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52 Cards in this Set

  • Front
  • Back
What is stable angina due to? What is coronary ischemia due to?
i)due to fixed narrowing of vessels due to atherosclerosis. ii)Due to imbalance b/w blood supply and O2 demand->inadequate perfusion.
What are the clinical presentations of CAD? x5
i)asymptomatic ii)stable angina pectoris iii)USA iv)MI v)sudden death
What are some risk factors for stable angina? x5
i)DM ii)High LDL iii)low HDL iv)homocysteinemia v)m>45; w>55
What are the prognostic indicators of CAD? x3
i)LV function (EF): <50% means bad ii)vessel: L MCA: poor b/c 2/3 of heart. iii)>1 vessel involved
when to use a stress EKG?
i)confirm angina DX ii)evaluate response of therapy iii)ID pts w/CAD who may have high risk of ACS
what are clinical features of stable angina?
i)pressure, squeezing, heaviness CP ii)brought on by exertion or emotion iii)relieved by nitro
What are the diagnostic modalities for stable angina? x5
i)1st: EKG-> ii)if +, exercise stress test or iii)pharm stress test iv)Holter monitoring: ambulatory EKG in silent ischemia. v)cardiac cath w/coronary angiography: if +stress test
What is normal EKG in stable angina, and what are 2 other situations?
i)nl: no changes ii)if Q wave: prior MI iii)If ST or T wave during CP, treat as if unstable angina
What is Syndrome X?
exertional angina w/nl coronary arteriogram (no stenosis at cardiac cath). ii)see evidence of MI. iii)excellent PX
What is a + stress test? x4 What do you do if +?
i)ST depression:subendocardial ischemia ii)CP iii)arrythmias iv)hypotension. Need cardiac cath
What are the types of the stress test? x3
i)stress EKG ii)stress echo: exercise induced ischemia seen in wall motion abnl not present at rest. Often favored over stress EKG (ischemia, LV size/fcn, valvular dz seen). iii)nuclear perfusion imaging: enhances info from stress test. Viable myocardial cells extract radioisotope from blood, so if no uptake, then no blood flow to area of mycardium. Need to figure out reversible areas vs irreversible b/c can use PTCA or CABG
What are the drugs in pharm stress test and how do they cause stress?
i)adenosine and dipyramidole: cause entire system to vasodilate, and since dz'd ones are maximally dilated at rest, they get less flow. ii)dobutamine: incr HR, BP, contractility
What are the 4 parts to the treatment plan in SAP
i)risk factor modification ii)medical therapy iii)revasc iv)management decisions
what are some risk factor modification methods for CHD? x3
i)smoking: cuts CHD risk by 1/2. ii)diabetes: more eff on microvasc iii)diet: decrease sat fat and chol
what are the main drugs used in CAD? x5
i)ASA: decreases morbidity (decr risk of MI) ii)B block: block symp stim of heart (decr HR, BP, and contractility). They decr freq of coronary events. iii)nitrates: decr preload. iv)CCB: afterload reduction and coronary vasodilation. Secondary treatment to B block or nitrates. v)CHF present: ACE or diuretic
what is the management of stable angina?
i)risk mod and ASA in all ii)B block and nitrates for mild. Possible CCB. iii)moderate dz: 2 vessel dz, mod angina: coronary angiography (PTCA or CABG?) iii)Severe: decr EF, severe angina, LMCA or 3 vessels do angio and CABG
What is ACS?
plaque rupture and occlusion. Used for USA and MI
Pathophysiology of USA?
Due to decreased coronary flow at rest: O2 demand is unchanged. It is due to stenosis that has enlarged via thrombosis, hemorrhage or plaque rupture
Definition of the patient that has USA? x3
i)pts w/chronic angina w/incr freq, duration, or intensity of CP. ii)pts w/new onset angina that is severe and worsening iii)pts w/angina at rest
How to DX USA?
