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Critical Care > Ch.19 Common Cardiovascular Disorders > Flashcards

Ch.19 Common Cardiovascular Disorders Flashcards

1
Q

Describe the pericardium. What are the different layers? How much fluid is in the pericardial space?

A

There are two layers: the tough fibrous lay and the inner serous layer

Inner serous layer has two sublayers: the parietal and visceral (epicardium)

The pericardial space holds anywhere from 10-50ml of serous fluid.

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2
Q

What is pericarditis? What defines any pericarditis as being an acute event?

A

Pericarditis is the inflammation of the percardium

Any pericarditis that lasts no longer than 1-2 weeks is considered acute.

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3
Q

Is most pericarditis (90%) found to be idiopathic?

A

YES YES YES

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4
Q

What is dressler syndrome?

A

pericarditis, malaise, fever, and elevated WBC count weeks to months after an MI

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5
Q

What is constrictive pericarditis? How is this treated? is this effective?

A

the formation of adhesions after repeated bouts of pericarditis that dont allow the heart to fill properly during diastole.

it is treated by removing the diseased portion of the pericardium, and it isnt very effective, most people even with successful removal dont have a long term survival rate.

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6
Q

What is the biggest symptom that occurs in patients with pericarditis?

A

chest pain that seems pleuritic and worsens by breathing deeply or lying supine, relieved by sitting up, leaning forward, and shallow breaths.

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7
Q

What can confirm but not rule out the diagnosis of pericarditis?

A

pericardial friction rub (rasping or scraping high-pitched sound that varies with cardiac cycle)

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8
Q

Where is a pericardial friction rub best heard?

A

diaphragm of stethescope over the lower to middle left sternal edge.

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9
Q

What are some complications of pericarditis to watch out for?

A

constrictive pericarditis

pericardial effusion possibly leading to tamponade

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10
Q

What labs would be ran to see about possible pericarditis?

A

CBC, cardiac enzymes (inflammation may extend to myocardium), CRP, sed rate, rheumatoid factors, antinuclear antibody titers, blood culture if evidence of infection, viral study if diagnostic workup is negative.

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11
Q

When do most cases of pericarditis abate? is recurrence common?

A

after 2-6 weeks

recurrence is rare

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12
Q

What is the basic treatment of pericaridits?

A

NSAIDS (aspirin or ibuprofen)

Colchicine

steroids (if seemingly autoimmune)

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13
Q

What is myocarditis?

A

myocarditis is the inflammation of the myocardium.

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14
Q

What is the difference between primary and secondary myocarditis?

A

Primary: acute viral infection or autoimmune response to the infection

Secondary:related to a specific organism

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15
Q

Why is myocarditis so devastating?

A

its prevalence is unknown because its clinical presentation is subacute most often. It is a progressive disease with a poor prognsis becuase of the high risk for dysrhythmias, CHF, and death.

it is a leading cause of sudden death in young athletes.

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16
Q

How is myocarditis definitively diagnosed, but not ruled out?

A

endomyocardial biopsy

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17
Q

What things could indicate a diagnosis of myocarditis?

Do these differ from viral?

A

fatigue, dyspnea, palpitations, precordial discomfort, slight rise in serum enzyme levels, non-specific ST-T wave changes

with viral there is typically a delay of onset of cardiac symptoms (CHF, dysrhythmias)

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18
Q

How is myocarditis treated and managed?

A

it is very similar to the treatment for heart failure.

Help the family deal with reality of the potentially lethal disease that often doesnt resolve.

heart transplant or mechanical circulation may be the end result.

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19
Q

If an athlete has myocarditis,can they return to competitive sports, is so, when?

A

withdraw from competitive sports for at least 6 months following the onset of the disease.

returning to sports depends on normalizing cardiac function and no clinical signs of abnormal function, such as dysrhythmias

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20
Q

Describe endocarditis.

A

an infection of the endocardial surface of the hear including the valves

caused by bacteria. viral, or fungal agents.

