HTN and cardiomyopathy Flashcards
normal BP
- < 120/80
stage 1 HTN
- SBP 130-139
- DBP 80-89
Stage 2 HTN
- SBP > 140
- DBP > 90
what is the gold standard for HTN dx
- 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
how to dx HTN
- 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
target end organ damage
- LVH
- HTN retinopathy
- ischemic CV disease
HTN screening
- anyone over 18 annually
- anyone with increased risk factors screen semi- annually
primary HTN
- no underlying cause
- aka essential HTN
- 95% of all HTN
- likely multifactorial cause
secondary HTN
- 5% of all HTN
- related to an identifiable cause
- common causes- renal disease, cushings, pregnancy, drugs, hyperthyroidism
masked HTN
- 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
white coat HTN
- BP that is consistently elevated at office readings but doesnt meet HTN dx criteria
- need to get BP readings out of office to dx
additional screenings for HTN
- 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
when do you treat for HTN
- 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
initial drug tx for HTN
- thiazide diuretic
- long acting CCB
- ACEI
- ARB
- no significant difference in CV mortality between the four classes
HTN tx for AA
- thiazide diuretic
- CCB
HTN for CKD pts
- ACE or ARB best tx- delays progression of kidney disease
- ACE avoided in acute kidney disease
HTN tx with diabetic nephropathy or non- diabetic kidney disease
- ACE or ARB initially
- more aggressive tx required d/t increased CV risk
- often require multiple agents
HTN combo tx principles
- 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
possible HTN combo tx
- ACE/ARB + CCB
- ACE/ARB + thiazide (less effective)
- DO NOT combine ACE + ARB
resistant HTN
- BP that isnt controlled to goal despite adherence to 3 drug regimen of dif classes
- requires at least 4 meds to achieve goal
HTN urgency
- SBP > 220 or DBP > 125 WITHOUT end organ damage
- must be reduced within few hours
- not a medical emergency
- often d/t noncompliance
malignant HTN
- encephalopathy or nephropathy with papilledema
HTN emergency
- 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
why do you slowly drop BP in HTN emergency
- reduce risk of coronary, cerebral, or renal ischemia
- requires meds that are easily titrated
medication choices for HTN emergency
- nitropursside
- NTG
- BB- labetalol or esmolol
- Nicardipine
- diuretics
- hydralazine
sx that qualify as end organ damage during HTN emergency
- HTN encephalopathy- HA, irritability, confusion, AMS, seizures
- HTN nephropathy- hematuria, proteinuria, progressive kidney dysfunction
- aortic dissection
- pre-eclampsia, eclampsia
- Pulmonary edema
- unstable angina, MI
classifications of cardiomyopathy
- dilated
- restrictive
- hypertrophic
- hypertrophic obstructive
- arrhythmogenic right ventricular cardiomyopathy/ displasia
dilated CMP
- 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
common causes of dilated CMP
- idiopathic- most common
- infections
- toxins
- tachycardia induced
- stress- Takotsubo
infectious dilated CMP
- begins as infectious myocarditis
- usually viral
- bacterial- lyme or mycoplasma
- protozoan- chagas
clinical manifestations of infectious dilated CMP
- fever, myalgias, muscle tenderness
- heart palpitations/ arrhythmias, heart block, HF
- chest pain
- presyncope, syncope
- severity ranges
- often self limited
- biopsy if sx dont improve
chagas disease
- causes infectious dilated CMP
- protozoa- trypanosoma cruzi
- prevalent in central and south america
clinical manifestations of chagas
- acute myocarditis
- cardiac enlargement
- nonspecific EKG abnormalities
- LV apical aneurysms
- HF
- all types of arrhythmias and heart block
- thromboembolism*
- chest pain
dx of chagas
- serology- IgG Ab vs. T. cruzi
- CXR- cardiomegaly
- EKG- RBBB or LBBB, ST- T changes
- echo
- cardiac MRI- detects myocardial fibrosis
treatment of chagas
- antitrypanosomal drugs for acute and intermed disease
- std tx for HF
- implantable cardiac pacer +/- defibrillator if arrhythmias dangerous
toxic dilated CMP
- 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
tachycardia induced CMP
- 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
Takotsubo
- aka stress induced dilated CMP
- d/t severe psychological stress
- more common in post menopausal women
- LV apical ballooning/ dilation
- ST elevation without CAD
restrictive CMP
- non-dilated ventricles with impaired ventricular filling
- rigid ventricular walls -> inability to relax
- no hypertrophy
- diastolic dysfunction
- biatrial enlargement
causes of restrictive CMP
- familial
- infiltrative- sarcoidosis or amyloidosis
- storage diseases
- scleroderma
- endomyocardial fibrosis
hypertrophic cardiomyopathy (HCM)
- genetic
- interventricular septum hypertrophy more than LV free wall
- LV volume is reduced or normal
- diastolic dysfunction
clinical manifestations of HCM
- HOCM
- diastolic dysfn
- myocardial ischemia
- mitral regurg
- systolic dysfun at end stage
- HF
- supraventricular and ventricular arrhythmias
- sudden death
hypertrophic obstructive cardiomyopathy (HOCM)
- 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
sx of HOCM
- harsh crescendo- decrescendo systolic murmur
- murmur increased with valsalva, decreased with squatting
- fatigue
- dyspnea
- chest pain
- palpitations
- presycope or sycope
management of HOCM
- stay hydrated
- limit intense activity
- medical tx for chest pain, dyspnea, arrhythmias
- invasive procedures to improve LV outflow tract
procedures to improve LV outflow tract in HOCM
- alcohol septal ablation
- septal myectomy*
arrhythmogenic RV cardiomyopathy (ARVC)
- 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
sx of AVRC
- may be silent
- palpitations
- syncope
- atypical chest pain
- dyspnea
diagnosis of AVRC
- echo
- cardiac MRI gold std
- genetic testing
- endomyocardial biopsy
tx for AVRC
- implantable cardiac defibrillator
- anti-arrhythmic drugs if not candidate for ICD
- no competitive sports
- cardiac transplant if progressive and debilitating