Cardiovascular Emergencies

Chapter 19 Cardiovascular Emergencies

Belinda B. Hammond

Chest pain is the chief complaint of many patients presenting to the emergency department (ED). If the chest pain is a result of cardiac problems, time to treatment is important, and management may be initiated before a complete medical history and full diagnostic workup have been completed. Because of the life-threatening nature of these emergencies, assessing airway, breathing, and circulation (ABC) is always given priority.

This chapter assumes that the reader possesses a basic knowledge of risk factors for cardiac disease, basic life support and cardiopulmonary resuscitation (BLS/CPR), and dysrhythmia detection.

Assessment of Chest Pain

• The PQRST mnemonic (Table 19-1) is useful in assessing the characteristics of chest pain and may be used to gather comprehensive information about the nature of the pain.

• Patients often deny “pain” but complain of burning, pressure, or tightness. Describe the patient’s pain or discomfort using his or her own words in the documentation.

• Assess for “anginal equivalents,” particularly in women, diabetics, and the elderly.

• Patients with anginal equivalents may report shortness of breath, fatigue, palpitations, near-syncope, and nausea and vomiting.

• These symptoms may be more bothersome to the patient than any chest discomfort.¹

• Discomfort is more likely to be localized outside the chest area.

• If angina is present, it is often precipitated by mental stress rather than physical exertion.

• Have the patient rate the pain or discomfort on a scale of 1 to 10.

• Obtain a 12-lead electrocardiogram (ECG) within 10 minutes of patient arrival; assess for dysrhythmias and ST segment elevation or depression.

• There are many possible etiologies for chest pain (Table 19-2); therefore it is important to rule out the most serious or life-threatening causes immediately.

• Document current medications, including prescriptions, over-the-counter medications, and herbal therapies.

• Determine compliance with prescribed medications.

• Specifically question the patient about recent use of phosphodiesterase inhibitors for erectile dysfunction.

• Recent cocaine use is a common cause of ischemic chest pain resulting from coronary vasospasm. It is important to ask the patient about recreational drug use.

• Document positive and negative risk factors for cardiovascular disease, including those for previous cardiac disease such as prior myocardial infarction (MI), coronary interventions such as stent placement, and presence of a pacemaker or implantable cardioverter defibrillator (ICD).

TABLE 19-1 THE PQRST MNEMONIC

P	What things provoke or precipitate or palliate or alleviate the pain or discomfort?
Q	What is the quality of the pain or discomfort? Document this characteristic in the patient’s own words.
R	Does the pain or discomfort radiate? If so, to what locations? What is the location or region of the pain or discomfort?
S	Rate the severity of the pain or discomfort. Are there associated symptoms?
T	What are the time elements of the pain or discomfort? When did it start? How long did it last? Did the pain or discomfort begin suddenly or gradually?

TABLE 19-2 LIFE-THREATENING AND NON–LIFE-THREATENING CAUSES OF CHEST PAIN

LIFE-THREATENING	NON–LIFE-THREATENING
Acute coronary syndrome	Pericarditis
Pulmonary embolism	Esophageal reflex (GERD)
Aortic dissection	Pneumonia
Tension pneumothorax	Spontaneous pneumothorax
Acute myocardial infarction	Costochondritis
	Pancreatitis
	Herpes zoster infection
	Cocaine use

GERD, Gastroesophageal reflux disease.

Cocaine stimulates both alpha- and beta-adrenergic receptors. Use of beta-blockers in the patient who has recently used cocaine leaves alpha activity unopposed, resulting in additional coronary vasoconstriction and systemic hypertension.¹

Diagnostic Procedures

• 12-lead ECG

• Records the heart’s electrical activity from twelve different views

• Determines rate, rhythm, and presence of dysrhythmias

• Examines contiguous leads for ST segment depression or ST segment elevation

• Continuous bedside ST monitoring

• Serum electrolytes, complete blood count, clotting times, and cardiac biomarkers

• Chest radiograph

• Cardiac catheterization with angiography

• Echocardiogram to determine left ventricular (LV) ejection fraction (EF); presence of hypertrophy, dyskinetic, or akinetic areas; structural abnormalities such as LV aneurysm or valvular dysfunction; and pericardial effusion

• Doppler studies of peripheral blood flow

• Stress testing

Contiguous leads are those leads that “look at” the same area of the heart.

