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PC705 Pathophysiology > Module 5 Cardiac Disorders > Flashcards

Module 5 Cardiac Disorders Flashcards

1
Q

Does cardiovascular disease “run in families”?

A

YES

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2
Q

What is the primary cause of CAD (coronary artery disease)?

A

Atherosclerosis

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3
Q

What % of atherosclerosis is attributed to genetics?

What are many of these genes associated with?

A

50%

Inflammation

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4
Q

What is multifactorial atherosclerosis?

A

many different genes working together to cause the problem

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5
Q

What are single gene causes of atherosclerosis/CAD?

A

Familial hypercholesterolemia- autosomal dominant
Familial hyperlipidemia- Autosomal recessive
Familial apolipoprotein A-deficienc- Autosomal recessive

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6
Q

What is an environmental risk factor for CAD that has genetic influence?

A

Tobacco / Smoking

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7
Q

What is the most common arrhythmia?

A

Atrial fibrillation

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8
Q

Is atrial fib caused more often by single gene or multifactorial?

A

Multifactorial. Very few single gene cases.

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9
Q

What is genetic heterogeneity?

A

Several different genes can independently cause disease.

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10
Q

What is long QT syndrome (LQTS)?

A

A group of disorders that involve a delay in repolarization during the cardiac cycle.

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11
Q

How many people are affected by LQTS?

A

1:2,000-3,000

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12
Q

What is considered a long QT interval for men and women?

A

Men: >440msec; Women .460msec

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13
Q

Is LQTS dangersous? What can occur?

A

Yes, potentially lethal. torsade de pointes (a lethal polymorphic ventricular tachycardia can occur.

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14
Q

What can trigger torsade de pointes (deadly arrhythmia) in someone with LQTS?

A

Electrolyte imbalance, swimming, sudden loud noises, bradycardia, etc.

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15
Q

What are channelopathies?

A

Arrhythmias caused by problems with genes coding for ion channels (sodium, potassium, and calcium)

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16
Q

Name one channelopathy.

A

Long QT Syndrome

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17
Q

What ion channel is responsible for the majority of Long QT Syndrome?

A

Potassium channel.

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18
Q

Besides channelopathy, what are other causes of LQTS?

A

Private mutation - in one individual
Congenital- present at birth. Can be autosomal recessive or autosomal dominant.
Drug induced- many different drugs are listed

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19
Q

What characterizes coronary heart disease?

A

Insufficient delivery of oxygenated blood to the myocardium (ischemia), because of atherosclerotic coronary arteries. (vascular disorder that narrows coronary arteries)

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20
Q

How many people die per year from heart disease?

A

600,000

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21
Q

What is the leading cause of death for men and women?

A

Heart disease.

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22
Q

What is the most common heart disease?

A

Coronary heart disease (CHD) also known as Coronary artery disease (CAD)

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23
Q

How many people have an MI per year? Is it usually the first MI of more often a repeat?

A

720,000. Most of the time it is a first MI.

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24
Q

Does CHD affect all ethnicities?

A

YES

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25
Q

What are the sequelae of CHD?

A 
Angina
MI
Dysrhythmias
Heart failure
Sudden cardiac death
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26
Q

Nonmodifiable risk factors for CHD.

A

Age: 45 and over for men; 55 and over for women
Gender: male
Family hx of premature CHD:
MI or sudden cardiac death in male 1st degree relative at age less than 55 or female 1st degree relative at age less than 65

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27
Q

Modifiable risk factors for CHD.

A

Dyslipidemia, hypertension, smoking, DM,obesity, sedentary lifestyle

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28
Q

Lipid Risk Factors

A

Total cholesterol >200mg/dl
LDL cholesterol >130mg/dl
Triglycerides >150mg/dl
HDL cholesterol <40mg/dl

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29
Q

Non-traditional risk factors for CHD.

