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Multaq Phase One > Module 4 - Common CoMorbidities Associated with Afib > Flashcards

Module 4 - Common CoMorbidities Associated with Afib Flashcards

1
Q

Adrenergic

A

activated by epinephrine or any of various substances having epinephrine-like activity

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2
Q

Bruit

A

an abnormal sound or murmur

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3
Q

Cardiac output

A

the amount of blood pumped out by the ventricles in a given period

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4
Q

Cavitary dilatation

A

abnormal enlargement of a cavity of the body

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5
Q

Cheyne-Stokes respiration

A

an abnormal type of breathing seen especially in comatose patients, characterized by alternating periods of shallow and deep breathing

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6
Q

Comorbid

A

existing simultaneously with and usually independently of another medical condition

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7
Q

Cor pulmonale

A

a heart condition resulting from disease of the lungs or of their blood vessels

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8
Q

Coronary artery bypass grafting

A

a type of surgery called revascularization, used to improve blood flow to the heart in people with severe coronary artery disease

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9
Q

Diaphoresis

A

perspiration, especially when copious and medically induced

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10
Q

Diastolic

A

in blood pressure, the arterial pressure during the interval between heartbeats

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11
Q

Dilatation

A

in cardiology, an abnormal enlargement of an atrium or ventricle

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12
Q

Dyspnea

A

shortness of breath, can be associated with exertion or may occur at rest

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13
Q

Ectopic

A

occurring in an abnormal position or place; displaced

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14
Q

Ejection fraction

A

the ratio of the volume of blood the heart empties during systole to the volume of blood in the heart at the end of diastole expressed as a percentage usually between 50% and 80%

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15
Q

Endocardial thickening

A

the thin membrane that lines the interior of the heart becomes thick

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16
Q

Hemochromatosis

A

a hereditary disorder of iron metabolism characterized by excessive accumulation of iron in tissues, diabetes mellitus, liver dysfunction, and a bronze skin pigmentation

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17
Q

Hypertrophy

A

abnormal enlargement of a part or organ; excessive growth

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18
Q

Mitral valve annulus

A

the circular or ring-shaped valve between the left atrium and left ven- tricle of the heart, consisting of two triangular flaps of tissue, that pre- vents the blood from flowing back into the atrium

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19
Q

Neurohumoral

A

pertaining to neural and cellular characteristics

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20
Q

Orthopnea

A

difficult or painful breathing except in an erect sitting or standing position

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21
Q

Percutaneous revascularization

A

treatments such as cryoplasty, stent placement, and atherectomy that restore blood circulation of an organ or area, achieved by unblocking obstructed or disrupted blood vessels or by surgically implanting replace- ments, specifically by way of the skin (by injection or transdermally)

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22
Q

Plasminogen

A

the blood substance that forms plasmin when activated

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23
Q

S3 gallop

A

a low-pitched heart sound that generally indicates the presence of left ventricular dysfunction

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24
Q

Sarcoidosis

A

a chronic, progressive, systemic granulomatous abnormal increase in reticuloendothelial cells of unknown etiology, characterized by hard tubercles

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25
Q

True or false: Extensive data show that a patient can be cured of AF after effective treatment or elimination of a condition that is considered to be potentially “reversible” (eg, myocardial infarc- tion).

A

False

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26
Q

Which of the following is NOT a cardiovascular condition associated with AF?

A

Hyperthyroidism

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27
Q

Vagally mediated atrial fibrillation generally occurs ___________.

A

At night AND after meals

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28
Q

Macroscopic and microscopic alterations in atrial tissue begin in the _______ of life.

A

First year*

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29
Q

Patients with coronary artery disease do not get an inadequate supply of blood and oxygen to a portion of  _______.

A

The Myocardium

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30
Q

All of the following factors have been shown to increase the risk of developing coronary artery disease ________

A
  • Family history
  • Overweight or obesity
  • Smoking
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31
Q

Idiopathic calcification of the mitral valve and annulus in elderly patients is generally associated with________

A

All of the following:

a. Systemic hypertension
b. Aortic stenosis
c. Diabetes

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32
Q

Cardiomyopathy is a type of heart disease in which __________

A

The heart becomes abnormally enlarged, thickened, or stiffened*

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33
Q

Hypertension precedes more than _______ of congestive heart failure occurrences

A

75%

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34
Q

Which of the following is a risk factor for congestive heart failure?

