occluding the coronary artery, thus reestablishing distal perfusion. The goal of fibrinolytic therapy is to halt the infarction process and salvage areas of ischemic and injured myocardium.

The indications or inclusion criteria for fibrinolytic therapy are summarized in Table VI. Although EMT-Basics and EMT-Intermediates are not usually trained to interpret ECG rhythms, they can, through index of suspicion based on the patient's signs and symptoms, suspect AMI and conduct a field screening, especially if the time of onset is less than 12 hours.

Because of the interaction of fibrinolytics with the body's hematologic system, strict criteria must be met before the patient can be eligible for fibrinolytic therapy. If given to the wrong patient, fibrinolytics can cause life-threatening hemorrhage. Table VII summarizes the absolute and relative contraindications or exclusion criteria for fibrinolytic therapy. Some patients with certain relative contraindications may still be eligible for fibrinolytic therapy, based on a careful evaluation by the physician.



5. Are there any special considerations for this patient?

There are several issues to consider when treating and monitoring this patient. As previously discussed, nitroglycerin (being administered to this patient via continuous IV infusion) can cause hypotension. Therefore, careful monitoring of the patient's blood pressure is essential. Hypotension in a patient with a sick heart can have disastrous consequences.

You have also administered a total of 4 mg of morphine to the patient. Morphine, a narcotic analgesic, can depress the central nervous system, resulting in a decreased level of consciousness, hypoventilation, bradycardia and hypotension. While most people will not experience significant CNS depression with low doses of morphine, you should have a BVM handy to assist ventilations, as well as naloxone (Narcan) to reverse the effects of the morphine. Narcan competitively binds with opiate receptor sites in the body and reverses the CNS depression associated with narcotic administration.

Continuous cardiac monitoring is an essential part of cardiac patient management, especially in this patient, whose 12-lead ECG indicates that an MI is in progress. You must be alert for the development of warning signs of a potentially lethal dysrhythmia, such as premature ventricular complexes (PVCs). You should also observe the patient for any sudden changes in his heart rate. Anterior wall MIs can result in significant tachycardia or bradycardia, both of which can further complicate the clinical picture.

When caring for a potentially unstable cardiac patient, especially when your transport time is lengthy, you must remain cognizant of the fact that because you are alone in the back with the patient, your capabilities are limited to defibrillation and one-person CPR if the patient develops cardiac arrest. Therefore, it would be prudent to request additional assistance or arrange to rendezvous with another EMT or paramedic while en route to the hospital.

Summary

This case study represented a patient with a relatively uncomplicated myocardial infarction that, after prompt prehospital care and transport, was successfully halted in the emergency department with fibrinolytic therapy.

This patient was provided excellent care in the prehospital setting because the paramedic and his EMT-B partner worked together effectively as a team. Although ECG monitoring, IV therapy and medication administration are beyond the usual scope of practice of an EMT-B, many EMS systems are training their EMT-Bs to assist with these important procedures and interventions. This involves preparing IV equipment and supplies, applying the cardiac monitor, and recognizing and handling the various paramedic medications. This enhanced role of the EMT-B allows the paramedic to perform a more focused and careful patient assessment.

A cohesive working relationship between BLS and ALS personnel is absolutely crucial to the outcome of the patient. Although each level of prehospital provider possesses a different knowledge of pathophysiology and patient management, it is the combined contributions and efforts of each provider that will afford patients the high quality of care they deserve.

Bibliography

  • ACLS for EMT-Basics. Jones and Bartlett, Publishers/AAOS, 2003.
  • Advanced Cardiac Life Support: Principles and Practice. American Heart Association, 2003.
  • Emergency Care and Transportation of the Sick and Injured, 8th Edition. Jones and Bartlett, Publishers/AAOS, 2002.
  • Prehospital Advanced Cardiac Life Support, 2nd Edition. Brady Publishing, 2004.

[column]Learning outcomes
Level 2 case study: You will be able to:

  1. interpret relevant lab and clinical data
  2. identify monitoring and referral criteria
  3. explain treatment choices
  4. describe goals of therapy, including monitoring and the role of the       pharmacist/clinician
  5. describe issues – counselling points, adverse drug reactions, drug interactions, complementary/alternative therapies and lifestyle advice.

Scenario

You  are  a  hospital  pharmacist  visiting  your  regular  general medical ward  to review patients  and  provide  pharmaceutical  advice. Mr  HA  is  a  50-year-old accountant who was admitted 2 days ago to hospital following a blackout whilst watching a  football match with his  son. His preliminary  examination  reveals bruising to his left arm and upper thigh for which he has been prescribed paracetamol  1 g  four  times  daily  and  as required  ibuprofen  400 mg  three  times a day.
His past medical history  indicates  that  that he  is on no medication and seemed to be a reasonably fit man for his age with no existing diagnosed medical conditions. On examination he is slightly overweight at 81 kg, he smokes 20 cigarettes per day and drinks approximately 30 units of alcohol per week. His blood pressure on admission was 165/80 mmHg with a heart rate of 90 beats per minute. This degree of raised blood pressure and heart rate has been maintained over the last 48 hours. He is subsequently diagnosed as having hypertension.

