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NURS 428: Evolution > Common Cardiovascular Disorders > Flashcards

Common Cardiovascular Disorders Flashcards

Exam 3

1
Q

Normal Structure of the Heart:

Composed of three layers:

A

Epicardium

Myocardium

Endocardium

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2
Q

Normal Structure of the Heart:

Where is the heart located?

A

Mediastinal space

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3
Q

Normal Structure of the Heart:

What is the heart covered by?

A

Covered by pericardium

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4
Q

Pericardium:

Where is it located?

A

Pericardium surrounds the external surface of the heart and the roots of the great vessels.

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5
Q

Pericardium:

What are the two layers of the pericardium?

A
  1. outer tough fibrous pericardium
  2. inner serous layer
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6
Q

Pericardium:

What are the two layers of the serous pericardium?

A
  1. The parietal layer
  2. Inner visceral layer (epicardium)
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7
Q

Pericardium:

Two layers of the serous pericardium: The parietal layer

A

The parietal layer lines the internal surface of the fibrous membrane.

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8
Q

Pericardium:

Two layers of the serous pericardium: The inner visceral layer

A

It extends to the great vessels, where it then folds over on itself to form the inner visceral layer (epicardium)

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9
Q

Pericardium:

What lies between the outer and inner layers?

A

10 to 50 mL of clear serous fluid lies between these layers and acts as a lubricant.

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10
Q

Pericardium:

What does the pericardium help do?

A

The pericardium helps restrain the heart and isolate it from infections in the surrounding structures.

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11
Q

Pericardium:

What is pericarditis?

A

Pericarditis is inflammation of the pericardium

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12
Q

PericarditisAssessment:

What are signs and symptoms?

A

Chest pain

Pericardial friction rub

Low grade fever

Shallow breaths

ST segment elevation in all 12 leads.

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13
Q

PericarditisAssessment:

What are signs and symptoms: What appears in EKG?

A

ST segment elevation in all 12 leads

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14
Q

PericarditisAssessment:

What are signs and symptoms: Pericardial friction rub- when is it noted?

A

on auscultation (raspy, high pitched- varies with the cardiac cycle)

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15
Q

PericarditisAssessment:

Signs and symptoms: What is the primary symptom? How is it?

A

The primary symptom in acute pericarditis is chest pain.

The pain tends to be pleuritic in nature and classically is made worse by breathing deeply or lying supine.

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16
Q

PericarditisAssessment:

What are signs and symptoms:
How is chest pain presented?

A

Chest Pain usually sharp & stabbing, but can be dull ache is minority of cases

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17
Q

PericarditisAssessment:

What are signs and symptoms:
How else does chest pain appear?

A

Pain that radiates to shoulder or back

Pain aggravated by breathing deeply

Pain aggravated by lying down

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18
Q

Pericarditisdiagnosis:

What appears on the EKG?

A

Diffuse ST-segment elevation with an upward concavity and PR-segment depression.

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19
Q

Pericarditisdiagnosis:

Lab test include:

A

CBC, cardiac enzyme levels, C-reactive protein, erythrocyte sedimentation rate, rheumatoid factors, and antinuclear antibody titers.

Blood cultures

Viral studies

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20
Q

Pericarditisdiagnosis:

Lab test include: Why would blood cultures be indicated?

A

Blood cultures may be indicated f there is evidence of infection

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21
Q

Pericarditisdiagnosis:

Lab test include: Why would viral studies be indicated?

A

Viral studies may be obtained if the rest of the diagnostic workup is negative

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22
Q

Pericarditisdiagnosis:

What confirms a diagnosis? What is important to know about this though?

A

The presence of a pericardial friction rub confirms the diagnosis;

however, absence of a rub does not rule out pericarditis.

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23
Q

Pericarditisdiagnosis:

Where and how is it best to hear a friction rub?

A

It is best heard with the diaphragm of the stethoscope placed over the lower to middle left sternal border.

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24
Q

Complicationsof Pericarditis include:

A

Pericardial effusion

Cardiac tamponade

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25
Q

Complicationsof Pericarditis include:

Pericardial effusion: What are signs and symptoms?

A

Distant heart sounds

Cough, dyspnea, tachypnea

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26
Q

Complicationsof Pericarditis include:

Cardiac Tamponade: What are signs and symptoms?

A

Agitation, confusion, restlessness

Tachycardia, tachypnea

Drop in blood pressure

Distended neck veins

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27
Q

Complicationsof Pericarditis:

Pericardial effusion: What is it?

A

A pericardial effusion is when excess fluid builds up in the pericardial sac around the heart.

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28
Q

Complicationsof Pericarditis:

Cardiac Tamponade: What is it?

A

a life-threatening medical emergency that occurs when fluid builds up in the sac around the heart, compressing the heart and preventing it from pumping blood properly.

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29
Q

Complicationsof Pericarditis:

Cardiac Tamponade: What is a key finding of this?

A

Key finding in cardiac tamponade is a drop in bp

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30
Q

Pericarditis management:

What should be done with symptoms?

A

Relieve symptoms, eliminate any possible causative agents, and monitor for complications.

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31
Q

Pericarditis management:

What meds could be used?

A

NSAIDs such as aspirin or ibuprofen

Colchicine (anti-inflammatory)

Steroids

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32
Q

Pericarditis management:

Meds: What does colchicine do?

A

Colchicine has been shown to successfully reduce the recurrence of pericarditis.

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33
Q

Pericarditis management:

Meds: What should be avoided? What cases?

A

Anticoagulants must be avoided in the patient recovering from MI.

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34
Q

Pericarditis management:

Meds: What does steroids do?

A

Steroids may be indicated in resistant cases

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35
Q

Pericarditis management:

With treatment, when do symptoms abate?

A

Abates over 2 to 6 weeks

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36
Q

Pericarditis management:

How common is it to have recurrent episodes?

A

Rare to have recurrent episodes

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37
Q

Myocarditis: What is it?

A

Inflammation of the myocardium

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38
Q

Myocarditis:

What is secondary myocarditis?

A

inflammation related to specific organism

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39
Q

Myocarditis: What is it due to?

A

Due to: Acute viral or autoimmune infection, radiation, meds

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40
Q

Myocarditis:

Due to: Acute viral or autoimmune infection, radiation, meds; what is an example of a viral infection?