A

ALL of the following:

a. Advancing age
c. Myocardial infarction
d. Hypertension

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35
Q

Risk factors that should be identified in _________ are coronary artery disease, chronic hypertension, diabetes, a history of heavy alcohol use, and/or advanced age.

A

High-risk patients*

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36
Q

The small number of individuals with hypertophic cardiomyopathy who develop atrial fibrillation can also suffer from ____________

A

All of the following:

a. Hemodynamic deterioration leading to chest pain
b. Dizziness and syncope
c. Sudden cardiac death

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37
Q

AF may be related to a number of acute, reversible causes. These include:

A

• Binge drinking • Cardiothoracic and noncardiac surgery • Myocardial infarction (MI) • Pericarditis • Myocarditis • Hyperthyroidism • Electrocution • Pneumonia • Pulmonary embolism

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38
Q

Specific cardiovascular conditions associated with AF include:

A

• Hypertension (particularly when left ventricular hypertrophy [LVH] is present) • CAD • Valvular heart disease • Cardiomyopathies • Heart failure

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39
Q

Atrial structural abnormalities (occur mostly in the setting of underlying heart disease associated with hypertension, CAD, valvular heart disease, cardiomyopathies, and heart failure).

A

Fibrosis Dilation Ischemia Infiltration Hypertrophy Inflammation

40
Q

Extra cardiac factors (have pathophysiologic effects on atrial cellular structure and/or function

A

Hypertension Obesity Sleep apnea Hyperthyroidism Alcohol/drugs

41
Q

Atrial electrical abnormalities

A

Increased heterogeneity Decreased conduction Decreased action potential duration/refractoriness Increase automaticity Abnormal intracellular calcium handling

42
Q

Is AF Inheritable?

A

AF is heritable, and having a family member with arrhythmias increases a persons’ risk of also having it. In addition, premature AF, defined as having a first-degree relative with the onset of AF before age 66, doubles a person’s risk of experiencing arrhythmias.

43
Q

What is vagally mediated AF?

A

in some patients, parasympathetic influences (sometimes referred to as “increased vagal tone”) may pre- dominate, causing slowing of the heart rate and inhibition of conduction through the AV node, whereas in others, sympathetic influences (sometimes referred to as increased adrenergic tone) may predominate, causing an increase in heart rate, blood pressure (BP), and contractility. Generally occurring at night or after meals, vagally mediated AF is more common than adrenergically induced AF, which often occurs during the day in patients with organic heart disease. In patients with vagally mediated AF, adrenergic blocking drugs or digitalis can worsen symptoms. Anticholinergic agents, such as disopyramide, may be help- ful in preventing recurrent AF in these patients.

44
Q

What types of histological changes may occur in association with aging?

A

• The quantity of epicardial fat may increase, particularly over the anterior surface of the right ventricle and in the atrial septum • The size of the left ventricular cavity may decrease, particularly in the base-to-apex dimension • The ascending aorta may shift to the right and become more tortuous • The mitral annulus and aortic valve may become calcified, leading to aortic stenosis in the latter case • Valves can develop fibrous thickening • Mitral leaflets tend to buckle back toward the left atrium during ven- tricular systole • Small filament-like processes may develop on the closure lines of aortic and mitral valves, probably arising from the organization of small thrombi on the valve contact margins

45
Q

What are the three major tenets of AF therapy:

A
  • Restoration and maintenance of sinus rhythm
  • Ventricular rate control
  • Prevention of thromboembolism
46
Q

View of the Progression of Atherosclerosis

A
47
Q

Epidemiology of CAD

A

CAD is the single greatest cause of death and disability in the devel- oped world. It is also responsible for higher economic costs than any other illness. In the United States, CAD is the most common serious, chronic, life-threatening illness:

  • 13 million persons have CAD
  • More than 6 million have angina pectoris
  • More than 7 million have sustained MIs

The increase of CAD is largely due to high-fat and energy-rich diets, smoking, and sedentary lifestyles.

