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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
What are the Sx seen with calcific aortic stenosis? What is the Tx?
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
Describe what happens with Mitral annular calcification.
Calcific deposits occur in fibrous annulus | -irregular stony hard, occasionally ulcerated nodules at base of leaflets
27
What effects does mitral annular calcification have?
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
What may happen to nodules in mitral annular calcification?
Sites for thrombus formation or infective endocarditis
29
When and in who is mitral annular calcification more common?
F > M >60 yo With mitral valve prolapse
30
What is mitral valve prolapse? When is it heard? Who does it affect more?
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
What DO is MVP associated with? What is the gene associated with it?
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
What is the characteristic anatomic change in MVP?
Interchordal ballooning (hooding) of mitral leaflets
33
What is MVP a complication of?
Of other causes of regurgitation Ex: Dilated hypertrophy Ischemic dysfunction
34
What are Sx of MVP?
Mostly asymptomatic, minority may experience: - CP mimicking angina (not exertional) - dyspnea
35
What are some complication s of MVP?
Infective endocarditis Mitral insufficiency Thromboembolism Arrhythmias
36
What tx can be done for MVP?
Valve repair or replacement therapy for sx pts or those with increase risk for signif complications
37
What is rheumatic fever (RF)?
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
What is the pathogenesis of RHD?
Immune response to Strep M proteins cross reacting with cardiac self-ags
39
When do you start seeing Sx of RHD? What are the Sx? What titers are associated with RHD?
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
What cardiac changes are seen with RHD?
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
What Cardiac features are seen with CHRONIC RHD?
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
What is infective endocarditis (IE)?
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
What is acute infective endocarditis?
Rapidly progressing, destructive infection of previously normal valve Requires surgery + abx
44
What is subacute infective endocarditis?
Slower, infection of previously deformed valve (ex: chronic RHD) Can be cured by Abx alone
45
What are predisposing conditions of IE?
Valvular abnormalities -RHD, prosthetic valves, MV prolapse, calcific stenosis, bicuspid AV Bacteremia -another site of infection, dental work, contam needle
46
What is the classic feature of IE? What does friability lead to?
Friable, bulky, destructive valvular vegetations Friability leads to septic emboli -PE if right side valve affected
47
What side valves are more affected? If the other side is affected, why?
Left-sided valves Right-sided valves more often involved in IV drug users
48
What are the vegetations seen in IE made of?
Mixtures of fibrin, inflammatory cells, and organisms Subacute vegetations may have a granulation tissue component
49
What do pts with IE present with?
Nonspecific Sx: -fever, weight loss, fatigue, flu-like (esp elderly) Acute endocarditis sx = fever, chills, weakness, lassitude
50
What can you observe on a PE in pts with IE?
If they have a left-sided lesion, murmurs are usually present (90%)
51
What organisms are involved with IE?
S. viridans (valve abnormalities) S. aureus (normal valves, abnormal valves, IV drug uses) S. epidermidis (prosthetic valves) HACEK (hemophilus, actinobacillus, cardiobacterium, eikenella, kingella)
52
What are some characteristic signs/indicators of IE?
Subungal splinter hemorrhages Osler nodes Janeway lesions Roth spots
53
What is Nonbacterial Thrombotic Endocarditis (NBTE)?
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
What is NBTE associated with?
Malignancies = especially mucinous adenocarcinoma Sepsis Catheter-induced endocardial trauma
55
What is Carcinoid Syndrome?
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
What is Carcinoid Heart Dz?
~50% of pts with systemic sx dev cardiac manifestations
57
How is the liver affected by carcinoid heart dz?
Liver normally catabolizes circulating mediators before they can affect the heart; thus usually massive metastatic hepatic burden
58
Which side of the heart is more affected by carcinoid heart dz?
Right endocardium and valves Left side protected due to pulmonary vascular bed degradation of mediators
59
When else as lesions similar to carcinoid heart dz seen?
Similar lesions as pts taking fenfluramine (appetite suppressant) or ergot alkaloids (migraine) Affects systemic serotonin metabolism
60
On a biopsy, what would you observe with carcinoid heart dz? What about histologically?
Glistening white intimal plaque-like thickenings of the endocardial surfaces of the cardiac chambers and valve leaflets Intimal thickening = acid mucopolysaccharide rich
61
What are complications of cardiac valve prostheses?
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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