Ch 14

Question 1

The location of infarction is determined by correlating the ECG leads with Q waves and the ST segment and T wave abnormalities
The ECG manifestations that are used to diagnose MI and pinpoint the area of damaged ventricle include inverted T waves, ST segment elevation, and pathologic Q waves in specific lead groupings, as described subsequently.
Anterior wall infarction.
Left lateral wall infarction.
Inferior wall infarction.
Right ventricular infarction.
Posterior wall infarction.

Answer 1

Myocardial Infarction Location

Question 2

Anterior wall infarction results from occlusion of the proximal left anterior descending artery
ST segment elevation is expected in leads V1 through V4 on the 12-
lead ECG, If the left main coronary artery is occluded, the ECG manifestations will involve almost all precordial leads V1 through V6 and leads I and aVL may be associated with left ventricular pump failure, cardiogenic shock, or death.

Answer 2

Anterior wall infarction.

Question 3

as a result of occlusion of the circumflex coronary artery. On a 12-lead ECG, new Q waves and ST segment T wave changes are seen in leads I, aVL, V5, and V6

Answer 3

Left lateral wall infarction.

Question 4

occurs with occlusion of the right coronary artery. This infarction manifests by ECG changes in leads II, III, and aVF
Conduction disturbances are expected with an inferior wall MI and are related to the anatomy of the coronary arterial supply.
Heart block and other conduction disturbances should be anticipated.

Answer 4

Inferior wall infarction.

Question 5

when a blockage occurs in a proximal section of the right coronary artery. This places the entire right ventricle and inferior wall at risk.
Leads can also be placed on the right side of the chest to assist in the diagnosis of right ventricular infarction and posteriorly to show a posterior infarction. To detect a right ventricular infarction, specific ECG lead placement is used. Electrodes are placed over the right precordium (chest) in a mirror image of the conventional left-sided leads.
The right ventricle has a very thin wall, which means that ST segment elevation is detected only in the right ventricular leads during the acute phase of the infarction.

Answer 5

Right ventricular infarction.

Question 6

because of a blockage in the right coronary artery or in the circumflex artery.
A posterior wall MI is difficult to detect but may be identified by specific leads placed in the left scapular area or by very tall R waves in leads V1 and V2

Answer 6

Posterior wall infarction.

Question 7

These complications may result from electrical dysfunction or from a cardiac contractility problem.
Electrical dysfunctions include bradycardia, bundle branch blocks, and various degrees of heart block. Pumping complications can cause heart failure, pulmonary edema, and cardiogenic shock.
new murmur in a patient with an acute MI warrants special attention, as it may indicate rupture of the papillary muscle. The murmur can be indicative of severe damage and impending complications such as heart failure and pulmonary edema.
Sinus bradycardia.
Sinus tachycardia.
Atrial dysrhythmias.
Ventricular dysrhythmias.
Atrioventricular heart block during myocardial infarction.
Ventricular aneurysm after myocardial infarction.
Ventricular septal rupture after myocardial infarction.
Papillary muscle rupture after myocardial infarction.
Cardiac wall rupture after myocardial infarction.
Pericarditis after myocardial infarction.
Heart failure and acute myocardial infarction.

Answer 7

Focus on Complications of Acute Myocardial Infarction

Question 8

(heart rate less than 60 beats/min) occurs frequently in patients who sustain an acute MI. It is more prevalent with an inferior wall infarction in the first hour after STEMI.
treated with atropine (0.5 to 1.0 mg by intravenous push), repeated every 3 to 5 minutes to a maximum dose of 0.03 mg/kg (e.g., 2 mg for a person who weighs 70 kg) per advanced cardiac life support guidelines.

Answer 8

Sinus bradycardia.

Question 9

(heart rate greater than 100 beats/min) most often occurs with an anterior wall MI.
reducing the ejection fraction and the stroke volume. In an attempt to maintain cardiac output, the heart rate increases.
by treating the underlying cause, as it greatly increases myocardial oxygen consumption, leading to further ischemia.

Answer 9

Sinus tachycardia.