Anterior left ventricle (LV)	Leads V1–V4
Ventricular septum	Leads V1 and V2
Inferior surface of LV	Leads II, III, aVF
Lateral LV wall	Leads I, aVL, V5, V6
Posterior LV	Leads V1 and V2

Specific Cardiac Emergencies

Acute Coronary Syndrome

Acute coronary syndrome (ACS) refers to the clinical presentations of acute myocardial ischemia. This continuum includes unstable angina, non–ST segment elevation myocardial infarction (non-STEMI), and ST segment elevation myocardial infarction (STEMI). These presentations represent varying degrees of myocardial oxygen supply and demand imbalance and refer to different stages of myocardial ischemia. Table 19-3 summarizes the characteristics of these three problems.

• Unstable angina—a change in the patient’s usual pattern of angina

• Ischemic chest pain becomes unpredictable, more intense, and more difficult to relieve. Unstable angina may occur at rest, even awakening the patient from sleep. It occurs more frequently and is longer in duration than the patient’s usual angina.

• Indicates an unstable atherosclerotic plaque with the potential for rupture.

• Transient (ST segment depression or T wave inversion) or negative ECG changes; negative cardiac biomarker results.

• Ischemic chest pain or anginal equivalent associated with ST segment depression and positive cardiac biomarkers.

• Indicates rupture of unstable atherosclerotic plaque and intermittent coronary occlusion.²

• Associated with complete occlusion of a coronary artery by a thrombus superimposed on a ruptured plaque.

• ECG shows 1-mm (or more) ST segment elevation in two or more contiguous leads or new (or presumed new) left bundle branch block (LBBB) pattern.

• Cardiac biomarkers will be positive.

TABLE 19-3 DIAGNOSTIC DIFFERENCES BETWEEN TYPES OF ACUTE CORONARY SYNDROME

	12-LEAD ECG FINDINGS	CREATINE KINASE TROPONIN TEST
Unstable angina	Normal or nondiagnostic changes such as ST depression and T wave inversion	Negative
Non-STEMI	ST depression or T wave changes	Positive
STEMI	ST elevation >1 mm in two contiguous leads New or presumably new LBBB	Positive

ECG, Electrocardiogram; LBBB, left bundle branch block; STEMI, ST segment elevation myocardial infarction.

Signs and Symptoms

• Chest pain or discomfort unrelieved by rest.

• Pain or discomfort may be described as burning, crushing, tightness, pressure, or aching.

• Patient may deny chest pain and complain of a toothache, pain in the jaw or elbow, or indigestion-like discomfort.

• Discomfort is often substernal.

• Radiation of pain to arm, neck, jaw, back, or shoulder is not uncommon.

• Associated with nausea, vomiting, shortness of breath, diaphoresis, weakness, dizziness, syncope, and palpitations.

• Patient may experience a sense of impending doom.

• Sign of LV failure (crackles, S₃ heart sound, respiratory distress) if infarct involves a large portion of the anterior left ventricle.

• Tachycardia may be the result of sympathetic stimulation; bradycardia or varying degrees of atrioventricular (AV) block often seen with inferior MI.

Diagnostic Procedures

• 12-lead ECG.

• Non-STEMI: ST depression.

• STEMI: 1-mm or more ST segment elevation in two or more contiguous leads. See Table 19-4 for localization of MI and potential complications associated with MI location.

• LBBB on the 12-lead ECG distorts the ST segment. In the presence of new or presumed new LBBB and ischemic chest discomfort, manage the patient as though STEMI is present.

• If initial ECG is nondiagnostic, repeat the 12-lead ECG in 1 hour; if the patient remains symptomatic or experiences new symptoms, obtain repeat ECGs at 5- to 10-minute intervals or initiate continuous ST segment monitoring.

• If inferior wall MI is present, obtain right-sided V-leads to detect possible right ventricular infarct (Fig. 19-1A).

• Patients experiencing right ventricular (RV) infarction are “preload dependent.”

• Administer nitroglycerin with caution because of potential for worsened hypotension.

• May require volume administration.

• The classic triad of RV failure because of RV infarct.

• Severe systemic hypotension.