(sim to stable angina). i)R/o MI ii)stabilize w/meds b/4 stress test or just do cardiac cath initially if high prob (TIMI)
How to treat USA?
i)admit and give IV and O2. Give nitrates and morphine for pain. ii)meds: ASA; B-Block; LMWH w/PTT 2-2.5 if nl Heparin; nitrates; GP2b/3a inhibitors (abciximab) iii)cardiac cath/revasc if no response to med therapy or if EKG has ischemia after 48 hrs on stress test. iv)post acute treatment: a)ASA, B block, nitrates; b)decr risk factors: esp statin; consider folic acid: good for endothelium and as antiox
What is variant angina?
i)transient coronary vasospasm that is accompanied by atherosclerotic lesion but can be in normals. ii)Get angina at rest and ass'd w/ventricular dysrhythmias iii)ST elevation: transmural.
How to DX Prinzmetal's? how to treat?
i)coronary angiography: vasospasm w/ergonovine. ii)vasodilate: CCBs and nitrates
What is MI due to?
i)necrosis of myocardium b/c of interuppted blood supply (thrombotic occlusion of coronary previously narrowed by athero).
What is mortality in MI?
i)30%. ii)1/2 are prehospital
What are the clinical features of MI?
i)CP: radiates to back, neck, jaw, arms ii)some have epigastric discomfort. (substernal CP lasting >30 min w/diaphoresis=usually MI) iii)can be asympto: old, DM, postop, women. iv)SCD due to VFib. v)other sxs: dysp, N/V, syncope, impending doom
How to DX MI?
i)EKG ii)cardiac enzymes: CKMB and Troponin I and T
i)What are markers for EKG changes in MI?
i)a)Peaked T waves early b)ST seg elevation: transmural c)Q waves: necrosis, seen late d)T wave inversion e)ST segment depression: subendocardial injury
What are categories of infarcts in MI?
i)ST segment elevation infarct: transmural; larger. ii)Non ST segment elevation infarct: subendocard (inner 1/3 to 1/2 of wall); smaller; presents like USA but cardiac enzymes differentiates
What are the diff cardiac enzymes; What is there pattern; how to manage and when to get the tests?
i)CKMB: gold std. incr w/in 4-8 and returns 48-72 w/peak at 24; measure at admission and q8 hrs. ii)Troponins (I and T): incr 3-5 hrs; returns 5-14 days w/peak at 24-48; better sn/sp; obtain at admission and q 8 hrs; falsely incr w/renal failure
W/cardiac enzymes, when is injury more severe and worse prognosis?
higher the peak and longer enzyme levels remain elevated
What drugs have been shown to decr mortality in MI?
i)ASA ii)B block iii)ACE-I
How do you treat MI?
i)admit to CCU and do IV access w/O2 and analgesics. ii)med TX iii)Revasc: earliness is more imp than type of reperfusion (tPA vs PTCA) iv)rehab:exercise and risk factor reduction; reduces sxs and prolongs survival
What meds do you use for MI?
i)ASA ii)B block: decr afterload iii)ACE-I: w/in hrs of admit iv)statins: maintenance; v)heparin: no decr in mortality but prevents thrombus progression (+IV, morphine, and O2)
What are the complications of MI? x5
i)CHF:mild case treat medically; severe may lead to cardiogenic shock ii)arrhythmia iii)rupture iv)pericarditis v)recurrent MI: CK MB used; and if repeat ST elevation w/in 1st 24 hrs, think recurrent infarct.
What type of arrhythmias may result from MI? (x10)Treatments?
i)Premature ventricular contractions (PVCs), sinus bradycardia, accelerated idioventricular rhythm, 1st and 2nd degree AV block: observe ii)A-fib iii)VT: cardioversion if unstable; antiarrhythmics (amio) if stable. iv)Vfib: defib/CPR v)PVST vi)sinus tach: treat cause (pain pills, ASA for fever). vii)asystole: defib for VFib if unclear; if clear, then pacemaker. viii)2nd/3rd degree AV block: ant MI needs pacemaker; inf MI can use atropine unless conduction not restored
What are the types of mechanical complications for MI x3? What are the sequelae, and when do they occur?