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21
Q

What are some risk factors for infectious endocarditis

A

prior cardiac condition (including congenital heart disease)

Bloodstream infection

Mitral valve prolapse

rheumatic heart disease

IV drug use (illicit)

patients with prosthetic valves or long-term indweling devices

VALVE DISEASE

> 60 y/o

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22
Q

Why might there be such a rise in incidence of IE in pediatrics?

A

an increase in pediatric survival of congenital heart disease

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23
Q

Briefly describe the pathophysiology of the development of IE.

A

enodothelial damage creates turbulent blood flow

This blood flow aggregates platelets (especially in patients in hypercoagulable state)

platelet or fibrin clot on valve leaflet forms

clot is exposed to bacteria in the blood (commonly from dental or urologic procedures)

bacteria proliferates and interferes with normal valve function and eventually damages structure

these non-functioning valves can eventually lead to heart failure an particles from the vegetations or valves can become thrombii.

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24
Q

How does bacteria manage to proliferate on vegetations and valves?

A

turbulent blood flow concentrates number of bacteria by vegetation

vegetation itself covers bacteria with layers of platelets and fibrin protecting the colony from bodies defenses

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25
Q

When will symptoms of endocarditis usually occur within in relation to a precipitating event?

A

2 weeks

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26
Q

What are the possible processes that can cause symtpoms of endocarditis in a 2 week period?

A

bacteremia

fungemia

valvulitis

immunologic response (?)

peripheral emboli

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27
Q

What are some initial, nonspecific complaints that someone presenting with endocarditis may have?

A

malaise

anorexia

fatigue

weight loss

night sweats

FOCUS ON HISTORY AND PHYSICAL EXAM WHEN NONSPECIFIC SYMPTOMS APPEAR

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28
Q

What is the one thing that is most common in all patients presenting with endocarditis?

A

fever and a new or changed heart murmur

29
Q

20% of patients with IE have a presenting symptom of what?

A

stroke from septic emboli

30
Q

What are some more specific features of endocarditis?

A

box 19-4!

31
Q

What offer a definitive diagnosis of I.E.?

A

Persistent bacteremia caused by common pathogens of I.E. And evidence of myocardial involvement, like echocardiographic imaging of vegetation or a new or worsening murmur

This is Duke criteria

32
Q

How many separate cultures are drawn to diagnose I.E.?

A

Two or three

Take extra care in preparation to avoid contamination.

33
Q

How is I.E. Treated?

A

Antibiotics based on culture results

Look out for resistance, most therapies have been modified to account for this

Treat before specimens are identified, as soon as cultures are drawn

34
Q

When is surgery recommended for I.E.?

A

Presence of native or prosthetic valve dysfunction or dehiscence, severe CHF secondary to valve dysfunction, and uncontrolled infections

35
Q

How is I.E. Cured most often cured?

A

Prolonged antibiotic therapy

Entire colony needs to be eradicated from vegetation

36
Q

What is the difference between cardiomyopathy and myocarditis?

A

Myocarditis is inflammatory in its cause of damage while cardiomyopathy continues to have an idiopathic cause.

37
Q

What is the definition of cardiomyopathy?

A

Diseases of the heart muscle that cause cardiac dysfunction such as heart failure, dysrhythmias, or sudden death.

38
Q

What are the different categories and sub-categories for cardiomyopathy?

A

Dilated - ischemic and nonischemic

Hypertrophic

39
Q

Describe dilated cardiomyopathy.

A

An increase in myocardial cavity size because of ventricular wall thinning leading to impaired systolic function. As the cavity gets bigger the heart takes a globular shape.

40
Q

What can cause a decrease in myocardial contractility which may be the cause of the dilation of the chamber and thinning of the ventricular wall in the first place?

A

Ischemia, alcohol abuse, endocrine disorders, pregnancy, viral infections, muscular dystrophy, valvular disease, Ect…

41
Q

Describe the pathophysiology of dilated cardiomyopathy.

A

Decrease in contractility (EF less than 40%) leads to increased end systolic volume. This increase in preload eventually causes the hearts ventricles to dilate to accommodate. This further decreases strike volume. Eventually the mitral and tricuspid valves become insufficient.