A

Most common: viruses (flu)

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41
Q

Myocarditis:

What are signs and symptoms?

A

S&S are benign to severe heart involvement (dysrhythmias, CHF, even sudden death among young athletes)

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42
Q

Myocarditis:

How long after viral infection can cardiac involvement be noted?

A

Cardiac involvement can be seen 7-10 days after viral infection

Delay in symptoms when viral is cause

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43
Q

Myocarditis

What are signs and symptoms?

A

fatigue,

dyspnea,

palpitations,

Pleuritic Chest pain,

friction rub,

S3,

crackles,

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44
Q

Myocarditis

Diagnosis: What can be done?

A

ECG & Lab findings

Endomyocardial Biopsy

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45
Q

Myocarditis

Diagnosis: What is important to know about ekg and lab findings?

A

ECG & Lab findings are vague

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46
Q

Myocarditis

Diagnosis: What is the most diagnostic measure? What is important to remember about it?

A

Endomyocardial Biopsy - most diagnostic but lack of positivity does not rule out myocarditis

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47
Q

Myocarditis

What is the goal of treatment?

A

Goal: Manage the symptoms of poor cardiac function

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48
Q

Myocarditis

What does treatment include?

A

Tx: Supportive (Oxygen, Rest, restricted activity).

Myocarditis may resolve without further sequelae.

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49
Q

Myocarditis:

What is nursing management:

A

Athletes with myocarditis should withdraw from competitive sports for a period of at least 6 months.

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50
Q

Myocarditis:

What is nursing management: Athletes with myocarditis should withdraw from competitive sports for a period of at least 6 months.

What does return to training and competition depend on?

A

Return to training and competition depends on:

normalization of cardiac function and absence of any significant clinical findings, such as dysrhythmias.

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51
Q

Endocarditis:

How is the endocardium normally?

A

Endocardium continuous with valves

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52
Q

Endocarditis: What is it?

A

Endocarditis is an infection of the endocardial surface of the heart, including the valves.

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53
Q

Endocarditis:

What are common organisms that cause it?

A

Common organisms:

streptococci,

enterococci,

staphylococcus aureus

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54
Q

Endocarditis:

Who is at risk for developing this?

A

Children with congenital heart disease are at risk.

Adults with mitral valve prolapse, rheumatic heart disease, illicit intravenous drugs, and patients with prosthetic valves or long-term indwelling devices

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55
Q

Endocarditis:

What can result from this?

A

Can result in proliferation of bacteria, damaging the valve structure, leading to heart failure

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56
Q

Assessment of Endocarditis:

When do symptoms appear?

A

Symptoms of endocarditis usually occur within 2 weeks of the precipitating event and are related to four underlying processes: bacteremia or fungemia, valvulitis, immunologic response, and peripheral emboli

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57
Q

Assessment of Endocarditis:

What are symptoms?

A

High fever and shaking chills

Night sweats, cough, weight loss

General malaise, weakness, fatigue, headache, musculoskeletal complaints

New murmurs

Symptoms of HF

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58
Q

Assessment of Endocarditis:

How is a diagnosis made?

A

echocardiogram,

transesophageal echocardiography,

persistent bacteremia,

visualization of vegetation,

or new or worsening murmur.

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59
Q

Assessment of Endocarditis:

How is blood drawn to make a diagnosis?

A

Blood is usually drawn for three separate sets of cultures.

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60
Q

Assessment of Endocarditis:

What is treatment?

A

Treatment: antibiotics (prolonged course), immediate surgery if CHF evolves secondary to valve dysfunction.

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61
Q

Cardiomyopathy: What is it?

A

Cardiomyopathies are diseases of the heart muscle that cause cardiac dysfunction resulting in heart failure, dysrhythmias, or sudden death.

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62
Q

Cardiomyopathy:

What could lead to structural changes that result in functional changes?

A

Current theories under investigate suggest that ischemic, immune, mechanical and neurohormonal effects on the pericardium, myocardium and endothelium lead to structural changes that result in functional changes.

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63
Q

Cardiomyopathy:

What do structural changes on the cellular level lead to?

A

Structural changes at the cellular level leads to stiffness of the ventricles and smooth muscle layers in the arteries.

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64
Q

Cardiomyopathy:

What does both stiffness and spherical remodeling occurring in the same heart lead to?

A

Both stiffness and spherical remodeling may occur in the same heart, leading to a compromised cardiac output from impaired relaxation and impaired emptying.

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65
Q

Cardiomyopathies:

What are the most common types?

A

The most common types of primary cardiomyopathies in Western countries:

dilated, ischemic, nonischemic and hypertrophic cardiomyopathies (HCMs)

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66
Q

Dilated cardiomyopathy:

What is it and why does it happen?

A

DCM is characterized by increased myocardial cavity size in the presence of normal or reduced left ventricular wall thickness and impaired systolic function.

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67
Q

Dilated cardiomyopathy:

What may lead to a decrease in contractility in DCM?

A

Ischemia

Alcohol abuse

Endocrine disorders

Pregnancy

Viral infections

Muscular dystrophy

Valvular disease

All may cause a decrease in contractility

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68
Q

Dilated cardiomyopathy:

What is a decrease in contractility?

A

Ejection fraction < 40%

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69
Q

Dilated cardiomyopathy:

What happens overtime? Why?

A

Overtime, the ventricle dilates to accommodate the increased intraventricular volumes (preload)

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70
Q

Dilated cardiomyopathy:

Overtime, the ventricle dilates to accommodate the increased intraventricular volumes (preload)

In the dilated heart, the increased volume leads to what?

A

In the dilated heart, the increased volume leads to a decreased stroke volume

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71
Q

Dilated cardiomyopathy:

What happens to the valves? Why?

A

Mitral and tricuspid insufficiency develop as the valve leaflets are stretched and separated.

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72
Q

Dilated cardiomyopathy:

What commonly occurs?

A

Dysrhythmias and conduction defects commonly occur

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73
Q

What is the third most common cause of heart failure?

A

Dilated cardiomyopathy

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74
Q

What is the most frequent cause of heart transplantation?

A

Dilated cardiomyopathy:

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75
Q

Dilated cardiomyopathy:

What is the specific cause most of the time?

A

In most cases, the specific cause is unknown

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76
Q

Dilated cardiomyopathy:

How are some patients- symptom-wise?