Question 10

Premature atrial contractions occur frequently in patients who sustain an acute MI. Atrial fibrillation is also common and may occur spontaneously or may be preceded by premature atrial contractions.
loss of organized atrial contraction decreases cardiac output by up to 20%.
loss of organized atrial contraction decreases cardiac output by up to 20%.

Answer 10

Atrial dysrhythmias.

Question 11

seen in almost all patients within the first few hours after MI. They are initially controlled through administration of oxygen to reduce myocardial hypoxia and by correcting acid base or electrolyte imbalances.
Ventricular fibrillation (VF) is a life-threatening dysrhythmia associated with high mortality in acute MI. Beta-blockers are prescribed after acute MI to decrease mortality from ventricular dysrhythmias.

Answer 11

Ventricular dysrhythmias.

Question 12

can occur in 6% to 14% of patients with STEMI, and these patients have increased mortality rates. In STEMI, AV block most often occurs after an inferior wall MI.
Most patients receive fibrinolysis or undergo PCI to open the occluded vessel. In most cases, transcutaneous pacing is the primary intervention; transvenous pacemakers are used less frequently.

Answer 12

Atrioventricular heart block during myocardial infarction.

Question 13

is a noncontractile, thinned left ventricular wall that results from an acute transmural infarction.
most often occurs in the setting of an acute left anterior descending artery occlusion with a wide area of infarcted myocardium.
Most effective prevention is early reperfusion of the myocardium, accomplished by opening the thrombosed coronary artery. The most common complications of a ventricular aneurysm are acute heart failure, systemic emboli, angina, and VT.
Treatment is directed toward management of these complications and surgical repair by left ventricular aneurysmectomy.

Answer 13

Ventricular aneurysm after myocardial infarction.

Question 14

Rupture of the ventricular septal wall after MI is a rare but potentially lethal complication of an acute anterior wall MI
is an abnormal communication between the right and left ventricle.
Most patients with septal rupture also have signs and symptoms of cardiogenic shock.
Ventricular septal rupture manifests as severe chest pain, syncope, hypotension, and sudden hemodynamic deterioration caused by shunting of blood from the high-pressure left ventricle into the low-pressure right ventricle through the new septal opening. A holosystolic murmur (often accompanied by a thrill) can be auscultated and is best heard along the left sternal border.
Rupture of the septum is a medical and surgical emergency.
Patient’s condition is stabilized with vasodilators and an intra-aortic balloon pump (IABP) to decrease afterload.

Answer 14

Ventricular septal rupture after myocardial infarction.

Question 15

can occur when the infarct involves the area around one of the papillary muscles that support the mitral valve.
Infarction of the papillary muscles results in ineffective mitral valve closure, and blood is forced back into the low-pressure left atrium during ventricular systole. The rupture may be partial or complete.
Complete rupture is catastrophic and precipitates severe acute mitral regurgitation, cardiogenic shock, and high risk of death.
Partial rupture also results in mitral regurgitation, but the condition can be stabilized with aggressive medical management using an IABP and vasodilators. Urgent surgical intervention is required to replace the mitral valve.

Answer 15

Papillary muscle rupture after myocardial infarction.

Question 16

has two peak times. The first occurs within the first 24 hours, and the second occurs between 3 and 5 days after infarction, when leukocyte scavenger cells are removing necrotic debris, thinning the myocardial wall.
onset is sudden and usually catastrophic.
Bleeding into the pericardial sac results in cardiac tamponade, cardiogenic shock, pulseless electrical activity, and death. Survival is rare.
The best prevention is early reperfusion of the myocardium.

Answer 16

Cardiac wall rupture after myocardial infarction.

Question 17

inflammation of the pericardial sac. It can occur during or after acute MI.
damaged epicardium becomes rough and inflamed and irritates the pericardium lying adjacent to it, precipitating pericarditis. Pain is the most common symptom of pericarditis, and a pericardial friction rub is the most common initial sign.
Pericarditis frequently produces a pericardial effusion.
Pericarditis is treated with nonsteroidal antiinflammatory drugs, aspirin, and rest.

Answer 17

Pericarditis after myocardial infarction.