i)free wall rupture: usually day 1-4 post-MI. leads to hemopericardium and tamponade. treat: stabilize, pericardiocentesis, SX repair. ii)IV septum rupture: 10 days post. treat: emergent surgery. iii)pap muscle rupture: produces MR; need echo immediately if suspect; treat: mitral valve replacement w/NaNitroprusside or IABP to decr afterload
What is diff b/w ventricular pseudoaneurysm and ventricular aneurysm and what are they complications of?
i)complication of MI. ii)pseudo: incomplete free wall rupture (contained by pericardium); due an echo and need surgery b/c becomes rupture. iii)aneurysm: no rupture but get v-tach; usually just meds given
what are the 2 types of pericarditis and what are their cure?
i)acute pericarditis: give ASA, NSAIDs and steroids contraind. ii)Dresslers: fever, malaise, pericarditis, leukocytosis. give ASA
What are the groups for the DDX of CP
i)heart, pericardium, vascular ii)pulmonary iii)GI iv)chest wall v)psych vi)cocaine: causes angina or MI
what is DDX of heart causes of CP?
i)3 kinds of angina ii)MI iii)pericarditis iv)dissection
pulm causes of DDX of CP?
i)pulm embolism (pain w/infarct). ii)pneumothorax iii)pleuritis iv)pneumonia v)status asthmaticus
DDX of GI causes of CP?
i)GERD ii)diffuse eso spas iii)PUD iv)eso rupture
DDX of chest wall causes of CP?
i)costochondritis ii)muscle strain iii)rib fracture iv)thoracic outlet syndrome v)herpes zoster
What is approach to treating pt w/CP?
i)r/o life threatening causes: MI, USA, dissect, PE, pneumothorax, rupture. ii)vitals iii)hx iv)PE v)tests: a)cardiac enzymes, b)EKG, c)CXR d)workup of PE if appropriate
What do you do if chronic angina becomes USA
i)EKG and enzymes ii)ASA iii)IV heparin
Describe FS relationship in CHF
i)Nl: increase preload->incr contractility/SV. at rest, no diff b/w CHF and nl. ii)exertion: increase preload w/o incr contractility.
Diff b/w systolic and diastolic dysfcn?
i)systolic: due to impaired contractility (decr EF); post MI, cardiomyopathy, myocarditis. ii)diastolic dysfcn: impaired relaxation or incr stiffness. Can see impaired relaxation on echo. Cause: HTN, valve dz, restrictive cardiomyopathy
What are some symptom (x3) and signs (x5) of LHF:
i)SX: nocturnal cough (nonprod) worse in recumbency; confusion and memory problem b/c of low brain perfusion; diaphoresis and cool ext at rest. ii)Signs: cardiomegaly->displaced PMI. S3: ken-tuck-Y (after S2). S3: rapid filling phase into stiff ventricle; at the apex. S4:a-kick into stiff ventricle. S4 b/4 S1 (TEN-nes-see); Left sternal border. crackles and rales at lung base. Pleural effusion (decr fremitus).
Sxs and signs of RHF
nocturia; rt ventricular heave.
How do you DX CHF? x6
i)CXR: cardiomegaly; Kerley B lines (lines near costophrenic angles due to pulm congestion b/c of dilation of pulm lymphatic vessels); interstitial markings; effusion. ii)echo: initial test for CHF! Can tell you if systolic or diastolic dysfcn; if CHF is pericardial, myocardial, valvular and estimates EF(imp). iii)EKG: for detection of chamber enlargement and if ischemic HD or prior MI. iv)radionuclide: precision for LV and RV EF (esp if echo suboptimal w/pulm dz). v)cardiac cath: clarifies cause of CHF if noninvasive results no good. can use angiograpy to exclude CAD as cause. vi)stress test
How to treat systolic dysfcn?
i)Na restrict ii)diuretics: no decr in mortality or improved px. lasix is best. iii)ACE-I: venous and arterial dilation to decr preload and afterload. ACE+diuretic should be initial treament. Ace reduce mortality; need to monitor BP, K, BIN, Cr. iv)B block: decrease mortality; slows tissue remodeling and given to stable patients only. v)digitalis: no improved mortality; need to check levels. Useful in bad EF, bad CHF, bad Afib. vi)hydralaine/isosorbide dinitrates: intolerable ACE-I. Improves CHF, but not as effective as ACE-I