A

Some patients remain asymptomatic or have minimal clinical findings.

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77
Q

Dilated cardiomyopathy:

How do symptoms usually develop?

A

Symptoms develop gradually and are typically related to left ventricular heart failure

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78
Q

Dilated cardiomyopathy:

The presence of what is associated with a poor prognosis?

A

The presence of right sided heart failure is associated with poor prognosis

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79
Q

Dilated cardiomyopathy:

What tests are done and why?

A

Lab tests

Echocardiogram

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80
Q

Dilated cardiomyopathy:

Why are lab tests for?

A

Lab tests include screening for potentially reversible causes, including HIV

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81
Q

Dilated cardiomyopathy:

Why are echocardiograms for?

A

The echocardiogram differentiates the primary abnormality and determines ejection fraction.

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82
Q

Dilated cardiomyopathy:

What procedure is done? Why?

A

Cardiac catheterization to rule out coronary artery disease

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83
Q

Treatment of dilated cardiomyopathy

Broadly includes?

A

Identify and eliminate potential causes of DCM

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84
Q

Treatment of dilated cardiomyopathy

What kind of damage is reversible?

A

Myocardial damage related to ingesting alcohol is reversible if detected early and the patient abstains from further drinking.

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85
Q

Treatment of dilated cardiomyopathy

What kind of damage is reversible?

A

Control of heart failure, dysrhythmias, or intracoronary thrombus

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86
Q

Treatment of dilated cardiomyopathy

What kind of treatment is done for severe cases? What are severe cases?

A

Biventricular pacing for severe symptomatic heart failure, prolonged QRS, dilated ventricle and poor ejection fraction.

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87
Q

Treatment of dilated cardiomyopathy

What do implantable cardioverter defibrillators (ICDs) do?

A

Implantable cardioverter defibrillators (ICDs) to prevent sudden death associated with lethal dysrhythmias

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88
Q

Treatment of dilated cardiomyopathy

What other treatments have been shown to prolong life?

A

Mechanical circulatory support, heart transplantation, and some medical therapies have been shown to prolong life.

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89
Q

Ischemic cardiomyopathy:

What causes this?

A

Result of oxygen levels that are inadequate to meet the metabolic demands of the myocardial cells.

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90
Q

Ischemic cardiomyopathy:

Result of oxygen levels that are inadequate to meet the metabolic demands of the myocardial cells.

Why do this occur? How is it?

A

Caused by obstruction in the coronary arteries;

may be acute or chronic

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91
Q

Ischemic cardiomyopathy:

What does severe, persistent ischemia lead to?

A

Severe, persistent ischemia causes the muscle tissue to die (MI)

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92
Q

Ischemic cardiomyopathy:

What happens to dead muscle?

A

Dead muscle is replaced with scar tissue.

The larger the scar, the greater the dysfunction.

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93
Q

Ischemic cardiomyopathy:

What does decreased muscle mass lead to?

A

Decreased muscle mass leads to decreased energy for pumping blood and decreased cardiac output.

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94
Q

Ischemic cardiomyopathy:

Decreased muscle mass leads to decreased energy for pumping blood and decreased cardiac output. What does this lead to?

A

Cardiogenic shock results

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95
Q

Ischemic cardiomyopathy:

What increases? What does this result in?

A

Left ventricular end-diastolic pressure increases, pulmonary artery pressure increase, and pulmonary edema results.

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96
Q

Ischemic cardiomyopathy:

Left ventricular end-diastolic pressure increases, pulmonary artery pressure increase, and pulmonary edema results. What occurs?

A

End-organ damage occurs

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97
Q

Non ischemic cardiomyopathy:

What are causes?

A

Idiopathic cardiomyopathy

Myocarditis

Pregnancy, heavy alcohol use, hypertension and tachycardia

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98
Q

Non ischemic cardiomyopathy:

Causes: Idiopathic cardiomyopathy- What is this?

A

heart dilates, remodels, and becomes ineffective to pump

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99
Q

Non ischemic cardiomyopathy:

How may this present?

A

May be acute or chronic

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100
Q

Hypertrophic cardiomyopathy(HCM)

What is this?

A

Hypertrophied, nondilated left ventricle not related to any obvious cause

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101
Q

Hypertrophic cardiomyopathy(HCM)

It is hypertrophied, nondilated left ventricle not related to any obvious cause

What would as obvious cause be?

A

Hypertension or aortic stenosis

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102
Q

Hypertrophic cardiomyopathy(HCM)

What is a characteristic feature of this?

A

Diastolic dysfunction is a characteristic feature

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103
Q

Hypertrophic cardiomyopathy(HCM)

How is the heart in this condition?

A

The heart can contract but cannot relax and remains abnormally stiff in diastole.

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104
Q

Hypertrophic cardiomyopathy(HCM)

What else may occur?

A

Septal wall hypertrophy may occur, leading to a left ventricular outflow tract obstruction during systole.

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105
Q

Hypertrophic cardiomyopathy(HCM)

What usually occurs in asymptomatic or mildly symptomatic people? What age?

A

Sudden death, usually from a ventricular dysrhythmia, in asymptomatic or mildly symptomatic people of any age group

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106
Q

HCM Assessment and treatment

Assessment: How is it usually found?

A

Often found unexpectedly during investigation of heart murmurs or family screening

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107
Q

HCM Assessment and treatment

Assessment: What is the most common symptom?

A

The most common symptom is dyspnea.

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108
Q

HCM Assessment and treatment

Assessment: What other symptoms frequently occurs?

A

Presyncope and syncope also frequently occur.

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109
Q

HCM Assessment and treatment

Assessment: What would confirm the diagnosis of this illness?

A

Left ventricular hypertrophy (LVH) present on the echocardiogram confirms the diagnosis.

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110
Q

HCM Assessment and treatment

Assessment: Who could this be a normal finding in?

A

Borderline LVH may be a normal finding in competitive athletes.

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111
Q

HCM Assessment and treatment

Treatment includes:

A

Control symptoms.

Prevent complications and reduce the risk for sudden death.

Genetic screening and counseling

ICD

Percutaneous ablation with ethanol or surgery to remove a portion of the septum may be necessary.

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112
Q

HCM Assessment and treatment

Treatment includes: Percutaneous ablation- what does it do? What is it used with?

A

Percutaneous ablation with ethanol or surgery to remove a portion of the septum may be necessary.

