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Cardio

ACS (Acute Coronary Syndrome)

Defi­nit­ion
Spectrum of problems ranging from unstable angina to MI
Symp­toms
Crushing pain/p­res­sure; radiation to jaw, back, and left arm; SOB, diapho­resis, N/V; impending sense of doom
Most common etiology of MI
Preexi­​sting athero­​sc­l​e­rotic plaque​ ➔ ​thr​ombus format­​ion​ ➔ ​pro​l­onged myocardial ischem​ia ➔ MI
EKG changes
Acute MI: progre­​ssion from peaked T- wave​s ➔ ST​-de­​gment elevat­​io­n​/­de​­pre­​ssi​on ➔ Q​-wa​ve ➔T​-wave inversions (hours­​-days)
Labo­ratory Tests
EKG (within 10 min), troponin levels, CK:CK-MB ratio, MRI with gadolinium
Stable Angina
Reprod­ucible pain, improved with rest, lasts <10min,
UA/N­STEMI
Occurs more often with less activity, not relieved with NTG, lasts >10min, EKG changes
STEMI
Complete occlusion, EKG changes
Initial Treatm­ent
ONAM: Oxygen, +/- nitro, antipl­atelets (ASA+P­2Y12), morphine (PRN), EKG monito­ring, IV access
Disc­harge Treatm­ent
1) ASA (life)
2) P2Y12 (1yr)
3) Statin
4) ß-blocker
5) ACE-I
6) Aldost­erone antagonist
Emer­gency Interv­ent­ion
Door-t­o-n­eedle within 30min; door-t­o-b­alloon within 90min
 

Congestive Heart Failure (CHF)

Defi­nit­ion
Inability of the heart to keep up the the demands on it and pump blood with normal efficiency
Result of one or more of the follow­ing
Contra­​ctile ability of heart muscle, preload and after load of the ventricle, and heart rate
Etio­logy
MI, perica­​rdial disorders, valvular disorders, congenital abnorm­​al­i​ties, and non cardiac causes (high-­​output heart failure from thyrot­​ox­i​cosis or severe anemia)
Clinical features of HFrEF/­LHF
Exertional dyspnea, non-pr­​od­u​ctive cough, fatigue, orthopnea, PND, basilar rales, gallops, exercise intole­​rance
Clinical features of HFpEF/­RHF
Distended neck veins, hepatic conges­​tion, nausea, dependent pitting edema, *edema + hepato­​me­galy, (R-sided failure often caused by L-sided failure)
Trea­tment
1) Loop
2) ACE-I
3) ß-blocker
4) Spiron­ola­ctone
5) Hydral­azine + ISDN (esp in blacks)

Hypert­ension

Primary HTN
Causes 95% of cases of HTN; multif­​ac­t​orial pathog­​enesis (genetics, salt, obesity, RAAS, NSAIDs, smoking, lack of exercise, metabolic syndrome)
Seco­ndary HTN
Narrowing of aorta, RAS, chronic steroids, Cushings syndrome, pregnancy, thyroid and parath­​yroid disease, primary hypera­​ld­o​s­te​­ronism, parenc­​hymal renal dz)
Trea­tment Goal
All ages with DM or CKD ≤140/90
Ages <60yo ≤140/90
Ages ≥60yo ≤150/90
Trea­tment
First line: ACE-I/ARB, CCB, thiazides
Other: alpha blockers, clonidine, guanfa­cine, hydral­azine, minoxidil,

Ischemic Heart Disease

Defi­nit­ion
Charac­​te­rized by insuff­​icient oxygen supply to cardiac muscle
Etio­logy
1) Athe​r­os​­cle­​rotic narrowing (most common). 2) Constr­​iction of coronary arteries. 3) (Rare) congen­​ital, emboli, arteritis, dissection
Risk Factors
Metabolic syndrome, male, older age, smoking, FmHx, HTN, DM, low-es­​trogen state, abdominal obesity, inacti­​vity, dyslip­​id­emia, EtOH, low fruits­​/v­e​ggies (cocai​ne ➔ MI)
Un/s­table Angina
See Above
Prin­zme­tal's (Variant) Angina
Caused by vasospasm at rest, exercise capacity preserved. Treated with CCBs, avoid ß-blockers
EKG Findings
Horizontal or downsl­​oping ST-segment depression
Trea­tment
Lifestyle changes, nitrates (nitro and LA), B-bloc­​kers, CCB, Ranola­​zine, ASA/Cl­​op­i​d­igrel, revasc­​ul­a​r­iz​­ation
  

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