Questions

1    What is hypertension?
2    What are the appropriate treatment targets for this patient’s blood pressure?
3    Besides blood pressure, what other advice and treatment does this patient require to ensure his risk of a cardiovascular event is reduced? Give clear reasons for your advice and explain the risks associated with not taking this advice.
4    What are the main classes of drug used to treat hypertension?
5    Which class of drug would be appropriate first-line treatment for Mr HA? How would this treatment choice be affected if the patient had been of Afro-Caribbean origin?
6    For one of the classes of drugs mentioned in question 4 indicate the following:

  • a drug from that class
  • a suitable starting dose and frequency
  • the maximum dose for hypertension
  • three contraindications
  • three common side-effects.

7    In view of Mr HA’s age he requires cardiovascular risk assessment. How would you assess this patient’s cardiovascular risks?

Answers

1       What is hypertension?
Hypertension  (in  people  without  diabetes)  is  defined  as  a  sustained  systolic blood  pressure  of  (SBP)  of  ≥140 mmHg,  or  sustained  diastolic  blood  pressure (DBP)  of  ≥90 mmHg  (Clinical  Knowledge  Summaries,  2007).
Note: Hypertension  is  considered  to  be  sustained  if  an  initial  raised  blood pressure measurement persists at two or more subsequent consultations).

2        What are the appropriate treatment targets for this patient’s blood pressure?
The  aim  of  treatment  is  to  reduce  blood  pressure  to  140/90 mmHg  or  below (NICE,  2006).
Note:  Patients  not  achieving  this  target,  or  for  whom  further treatment  is  inappropriate,  declined  or  not  tolerated  will  still  receive  some worthwhile benefit from the drug treatments if these lower blood pressure.

3         Besides blood pressure, what other advice and treatment does this patient require to ensure his risk of a cardiovascular event is reduced? Give clear reasons for your advice and explain the risks associated with not taking this advice.
This patient should receive appropriate advice on a range of lifestyle measures that may reduce his overall cardiovascular disease risk. In particular he needs to be encouraged  to  lose weight,  stop  smoking and  to  reduce his alcohol  intake to within recommended limits.
The Clinical Knowledge Summary on Hypertension  (2007)  suggests  that people with hypertension should be advised on appropriate lifestyle modifications to reduce cardiovascular disease risk. Advice should be given on:

  • alcohol consumption
  • diet
  • physical activity
  • smoking cessation
  • weight reduction.

[/column]
There is evidence that a healthy diet, regular exercise and moderation of alcohol intake can reduce, delay or remove the need for long-term antihypertensive drug  treatment  (North  of  England  Hypertension  Guideline  Development Group, 2006).
Combining dietary and exercise interventions reduces blood pressure by at least  10 mmHg  in  about  a  quarter  of  people  with  hypertension  (North  of England Hypertension Guideline Development Group, 2006). Detailed dietary, exercise  and  weight-loss  advice  is  given  in  the  Dietary  Approaches  to  Stop Hypertension  (DASH)  eating  plan  (available  from  www.nhlbi.nih.gov/health/public/heart/hbp/dash).

Individual lifestyle modifications that are known to reduce blood pressure include (North of England Hypertension Guideline Development Group, 2006):

i. Regular aerobic exercise for 30–60 minutes, three to five times each week

ii. Moderating alcohol intake to recommended levels (less than 21 units per week for men; and less than 14 units per week for women)

iii. Restriction of dietary sodium salt to less than 6 g per day by reducing intake or substitution with low-sodium salt alternative

iv. Weight reduction in people who are overweight (body mass index [BMI] over   25 kg/m2)

v. Restricting coffee consumption (and other caffeine-rich drinks) to fewer than five cups per day

vi. Relaxation therapies (e.g. stress management, meditation, cognitive therapies, muscle relaxation, biofeedback) – can reduce the blood pressure, and individuals might wish to pursue these as part of their treatment (though routine provision by primary care teams is neither widely available nor currently recommended).