• Absence of pulmonary congestion.

• Increased central venous pressure (CVP) and jugular venous distension.

• If inferior MI is associated with ST depression in V2 and R wave larger than S wave in leads V1 and V2, obtain posterior ECG to detect possible posterior wall MI (Fig. 19-1B).

• Cardiac biomarkers.

• Troponin I elevates 3 to 12 hours after infarct; level peaks between 10 and 24 hours.

• Creatine kinase-MB elevates 4 to 12 hours after infarct; level peaks between 10 and 24 hours.

• Chest radiograph to detect pulmonary congestion or cardiac enlargement.

• Complete blood count, blood chemistries, and coagulation studies.

TABLE 19-4 DIFFERENCES BETWEEN TYPES OF MYOCARDIAL INFARCTION

Fig. 19-1 A, Right precordial leads. B, Posterior chest leads.

(From Moser, D., & Reigel, B. [2008]. Cardiac nursing: A companion to Braunwald’s heart disease. Philadelphia, PA: W.B. Saunders.)

Creatine kinase-MB (CK-MB) levels return to normal within approximately 72 hours; on the other hand, troponin values remain elevated up to 9 days. This is significant in the patient who “infarcts at home” and comes to the ED several days after experiencing chest pain or angina equivalents; the troponin remains elevated but the CK-MB has returned to normal.

Therapeutic Interventions

• Administer supplemental oxygen to maintain oxygen saturation above 92%.

• Maintain intravenous (IV) access.

• Give non–enteric coated aspirin, 162 to 325 mg; have patient chew and swallow aspirin if possible. Administer aspirin as rectal suppository if necessary.

• Administer nitroglycerin sublingual tablet or spray if systolic blood pressure greater than 90 mm Hg and heart rate greater than 50 beats per minute. If the patient experiences no relief from pain, the emergency nurse may repeat nitroglycerin every 5 minutes up to three doses.

• The American Heart Association does not recommend the routine use of IV nitroglycerin in patients with STEMI.² If it is used, monitor the patient closely for drug-induced hypotension that can decrease coronary perfusion and worsen myocardial ischemia.

• If the patient has used a phosphodiesterase inhibitor within the past 24 hours, nitroglycerin administration may result in severe hypotension refractory to vasopressors.

• Nitroglycerin must be administered with caution in patients with inferior wall MI and possible RV involvement. These patients are often highly dependent on RV filling pressures; venodilation and decreased preload can precipitate a dramatic and irreversible decrease in cardiac output.

• Use of morphine is indicated for STEMI when chest discomfort is unresponsive to nitrates. It should be used with caution in unstable angina and non-STEMI because of an association with increased mortality.

• Medications to limit platelet aggregation are important treatment modalities.

• Aspirin (see above)

• Clopidogrel (Plavix) or prasugrel (Effient)

• In STEMI, early reperfusion of the myocardium, by pharmacologic or mechanical means, has been shown to reduce mortality.

• Opening the infarct-related artery restores myocardial perfusion and therefore limits infarct size and reduces complications (including death) associated with acute MI.

• The goal for “total ischemic time” (from time of symptom onset to intervention) is under 90 minutes.

• Percutaneous coronary intervention (PCI) is the preferred method of reperfusion.³

• Bivalirudin (Angiomax), a direct thrombin inhibitor, can be used for anticoagulation in patients undergoing primary PCI.³

• Glycoprotein IIb/IIIa inhibitors are antiplatelet agents that may be considered at the time of PCI.³

• Abciximab (ReoPro)

• Eptifibatide (Integrilin)

• Tirofiban (Aggrastat)

• If the patient is unable to undergo primary PCI within 90 to 120 minutes of first medical contact, immediate fibrinolytic therapy should be administered.

• Patients who receive fibrinolytics as primary reperfusion therapy should be transferred as soon as possible to a PCI-capable facility.³

• Prehospital administration of half-dose fibrinolytics, followed by urgent PCI, is being implemented in some areas of the country.

• Medical management.

• Beta-blockers—oral beta-blockers are recommended for all types of ACS unless contraindicated by signs of heart failure or low output states.

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Tags: Sheehys Manual of Emergency Care

Aug 9, 2016 | Posted by admin in EMERGENCY MEDICINE | Comments Off

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