A

Non-traditional – markers of inflammation and thrombosis – C-reactive protein, fibrinogen, protein C, and plasminogen activtor inhibitor; hyperhomocysteinemia (Lee, 2008), and infection

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30
Q

Differentiate between stable plaques and vulnerable plaques in artherosclerosis.

A

Stable plaques - have more collagen and fibrin with a stable cap; usually asymptomatic or may be associated with exercise induced angina (stable angina)

Vulnerable plaques - have large lipid core and thin caps; hypertension causes high shear on the thin cap.

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31
Q

Pathogenesis of unstable plaque / thrombus formation

A

Thin cap - shear/ inflammation, apoptis- rupture of plaque - increased inflammation with release of multiple cytokines / platelet adherance - thrombus formation and vasoconstriction of vessel - decrease in coronary blood flow - unstable angina or MI

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32
Q

When does ischemia of the cardiac cells occur?

A

When the oxygen supply is insufficient to meet metabolic needs.````

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33
Q

What are two factors that can cause ischemia?

A

Impaired coronary perfusion: large, stable atherosclerotic plaque, acute platelet aggregation and thrombosis, vasospasm, and failure of autoregulation by microcirculation (Chronic - stable angina; Acute- MI or cardiac arrest)

Increased myocardial workload: heart rate, preload, afterload, and contractility (increasing in these)

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34
Q

What is angina pectoris?

A

Means chest pain and is associated with intermittent myocardial ischemia.

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35
Q

Stable angina facts.

A
  • Most common
  • Predictable, elicited by similar stimuli each time (physical exertion, emotional stress)
  • Relieved by rest or nitroglycerin
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36
Q

Prinzmetal variant angina facts.

A
  • Unpredictable
  • Unrelated to exertion
  • Occurs at rest
  • Most people affected have significant coronary artherosclerosis
  • Vasospasm is probable cause
  • Treated with calcium channel blockers
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37
Q

List the two Acute Coronary Syndrome conditions.

A

Unstable angina and Myocardial infarction

38
Q

Unstable angina facts.

A
  • Occlusion is partial or clot is dissolved before death of myocardial tissue.
  • Unpredictable; worsens over time
39
Q

What happens in myocardial infarction?

A

Total loss of flow to an area of the heart; no oxygen

40
Q

Signs and symptoms of MI.

A

Severe crushing chest pain that may radiate to shoulder, back , jaw, or down arm, nausea, vomiting, diaphoresis, and anxiety

41
Q

Describe pain of MI.

A

Severe crushing pain that last >15min despite rest or nitro.

42
Q

What EKG changes occur with an MI?

A

ST segment elevation due to injury and ischemia.

Large Q waves and inverted T waves are caused by necrotic tissue.

43
Q

What are the serum markers for diagnosing an MI?

A

Elevated CK-MB

Elevated Troponin I & T - markers of choice

44
Q

Events of MI (3 things happen)

A
  1. Inflammation of cardiac muscle- fever, leukocytosis & elevated sedimentation rate.
  2. Decreased cardiac output- fatigue, restlessness, anxiety & weakness
  3. Sympathetic nervous system activation (compensatory)- increased heart rate, vasoconstriction
45
Q

What factors affect prognosis after MI?

A

extent and location of infarct, previous CV health, age, comorbidities, & particularly how quickly tx is sought.

46
Q

MI causes decreased SV(stroke volume). What does this cause?

A

Enhanced preload, hypertrophy of cardiacmyocytes and Activation of SNS, which increases HR, BP and fluid retention by kidney. Imposes greater workload on heart and may contribute to further ischemic damage

47
Q

What is sudden cardiac death?

A

Unexpected death within 1 hour of onset of symptoms

48
Q

What is primary cause of sudden cardiac death?

A

Lethal dysrhythmia like v-fib

49
Q

What is heart failure?

A
  • Chronic Ischemia Cardiomyopathy- heart failure develops insidiously as a consequence of progressive ischemic myocardial damage.
  • Due to progressive apoptotic death of myocytes
  • More common in older adults
50
Q

What is the cause of rheumatic heart disease?