Question 18

Many patients with acute STEMI also have acute heart failure on admission to the hospital.

Answer 18

Heart failure and acute myocardial infarction.

Question 19

Clinical guidelines address the issues of interventions to open the coronary artery, anticoagulation, prevention of dysrhythmias, intensive glucose control, and prevention of ventricular remodeling after STEMI. To facilitate rapid coronary artery revascularization in STEMI, local hospitals are encouraged to develop a coordinated patient transfer strategy between PCI-capable and non PCI-capable hospitals
Recanalization of Coronary Artery
Anticoagulation
Dysrhythmia Prevention
Prevention of Ventricular Remodeling

Answer 19

Medical Management

Question 20

The essential immediate interventions for a patient with an acute STEMI are fibrinolytic therapy or PCI to open the occluded artery.
patients with symptoms of ACS to be rapidly triaged and treated.

Answer 20

Recanalization of Coronary Artery

Question 21

The acute phase after STEMI, heparin is administered in combination with fibrinolytic therapy to recanalize (open) the coronary artery.
an initial heparin bolus of 60 units/kg (maximum 5000 units) is given intravenously, followed by a continuous heparin drip at 12 units/kg per hour (maximum 1000 units/h) to maintain an activated partial thromboplastin time (aPTT) between 50 and 70 seconds (1.5 to 2.0 times control) for 48 hours or until revascularization.
intravenous unfractionated heparin (UFH) or subcutaneous low molecular-weight heparin (LMWH) if the patient is at risk for thrombus development.
patients with known heparin-induced thrombocytopenia, as an alternative to LMWH or UFH, a third class of antithrombotic medications is available: direct antithrombotic agents at risk for thrombotic emboli include patients with an anterior wall infarction, atrial fibrillation, previous embolus, cardiomyopathy, or cardiogenic shock.

Answer 21

Anticoagulation

Question 22

Antidysrhythmic with the best safety record after STEMI is amiodarone. Beta-blockers are another class of antidysrhythmics that are recommended for all patients after STEMI. Beta-blockers prevent ventricular dysrhythmias, lower BP, and prevent reinfarction, especially in patients with left ventricular dysfunction.

Answer 22

Dysrhythmia Prevention

Question 23

Vasodilating medications (angiotensin-converting enzyme inhibitors [ACEIs] or angiotensin II receptor blockers [ARBs]) can stop or limit the ventricular remodeling that leads to heart failure.
Ventricular remodeling refers to progressive changes in the size, architecture, and shape of the myocardium and occurs because of an injury such as MI.
The heart chamber walls ultimately become dilated, thinned, and poorly contractile. An ACEI or, if it is not tolerated, an ARB is indicated for all patients after STEMI.

Answer 23

Prevention of Ventricular Remodeling

Question 24

Nursing interventions focus on achieving a balance between myocardial oxygen supply and demand, preventing complications, and providing patient and family education.
Balance of Myocardial Oxygen Supply and Demand
Prevention of Complications
Depression After Myocardial Infarction
Educate the Patient and Family

Answer 24

Nursing Management

Question 25

In the acute period, if severe heart muscle damage has occurred, myocardial oxygen supply is increased by the administration of supplemental oxygen to prevent tissue hypoxia.
Cardiac medications play an increasingly important role in balancing supply and demand, and the critical care nurse administers and monitors the effectiveness of these agents.
Low cardiac output, positive inotropic medications such as dobutamine, dopamine, or both may be administered. Milrinone, a phosphodiesterase inhibitor that increases contractility by improving sarcolemma calcium uptake and causes positive inotropic effects in the myocardium may be prescribed.
In contrast to dobutamine and dopamine, milrinone does not compete for receptor sites in patients taking beta-blockers.
Myocardial oxygen supply can be further enhanced by the use of coronary artery vasodilators. Nitroglycerin is often administered for the first 48 hours to increase vasodilation and prevent myocardial ischemia.
However, if the patient is in cardiogenic shock, beta-blockers are withheld until the cardiac output has improved. Other interventions to decrease cardiac work and myocardial oxygen consumption include bed rest with bedside commode privileges when the patient is clinically stable.

