Cardio Flashcards
Gold standard for assessing LV mass and volume
Cardiac MRI
Most useful index of LV function
EF
EF =
Stroke volume/EDV
Normal EF
> /=50 %
Biomarkers sensitive for presence of HF
Useful in diagnosis and establishing prognosis and severity
May inc with age, renal impairment and women but falsely low in obese
B type natriuretic peptide
N-terminal pro BNP
Diagnostics for HF (6)
1 laboratory (CBC, electro, BUN, Crea, AST/ALT, UA and/or fasting glucose, OGTT, dyslipidemia, tsh) 2 ECG 3 CXR 4 2D Echo/Doppler 5 BNP, NT Pro BNP 6 Exercise testing
ECG in severe pulmonary hypertension (3)
P pulmonale
R axis deviation
RVH
Best for diagnosing chronic thromboembolic disease
Ventilation/Perfusion scan
Confirms diagnosis of pulmonary hypertension
Cardiac cath
Therap targets in HFpEF (3)
1 control congestion
2 stabilize heart rate and bp
3 improve exercise tolerance
Showed stat significant reduction in hosp but no diff in all cause mortality in HFpEF
Candesartan ARB
ADHF typical HTN Mx
Vasodilators (usually not volume overloaded)
ADHF Typical Normotensive
Diuretics (usually volume overloaded)
ADHF Pulmonary edema with pulmo congestion and hypoxia (4)
Opiates
Vasodilators
Diuretics
O2 non invasive ventilation
ADHF Low output hypoperfusion, with end-organ dysfunction
Vasodilators
Hemodynamic monitoring
Inotropic therapy
ADHF Cardiogenic shock hypotension, low cardiac output, EOF
Inotropic therapy catecholamine
Mech circ support
Interplay of neurohormonal factors with deteriorating function of kidney while therapy is adminstered to preserve the heart
Exacerbated by backward failure, inc intraabd pressure and impairment of venous return
Cardiorenal syndrome
In diabetics with HF, this drug demonstrated dec in CV mortality and hospitalizations for
HF
Empagliflazone SGLT2
induces osmotic diuresis and ketosis
Candidates for ICD prophylactic therapy
NYHA Class II and III
LVEF <35% irrespect of etiology
ICD is appropriate in
Patients with MI
Residual LVEF =30% even asymptomatic
Serious infection from colonization or invasion of heart valves or the mural endocardium by microbe
Infective endocarditis
IE Pathophy
Endothelial injury
Direct infection by virus
Development of platelet fibrin thrombus (bacterial attachment during transient bacteremia)
Organisms enter bloodstream from mucosal surface, skin or site of focal infection
Causes native valve endocarditis
S viridans
Endocarditis in IV drug user
S aureus
Prosthetic valve endocarditis
S epidermidis
Miscellaneous virulent organisms causing IE
Gram neg
Fungi
HACEK
Viridans, strep, staph and HACEK enter via
oral cavity, skin, upper respiratory tract
Streptococcus gallolyticus
Subspecies gallolyticus enter via
GI tract
Enterococci enter via
urinary tract
Endocarditis and Colon CA
strep bovis
The organisms causing IE contain
which adhere to nonbacterial thrombotic endocarditis NBTE sites or
injured epithelium
Microbial surface components recognizing adhesins matrix molecules (MSCRAMMS)
Normal valve
Necrotic, ulcerative, destructive in days
Fever of >/= 39.4
Mx: Surgery
Acute IE
Deformed valve
Insidious, less destructive, weeks to months
Fever of <39.4
Mx: antibiotic
Subacute
Injection drug use associated endocarditis involves the
and is caused by
Occurs among injection drug users
tricuspid valve
s aureus
Polymicrobial endocarditis
Dx of IE is established only
when vegetations are examined histologically and microbiologically
Highly sensitive and specific diagnostic schema
Based on clinical, lab and 2D ECHO
Modified Duke Criteria
Duke Major Criteria
1 Positive blood culture (2 separate)
Viridans, strep gallolyticus, HACEK, staph aureus or CA enterococci in absence of primary focus
Persistently positive
2 Evidence of endocardial involvement
Intracardiac mass on valve or structure in path of regurgitant jet new partial dehiscence of prosthetic valve in 2DECHO
3 New valvular regurgitation (sufficient inc or change in preexisting murmur)