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CPR Exam 1 > Arrhythmias, Hypertensive heart dz, Valvular heart dz > Flashcards

Arrhythmias, Hypertensive heart dz, Valvular heart dz Flashcards

1
Q

What is the most common cause of rhythm DOs?

A

Ischemic injury

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2
Q

Name and describe some rhythm DOs.

A

Sick sinus syndrome = SA node damaged –> bradycardia

Atrial fibrillation = myocytes depolarize independently and sporadically (atrial dilation) with variable transmission thru AV node

Heart Block = dysfunctional AV node

  • 1st degree = prolonged PR interval
  • 2nd degree = intermittent transmission
  • 3rd degree = complete failure
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3
Q

What is the buzz word for atrial fibrillation?

A

Irregular irregular HR

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4
Q

Why would you get arrhythmias?

A

Abnormalities in gap junction structure or spatial relationship
-ischemic heart dz, dilated cardiomyopathies, myocyte hypertrophy, inflammation, amyloid, etc.

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5
Q

Describe the genetics behind rhythm DOs.

A

Hereditary
Autosomal dominant
Primary electrical DOs, dx thru genetic testing

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6
Q

What are channelopathies?

A

Mutations in genes that are required for NL ion channel function

Can be assoc with skeletal muscle DOs and diabetes; most common isolated to heart

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7
Q

What is the most common inherited arrhythmogenic Dz? Describe it. What are some others?

A

Long QT syndrome

  • assoc with excessive repolarization
  • seen in swimmers
  • affects K+ and Na+ channels

Short QT syndrom
Brugada syndrome
CPVT syndrome

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8
Q

What is sudden cardiac death (SCD)?

A

Unexpected death form cardiac cause, either

  • without sx
  • within 1-24 hrs of sx onset

80-90% of successively resuscitated pts show NO lab or ECG changes

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9
Q

What Dz precipitates SCD in 80-90% of cases?

A

Coronary artery dz

  • usually >75% stenosis or one or more of the 3 main coronary arteries
  • SCD often first manifestation of IHD
  • healed remote MIs seen in about 40%
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10
Q

What are some other causes of SCD?

A

Cardiomyopathies

Myocarditis

Congenital abnormalities of the conduction system

Myocardial hypertrophy

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11
Q

What is SCD pathogenesis often due to?

A

Fatal arrhythmia most often arising from ischemia-induced myocardial irritability

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12
Q

What is left-sided (systemic) hypertensive heart dz (HHD)?

A

Pressure overload results in left ventricular hypertrophy (LHV)

LV wall is concentrically thickened (>1.5cm, weight >500gm)

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13
Q

What conditions eventually results from left-sided HHD?

A

Diastolic dysfunction can result in left atrial enlargement

Leads to AFIB

May also lead to CHF, as is a risk factor for SCD

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14
Q

How does right-sided (pulmonary) HHD arise? What about acute cor pulmonale?

A

Arises in setting of pulmonary HTN

Acute cor pulmonale may arise from a large pulmonary embolus
-marked dilation of RV without hypertrophy

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15
Q

What is the most common cause of pulmonary HTN leading to right-sided HHD?

A

Left-sided heart dz

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16
Q

Why can valvular dz come into clinical attention?

A

Stenosis

Insufficiency (regurgitation or incompetence)

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17
Q

What is functional regurgitation?

A

Used to describe the incompetence of a valve stemming from an abnormality in one of its support structures

Functional mitral valve regurgitation is common and clinically important in IHD and dilated cardiomyopathy

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18
Q

Valvular dz present with stenosis and/or insufficiency. Describe both.

A

Stenosis = valve doesn’t open completely, occurs chronically

  • impedes forward flow
  • chronic stenosis may cause PRESSURE overload hypertrophy —> CHF

Insufficiency = valve doesn’t close completely, occurs acutely or chronically

  • allows reverse flow
  • chronic insufficiency may cause VOLUME overload hypertrophy —> CHF
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19
Q

What is the common cause of mitral valve stenosis?

A

Postinflammatory scarring = rheumatic heart dz

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20
Q

What is the common cause of Aortic stenosis? What are some others?

A

Calcification of congenitally deformed valve

Postinflammatory scarring due to RHD
Senile calcific aortic stenosis

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21
Q

What is the common cause of Mitral regurgitation? What are some others?