48
Q

The annual mortality rate from MI has decreased significantly over the past 30 years for several reasons

A
  • Lifestyle changes such as decreased smoking, changes in diet, and increased exercise
  • Modification of risk factors with or without drug treatment
  • Advances in the treatment of CAD and acute MI
49
Q

CAD Mortality Rates

A

Approximately 1.5 million Americans have acute MIs each year. Almost one-third of those cases result in death. Nearly half of the deaths occur before the patients receive emergency medical care of any type.8

50
Q

CAD Risk Factors

A

Cigarette smoking

Serum cholesterol

  • Total >240 mg/dL
  • LDL >130 mg/dL
  • HDL <35 mg/dL

Triglycerides >200 mg/dL Male gender

Diabetes mellitus

Hypertension

Family history of early heart disease

Obesity

Inactivity

51
Q

Chronic Stable Angina Pectoris

A

Stable angina pectoris is the most benign of three syndromes. It occurs as a result of an imbalance between oxygen supply and demand in the myocardium.

This mismatch of coronary blood supply and myocardial metabolic demand can result in no symptoms or minimum myocardial damage in some patients or in full-blown isch- emia and infarction in others.17

52
Q

Primary treatment of CAD

A
  • Lower blood lipids by dietary and pharmacologic methods
  • systemic hypertension should be treated to target BPs consistent with treatment guidelines
  • Patients should also be strongly encouraged to lose weight, stop smoking, and increase their level of daily exercise.
53
Q

Unstable angina/NSTEMI

A

is unpredictable and is classified as an acute coro- nary syndrome and should be treated as an emergency. This is some- times described as17:

  • Angina at rest
  • Severe angina of new onset
  • Increased severity or frequency of previously stable angina

The most common cause is reduced myocardial perfusion resulting from coronary artery narrow- ing due to a nonocclusive thrombus that has developed on a disrupted atherosclerotic plaque.

54
Q

Unstable angina or NSTEMI presents clinically in one of several ways:

A
  • Prolonged angina at rest, usually lasting less than 20 minutes
  • New-onset angina that is severe, disabling, and prolonged or frequent
  • More frequent occurrences of established angina
  • Angina that is longer in duration
  • Angina that occurs with less provocation
55
Q

Pts. with unstable angina or NSTEMI are handled in one of three ways:

A
  1. Admitted to a cardiac care unit that provides continuous ECG moni- toring and specialized nursing
  2. Hospitalized in an institution that offers mechanical revascularization
  3. High-risk patients should receive interim treatment with an intensive pharmacologic regimen until arrangements can be made for trans- fer to a facility with interventional capability
56
Q

Acute Myocardial Infarction

A

nearly all cases of acute MI are caused by thrombotic occlusion of a coronary artery, often in the presence of fixed narrowing caused by atherosclerotic plaque.

We now know that, in most cases, acute coronary artery occlusion occurs at sites in the coronary artery circulation that have stenosis of less than 70%.

Patients are at increased risk for MI if they have unstable angina with increasingly frequent and severe symptoms.

57
Q

TX Protocol for AMI

A

one of the key tenets of the therapeutic approach to patients with suspected MI is to reduce the time from onset of symptoms to initiation of treat- ment, which generally involves some form of reperfusion therapy. The protocol that has been used includes the following recommendations8:

  • All patients with definite or suspected MI should be admitted to the hospital and undergo preparation for intravenous access
  • All should be placed on continuous ECG monitoring
  • High-risk patients should be admitted to a coronary care unit

Lidocaine, atropine, an external or internal pacemaker, and a defibrillator are readily available because of the chance of tachyarrhythmia and bradyarrhythmia, particularly in the first 24 hours.

58
Q

How Coronary Artery Disease
May Contribute to Atrial Fibrillation

A

AF is not commonly associated with CAD. The exceptions are when it is complicated by acute MI or heart failure. AF occurs transiently in only 6% to 10% of patients with acute MI. This type of occurrence is pre- sumed to be due to atrial ischemia or atrial stretching after heart failure.

There is evidence, however, from several studies that AF is an independent predictor of increased mortality in patients with stable CAD. In the CASS study, the relative risk was 1.98 at 7 years.