A
  • Consequence of rheumatic fever, which is an acute inflammatory disease (immune response) to group A beta hemolytic strep
  • Rheumatic fever affects heart, joints, and skin, & kidneys.
  • Has a genetic predisposition
51
Q

At what rate and who does rheumatic fever affect?

A

Age 5-15 and 3% of those with strep throat will develop rheumatic fever.

52
Q

What are the clinical manifestations of rheumatic fever?

A
  • endocardial inflammation, which damages valves

- joint inflammation, involuntary movements (Sydenham chorea), and a distinctive truncal rash

53
Q

What % of people with rheumatic fever will develop rheumatic heart disease?

A

10%

54
Q

What are the rates for valvular damage in rheumatic heart disease?

A
  1. Mitral valve alone- 50-60%
  2. Mitral and aortic valve- 20%
  3. Mitral, aortic, and tricuspid- 10%
55
Q

How are the valves damaged in Rheumatic heart disease?

A

Causes rigidity and deformity of the cusps and shortens and fuses the cordate tendinae. Results in valvular stenosis or regurgitation.

56
Q

What three things can cause endocardial and valvular structure damage?

A
  1. Inflammation and scarring
  2. calcification
  3. Congenital malformations
57
Q

What is the result of valvular structure damage?

A

Altered hemodynamics which lead to increased myocardial workload, ultimately resulting in heart failure.

58
Q

Define stenosis and give results.

A

Falure of valve to open completely. Results in extra pressure & work for the heart; progresses slowly, heart chambers compensate through myocardial cell hypertrophy.

59
Q

Define regurgitation and give results.

A

Inability of a valve to close completely, causing a backward flow; Results in extra volume work for the heart; may develop suddenly from infection and is poorly tolerated (little compensation)

60
Q

Define Mitral stenosis & list clinical manifestations.

A

Blood flow from left atrium into left ventricle is impaired, because mitral valve does not open completely. (major etiology- Rheumatic heart disease)
-Left atrial chamber enlargement and hypertrophy; if left uncorrected can result in chronic pulmonary hypertension, right ventricular hypertrophy and right sided heart failure.

61
Q

Describe mitral stenosis murmur.

A

Low-pitched rumble, diastolic; at apex

62
Q

Most common complaint with mitral stenosis.

A

Exertional dyspnea.

63
Q

Define mitral regurgitation and list clinical manifestations.

A

Backflow of blood from left ventricle to left atrium during ventricular systole, caused by inability of mitral valve to close completely. Results in hypertrophy of left atrium and ventricle, which may lead to left sided heart failure.

64
Q

Describe mitral regurgitation murmur.

A

Loud, pansystolic, high pitched, blowing; loudest at apex, transmitted to left axilla

65
Q

Most common complaints with mitral regurgitation.

A

Chronic weakness and fatigue.

66
Q

Define mitral valve prolapse and list clinical manifestations.

A

Most common valvular problem- 2-3% of population.
Mitral valves that balloon into the left atrium during ventricular systole.
Women affected twice as much.
Typically asymptomatic

67
Q

Sounds heard with MVP.

A

Midsystolic click; systolic murmur

68
Q

Define and list clinical manifestations of aortic stenosis.

A
  • Failure of the aortic valve to open completely.
  • Results in obstruction of aortic outflow and compensatory left ventricular hypertrophy. Predisposes to ischemia and angina. Continued high left ventricular afterload my lead to left sided HF. slow HR
69
Q

Describe murumr in aortic stenosis.

A

Harsh midsystolic crescendo-decrescendo; at right 2nd intercostal space, transmitted to neck

70
Q

What is the most common cause of aortic stenosis?

A

Senile calcification.

71
Q

Define and list clinical manifestations for aortic regurgitation.

A
  • Incompetent aortic valve (does not close completely) causes backflow from the aorta into the left ventricle during daistole.
  • Results in left ventricular hypertrophy increasing stroke volume and causes high systolic pressure. Diastolic lower than normal. Bounding peripheral pulsation.
72
Q

Most common cause of aortic regurgitation?

