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Clin Med II > HTN and cardiomyopathy > Flashcards

HTN and cardiomyopathy Flashcards

1
Q

normal BP

A
  • < 120/80
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2
Q

stage 1 HTN

A
  • SBP 130-139

- DBP 80-89

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3
Q

Stage 2 HTN

A
  • SBP > 140

- DBP > 90

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4
Q

what is the gold standard for HTN dx

A
  • ambulatory BP monitoring (ABPM)
  • records BP over time, usually 24 hours
  • requires mean of 125/75
  • daytime mean 130/80
  • nighttime mean 110/65
  • not used often
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5
Q

how to dx HTN

A
  • ABPM
  • 3 office based readings of >130 and/or > 80 over course of weeks or months
  • if pt presents with HTN urgency or emergency
  • if pt has >160 SBP or > 100 DBP and has target end organ damage
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6
Q

target end organ damage

A
  • LVH
  • HTN retinopathy
  • ischemic CV disease
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7
Q

HTN screening

A
  • anyone over 18 annually

- anyone with increased risk factors screen semi- annually

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8
Q

primary HTN

A
  • no underlying cause
  • aka essential HTN
  • 95% of all HTN
  • likely multifactorial cause
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9
Q

secondary HTN

A
  • 5% of all HTN
  • related to an identifiable cause
  • common causes- renal disease, cushings, pregnancy, drugs, hyperthyroidism
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10
Q

masked HTN

A
  • BP that is constantly elevated at out of office measurements
  • doesnt meet in office dx criteria
  • associated with increased all cause mortality
  • increased long term risk of sustained CV morbidity
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11
Q

white coat HTN

A
  • BP that is consistently elevated at office readings but doesnt meet HTN dx criteria
  • need to get BP readings out of office to dx
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12
Q

additional screenings for HTN

A
  • chem 10- electrolytes and renal fn
  • fasting glucose and/or Hb A1C
  • CBC
  • TSH
  • Lipid profile
  • EKG (LVH)
  • dont need to do routine screenings for secondary causes
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13
Q

when do you treat for HTN

A
  • when avg office BP is > 140/90
  • when out of office avg is > 135/85
  • when comorbidities plus out of office avg > 130/80
  • lifestyle modifications should be first line but often need medications
  • close follow up within 3 mo to monitor progress
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14
Q

initial drug tx for HTN

A
  • thiazide diuretic
  • long acting CCB
  • ACEI
  • ARB
  • no significant difference in CV mortality between the four classes
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15
Q

HTN tx for AA

A
  • thiazide diuretic

- CCB

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16
Q

HTN for CKD pts

A
  • ACE or ARB best tx- delays progression of kidney disease

- ACE avoided in acute kidney disease

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17
Q

HTN tx with diabetic nephropathy or non- diabetic kidney disease

A
  • ACE or ARB initially
  • more aggressive tx required d/t increased CV risk
  • often require multiple agents
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18
Q

HTN combo tx principles

A
  • majority of pts need more than 1 agent
  • combo of drugs from different classes better than doubling dose of single agent
  • combo of 2 first line agents of dif classes when 20 SBP or 10 DBP away from goal
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19
Q

possible HTN combo tx

A
  • ACE/ARB + CCB
  • ACE/ARB + thiazide (less effective)
  • DO NOT combine ACE + ARB
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20
Q

resistant HTN

A
  • BP that isnt controlled to goal despite adherence to 3 drug regimen of dif classes
  • requires at least 4 meds to achieve goal
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21
Q

HTN urgency

A
  • SBP > 220 or DBP > 125 WITHOUT end organ damage
  • must be reduced within few hours
  • not a medical emergency
  • often d/t noncompliance
22
Q

malignant HTN

A
  • encephalopathy or nephropathy with papilledema
23
Q

HTN emergency

A
  • SBP > 220 or DBP > 120 WITH evidence of end organ damage
  • requires substantial reduction in BP within 1 hour
  • reduce BP by no more than 25% within minutes to 1-2 hours
  • work towards goal of 160/100 within 2-6 hours
24
Q

why do you slowly drop BP in HTN emergency

A
  • reduce risk of coronary, cerebral, or renal ischemia

- requires meds that are easily titrated

25
Q

medication choices for HTN emergency

A
  • nitropursside
  • NTG
  • BB- labetalol or esmolol
  • Nicardipine
  • diuretics
  • hydralazine
26
Q

sx that qualify as end organ damage during HTN emergency

A
  • HTN encephalopathy- HA, irritability, confusion, AMS, seizures
  • HTN nephropathy- hematuria, proteinuria, progressive kidney dysfunction
  • aortic dissection
  • pre-eclampsia, eclampsia
  • Pulmonary edema
  • unstable angina, MI
27
Q

classifications of cardiomyopathy

A
  • dilated
  • restrictive
  • hypertrophic
  • hypertrophic obstructive
  • arrhythmogenic right ventricular cardiomyopathy/ displasia
28
Q