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113
Q

HCM Assessment and treatment

Treatment includes: How are symptomatic patients?

A

Most symptomatic patients can be medically managed.

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114
Q

Peripheral Vascular Disease:

What is it?

A

A group of distinct disorders involving the arteries, veins, and lymphatic vessels of the peripheral circulation.

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115
Q

Peripheral Vascular Disease:

What is this considered?

A

Noncardiac diseases that affect the circulation as a whole

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116
Q

Peripheral Vascular Disease:

Noncardiac diseases that affect the circulation as a whole: What does this include?

A

Peripheral arterial disease (PAD)

Venous disease

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117
Q

Peripheral Arterial Disease:

What is this?

A

Processes that obstruct the blood supply of the lower or upper extremities

118
Q

Peripheral Arterial Disease:

Who is it common in?

A

Symptomatic PAD is a disease of the elderly found more commonly in men aged 70 years and older.

Patients of any age with risk factors for atherosclerosis, such as smoking or diabetes

119
Q

Peripheral Arterial Disease:

What are other risk factors of PAD?

A

Other risk factors: hypertension, lipid disorders, family history, postmenopausal state, and hyperhomocysteinemia

120
Q

Peripheral Arterial Disease:

How does the disease develop?

A

The disease develops in major bifurcations and areas of acute angulations.

121
Q

Peripheral Arterial Disease:

What are symptoms? What is the main symptom?

A

Intermittent claudication is classic symptom, and is cramping, burning or aching pain in the legs or buttocks, relieved with rest (when legs dangle, when elevated,)

122
Q

Peripheral Arterial Disease:

What are other symptoms?

A

Other symptoms: cool to touch, hair loss on extremities, nail thickening, drying of the skin

123
Q

Peripheral Arterial Disease:

What are some results to monitor?

A

Ankle brachial index: Ratio of ankle to brachial systolic blood pressure (normal 1.0 or greater).
Critical limb ischemia = ABI less than 0.518

124
Q

Peripheral Arterial Disease:

What is management of this disease?- Broadly

A

Modifying or eliminating risk factors

125
Q

Peripheral Arterial Disease:

What is management of this disease?

A

Smoking cessation, aggressive treatment of hypertension, diabetes, and lipid disorders

Antiplatelets (aspirin or clopidogrel [Plavix]) to reduce the risk for MI and stroke and cilostazol (Pletal) to increase walking distance

Peripheral balloon angioplasty

Surgical bypass in severe obstruction

126
Q

Peripheral Arterial Disease:

Management of this disease: What is used in severe obstruction?

A

Surgical bypass in severe obstruction

127
Q

Peripheral Arterial Disease:

Management of this disease: What do platelets do? What are examples of platelets?

A

Antiplatelets (aspirin or clopidogrel [Plavix]) to reduce the risk for MI and stroke and cilostazol (Pletal) to increase walking distance

128
Q

Venous disease:

What is phlebitis?

A

Phlebitis: vessel wall inflammation as a result of injury related to varicose veins

129
Q

Venous disease:

What can phlebitis lead to?

A

Can lead to VTE

It can lead to the formation of a thrombus, a solid obstruction within the vein that can break loose and form a venous thromboembolism (VTE).

130
Q

Superficial thrombophlebitis- What is it?

A

Superficial thrombophlebitis is a condition in which an injury to the vessel wall causes inflammation and clot formation in the superficial blood vessels.

131
Q

Venous disease:

What are factors that predispose someone to thrombus formation?

A

Factors that predispose a patient to thrombus formation are vessel wall injury, stasis of blood, and increased blood coagulability (Virchow triad).

132
Q

Venous disease:

What are symptoms of DVT?

A

Deep venous thrombosis (DVT) is characterized by pain, swelling, tenderness, and increased temperature over the affected area

Brownish in color

133
Q

Venous disease:

What is accurate diagnosis of DVT?

A

Accurate diagnosis usually requires diagnostic testing such as compression ultrasonography.

134
Q

Venous disease:

What is treatment for VTE?

A

The focus of care for the patient with VTE is to relieve symptoms, increase blood flow, and prevent complications.

135
Q

Venous disease

Patients with DVT are at high risk for what?

A

Patients with DVT are at high risk for pulmonary embolism.

136
Q

Venous disease

What is included in treatment strategies? What meds?

A

Treatment strategies include anticoagulant therapy to prevent the formation of emboli, followed by long-term warfarin or direct oral anticoagulant (DOAC; e.g., apixaban, dabigatran, edoxaban, and rivaroxaban) use to prevent recurrence.

.

137
Q

Venous disease

The type of therapy used in patients depend on what?

A

Specific therapy depends on the patient’s history and clinical setting.

138
Q

Venous disease

What is the most common complication of therapy for venous diseases?

A

Bleeding is the most common complication of therapy, and major hemorrhage can be fatal.

139
Q

Venous disease

What kind of orders should be anticipated for venous diseases?

A

Anticipate orders for VTE prophylaxis based on daily interdisciplinary patient assessment for VTE risks.

This risk assessment includes determining need for ongoing central venous catheter use, current VTE prophylaxis, bleeding risks, and treatment responsiveness.

Also, aim to reduce the amount of time the patient is immobile because of the effects of treatment (e.g., analgesia, sedation, neuromuscular blockade, mechanical ventilation).

140
Q

Venous disease

Anticipate orders for VTE prophylaxis based on daily interdisciplinary patient assessment for VTE risks. What is included in risk assessment?

A

This risk assessment includes determining need for ongoing central venous catheter use, current VTE prophylaxis, bleeding risks, and treatment responsiveness.

141
Q

Venous disease

How should mechanical prophylaxis devices fit??

A

Mechanical prophylaxis devices should fit properly and should only be removed for cleaning and skin inspection.

142
Q

What is the longest and strongest artery in the body?

A

The aorta

143
Q

Aortic disease:

Overtime, what can happen to the aorta?

A

Over time, congenital, degenerative, hemodynamic, and mechanical factors stress this elastic vessel.

The result is dilation of the aortic wall, leaving the patient at risk for aortic dissection or rupture.

144
Q

Aortic disease:

Over time, congenital, degenerative, hemodynamic, and mechanical factors stress this elastic vessel. What does this lead to?

A

The result is dilation of the aortic wall, leaving the patient at risk for aortic dissection or rupture.