A

Abnormal aortic valve or **aortic root dilation

73
Q

Describe murmur in aortic regurgitation.

A

Faint, high pitched blowing, diastolic; Left sternal border, aortic area, apex

74
Q

Patient complaint in aortic regurgitation?

A

May be asymptomatic. But may have palpitations and throbbing or pounding heart.

75
Q

What is a cardiac dysrhythmia?

A

A cardiac rhythm abnormality affecting impulse generation or conduction

76
Q

Two reasons dysrhythmias are significant.

A
  1. Indicate underlying pathphysiologic disorder

2. They can impair normal cardiac output

77
Q

What are the characteristics of Normal Sinus rhythm?

A

Initiates in sinus node. Rate between 60-100.

78
Q

What is tachycardia? Causes?

A

Rate above 100. Sympathetic activation, decreased parasympathetic activity, fever, hyperthyroidism, pain, increased metabolism, low blood pressure, and hypoxia. Also is a compensatory response to reduced stroke volume.

79
Q

What is bradycardia? Causes?

A

Rate less than 60. Increased parasympathetic activity, sleep, drugs, increased stroke volume, or acute hypertension. Also occurs in well conditioned individuals. Valsalva, carotid sinus massage.

80
Q

Sinus arrest.

A

Absence of impulse. asystole. Escape rhythm will usually fire after several seconds. MI, electrical shock, electrolyte imbalance, acidosis.

81
Q

Abnormal site of Impulse Initiation - List both, site, and rate

A
  1. Junctional - arises from A-V node, rate 40-60

2. Ventricular - arises from purkinjie fibers, rate 15-40, wide qrs

82
Q

Describe Premature atrial complexes

A

Originate in atria but not from s-a node. May be a precursor for more severe dysrhythmias.

83
Q

Atrial flutter and atrial fibrillation: rates, characteristics, causes and concerns.

A

Rates: 240-350 beats/min
Causes: underlying heart disease, fluid overload, or atrial ischemia.
Atrial fib is irregularly irregular and increases risk for stroke.

84
Q

Describe junctional dysrhythmia; junctional tachycardia.

A

Initiates just proximal or distal to the A-V node.

Junctional tach: junctional rate of 70-140

85
Q

Premature ventricular complexes.

A

Arise from ventricular myocardium- depolarizes ventricle but doesn’t activate atria.
Associated with CAD, drug overdose, and electrolyte disturbance (esp. hypokalemia).
Not clinically significant unless they are frequent.

86
Q

Describe ventricular tachycardia.

A
  • 3 or more ventricular complexes at rate over 100 beats/min
  • Associated with myocardial ischemia and infarction
  • High catecholemine levels and electroly balance may contribute.
  • Can be lethal
87
Q

Describe ventricular fibrillation.

A
  • Rapid, uncoordinated cardiac rhythm that results in ventricular quivering (lacks effective contraction)
  • Will result in death within minutes if not reversed.
88
Q

What is the most common type of heart failure?

A

Left sided

89
Q

Differentiate between systolic dysfunction and diastolic dysfunction in left sided heart failure.

A

Systolic heart failure = Inability of the heart to generate adequate Cardiac Output (low ejection fraction) to perfuse tissues
Diastolic heart failure – reduced ventricular compliance during diastole resulting in a ventricle that does not fill effectively – the ejection fraction remains normal

90
Q

Define Right sided heart failure.

A

Right sided heart failure
Inability of the right ventricle to provide adequate blood flow into the pulmonary circulation at normal central venous pressure.

91
Q

Define preload.

A

Pressure created at the end of systole; volume of blood in the ventricle after atrial contraction & ventricular filling.

92
Q

Define afterload.

A

Resistance to ejection during systole; the tension or pressure that must be generated by a chamber of the heart in order to contract and eject blood

PC705 Pathophysiology (8 decks)

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