59
Q

VALVULAR HEART DISEASE

A

The most common are:

  • Rheumatic carditis
  • Degenerative conditions of the valve collagen
  • Infection

Less frequently, valves may be involved with:

  • Collagen vascular disorders
  • Tumors
  • Carcinoid
  • Marfan’s syndrome
60
Q

Signs and Symptoms of Valvular Disease

A

include signs and symptoms of cardiac illness, such as:

  • Shortness of breath
  • Pulmonary edema
  • Angina pectoris
  • Syncope

It is common for patients with valvular abnormalities to show no symp- toms until the onset of an underlying medical illness precipitates heart failure

61
Q

Two Categories of Valve Lesions

A

Valvular heart disease lesions are generally categorized as stenotic and regurgitant.

62
Q

Valvular Stenosis

A

Often due to infection that causes inflammation that heals as fibrous tissue

leaflets of the valves and supporting structions can become fibrotic and thick, possible fusing and then becomming calcified

Impact is greatest on the RV ans pulmonary vasculature

63
Q

Valvular Regurgitation

A

Competence of the mitral valve depends on integrated functioning of the:

  • Mitral annulus
  • Valve leaflets
  • Chordae tendineae
  • Papillary muscles
  • Ventricular wall

**Incompetence can be caused by abnormalities of any of these structures. **

During regurgitation, chordae tendineae become fibrotic, fused, and shortened.

Idiopathic calcification of the mitral valve and annulus in elderly patients can be an important cause of regurgitation. It is generally associated with:

  • Systemic hypertension
  • Aortic stenosis
  • Diabetes
  • Chronic renal failure
64
Q

How Valvular Heart Disease Contributes to Atrial Fibrillation

A

A study evaluated the frequency of AF in approximately 1100 patients with rheumatic heart disease. The prevalence varied with the type of valve disease:

  • Mitral stenosis, mitral regurgitation, and tricuspid regurgitation — 70%
  • Mitral stenosis and mitral regurgitation — 52%
  • Isolated mitral stenosis — 29%
  • Isolated mitral regurgitation — 16%

However, only about 1% of patients with aortic stenosis who did not have heart failure also had AF.

The rate at which AF occurs was evaluated in a study of 89 patients with mitral valve prolapse and 360 patients with flail leaflets. Every patient was in sinus rhythm at the time of diagnosis. The rate of AF development was about 5% per year for both types of lesions

65
Q

When to Treat High Blood Pressure

A

JNC 8: Treatment for high blood pressure

60+ years and older should be started when blood pressure reaches ≥150/≥90 mm Hg. Treatment goals should be to reach a blood pressure level <150/90 mm Hg.

<60 years, treatment should be started when blood pressure reaches ≥140/≥90 mm Hg, with a treatment goal of <140/90 mm Hg.

66
Q

Hypertension Epidemiology

A

About 1 in every 3 Americans has hypertension, a disease that costs the nation more than $47 billion a year.

  • average systolic BP is higher for men than for women
  • aged 65 and older, women have higher systolic BPs than do men
  • Among adults, blood pressure increases progressively with age

In men and women in the United States, respectively, hypertension affects23:

  • 43% and 46% of African Americans
  • 28% and 29% of Mexican Americans
  • 34% and 31% of White Americans
67
Q

HTN Risk Factors

A

Certain medical conditions and unhealthy lifestyle habits increase the risk for hypertension.23

• Medical conditions

o Pre-hypertension (blood pressure that is higher than normal but not yet in the range of high blood pressure)23

o Diabetes
• Unhealthy lifestyle habits

o Tobacco
o Eating foods high in sodium and low in potassium o Not getting enough physical activity
o Obesity
o Excessive alcohol intake

68
Q

Blood Pressure Measurements Related to Risk

A

An analysis of the Framingham Heart Study data revealed that the best predictor of risk was a high diastolic pressure in subjects younger than 50 years but high systolic pressure was the best predictor in those older than 60 years, when the relationship between diastolic pressure and risk changed, such that low diastolic pressure was related to higher risk.

69
Q

How Hypertensive Heart Disease Contributes to Atrial Fibrillation

A

Hypertension is associated with LVH, impaired ventricular filling, left atrial enlargement, and slowing of atrial conduction velocity. These changes in cardiac structure and physiology favor the development of AF .