145
Q

Abdominal Aortic Aneurysm (AAA): What are they more common than?

A

More common than thoracic aortic aneurysms

146
Q

Abdominal Aortic Aneurysm (AAA):

Who does it occur more in (what population)?

A

More frequent in males

147
Q

Abdominal Aortic Aneurysm (AAA):

What is the leading risk factor for AAAs? What are other issues leading to AAAs?

A

Smoking is the leading risk factor for AAAs, followed closely by age, hypertension, lipid disorders, and atherosclerosis.

genetic, and environmental influences

148
Q

Abdominal Aortic Aneurysm (AAA):

What is a major risk of AAA?

A

The major risk from AAAs is rupture, which is associated with a high rate of mortality (up to 90%).

149
Q

AAA—Assessment and Management

Assessment: How do most people with AAA present?- symptomwise?

When is it typically identified?

A

Most patients with AAAs are asymptomatic; they are typically identified during health screening for another problem.

150
Q

AAA—Assessment and Management

Assessment: What is the most common complaint?

A

Abdominal or back pain is the most common complaint.

151
Q

AAA—Assessment and Management

Assessment: What is assessed?

A

Abdomen assessed for bruits or masses and assessment of peripheral pulses

152
Q

AAA—Assessment and Management

Assessment: What is associated with worsening symptoms?

A

Worsening of symptoms is usually related to expansion or rupture of the aneurysm.

153
Q

AAA—Assessment and Management

Assessment: What is the most practical method of confirming the diagnosis?

A

Abdominal ultrasonography is the most practical method of confirming the diagnosis

154
Q

AAA—Assessment and Management

Management

A

Management of AAAs includes control of hypertension and elimination of risk factors, such as smoking.

155
Q

AAA—Assessment and Management

Management: How should the patient be followed?

A

The patient should be followed with serial noninvasive tests, such as ultrasonography.

156
Q

AAA—Assessment and Management

Management: What does treatment involve?

A

Treatment of aneurysms involves surgical repair, which is usually indicated for AAAs larger than 5.5 cm

157
Q

AAA—Assessment and Management

Management: In addition to surgery, how may AAAs be repaired?

A

In addition to surgery, AAAs may be repaired by a minimally invasive approach using an endovascular graft.

158
Q

Thoracic Aortic Aneurysm: What is the most common cause?

A

Most ascending thoracic aortic aneurysms are due to conditions that cause remodeling and cystic medial degeneration.

159
Q

Thoracic Aortic Aneurysm: What are they also associated with?

A

Ascending thoracic aortic aneurysms are also associated with connective tissue disorders, genetic disorders, bicuspid aortic valve, infections, inflammatory diseases, chronic aortic dissection, and trauma.

160
Q

Thoracic Aortic Aneurysm—Assessment and Management

Assessment: How do most patients present?

A

Like most patients with AAAs, most patients with thoracic aortic aneurysms are asymptomatic at the time of diagnosis.

161
Q

Thoracic Aortic Aneurysm—Assessment and Management

Assessment: What are symptoms related to? What do these include?

A

Symptoms are related to the size and location of the aneurysm; these include aortic insufficiency and signs of compression of adjacent structures

162
Q

Thoracic Aortic Aneurysm—Assessment and Management

Assessment: Symptoms are related to the size and location of the aneurysm; these include aortic insufficiency and signs of compression of adjacent structures

Which can lead to?

A

which can lead to symptoms such as hoarseness, dysphagia, dyspnea, and heart failure

163
Q

Thoracic Aortic Aneurysm—Assessment and Management

Assessment: What can be fatal?

A

Rupture or acute dissection of a thoracic aneurysm can be fatal.

164
Q

Thoracic Aortic Aneurysm—Assessment and Management

Management: What does it include?

A

For most ascending thoracic aortic aneurysms, surgical repair is indicated at a diameter of 5.5 cm or more.

165
Q

What is the most common and lethal condition involving the aorta?

A

Acute aortic dissection, which occurs when the aortic wall tears, is the most common and the most lethal condition involving the aorta.

166
Q

Aortic Dissection—Assessment and Management

Who is the incidence of aortic dissection highest in?

A

The incidence is highest in males older than 60 years with a history of hypertension.

167
Q

Aortic Dissection—Assessment and Management

What are other risk factors to developing aortic dissection?

A

Other risk factors include connective tissue disorders (i.e., Marfan syndrome, Turner syndrome), a preexisting aortic aneurysm, cardiac surgery (aortic valve or coronary bypass), cardiac catheterization, illicit use of stimulants (cocaine, crack, methamphetamine), preexisting vasculitis, strenuous isometric resistance exercises, and trauma.

168
Q

Aortic Dissection—Assessment and Management

How do most patients present?

A

More than 90% of patients present with sudden, intense chest pain.

169
Q

Aortic Dissection—Assessment and Management

How do most patients describe symptoms?

A

The pain is described as “ripping” or “tearing” and may be accompanied by syncope

170
Q

Aortic Dissection—Assessment and Management

How can the diagnosis be determined in most patients?

A

In most patients, the diagnosis can be determined with a careful history and physical examination.

171
Q

Aortic Dissection—Assessment and Management

In most patients, the diagnosis can be determined with a careful history and physical examination. What would this show?

A

The patient will have a murmur of aortic regurgitation or alteration of the peripheral pulses with known risk factors, such as hypertension.

172
Q

Aortic Dissection—Assessment and Management

What may a chest radiograph show?

A

The chest radiograph may show a widened mediastinum.

173
Q

Aortic Dissection—Assessment and Management

If the aortic dissection involves the coronary arteries, what may be present?

A

Cardiac ischemia may be present if the dissection involves the coronary arteries.

174
Q

Aortic Dissection—Assessment and Management

What may be another complication of aortic root?

A

Cardiac tamponade may be another complication of dissection involving the aortic root.

175
Q

Aortic Dissection—Assessment and Management

What may be another complication if the aortic arch vessels are involved?

A

Neurologic deficits may occur if the aortic arch vessels are involved.

176
Q

Aortic Dissection—Assessment and Management

Dissections extending to the renal arteries result in:

A

Dissections extending to the renal arteries result in:

elevated serum creatinine,

decreased urine output, and severe hypertension that is difficult to manage.

