Cardiology Emergenncy Medicine

CardiologyEmergencyMedicine

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AlejandroGarcíaRoblesOrtiz


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Myocardial infarction (MI) is the rapid development of myocardial necrosis caused by a critical imbalance between oxygen supply and demand of the myocardium. This usually results from plaque rupture with thrombus formation in a coronary vessel, resulting in an acute reduction of blood supply to a portion of the myocardium.

Although the clinical presentation of a patient is a key component in the overall evaluation of the patient with MI, many events are either "silent" or are clinically unrecognized, evidencing that patients, families, and health care providers often do not recognize symptoms of a MI. The appearance of cardiac markers in the circulation generally indicates myocardial necrosis and is a useful adjunct to diagnosis.

Cardiac markers help to categorize MI, which is considered part of a spectrum referred to as acute coronary syndrome that includes ST-elevation MI (STEMI), non–ST-elevation MI (NSTEMI), and unstable angina.


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This categorization is valuable because patients with ischemic discomfort may or may not have ST-segment elevations on their electrocardiogram. Those without ST elevations may ultimately be diagnosed with NSTEMI or with

unstable angina based on the presence or absence of cardiac enzymes. Additionally, therapeutic decisions, such as administering an intravenous thrombolytic or performing percutaneous coronary intervention (PCI), are often made based on this categorization.


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Pathophysiology

The most common cause of MI is narrowing of the epicardial blood vessels due to atheromatous plaques. Plaque rupture with subsequent exposure of the basement membrane results in platelet aggregation, thrombus formation, fibrin accumulation, hemorrhage into the plaque, and varying degrees of vasospasm. This can result in partial or complete occlusion of the vessel and subsequent myocardial ischemia. Total occlusion of the vessel for more than 4-6 hours results in irreversible myocardial necrosis, but reperfusion within this period can salvage the myocardium and reduce morbidity and mortality.

Nonatherosclerotic causes of MI include coronary vasospasm as seen in variant (Prinzmetal) angina and

in patients using cocaine and amphetamines; coronary emboli from sources such as an infected heart valve; occlusion of the coronaries due to vasculitis; or other causes leading to mismatch of


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oxygen supply and demand, such as acute anemia from GI bleeding. MI induced by chest trauma has also been reported,

usually following severe chest trauma such as motor vehicle accidents and sports injuries. For additional information, see Medscape's article"


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Frequency

United States

MI is a leading cause of morbidity and mortality in the United States. Approximately 1.3 million cases of nonfatal MI are reported each year, for an annual incidence rate of approximately 600 cases per 100,000

people. The proportion of patients diagnosed with NSTEMI compared with STEMI has progressively increased.

International

Cardiovascular diseases account for 12 million deaths annually worldwide. MI continues to be a significant problem in industrialized countries and is becoming an increasingly significant problem in developing countries.


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Mortality/Morbidity

Approximately 500,000-700,000 deaths are caused by ischemic heart disease annually in the United States.

One third of patients who experience STEMI die within 24 hours of the onset of ischemia, and many of the survivors experience significant morbidity. For many patients, the first manifestation of coronary artery disease is sudden death likely from malignant ventricular dysrhythmia.

• More than one half of deaths occur in the prehospital setting.

• In-hospital fatalities account for 10% of all deaths. An additional 10% of deaths occur in the first year postinfarction.


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• A steady decline has occurred in the mortality rate from STEMI over the last several decades. This appears to be due to a combination of a fall in the incidence of MI (replaced in part by an increase in the incidence of unstable angina) and a reduction in the case-fatality rate once an MI has occurred.

Emergency Medical Services Around the World are trained roughly everyday in order to save people’s lives.


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Sex

A male predilection exists in persons aged 40-70 years. Evidence exists that women more often have MIs without atypical symptoms. The atypical


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presentation in women might explain the sometimes delayed diagnosis of MIs in women. In persons older than 70 years, no sex predilection exists.

Age

MI most frequently occurs in persons older than 45 years.

Certain subpopulations younger than 45 years are at risk, particularly cocaine users, persons with type 1 diabetes mellitus, patients with hypercholesterolemia, and those with a positive family history for early coronary disease. A positive family history includes any first-degree male relative aged 45 years or younger or any first-degree female relative aged 55 years or younger who experienced a myocardial infarction. In younger patients, the diagnosis may be hampered if a high index of suspicion is not maintained.