70
Q
A

Currently, hypertension is the most prevalent, independent, and poten- tially modifiable risk factor for AF26:

  • The relative risk for development of AF in patients with hypertension is modest (relative risk, 1.4 to 2.1) compared with other conditions, including heart failure (relative risk, 6.1 to 17.5) and valve disease (relative risk, 2.2 to 8.3)
  • However, because almost 31% of people in the United States have high BP23, hypertension is the primary risk factor for AF in North America

Cohort studies have suggested that hypertension was present in over 50% of North American patients with AF and was believed to be causative in 15%.

71
Q

Left Ventricular Hypertrophy and HTN

A

One effect of hypertension on the heart is hypertrophy of the left ven- tricle. Currently, hypertension is the most prevalent, independent, and potentially modifiable risk for AF and leads to LVH.

The risk of developing AF also increases by 28% for each 4-mm increase in left ven- tricular thickness as measured by echocardiography.

72
Q

Left Atrial Enlargement and HTN

A

Once patients develop LVH that can be detected by ECG, the prevalence of left atrial enlargement is high, and studies have shown that the magnitude of atrial enlargement correlates with the degree of hypertension and increases the risk of AF.

73
Q

Atrial Electrophysiology and HTN

A

Two distinct abnormalities have been described:

  • Prolongation of atrial conduction velocity
  • Decrease in atrial refractoriness

Both of these changes are associated with the development and main- tenance of AF.

74
Q

Congestive Heart Failure - CHF

A

a clinical syndrome that occurs in patients who, because of an inherited or acquired abnormality of cardiac structure and/or function, develop a constellation of clinical symptoms and signs (dyspnea, rales, elevated jugular venous pressure, and edema) and/or manifestations of inadequate tissue perfusion (impaired exer- cise tolerance, fatigue, signs of hypoperfusion, renal dysfunction) that lead to **frequent hospitalizations, poor quality of life, and a shortened life expectancy **

75
Q

Causes of CHF

A

CHF may result from any of the following:

  • Impaired myocardial contractility (systolic dysfunction, commonly characterized as reduced LVEF)
  • Increased ventricular stiffness or impaired myocardial relaxation (diastolic dysfunction, which is commonly associated with a rela- tively normal LVEF)
  • Other cardiac abnormalities, including obstructive or regurgitant val- vular disease, intracardiac shunting, and disorders of heart rate or rhythm
  • States in which the heart is unable to compensate for increased peripheral blood flow or metabolic requirements
  • An acute insult to cardiac function, such as a large MI, but, more commonly, from a chronic process often referred to as ischemic cardiomyopathy
76
Q

CHF is not a separate disease entity

A

It is a pathophysiological state characterized by congestion in the pulmonary and/or systemic circulation. This congestion occurs when the heart is unable to pump enough oxygenated blood to meet the metabolic needs of the tissues.

CHF is a syndrome or physiological state, whereas the other disorders described in this chapter are actual car- diac diseases

77
Q

Epidemiology of CHF

A

Both the incidence and the prevalence of heart failure are growing, as is the resulting burden of deaths and hospitalizations.

The incidence of heart failure increases with age

Although the relative incidence of heart failure is lower in women than in men,31 the rate of mortality in women with heart failure is greater than the rate in men

78
Q

CHF Common Causes

A

The most common causes of CHF in the United States are32:

  • CAD
  • Systemic hypertension
  • Nonischemic dilated cardiomyopathy
79
Q

Risk Factors for CHF

A

Risk factors for CHF include:

  • Advancing age
  • Previous MI
  • Hypertension (precedes over 75% of CHF occurrences )
  • Diabetes mellitus
  • Valvular heart disease
  • Obesity
80
Q

New York Heart Association Classification for CHF

A

The New York Heart Association (NYHA) functional classification scheme is used to assess the severity of functional limitations and cor- relates fairly well with prognosis

81
Q

Other Clinical Manifstations of CHF

A

Other clinical manifestations that occur in some patients with CHF include:

  • Nocturnal angina resulting from increased cardiac work (secondary to increased venous return)
  • Cheyne-Stokes respiration — alternating phases of apnea and hyper- ventilation caused by prolonged circulation time from lungs to brain
  • Fatigue and lethargy resulting from low cardiac output
  • Patients with failure of the left side of the heart will have the following abnormalities on physical examination: pulmonary rales, tachy- pnea, S3 gallop, cardiac murmurs (aortic stenosis, aortic regurgitation, mitral regurgitation), paradoxical splitting of S2
  • Acute precipitants of CHF exacerbations include noncompliance with salt restriction, pulmonary infections, arrhythmias, medications (e.g., calcium channel blockers, antiarrhythmic agents), and inappro- priate reductions in CHF therapy
82
Q

ACC/AHA Classifications for CHF

A

The ACC and AHA have developed a classification of heart failure based on stages of the syndrome (Table 4-8).