dilated CMP

A
  • dilation of LV
  • normal or decreased wall thickness
  • LA and RV enlargement possible
  • impaired contraction of one or both ventricles
  • impaired systolic fn- EF < 40%
  • possible conduction abnormalities and arrhythmias
29
Q

common causes of dilated CMP

A
  • idiopathic- most common
  • infections
  • toxins
  • tachycardia induced
  • stress- Takotsubo
30
Q

infectious dilated CMP

A
  • begins as infectious myocarditis
  • usually viral
  • bacterial- lyme or mycoplasma
  • protozoan- chagas
31
Q

clinical manifestations of infectious dilated CMP

A
  • fever, myalgias, muscle tenderness
  • heart palpitations/ arrhythmias, heart block, HF
  • chest pain
  • presyncope, syncope
  • severity ranges
  • often self limited
  • biopsy if sx dont improve
32
Q

chagas disease

A
  • causes infectious dilated CMP
  • protozoa- trypanosoma cruzi
  • prevalent in central and south america
33
Q

clinical manifestations of chagas

A
  • acute myocarditis
  • cardiac enlargement
  • nonspecific EKG abnormalities
  • LV apical aneurysms
  • HF
  • all types of arrhythmias and heart block
  • thromboembolism*
  • chest pain
34
Q

dx of chagas

A
  • serology- IgG Ab vs. T. cruzi
  • CXR- cardiomegaly
  • EKG- RBBB or LBBB, ST- T changes
  • echo
  • cardiac MRI- detects myocardial fibrosis
35
Q

treatment of chagas

A
  • antitrypanosomal drugs for acute and intermed disease
  • std tx for HF
  • implantable cardiac pacer +/- defibrillator if arrhythmias dangerous
36
Q

toxic dilated CMP

A
  • most often d/t alcohol
  • correlated to the amount and duration of daily drinking
  • abstinence -> improved fn if dx early
  • can also be d/t cocaine or other meds
37
Q

tachycardia induced CMP

A
  • afib with RVR or AVNRT
  • preexcitation syndromes
  • reduced contractility -> reduced EF
  • abnormalities in myocardial architecture
  • decreased response to calcium
  • tx of arrhythmias -> reversal of myocardial dysfunction
38
Q

Takotsubo

A
  • aka stress induced dilated CMP
  • d/t severe psychological stress
  • more common in post menopausal women
  • LV apical ballooning/ dilation
  • ST elevation without CAD
39
Q

restrictive CMP

A
  • non-dilated ventricles with impaired ventricular filling
  • rigid ventricular walls -> inability to relax
  • no hypertrophy
  • diastolic dysfunction
  • biatrial enlargement
40
Q

causes of restrictive CMP

A
  • familial
  • infiltrative- sarcoidosis or amyloidosis
  • storage diseases
  • scleroderma
  • endomyocardial fibrosis
41
Q

hypertrophic cardiomyopathy (HCM)

A
  • genetic
  • interventricular septum hypertrophy more than LV free wall
  • LV volume is reduced or normal
  • diastolic dysfunction
42
Q

clinical manifestations of HCM

A
  • HOCM
  • diastolic dysfn
  • myocardial ischemia
  • mitral regurg
  • systolic dysfun at end stage
  • HF
  • supraventricular and ventricular arrhythmias
  • sudden death
43
Q

hypertrophic obstructive cardiomyopathy (HOCM)

A
  • hypertrophy of interventricular septum
  • significant LV outflow tract obstruction- aortic valve
  • preload dependent condition
  • common in teens and young adults
  • most common cause of sudden death in young people
44
Q

sx of HOCM

A
  • harsh crescendo- decrescendo systolic murmur
  • murmur increased with valsalva, decreased with squatting
  • fatigue
  • dyspnea
  • chest pain
  • palpitations
  • presycope or sycope
45
Q

management of HOCM

A
  • stay hydrated
  • limit intense activity
  • medical tx for chest pain, dyspnea, arrhythmias
  • invasive procedures to improve LV outflow tract
46
Q

procedures to improve LV outflow tract in HOCM

A
  • alcohol septal ablation

- septal myectomy*

47
Q

arrhythmogenic RV cardiomyopathy (ARVC)

A
  • myocardium in RV is replaced by fibrous and/or fibro- fatty tissues
  • rare genetic disease
  • can cause gentricular arrhythmias
  • RV dysfunction, akinesis, dyskinesis
  • global RV dilation if severe
  • can cause sudden cardiac death in young people
48
Q

sx of AVRC

A
  • may be silent
  • palpitations
  • syncope
  • atypical chest pain
  • dyspnea
49
Q

diagnosis of AVRC

A
  • echo
  • cardiac MRI gold std
  • genetic testing
  • endomyocardial biopsy
50
Q

tx for AVRC

A
  • implantable cardiac defibrillator
  • anti-arrhythmic drugs if not candidate for ICD
  • no competitive sports
  • cardiac transplant if progressive and debilitating

Clin Med II (16 decks)

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