177
Q

Aortic Dissection—Assessment and Management

To confirm the diagnosis of acute aortic dissection, what is ordered?

A

To confirm the diagnosis of acute aortic dissection,

transesophageal echocardiography or

contrast medium–enhanced CT

may be ordered

178
Q

Aortic Dissection—Assessment and Management

What does survival depend on?

A

Survival of the acute phase depends on the location of the dissection, the severity of the complications, and the rapidity with which the diagnosis is confirmed.

179
Q

Aortic Dissection—Assessment and Management

What does clinical management focus on?

A

Clinical management focuses on controlling blood pressure and managing pain.

180
Q

Aortic Dissection—Assessment and Management

What is treatment when the ascending aorta is involved in the dissection?

A

Surgery is the treatment of choice when the dissection involves the ascending aorta.

181
Q

Hypertension

Medical Management- Diagnosis

How is HTN defined?

A

Hypertension is defined as a systolic blood pressure greater than 130 to 139 mm Hg in stage 1 and greater than 140 mm Hg in individuals in stage 2, and a diastolic blood pressure greater than 90 mm Hg in all age groups.

182
Q

Hypertension

Treatment:

A

Lifestyle changes

Medications

183
Q

Hypertension

Treatment: What are medications used?

A

Diuretics

Antihypertensives

184
Q

Hypertension

Clinical Manifestations include

A

Headaches

Chest pain

Vision changes

Shortness of breath

Renal dysfunction

Dizziness

Fatigue

Nosebleeds

185
Q

Hypertension- Complications include

A

Dilated cardiomyopathy

Systolic dysfunction

Renal failure

Stroke

Hypertensive crisis

186
Q

Hypertensive Crisis:

Who is at risk for developing this?

A

Patients with high blood pressure are at risk for experiencing a hypertensive crisis.

187
Q

Hypertensive Crisis:

What is it?

A

A hypertensive crisis or emergency is defined as an acute elevation of blood pressure (greater than 180/120 mm Hg) that is associated with acute or imminent target organ damage.

188
Q

Hypertensive Crisis:

How common is it? Who does it occur in mostly?

A

This rare but potentially fatal condition strikes about 1% to 2% of hypertensive patients, occurring more frequently in African American males and in older adult patients.

189
Q

Hypertensive Crisis-Assessment

Signs and symptoms include:

A

Signs of encephalopathy include headache, visual disturbances, confusion, nausea, and vomiting.

190
Q

Hypertensive Crisis-Assessment

Signs and symptoms include: What happens to eyes?

A

Examination of the retina of the eyes may reveal cotton-wool spots and hemorrhages, indicating damage to retinal nerves and rupture of retinal blood vessels;

191
Q

Hypertensive Crisis-Assessment

What else may occur? What would this indicate?

A

Chest pain may represent acute coronary syndrome or aortic dissection.

192
Q

Hypertensive Crisis-Assessment

What happens to kidneys?

A

Depending on the damage to the kidneys, the patient may present with decreased urine output (oliguria) or azotemia (excess urea in the blood).

193
Q

Hypertensive Crisis-Management

What is the goal of treatment?

A

The goal is to reduce the bp by not more than 25% within 1 hour.

194
Q

Hypertensive Crisis-Management

What is treatment?

A

Several intravenous medications are indicated in treating hypertensive crises; the choice depends on availability and the clinical situation.

195
Q

Hypertensive Crisis-Management

Several intravenous medications are indicated in treating hypertensive crises; the choice depends on availability and the clinical situation. What are examples of drugs?

A

The selected drug may be a vasodilator, adrenergic blocker, calcium channel blocker, or an angiotensin-converting enzyme inhibitor.

196
Q

Hypertensive Crisis-Management

What is necessary to avoid lowering the blood pressure too quickly? How is this accomplished?

A

Constant monitoring is necessary to avoid lowering the blood pressure too quickly;

this is best accomplished with an intra-arterial catheter.

197
Q

Hypertensive Crisis-Management

What should be done about the cause of HTN crisis?

A

Identify the cause

198
Q

Hypertensive Crisis-Management

Identify the cause: What could they be?

A

Acute or chronic kidney disease

Exacerbation of chronic hypertension

Sudden withdrawal of antihypertensive medications

199
Q

Heart Failure: What is it?

A

Heart failure is a clinical syndrome characterized by fatigue and dyspnea on exertion (DOE), edema, orthopnea, and paroxysmal nocturnal dyspnea.

200
Q

Heart Failure: What is it used to describe?

A

Heart failure is the term used to describe the general clinical syndrome regardless of the kind of heart failure or the etiology that produces the symptoms.

201
Q

Heart Failure: Why is this the term used?

A

The revised guidelines recently published by a joint American College of Cardiology (ACC) and American Heart Association (AHA) task force use the preferred term heart failure rather than congestive heart failure as not all patients present with symptoms suggestive of fluid retention.

202
Q

Acute Versus Chronic Heart Failure:

What does it describe?

A

Describes the onset and intensity of symptoms

203
Q

Acute Versus Chronic Heart Failure:

Acute HF: What is it ?

A

Acute: sudden onset over days or hours

204
Q

Acute Versus Chronic Heart Failure:

Chronic HF: What is it ?

A

Chronic: develop over months to years

205
Q

Acute Versus Chronic Heart Failure:

Chronic HF: How may heart failure become chronic?

A

If the cause of acute symptoms is not reversed, then heart failure will become chronic.

206
Q

Left-Sided Heart Failure: What is it?

A

Failure of the left ventricle to fill or empty properly

207
Q

Left-Sided Heart Failure: What does it lead to?

A

Leads to increase in ventricular pressures and pulmonary vascular congestion

208
Q

Left-Sided Heart Failure: How can it further be classified as?

A

systolic and diastolic dysfunction.

209
Q

Left-Sided Heart Failure:

Systolic dysfunction: How is it defined? What is it caused by?

A

Systolic dysfunction is defined as an ejection fraction (EF) of less than 40% and is caused by a decrease in contractility.

210
Q

Left-Sided Heart Failure:

Diastolic dysfunction: What is the cause of this?

A

Diastolic dysfunction is caused by impaired relaxation and filling.

211
Q

Left-Sided Heart Failure:

Diastolic dysfunction: How is EF?

A

EF may be as high as 80%.

212
Q

Right-Sided Heart Failure: What is it?