83
Q

Goals in the management of CHF are :

A

Goals in the management of CHF are:

  • Preventing or eliminating symptoms
  • Improving quality of life
  • Prolonging survival
84
Q

Approaches to Achieving Therapeutic Goals

for Congestive Heart Failure

A

Three general approaches to achieving therapeutic goals include recognition and treatment of underlying cardiac disease, removal of precipitating factors, and management of heart failure symptoms.

85
Q

How Congestive Heart Failure Contributes to Atrial Fibrillation

A

The pathophysiology of heart failure is linked to the pathophysiology of AF in several ways, including neurohormonal modulation, mechanical remodeling, and ion-channel remodeling.

86
Q

Neurohumoral Modulation

A

In CHF, neurohumoral modulation with elevated concentrations of catecholamine and angiotensin II may promote atrial fibrosis, which impairs atrial conduction.

87
Q

Structural Remodeling

A

Heart failure is associated with enlargement of the left atrium in many patients, a structural change that promotes the development of AF and multiple electrical wavefronts.

88
Q

Atrial Ionic Channel Remodeling

A

Changes in atrial ionic channels may contribute to structural changes in HF. In addition, calcium currents and potassium currents play an important role in the electrical remodeling that takes place in AF.

89
Q

Effects of Atrial Fibrillation on Heart Failure

A

The adverse effects of AF on heart failure include38:

  • A loss of atrial contribution to ventricular filling
  • A non-physiological heart rate response
  • Irregular periods of ventricular filling

The resultant hemodynamic changes can lead to further deterioration of cardiac function by reducing stroke volume, cardiac output, and peak oxygen consumption. In addition, impaired contraction of the atria increases the risk of thromboembolism.

90
Q

Cardiomyopathy

A

The term “cardiomyopathy” means “disease of the cardiac muscle.”

It is a type of heart disease in which the heart becomes abnormally enlarged, thickened, and/or stiffened. As a result, the cardiac muscle’s ability to pump and/or receive blood is usually decreased. This condi- tion is generally progressive and may lead to heart failure.

91
Q

Cardiomyopathies cause symptoms such as:

A
  • dyspnea,
  • chest pain,
  • fainting,
  • dizziness,
  • exercise intolerance.
92
Q

Ischemic Cardiomyopathy

A

Ischemic cardiomyopathy is a chronic disorder caused by either MI or CAD. CAD often leads to episodes of cardiac ischemia, in which the cardiac muscle does not receive enough oxygen-rich blood.

Additionally, as a result of one or more MIs, the heart enlarges because of the fibrosis, which results in a decreased quantity of func- tioning cardiac muscle to pump blood.

93
Q

Congestive Cardiomyopathy

A

Congestive cardiomyopathy (also called “dilated” cardiomyopathy) occurs when the cardiac muscle is enlarged and weakened and can- not pump adequate oxygen-rich blood to the body.

94
Q

Nonischemic Cardiomyopathies

A

Nonischemic cardiomyopathies tend to be progressive diseases, although they are less common than ischemic cardiomyopathies.

95
Q

Hypertrophic Cardiomyopathy

A

Hypertrophic cardiomyopathy is characterized by the abnormal growth of muscle fibers on the cardiac muscle, often causing a thickened wall between the right and left ventricles.

It is generally considered a genetic disease that affects about 0.2% of the population.

96
Q

How Cardiomyopathy Contributes to Atrial Fibrillation

A

Approximately 15% of patients with hypertrophic cardiomyopathy develop AF. In these individuals, AF can result in profound hemodynamic deterioration, leading to chest pain, dizziness, syncope, and even sudden cardiac death. **Dilatation of the left ventricle and left atrium in patients with cardiomyopathy and heart failure can cause AF through tissue stretching and fibrosis. **

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