42
Q

What is the third most common cause of heart failure, the most common cause of heart failure in the young, and the most common cause of heart transplantation?

A

DCM

43
Q

Is DCM familial?

A

Yes, 30-50% of cases are

44
Q

What is the most prevalent toxic cause of DCM?

A

Alcohol abuse

45
Q

What are the two different types of DCM?

A

Ischemic and nonischemic

46
Q

Describe ischemic cardiomyopathy.

A

Oxygen levels are inadequate enough to meet metabolic demands of myocardial cells. Decrease in oxygen = less ATP. Electrolyte pumps stop working which leads to mechanical and electrical dysfunction

47
Q

What can happen to myocardial tissue if it becomes very ischemic, but doesn’t die?

A

It can hibernate. Restoring the flow to this hibernating tissue can greatly increase myocardial function.

48
Q

What may happen if the chordae tendineae are damaged after an infarct?

A

This can lead to acute mitral regurge that may be life threatening if large enough

49
Q

Describe the pathophysiology of cardiogenic shock and how the body compensates.

A

Left ventricle empties poorly

End-diastolic pressure increases

Pulmonary artery pressure increases

Pulmonary edema results

Organ damage begins

Respiratory rate increases to supply more oxygen to blood because of poor gas exchange because of edema, also because of metabolic acidosis because of lactic acid production with damaged organs

50
Q

What is azotemia? What is it a sign of?

A

High levels of nitrogen containing products (like BUN and creatinine), higher than 20:1

51
Q

Pre renal Azotemia indicates that the kidneys have started to have decreased perfusion or function, what can happen if it is prolonged? What is this known as?

A

The ratio may be normalized, however creatinine and BUN will continue to rise. This is known as tubular necrosis.

52
Q

Other than damage to the kidneys, what else can happen with prolonged episodes of low cardiac output?

A

Ileus, bowel infarction, liver failure, pneumonia, skin breakdown

53
Q

How does nonischemic DCM develop?

A

Many times it is idiopathic, but there are many other causes that directly damage the heart muscle that arent due to ischemia.

54
Q

Can both ischemic and nonischemic DCM be acute or chronic?

A

Yes they can, both of which in chronic the symptoms come on more subtle and the body has time to compensate in most cases (for a while), acute not so much

55
Q

What may cause acute nonischemic DCM?

A

Myocarditis

56
Q

What may cause chronic nonischemic DCM?

A

Alcoholism and HTN

57
Q

When do people most often get treatment for their DCM?

A

After HF becomes uncompensated (interferes with daily activities)

58
Q

Can medications slow progression of DCM?

A

No, they will treat symptoms, structural changes are progressive in most cases (unless hyperthyroidism, hypothyroidism, hemochromatosis, valvular disease, and tachycardia are causes it may be reversed)

59
Q

What are the final treatments for advanced DCM?

A

Heart transplant or ventricular assist devices

60
Q

When would an ICD be placed?

A

If there is a risk for sudden death due to dysrhythmias.

61
Q

Describe hypertrophic cardiomyopathy.

A

This is due to a dysfunction in diastole because of limited space in the dilated ventricle that doesn’t fully relax in diastole.

Sometimes the septal wall can hyper trophy, causing a dysfunction in the outflow of blood from the left ventricle during systole

62
Q

Is HCM genetic?

A

Yes, it is the most common genetic cardiovascular disorder.

63
Q

Is HCM a secondary disorder?

A

NO

64
Q

What is HCM the leading cause of in the US?

A

Sudden death in athletes in competitive and recreational sports. Due to the risk for sudden death from ventricular dysrhythmias.

65
Q

How is HCM often found?

A

Investigation of a murmur or during a family screening.

66
Q

What is the most common symptom of HCM?

A

Dyspnea especially on exertion

67
Q

How is HCM confirmed?

A

LVH on echo, borderline LVH may be normal in competitive athletes

68
Q

Do patients with HCM get ICDs?

A

Yes, if they have had ventricular dysrhythmias before or have survived sudden death.

69
Q

What can be done with septal hypertrophy?

A

Ablation or surgical removal of portion of septum.

Critical Care (11 decks)

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