A

Mitral valve prolapse

Abnormalities of leaflets/commissures (postinflamm scarring, infective endocarditis, drugs)

Abnormalities of tensor apparatus (rupture of papillary muscle/chordae tendinae)

Abnormalities of LV/Annulus (LV enlargement, calcification fo mitral ring)

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22
Q

What is the common cause of Aortic regurgitation? What are some others?

A

Aortic insufficiency = dilation of ascending aorta (secondary to HTN/aging)

Rheumatic heart dz
Degenerative aortic dilation 
Syphilic aortitis 
Marfan syndrome 
Ankylosing spondylitis
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23
Q

What is the most common valve abnormality? When does it manifest? What is it associated with?

A

Calcific aortic stenosis

Prevalence increases with age (at around 60-80 yrs)

Wear and tear associated with chronic HTN, hyperlipidemia, inflammation

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24
Q

How does the valve appear with calcific aortic stenosis?

A

Bicuspid valve (should be 3) = shows accelerated course (increase in mechanical stress)

Bicuspid clinical sx 1-2 decades earlier than normal valve

Affected valves contain osteoblast-like cells, which deposit on osteoid-like substance –> ossifies

Mounded calcification in cusps prevent complete opening of the valve

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25
Q

What are the Sx seen with calcific aortic stenosis? What is the Tx?

A

Angina
CHF
Syncope

LV hypertrophy develops form increased pressure

Most pts with aortic stenosis will die within 5 yrs of developing angina, 3 yrs of syncope, and 2 yrs of CHF

Tx: surgical replacement

26
Q

Describe what happens with Mitral annular calcification.

A

Calcific deposits occur in fibrous annulus

-irregular stony hard, occasionally ulcerated nodules at base of leaflets

27
Q

What effects does mitral annular calcification have?

A

Normally doesn’t affect valve function

However, exceptions:

  • regurgitation by interfering with physiologic contraction of valve ring
  • stenosis by impairing opening of mitral leaflets
  • arrhythmias and occasionally sudden death by penetration of Ca deposits to depth sufficient to impinge on AV conduction system
28
Q

What may happen to nodules in mitral annular calcification?

A

Sites for thrombus formation or infective endocarditis

29
Q

When and in who is mitral annular calcification more common?

A

F > M

> 60 yo

With mitral valve prolapse

30
Q

What is mitral valve prolapse? When is it heard? Who does it affect more?

A

Floppy - Valve leaflets prolapse back into LA during systole

Leaflets become thickened and rubbery, due to proteoglycan deposits (myxomatous degeneration) & elastic fiber disruption

Mid-systolic click

2-3% of adults in US
Females more than males

31
Q

What DO is MVP associated with? What is the gene associated with it?

A

Marfan syndrome

Fibrillin-1 (FBN-1) mutations = loss of CT support in mitral valve leaflets makes them soft and billowy, creating so called floppy valve

32
Q

What is the characteristic anatomic change in MVP?

A

Interchordal ballooning (hooding) of mitral leaflets

33
Q

What is MVP a complication of?

A

Of other causes of regurgitation

Ex:
Dilated hypertrophy
Ischemic dysfunction

34
Q

What are Sx of MVP?

A

Mostly asymptomatic, minority may experience:

  • CP mimicking angina (not exertional)
  • dyspnea
35
Q

What are some complication s of MVP?

A

Infective endocarditis
Mitral insufficiency
Thromboembolism
Arrhythmias

36
Q

What tx can be done for MVP?

A

Valve repair or replacement therapy for sx pts or those with increase risk for signif complications

37
Q

What is rheumatic fever (RF)?

A

Multisystem inflammatory DO following pharyngeal infection with Group A Strep

Acute rheumatic fever may include a carditis component, and over time may evolve to chronic rheumatic heart dz (RHD)

38
Q

What is the pathogenesis of RHD?

A

Immune response to Strep M proteins cross reacting with cardiac self-ags

39
Q

When do you start seeing Sx of RHD? What are the Sx? What titers are associated with RHD?

A

Acute RF occurs 1.5-6 weeks after infection

Titers = Anti-streptolysin O & anti-DNase B

Sx:
Pancarditis
Migratory polyarthritis (large jts) 
Subcutaneous nodules 
Rash (erythema marginatum)
Syndenham chorea = neurologic DO with involuntary rapid, purposeless movements
40
Q

What cardiac changes are seen with RHD?

A

Pancarditis w/ Aschoff bodies = T-cells, occ plasma cells & activated macrophages (Anitschkow cells)

Inflammation and fibroid necrosis of endocardium and left-sided valves with verrucae (vegetations)

Repeated infections cause these to recur

41
Q

What Cardiac features are seen with CHRONIC RHD?