Answer 25

Balance of Myocardial Oxygen Supply and Demand

Question 26

Cardiac monitoring for early detection of ventricular dysrhythmias is ongoing.
Assessment for signs of continued ischemic pain is important, because angina is a warning sign of the myocardium being at risk.
Heart failure is a serious complication after STEMI. When the patient’s BP is stable, treatment with ACEIs is initiated.
These vasodilators are used to prevent left ventricular remodeling and dilation that occurs in many patients after acute MI.
Preventing hospital-acquired pneumonia and deep vein thrombosis (DVT) is facilitated by early mobilization and raising the head of the bed 30 degrees or more.
Stool softeners may be given to the patient to lessen the risk of constipation from analgesics and bed rest and to decrease the risk of straining. Providing a calming and quiet environment that focuses on the well-being of the patient assists in the recovery phase.

Answer 26

Prevention of Complications

Question 27

Depression is a condition that occurs across a wide spectrum of human experiences. Depression is a risk factor for development of CAD and impedes recovery after acute MI. Key symptoms of depression mentioned frequently by cardiac patients are fatigue, change in appetite, and sleep disturbance.

Answer 27

Depression After Myocardial Infarction

Question 28

Education focuses on the following key elements: (1) risk factor reduction, (2) manifestations of angina, (3) when to call a physician or emergency services, (4) medications, and (5) resumption of physical and sexual activities referral be made to a cardiac rehabilitation program to reinforce education that was initiated during hospitalization.

Answer 28

Educate the Patient and Family

Question 29

Patients are assigned into four groups, I through IV, according to the severity of symptoms and degree of patient activity eliciting symptoms
Heart failure can manifest in many different ways, depending on how far ventricular remodeling and dysfunction have advanced. Heart failure may be discovered because of a known clinical syndrome such as acute MI or because of decreased exercise tolerance, fluid retention, or admission to the critical care unit for an unrelated condition. For patients with fluid retention, the most reliable clinical sign of fluid volume overload is jugular venous distention.
The first step in the diagnosis is to determine the underlying structural abnormality creating the ventricular dysfunction and symptoms.
Various imaging tests are available to visualize cardiac anatomy, and laboratory tests

Answer 29

Assessment and Diagnosis - Heart Failure

Question 30

defined as a disturbance of the contractile function of the left ventricle, resulting in a low cardiac output state. This leads to vasoconstriction of the arterial bed that increases systemic vascular resistance (SVR),
creates congestion and edema in the pulmonary circulation and alveoli. Patients presenting with left ventricular failure have one of the following: (1) decreased exercise tolerance, (2) fluid retention, or (3) discovery made during examination of noncardiac problems. Clinical manifestations of left ventricular failure include decreased peripheral perfusion with weak or diminished pulses; cool, pale extremities; and, in later stages, peripheral cyanosis fluid accumulation behind the dysfunctional left ventricle elevated pulmonary pressures, contributes to pulmonary congestion and edema, and produces dysfunction of the right ventricle, resulting in failure of the right side of the heart.

Answer 30

Left Ventricular Failure - Heart Failure

Question 31

Pure failure of the right ventricle may result from an acute condition such as a pulmonary embolus or a right ventricular infarction, but it is most commonly caused by failure of the left side of the heart.
Pure failure of the right ventricle may result from an acute condition such as a pulmonary embolus or a right ventricular infarction, but it is most commonly caused by failure of the left side of the heart.

Answer 31

Right Ventricular Failure - Heart Failure

Question 32

Acute or chronic heart failure is determined by the rapid progression of the syndrome, the presence and activation of compensatory mechanisms, and the presence or absence of fluid accumulation in the interstitial space
Acute heart failure has a sudden onset with no compensatory mechanisms. The patient may experience acute pulmonary edema, low cardiac output, or cardiogenic shock. Patients with chronic heart failure are hypervolemic, have sodium and water retention, and have structural heart chamber changes such as dilation or hypertrophy.
Chronic heart failure is an ongoing process, with symptoms that may be made tolerable by medication, diet, and a reduced activity level. The deterioration into acute heart failure can be precipitated by the onset of dysrhythmias, acute ischemia, sudden illness, or cessation of medications. This may necessitate admission to a critical care unit. Hypertension is the primary precursor of heart failure in women, whereas CHD, specifically MI, is the primary cause of heart failure in men.