Weight reduction
Up to 30% of all coronary heart disease deaths have been attributed to unhealthy diets. In 1980, 8% of women were obese and 6% of men. By 1998, however, the prevalence had almost trebled to 21% of women and 17% of men. The four most common problems linked to obesity are heart disease, type 2 diabetes, hypertension and osteoarthritis (National Audit Office, 2001). Healthy, low-calorie diets had a modest effect on blood pressure in over weight individuals with raised blood pressure, reducing systolic and diastolic blood pressure on average by about 5–6 mmHg in trials. However, there is variation in the reduction in blood pressure achieved in trials and it is unclear why. About 40% of patients were estimated to achieve a reduction in systolic blood pressure of 10 mmHg systolic or more in the short term, up to 1 year (NICE, 2006).

Reducing alcohol consumption
Excessive alcohol consumption (men >21 units/week; women >14 units/ week) is associated with raised blood pressure and poorer cardiovascular and hepatic outcomes. Structured interventions to reduce alcohol consumption can reduce on average SBP and DBP by 3–4 mmHg in clinical trials.

Smoking cessation
There is no strong link between smoking and blood pressure. But the evidence of the link between smoking and cardiovascular and pulmonary diseases is overwhelming. In addition there is evidence that smoking cessation strategies are cost-effective (NICE, 2006).

4     What are the main classes of drug used to treat hypertension?
Thaizide  diuretics,  calcium  channel  blockers,  angiotensin-converting  enzyme (ACE) inhibitors, beta-blockers and angiotensin II receptor blockers.

5     Which class of drug would be appropriate first-line treatment for Mr HA? How would this treatment choice be affected if the patient had been of Afro Caribbean origin?

Angiotensin-converting  enzyme  inhibitors  (ACE  inhibitors)  would  be  the appropriate  initial  choice  in  this  patient.  If  the  patient  had  been  of  Afro Caribbean origin then a thiazide diuretic or calcium channel blocker would be an appropriate choice.

6        For one of the classes of drugs mentioned in question 4 indicate the following:

i. a drug from that class

ii. a suitable starting dose and frequency

iii. the maximum dose for hypertension

iv. three contraindications

v. three common side-effects.

Suitable starting doses,  frequencies and maximum doses  for some appropriate drugs are listed in Table A2.2.

Table  A2.2 Suitable  starting  doses,  frequencies  and  maximum  doses  for  some appropriate drugs for Mr HA (hypertension)[end_columns]

DrugDoseFrequencyMaximum dose
Ramipril1.25 mgOnce daily, increased at
intervals of 1–2 weeks
10 mg once daily
Lisinopril10 mgDaily40 mg daily
Enalapril5 mgOnce daily40 mg once daily
Perindopril4 mgDaily8 mg daily

 

[column]Three  contraindications  are:  (a)  patients with  a hypersensitivity  to ACE inhibitors (including angioedema), (b) patients with known or suspected reno vascular disease, and (c) pregnancy.

Three  common  side-effects  are:  (a) first-dose hypotension, (b) persistent dry  cough  and  (c)  hyperkalaemia. Other  side-effects  include:  gastrointestinal effects  (nausea,  vomiting,  dyspepsia,  diarrhoea,  altered  liver  function  tests, blood disorders, angioedema, rash, loss of sense of smell (more likely if also on potassium-sparing agents or potassium supplements).

7       In view of Mr HA’s age he requires cardiovascular risk assessment. How would you assess this patient’s cardiovascular risks?

According to the Joint British Societies Guidelines on prevention of cardiovascular disease (CVD) in clinical practice (British Cardiac Society et al., 2005) the following patients should be assessed:[/column]

i. Adults >40 years with no history of CVD or diabetes who are not already on treatment for blood pressure or lipids should be opportunistically reviewed.

ii. Patients <40 years with a family history of premature atherosclerotic disease should also have their cardiovascular risk assessed.

Cardiovascular risk over 10 years >20% is high risk and patients should be targeted for advice to reduce this risk (i.e. blood pressure reduction, aspirin, dietary modification and drug treatment for modification of lipids, stop smoking, etc.).
In order to calculate cardiovascular risk for a primary prevention patient such as Mr HA, use a validted risk calculator. These are JBS CVD Risk Predictor Charts  (Heart,  2005,  91:  1–52);  BNF  Extra  (contains  JBS CVD  risk  prediction programme.  Available  at  http://www.bnf.org/bnf/extra/current/450024.htm); QRISK (Available at http://www.qrisk.org/).[end_columns]

General references

  1. Joint Formulary Committee (2008) British National Formulary 55. London: British            Medical Association and Royal Pharmaceutical Society of Great Britain, March.
  2. National Prescribing Centre (NPC) (2002) MeReC Briefing – Lifestyle measures to reduce cardiovascular  risk.  Available  at  http://www.npc.co.uk/MeReC_Briefings/2002/  briefing_no_19.pdf [Accessed 3 July 2008].

Author: Narinder Bhalla; BSc (Hons), MSc, MRPharmS. Pharmacist,Cambridge University Hospital.

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