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Clinical

History

The history is critical in making the diagnosis of MI and sometimes may provide the only clues that lead to the diagnosis in the initial phases of the patient presentation.

• Chest pain, usually across the anterior precordium is typically described as tightness, pressure, or squeezing.

• Pain may radiate to the jaw, neck, arms, back, and epigastrium. The left arm is more frequently affected; however, a patient may experience pain in both arms.

• Dyspnea, which may accompany chest pain or occur as an isolated complaint, indicates poor ventricular compliance in the setting of acute ischemia. Dyspnea may be the patient's anginal equivalent, and, in an elderly person or a patient with diabetes, it may be the only complaint.

•


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• Nausea, abdominal pain, or both often are present in infarcts involving the inferior or posterior wall.

• Anxiety • Lightheadedness with or without syncope • Cough • Nausea with or without vomiting • Diaphoresis • Wheezing • Elderly patients and those with diabetes may

have particularly subtle presentations and


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may complain of fatigue, syncope, or weakness. The elderly may also present with only altered mental status. Those with preexisting altered mental status or dementia may have no recollection of recent symptoms and may have no complaints whatsoever.

• As many as half of MIs are clinically silent in that they do not cause the classic symptoms described above and consequently go unrecognized by the patient. A high index of suspicion should be maintained for MI especially when evaluating women, patients with diabetes, older patients, patients with dementia, and those with a history of heart failure. Patients with a permanent pacemaker in place may confound recognition of STEMI by 12-lead ECG due to the presence of paced ventricular contractions.


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Physical

The physical examination can often be unremarkable.

• Patients with ongoing symptoms usually lie quietly in bed and appear pale and diaphoretic.

• Hypertension may precipitate MI, or it may reflect elevated catecholamine levels due to anxiety, pain, or exogenous sympathomimetics.

• Hypotension may indicate ventricular dysfunction due to ischemia. Hypotension in the setting of MI usually indicates a large infarct secondary to either decreased global cardiac contractility or a right ventricular infarct.

• Acute valvular dysfunction may be present. Valvular dysfunction usually results from infarction that involves the papillary muscle. Mitral regurgitation due to papillary muscle ischemia or necrosis may be present.

• Rales may represent congestive heart failure.


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• Neck vein distention may represent pump failure. With right ventricular failure, cannon jugular venous a waves may be noted.

• Third heart sound (S3) may be present.

• A fourth heart sound is a common finding in patients with poor ventricular compliance that is due to preexisting heart disease or hypertension.

• Dysrhythmias may present as an irregular heartbeat or pulse.

• Low-grade fever is not uncommon.


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Causes

The most frequent cause of MI is rupture of an atherosclerotic plaque within a coronary artery with subsequent arterial spasm and thrombus formation.

Other causes include the following:

• Coronary artery vasospasm • Ventricular hypertrophy (eg, left ventricular

hypertrophy [LVH], idiopathic hypertrophic subaortic stenosis [IHSS], underlying valve disease)

• Hypoxia due to carbon monoxide poisoning or acute pulmonary disorders (Infarcts due to pulmonary disease usually occur when demand on the myocardium dramatically increases relative to the available blood supply.)

• Coronary artery emboli, secondary to cholesterol, air, or the products of sepsis

• Cocaine, amphetamines, and ephedrine • Arteritis


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• Coronary anomalies, including aneurysms of the coronary arteries

• Increased afterload or inotropic effects, which increase the demand on the myocardium

• Aortic dissection, with retrograde involvement of the coronary arteries

• Although rare, pediatric coronary artery disease may be seen with Marfan syndrome, Kawasaki disease, Takayasu arteritis, progeria, and cystic medial necrosis (see Myocardial Infarction in Childhood).

Risk factors for atherosclerotic plaque formation include the following:

• Age • Male gender • Smoking


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• Hypercholesterolemia and hypertriglyceridemia, including inherited lipoprotein disorders

• Diabetes mellitus • Poorly controlled hypertension • Type A personality • Family history • Sedentary lifestyle


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CardiogenicShock


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Cardiogenic shock occurs when there is failure of the pump action of the heart resulting in reduced cardiac output. This leads to acute hypoperfusion and hypoxia of the tissues and organs, despite the presence of an adequate intravascular volume. Cardiogenic shock can be defined as the presence of the following (despite adequate left ventricular filling pressure):

• Sustained hypotension (systolic blood pressure < 90 mmHg for more than 30 minutes)

• Tissue hypoperfusion (cold peripheries, or oliguria < 30 ml/hour, or both)

Cardiogenic shock most commonly occurs as a complication of acute myocardial infarction. It occurs in 7% of patients with ST segment elevation myocardial infarction and 3% with non-ST segment elevation myocardial infarction. It is a medical emergency requiring immediate resuscitation.