Answer 32

Acute Heart Failure Versus Chronic Heart Failure - Heart Failure

Question 33

clinical manifestations of acute heart failure result from tissue hypoperfusion and organ congestion and are progressive.
The severity of clinical manifestations increases as heart failure worsens.
Shortness of Breath in Heart Failure
Pulmonary Edema in Heart Failure

Answer 33

Pulmonary Complications in Heart Failure - Heart Failure

Question 34

The patient experiences the feeling of shortness of breath first with exertion, but as heart failure worsens, symptoms are also present at rest.
The more severe the heart failure, the higher the BNP value.
Breathlessness in heart failure is described by these terms:
Dyspnea: sensation of shortness of breath from pulmonary vascular congestion and decreased lung compliance
Orthopnea: difficulty breathing when lying flat because of an increase in venous return that occurs in the supine position
Paroxysmal nocturnal dyspnea: severe form of orthopnea in which the patient awakens from sleep gasping for air
Cardiac asthma: dyspnea with wheezing, a nonproductive cough, and pulmonary crackles that progress to the gurgling sounds of pulmonary edema

Answer 34

Shortness of Breath in Heart Failure

Question 35

protein-laden fluid in the alveoli, inhibits gas exchange by impairing the diffusion pathway between the alveolus and the capillary caused by increased left atrial and ventricular pressures and results in an excessive accumulation of serous or serosanguineous fluid in the interstitial spaces and alveoli of the lungs.
first stage is not as severe and is characterized by interstitial edema, engorgement of the perivascular and peribronchial spaces, and increased lymphatic flow later stage is characterized by alveolar edema resulting from fluid moving into the alveoli from the interstitium
Patients experiencing heart failure and pulmonary edema are extremely breathless and anxious and have a sensation of suffocation. They expectorate pink, frothy sputum and feel as if they are drowning
reflects low cardiac output, increased sympathetic stimulation, peripheral vasoconstriction, and desaturation of arterial blood.
Arterial blood gases in pulmonary edema.
Cardiogenic pulmonary edema versus noncardiogenic pulmonary edema.

Answer 35

Pulmonary Edema in Heart Failure

Question 36

variable. In the early stage of pulmonary edema, respiratory alkalosis may be present because of hyperventilation, which eliminates carbon dioxide.
As the pulmonary edema progresses and gas exchange becomes impaired, acidosis (pH less than 7.35) and hypoxemia ensue.

Answer 36

Arterial blood gases in pulmonary edema.

Question 37

When a patient develops pulmonary edema, it is often a challenge to determine whether the cause is cardiac, known as cardiogenic pulmonary edema, or pulmonary or systemic in origin. The latter is referred to as noncardiogenic pulmonary edema or, more commonly, acute respiratory distress syndrome (ARDS).
serum BNP level or insertion of a pulmonary artery catheter
A pulmonary artery catheter is used to determine the patient’s pulmonary artery occlusion pressure.

Answer 37

Cardiogenic pulmonary edema versus noncardiogenic pulmonary edema.

Question 38

goals of the medical management of heart failure are to relieve symptoms, enhance cardiac performance, and correct known precipitating causes
Relief of Symptoms and Enhancement of Cardiac Performance
Correction of Precipitating Causes
Palliative Care for End-Stage Heart Failure