A

Failure of the right ventricle to pump adequately

213
Q

Right-Sided Heart Failure: What is the most common cause of this?

A

Left-sided heart failure is the most common cause.

214
Q

Right-Sided Heart Failure: How else can this disease exist?

A

Can also exist with normal left ventricle.

215
Q

Right-Sided Heart Failure: What else can cause this?

A

Can result from pulmonary disease (cor pulmonale) and primary pulmonary artery hypertension

216
Q

Right-Sided Heart Failure: What is the most common cause of ACUTE right sided heart failure?

A

PE is a common cause of acute right-sided heart failure.

217
Q

What is the underlying result of all types of heart failure?

A

insufficient CO

218
Q

Factors that determine Cardiac output include:

A

Oxygen demand

Mechanical factors

Neurohormonal mechanisms

219
Q

Factors that determine Cardiac output include:

Oxygen demand

A

CO increases to meet increased O2 demand

220
Q

Factors that determine Cardiac output include:

Mechanical factors:

A

Stroke volume and heart rate

221
Q

Factors that determine Cardiac output

Neurohormonal mechanisms:

A

Catecholamines

Renin-angiotensin- aldosterone system

222
Q

Heart Failure:

Assessments include:

A

Vital signs

Breath sounds

Monitor rate and rhythm

Skin color, temperature, peripheral pulses

Dry, persistent cough

Activity intolerance

Laboratory data

Diagnostic studies

223
Q

Heart Failure:

Assessments include: Diagnostic studies like

A

Electrocardiography (ECG)

Echocardiography (with and without Doppler ultrasound)

Transesophageal echocardiogram (TEE)

224
Q

Heart Failure

Nursing Interventions

A

Rest, and activity as tolerated.

Improve pump function (contractility, heart rate and rhythm)

Patient education:

225
Q

Heart Failure

Nursing Interventions: Improve pump function (contractility, heart rate and rhythm)

How?

A

Diuretics

ACE inhibitors

Nitrates/hydralazine

Angiotensin converting enzyme inhibitors

Beta blockers (carvedilol [Coreg])

Digoxin

226
Q

Heart Failure

Nursing Interventions: Patient education

A

Sodium restriction,

alcohol cessation,

exercise,

medication adherence,

fluid restriction

227
Q

Heart Failure Complications

A

Pulmonary edema

Cardiogenic shock

Pleural effusion

Arrhythmias

Thrombus formation

Hepatomegly

Renal failure

228
Q

Cardiovascular Disease: What does it encompass?

A

Cardiovascular disease encompasses both cardiac and peripheral vascular diagnoses, including coronary artery disease (CAD).

229
Q

Cardiovascular Disease: CAD exists across a spectrum of severity, which includes

A

CAD exists across a spectrum of severity,

which includes stable angina and three diagnoses that are categorized as acute coronary syndrome (ACS):

unstable angina (UA),

non-ST-elevation myocardial infarction (NSTEMI), and

ST-elevation myocardial infarction (STEMI).

230
Q

Cardiovascular Disease:

CAD exists across a spectrum of severity, which includes stable angina and three diagnoses that are categorized as acute coronary syndrome (ACS):

A

unstable angina (UA),

non-ST-elevation myocardial infarction (NSTEMI)

ST-elevation myocardial infarction (STEMI).

231
Q

Cardiovascular Disease: What is a major cause of CAD?

A

Atherosclerosis is a major cause of CAD.

232
Q

Cardiovascular Disease:

Major risk factors are those that have been shown through research to significantly increase the risk of cardiovascular disease.

What are the two broad groups?

A

Modifiable

Nonmodifiable risk factors

233
Q

Cardiovascular Disease:

Modifiable includes

A

Smoking

Inactivity

Overweight

Cholesterol
- High LDL
- Low levels of HDL

Diabetes

Hypertension

234
Q

Cardiovascular Disease:

NonModifiable includes

A

Age

Greater than 65 y/o

Heredity (including race)
Higher in African Americans, Mexican Americans, Native Americans, Native Hawaiians, and some Asian Americans

Gender
Men;
after menopause, the death rate rises in women

235
Q

Angina- Classification

What are the groups?

A

Stable angina/angina pectoris

Variant (Prinzmetal) angina

Microvascular angina

Unstable angina

236
Q

Angina- Classification

Stable angina/angina pectoris:
How does it occur? How is it relieved?

A

Physical exertion or emotional stress; relieved by rest or nitroglycerin

237
Q

Angina- Classification

Variant (Prinzmetal) angina:
How does it occur? What is it the result of? What may cause this?

A

At rest, between midnight and 8 a.m.;

result of coronary artery spasm;

usually have severe atherosclerosis of at least one major coronary artery

238
Q

Angina- Classification

Microvascular angina

A

Chest pain with normal epicardial coronary arteries

239
Q

Acute Coronary Syndrome (ACS): What is it?

A

ACS is a spectrum that includes unstable angina (UA) and acute myocardial infarction (AMI).

240
Q

Acute Coronary Syndrome (ACS):

ACS is a spectrum that includes unstable angina (UA) and acute myocardial infarction (AMI).

What does AMI include?

A

With STEMI (ST-elevation myocardial infarction)

Without STEMI (Non-ST-elevation myocardial infarction (NSTEMI))

241
Q

Acute Coronary Syndrome (ACS):

ACS is a spectrum that includes unstable angina (UA) and acute myocardial infarction (AMI).

Unstable (preinfarction) angina: What is it?

A

Cardiac chest pain that can present as angina at rest, new-onset angina, or worsening angina

242
Q

Acute Coronary Syndrome (ACS):

ACS is a spectrum that includes unstable angina (UA) and acute myocardial infarction (AMI).

Unstable (preinfarction) angina: What does it require?

A

Requires immediate treatment

243
Q

Acute Coronary Syndrome (ACS):

ACS is a spectrum that includes unstable angina (UA) and acute myocardial infarction (AMI).

MI: What is it?

A

Prolonged ischemia related to an imbalance between oxygen supply and oxygen demand

244
Q

Myocardial Infarction:

What is triggered and how?

A

Plaque rupture triggers thrombus formation at the site of an atherosclerotic lesion

245
Q

Myocardial Infarction:

What results in an MI?

A

Occlusion of blood flow

246
Q

Myocardial Infarction:

How long until irreversible damage by MI occurs?