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Causes

Due to an intrinsic heart problem

• Myocardial infarction (MI) • Myocardial contusion (often from steering

wheel impact) • Acute dysrhythmia compromising cardiac

output • Acute mitral regurgitation (usually as a

complication of MI due to ruptured chordae tendinae)


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• Ventricular septal rupture (usually occurring as post-MI complication)

• Cardiac rupture (rupture of the wall of the left ventricle can occur post-MI or due to cardiac trauma)

• Hypertrophic obstructive cardiomyopathy or end-stage cardiomyopathy of other cause

• Myocarditis • Post-cardiac surgery requiring prolonged

cardioplegia/cardiopulmonary bypass • Severe valvular heart disease, particularly

aortic stenosis

Due to other causes

• Acute, severe pulmonary embolism (PE) • Pericardial tamponade/severe constrictive

pericarditis • Tension pneumothorax • Myocardial suppression due to

bacteraemia/sepsis (although, strictly speaking, this may be defined as septic shock)


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• Suppression of myocardial contractility by drugs, e.g. beta-blockers

• Suppression of myocardial contractility due to metabolic disturbance, e.g. acidosis, hypo or hyperkalaemia, hypocalcaemia

• Thyrotoxic crisis

Risk factors

• It is more likely to develop in the elderly and diabetics.

• Anterior and right-ventricular myocardial infarction are associated with an increased risk.

• History of previous infarction, peripheral vascular disease, cerebrovascular disease and multi-vessel atheroma increase the


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likelihood of the development of cardiogenic shock.

Presentation

Shock is due to an inability to adequately perfuse vital organs and tissues. The skin, brain, heart and kidneys are usually most severely affected by this. The symptoms and signs can present abruptly or develop insidiously over the course of many hours.

Symptoms

As many patients with cardiogenic shock have had an acute myocardial infarction, symptoms can include:

• Chest pain • Nausea and

vomiting


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• Dyspnoea • Profuse sweating • Confusion/disorientation • Palpitations

• Faintness/syncope

Signs

• Pale, mottled, cold skin with slow capillary refill and poor peripheral pulses

• Hypotension • Tachycardia/bradycardia • Raised JVP/distension of neck veins • Peripheral oedema • Quiet heart sounds or presence of third and

fourth heart sounds • Heaves, thrills or murmurs may be present

and may indicate the cause such as valve dysfunction

• Bibasal pulmonary crackles or wheeze may occur

• Oliguria (catheterisation is a useful early monitoring intervention)


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• Altered mental state

Assessment and initial management • Potentially correctable underlying causes

such as tension pneumothorax, massive PE, occult haemorrhage or hypovolaemia, sepsis, pericardial tamponade, anaphylaxis or

• respiratory failure should be kept in mind.

• First-line investigations can help to determine the underlying cause of cardiogenic shock.

• The aim of management is to make the diagnosis, prevent further ischaemia, and treat the underlying cause.

• Assess Airway, Breathing and Circulation. o Initiate oxygen/ventilatory support:

intubation and mechanical ventilation may be needed.

o Insertion of a Swan-Ganz catheter: allows monitoring of central venous


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pressure (CVP) and pulmonary capillary wedge pressure. This can guide the need for fluid resuscitation. Haemodynamic monitoring using a Swan-Ganz catheter can help to differentiate cardiogenic shock from other causes of shock such as hypovolaemia. (Arterial line, simple central venous line for CVP monitoring and a PiCCO line are alternatives to a Swan-Ganz catheter.)


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• Opiate analgesia such as diamorphine 2.5–5mg can be given if sufficient respiratory effort/rate and if blood pressure can support it.

• Treat any electrolyte abnormalities. • Treat any arrhythmias. • Perform an ECG early: this can show acute

MI. ECG may be normal in other causes of cardiogenic shock.

• Chest X-ray: can show tension pneumothorax, widened mediastinum in aortic dissection, signs of LVF.