Answer 38

Medical Management - Heart Failure

Question 39

goals of the medical management of heart failure are to relieve symptoms, enhance cardiac performance, and correct known precipitating causes
Control of symptoms involves management of fluid overload and improvement of cardiac output by decreasing SVR and increasing contractility.
Diuretics are administered to decrease preload and to eliminate
Morphine is given to facilitate peripheral dilation and decrease anxiety.
Afterload is decreased by vasodilators such as sodium nitroprusside (Nipride) and nitroglycerin.
Nitrates are used to decrease preload and vasodilate the coronary arteries if CAD is an underlying cause of the acute heart failure. For some patients, an IABP is temporarily required.
Contractility is initially increased by continuous infusion of positive inotropic medications (dopamine) or by combination inodilators such as dobutamine or milrinone, which have both inotropic and vasodilatory effects
Before transitioning out of the critical care unit, the patient with heart failure receives ACEIs to inhibit left ventricular chamber remodeling and slow left ventricular dilation. If the patient does not tolerate ACEIs, ARBs may be substituted.
Low-dose beta-blockers such as carvedilol may also be prescribed, although strict surveillance is required to anticipate and avoid untoward negative inotropic effects. Digoxin may be added to the regimen, especially if the patient has concomitant atrial fibrillation.

Answer 39

Relief of Symptoms and Enhancement of Cardiac Performance

Question 40

symptoms of heart failure are controlled, diagnostic studies such as cardiac catheterization, echocardiography, and diagnostic imaging tests to determine myocardial perfusion are undertaken to uncover the cause of the heart failure and tailor long-term management to treat the cause.

Answer 40

Correction of Precipitating Causes

Question 41

Heart failure is a progressive disease, and patients do not recover.
Primary aim of palliative care is symptom management and relief of suffering. Fundamental to all symptom management strategies for heart failure is the optimization of medications according to current guidelines. The most common symptoms of advanced heart failure are dyspnea, pain, and fatigue.

Answer 41

Palliative Care for End-Stage Heart Failure

Question 42

Nursing interventions are designed to achieve optimal cardiopulmonary function, promote comfort and emotional support, monitor the effectiveness of pharmacologic therapy, ensure nutrition intake is sufficient, and provide patient and family education.
Optimizing Cardiopulmonary Function
Promoting Comfort and Emotional Support
Monitoring Effects of Pharmacologic Therapy
Nutritional Intake
Educate the Patient and Family

Answer 42

Nursing Management - Heart Failure

Question 43

The patient’s ECG is evaluated for dysrhythmias that may be present as a result of medication toxicity or electrolyte imbalance.
The patient’s ECG is evaluated for dysrhythmias that may be present as a result of medication toxicity or electrolyte imbalance.
Diuretics or vasodilators are used to decrease excessive preload and afterload.
Generally, the daily weight is used in fluid management, and a weekly weight is optimally used for tracking body weight

Answer 43

Optimizing Cardiopulmonary Function

Question 44

Activity must be restricted during periods of breathlessness.
Bed rest usually is prescribed for the patient
Rest periods must be carefully planned and adhered to, and independence within the patient’s activity prescription must be fostered.
Vital signs are recorded before an activity is begun and after it is completed. Signs of activity intolerance such as dyspnea, fatigue, sustained increase in pulse, and onset of dysrhythmias are documented and reported to the physician.
Skin breakdown is a risk because of the combination of bed rest, inadequate nutrition, peripheral edema, and decreased perfusion to the skin and subcutaneous tissue.

Answer 44

Promoting Comfort and Emotional Support

Question 45

Patients experiencing acute heart failure require aggressive pharmacologic therapy.
The patient’s hemodynamic response to these agents is closely monitored. Fluid intake and output balances are tabulated daily or hourly in the critical care unit.

Answer 45

Monitoring Effects of Pharmacologic Therapy

Question 46

The patient’s hemodynamic response to these agents is closely monitored. Fluid intake and output balances are tabulated daily or hourly in the critical care unit.
Favorite foods and foods from home may be incorporated into the diet as long as the foods are compatible with nutritional restrictions such as low levels of sodium to decrease the risk of fluid retention.
Each patient must be assessed for nutritional imbalance individually.

Answer 46

Nutritional Intake

Question 47

assesses the patient’s and family’s understanding of the pathophysiology and individual risk factor profile for heart failure. Primary topics of education include (1) the importance of a daily weight, (2) fluid restrictions, (3) written information about the multiple medications used to control the symptoms of heart failure, (4) physical activity, and (5) when to call a healthcare provider
require education about lifestyle changes
Achieving the optimal outcomes for a patient with heart failure requires contributions from a team of educated health care clinicians

Answer 47

Educate the Patient and Family