A

Mitral leaflet thickening
Fusion of commissionaires
Shortening, fusion, thickening of cords

MITRAL STENOSIS (RHD only cause)

LA enlargement = afib, thromboembolic events
Pulm congestion/RHF; right ventricular hypertrophy
Infective endocarditis

42
Q

What is infective endocarditis (IE)?

A

Infection of valves or endocardium

Characterized by vegetations consisting of microbes and debris, assoc with underlying tissue destruction

Aorta, aneurysms, other blood vessels and prosthetic devices can become infected

43
Q

What is acute infective endocarditis?

A

Rapidly progressing, destructive infection of previously normal valve

Requires surgery + abx

44
Q

What is subacute infective endocarditis?

A

Slower, infection of previously deformed valve (ex: chronic RHD)

Can be cured by Abx alone

45
Q

What are predisposing conditions of IE?

A

Valvular abnormalities
-RHD, prosthetic valves, MV prolapse, calcific stenosis, bicuspid AV

Bacteremia
-another site of infection, dental work, contam needle

46
Q

What is the classic feature of IE? What does friability lead to?

A

Friable, bulky, destructive valvular vegetations

Friability leads to septic emboli
-PE if right side valve affected

47
Q

What side valves are more affected? If the other side is affected, why?

A

Left-sided valves

Right-sided valves more often involved in IV drug users

48
Q

What are the vegetations seen in IE made of?

A

Mixtures of fibrin, inflammatory cells, and organisms

Subacute vegetations may have a granulation tissue component

49
Q

What do pts with IE present with?

A

Nonspecific Sx:
-fever, weight loss, fatigue, flu-like (esp elderly)

Acute endocarditis sx = fever, chills, weakness, lassitude

50
Q

What can you observe on a PE in pts with IE?

A

If they have a left-sided lesion, murmurs are usually present (90%)

51
Q

What organisms are involved with IE?

A

S. viridans (valve abnormalities)

S. aureus (normal valves, abnormal valves, IV drug uses)

S. epidermidis (prosthetic valves)

HACEK (hemophilus, actinobacillus, cardiobacterium, eikenella, kingella)

52
Q

What are some characteristic signs/indicators of IE?

A

Subungal splinter hemorrhages
Osler nodes
Janeway lesions
Roth spots

53
Q

What is Nonbacterial Thrombotic Endocarditis (NBTE)?

A

Small, sterile thrombi on cardiac valve leaflets, along line of closure

Loosely attached, not invasive, do not illicit an inflammatory reaction

May be source of emboli = produce infarcts in brain, heart

54
Q

What is NBTE associated with?

A

Malignancies = especially mucinous adenocarcinoma

Sepsis

Catheter-induced endocardial trauma

55
Q

What is Carcinoid Syndrome?

A

A systemic DO marked by flushing, diarrhea, dermatitis, and bronchoconstriction; bioactive compounds such as seratonin released by carcinoid tumors

Plasma levels of serotonin and urinary excretion of serotonin metabolite (5-hydroxyindoleacetic acid) correlate with severity of cardiac lesion

56
Q

What is Carcinoid Heart Dz?

A

~50% of pts with systemic sx dev cardiac manifestations

57
Q

How is the liver affected by carcinoid heart dz?

A

Liver normally catabolizes circulating mediators before they can affect the heart; thus usually massive metastatic hepatic burden

58
Q

Which side of the heart is more affected by carcinoid heart dz?

A

Right endocardium and valves

Left side protected due to pulmonary vascular bed degradation of mediators

59
Q

When else as lesions similar to carcinoid heart dz seen?

A

Similar lesions as pts taking fenfluramine (appetite suppressant) or ergot alkaloids (migraine)

Affects systemic serotonin metabolism

60
Q

On a biopsy, what would you observe with carcinoid heart dz? What about histologically?

A

Glistening white intimal plaque-like thickenings of the endocardial surfaces of the cardiac chambers and valve leaflets

Intimal thickening = acid mucopolysaccharide rich

61
Q

What are complications of cardiac valve prostheses?

A

Thrombosis/thromboembolism

Coagulant-related hemorrhage

Prosthetic valve endocarditis

Structural deterioration (intrinsic)

  • wear, fracture, poppet failure in ball valves, cuspal tear, calcification
  • other forms of dysfunction

Inadequate healing (paravalvular leak), exuberant healing (obstruction), hemolysis

CPR Exam 1 (11 decks)

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