• Blood tests: o Urea, electrolytes and creatinine can

assess renal function o Liver function tests o Full blood count to exclude anaemia o Cardiac enzymes including troponins o Arterial blood gases o Brain natriuretic peptide (BNP): low BNP

levels may help to rule out cardiogenic shock in the setting of hypotension but a high BNP level isn't diagnostic of


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cardiogenic shock (e.g. there may be high BNP levels in pulmonary embolism, atrial fibrillation and sepsis); BNP levels may be more practical in monitoring progression in CCU/ICU

• Echocardiography: this can establish the cause of cardiogenic shock, e.g. acute ventricular septal defect, pericardial tamponade

Cardiogenic shock secondary to MI

Usual management of acute myocardial infarction

This should also take place including:

• Aspirin ± clopidogrel • Heparin


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• Glycoprotein IIb/IIIa inhibitors (for high-risk patients with non-ST-segment-elevation myocardial infarction).

• Glycaemic control • Nitrates may be a

useful treatment as they can effectively lower preload and afterload, provided the blood pressure can support them. Care must be taken as vasodilators and beta-blockers usually used in the treatment of MI may cause hypotension and worsen tissue perfusion.

Pharmacological inotropic support

• Vasopressor/inotropic support with dopamine, dobutamine, levosimendan or epinephrine may be needed.

• However, one study suggested that dopamine might be associated with increased mortality.


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• Another study suggested that levosimendan improves haemodynamic performance when compared to dobutamine and may lower mortality in patients with low-output heart failure.

Intra-aortic balloon pump counterpulsation

• Intra-aortic balloon pump counterpulsation (IABP) increases cardiac output and improves coronary artery blood flow.

• It can help to stabilise patients so that a diagnosis can be established and treatment initiated. It is not in itself definitive therapy.

• Its impact on long-term survival is controversial.


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Revascularisation

• Revascularisation with thrombolysis, percutaneous intervention or coronary artery bypass surgery should be considered.

• The SHOCK trial found that early revascularisation (angioplasty or coronary artery bypass graft) improves 1-year survival in patients under the age of 75 with acute myocardial infarction and cardiogenic shock when compared to medical treatments (including thrombolysis and intra-aortic balloon counterpulsation). This survival advantage seems to persist at 3 and 6 years.

• The American College of Cardiology and American Heart Association Guidelines suggest that patients who arrive at hospital in cardiogenic shock, or who develop it after arrival, are transferred to a centre where revascularisation can take place.

See Acute Myocardial Infarction Management for further details.


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Other management options

• Ventricular assist devices: these are essentially prosthetic ventricles that can support right and left ventricle performance. They may allow survival to cardiac transplantation. They are generally used when medical treatment and IABP fails and the cause of the cardiogenic shock is potentially reversible. A recent study has found them to be a safe and effective therapy.

• Non-invasive positive pressure ventilation (NIPPV) may be helpful in mild-moderate cases of cardiogenic shock (provided the blood pressure can support it).


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Prognosis

• Cardiogenic shock is the leading cause of death

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• • • •

• in acute myocardial infarction. • Mortality rates may be 70-90%, reduced to

40-60% if patients are treated aggressively. •


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• A recent study showed that among patients with cardiogenic shock who survive for 30 days after an ST-segment elevation myocardial infarction,

annual mortality rates of 2% to 4% are approximately the same as those of patients without shock. Percutaneous revascularisation was associated with a reduced risk of death.

Prevention

• Early coronary revascularisation in patients post-MI and adequate treatment of patients with structural heart disease may help to prevent cardiogenic shock.

• Better treatment of acute coronary syndrome seems to be reducing the rates of cardiogenic shock.

References


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MA Pfeffer, E Braunwald, LA Moye, L Basta, EJ … - New England Journal of Medicine, 1992 - content.nejm.org

FM Sacks, MA Pfeffer, LA Moye, JL Rouleau, JD … - New England Journal of Medicine, 1996 - content.nejm.org

SM Haffner, S Lehto, T Ronnemaa, K Pyorala, M … - New England Journal of Medicine, 1998 - content.nejm.org

MA Pfeffer, E Braunwald - Circulation, 1990 - Am Heart Assoc

B Assmus, V Schachinger, C Teupe, M Britten, R … - Circulation, 2002 - Am Heart Assoc

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