A

irreversible damage after 20 to 40 minutes

247
Q

Myocardial Infarction:

How can tissue be salvaged?

A

Tissue can be salvaged if flow is restored within 6 hours

248
Q

Myocardial Infarction:

Cellular changes depend on what?

A

Cellular changes depend on extension and expansion of infarct and ventricular remodeling

249
Q

Assessment of MI: What is noted?

A

Midsternal chest pain

Pale and diaphoretic

Dyspnea, tachypnea, and/or hypotension

Syncope

Feeling of impending doom

Nausea and vomiting

Dysrhythmias

250
Q

Assessment of MI:

Midsternal chest pain- how is it? How is it relieved?

A

Severe, crushing, and squeezing pressure

May radiate

Unrelieved with nitroglycerin

251
Q

Physical examination of MI:

How may patient appear? How is skin?

A

May appear restless, agitated, in distress

Skin is cool and moist

252
Q

Physical examination of MI:

How is breathing?

A

Labored breathing,

Crackles

Rhonchi

253
Q

Physical examination of MI:

How is heart?

A

Diminished S1, S3 and S4,

Pericardial friction rub

254
Q

Physical examination of MI:

What is there a lack of?

A

Lack of point o maximal impulse

255
Q

Physical examination of MI:

What is irregular?

A

Irregular, faint pulse

256
Q

Physical examination of MI:

What else is present?

A

VS

low grade fever

HTN

tachycardia,

hypotension and bradycardia

257
Q

Diagnostic Tests for MI:

A

ECG

258
Q

Diagnostic Tests for MI: ECG

What does it detect?

A

Detects patterns of ischemia, injury, and infarction

259
Q

Diagnostic Tests for MI: ECG

What causes ECG changes?

A

Depolarization and repolarization of cardiac cells are altered, causing ECG

260
Q

Diagnostic Tests for MI: ECG

ECG: What does ischemia looks like?

A

T-wave inversion,

ST depression

261
Q

Diagnostic Tests for MI: ECG

ECG: What does injury look like?

A

ST segment elevation

262
Q

Diagnostic Tests for MI: ECG

ECG: What does infarction look like?

A

T -wave

ST segment

Q wave changes

263
Q

Diagnostic Tests for MI: ECG

ECG: What does it reveal?

A

Reveals anatomical region involved

264
Q

Lab tests for MI:

A

Troponin

Other blood tests

265
Q

Lab tests for MI:

What is the preferred biomarker?

A

Troponin

266
Q

Lab tests for MI:

Troponin levels include?

A

Troponin I

Troponin T

267
Q

Lab tests for MI:

Troponin levels: Troponin I= rises? peaks? remains elevated?

A

Troponin I rises in 3 to 12 hours,

Peaks at 24 hours

remains elevated for 5-10 days.

268
Q

Lab tests for MI:

Other blood tests include?

A

Chemistry

CBC

Coagulation studies

full lipid profile

269
Q

Lab tests for MI:

Other diagnostic tests include:

A

Exercise stress testing

CXR

PET scan

Echocardiogram

MRI

Coronary angiography

270
Q

Management of MI:

When should you evaluate pt?

A

Evaluate within 10 minutes of arrival

271
Q

Management of MI

When patient arrives what do you do?

A

Patient history and 12 lead ECG elevation greater than 1 mm or two or more contiguous leads = MI

272
Q

MI management

When patient arrives what meds do you give?

A

ASA

Oxygen

Nitroglycerin

Morphine

B-blocker VS

IV access

Continuous cardiac monitoring

273
Q

MI management

When patient arrives what should you check

A

Serum cardiac markers

CBC

Chemistry and lipid profile

CXR echo

274
Q

MI management

What other interventions are done?

A

Percutaneous coronary intervention

Fibrinolytic therapy

Surgical intervention

275
Q

MI management

Percutaneous coronary intervention:
What does it do?

A

Reestablishes blood flow

276
Q

MI management

Percutaneous coronary intervention:
What is the procedure?

A

Artery is opened by balloon and stent is placed

277
Q

MI management

Fibrinolytic therapy:
In STEMI, when do you give drug by?

A

In STEMI, door to drug within 30 minutes

278
Q

MI management

Fibrinolytic therapy:
When should drug be given?

A

Given within 3 hours of onset of symptoms

279
Q

MI management

What is the surgical intervention?

A

CABG

280
Q

Complications of Acute MI

Include what two broad groups?

A

Hemodynamic complication

Mechanical complication

281
Q

Complications of Acute MI

Hemodynamic complications is what?

A

Cardiogenic shock

282
Q

Complications of Acute MI

Hemodynamic complications- Cardiogenic shock- what are symptoms?

A

S/S of cardiogenic shock include:

rapid, thready pulse, cool, moist skin, chest pain, dyspnea, tachypnea, inspiratory crackles, systolic bloop pressure less than 85 mmHg

283
Q

Complications of Acute MI

What is the most serious complication of MI?

A

Cardiogenic shock

284
Q

Complications of Acute MI

Mechanical complication- What is it?

A

Ventricular Septal Rupture

285
Q

Complications of Acute MI

When is the greatest risk for ventricular septal rupture?

A

Ventricular Septal Rupture. The greatest risk is within the first 24 hours and up to 5 days.

286
Q

Complications of Acute MI

Assessment findings for ventricular septal rupture?

A

Assessment finding of Ventricular Septal Rupture includes a new, loud systolic murmur.

287
Q

Surgical Revascularization- When is it indicated?

A

Unstable angina

AMI

Failure of percutaneous interventions

288
Q

Surgical Revascularization-

Includes:

A

Coronary artery bypass graft (CABG) surgery

Minimally invasive direct coronary artery bypass (MIDCAB) surgery

Transmyocardial revascularization (TMR)

289
Q

Surgical Revascularization-

CABG: Increased mortality associated with:

A

Left ventricle dysfunction

Emergency surgery

Age

Sex (female)

Number of diseased vessels

Decreased ejection fraction with congestive heart failure

290
Q

Surgical Revascularization-

CABG Surgery: What does it do?

A

Provides additional conduits for blood flow

Arteries longer patency

291
Q

Surgical Revascularization-

CABG Surgery: Provides additional conduits for blood flow- Where?

A

Saphenous vein

Internal mammary artery

Radial artery

NURS 428: Evolution (13 decks)

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