Clin Med- Cardio
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- What is the definition of Unstable Angina?
- -angina occuring at rest for a prolonged period of time
- What is angina pectoris?
-
-new onset angina
-constricting pain usually referring to the pectoral region - Class I Angina
- -Angina occuring with more than regular activity
- Class II Angina
- -Angina occuring during daily routines
- Class III Angina
- -Angina occuring with limitation of daily activity
- Class IV Angina
- -Angina occuring at rest or when doing anything
- Etiology of Angina
-
1. Atherosclerotic plaque
2. Coronary Vasospasm
3. inadequate Hb
4. reduced coronary blood flow
5. increased O2 demand - Clinical features of Angina
-
-radiating, substernal CP
-duration <20 min
-relieved by NTG
-angina equivalents - Risk Factors for Angina
-
- >70 yo
-male
-HTN > 140/90
-DM
-tobacco
-PVD - It isn't Angina if...
-
-pleuretic CP
-lower Abd pain
-localized pain
-CP related to mvmt
-lasts forever or for two seconds
-radiates to lower extremities - Physical findings of Angina
-
-JVD
-Rales
-S4
-murmur - You have an EKG of someone with angina. What do you see?
-
-ST depression
-T wave inversion
-dysrhythmias
-blocks - TX of Angina
-
-O2
-ASA
-NTG
-platelet inhibitors
-morphine
-BB
-CCB
-ACEI
-Heparin
-GIIbIIIaI
-IABP
-cath - H&P of MI
-
-radiating, substernal CP
-dyspnea
-diaphoresis
-nausea
-Hypo/HTN
-murmurs
-feeling of doom - What will you see on an EKG of someone having a MI?
-
-ST changes > 1mm in 2 consecutive leads
-dysrhythmias - TX of MI
-
-O2
-NTG
-ASA
-BB
-CCB
-ACEI
cath/lytics
-heparin
-diuretics
-monitor EKG, vitals, cardiac enzymes - What you find with a R sided MI
-
-usually with an inferior MI
-hypotn
-dec CO
-JVD
-RV dilitation upon ECHO - TX of a right sided MI
-
-ASA
-O2
-volume replacement (fluids)
-reperfusion (lytics)
-inotropes
-NO diuretics - Complications of MI
-
-V wall rupture
-V septal rupture
-Mitral dysfunction - Which chamber is most commonly affected with a myocardial contusion
- -RV
- Clinical presentation of myocardial contusion
-
-dysrhythmias
-ECHO abn
-ST changes on EKG - A Pt with a possible MI rolls up to your ER. How long do you have to get an EKG? Lytics? Cath lab?
-
-EKG- 10min
-Lytics- 30 min
-Cath-90 min - NL Aortic valve area
- 3-4 cm
- area when have mild AS? mod? severe?
-
-mild: 1.5-2.9cm
-mod: 1-1.5cm
-severe: <1cm - subvalvular AS
-
-fibromusclar ring
-ex: IHSS - Supravalvular AS
-
-coarctation of the aorta
-congenital - Valvular AS
- -common in adults
- pathology of AS
- -stenotic valve to LVH to mitral prob to LAH to A fib
- Most common etiology of AS in <50 yo
- -biscuspid problems
- Most common etiology of As in >50 yo
- -degenerative
- Clinical presentation of AS
-
-Angina/CAD/CHF
-systolic murmur
-CO is fixed
-EKG shows LVH
-CXR shows large heart and calcification of valve - Tx of AS
-
-valve replacement
-NO afterload reduction - SXS of AR
-
-hypotn (dec in CO)
-DOE
-CHF/ Pulm edema
-shock
-PND/orthopnea - Physical exam of AR
-
-diastolic murmur
-water hammer pulse
-wide pulse pressure - TX of AR
-
-surgery (NO IABP)
-vasodilators
-diuretics
-digitalis - NL area of Mitral valve
- -4-6 cm sq
- At what area do sxs of MS develop?
- -2.5cm sq
- Physical of MS
-
-post RF
-pulm edema
-A fib
-hemoptysis
-diastolic rumble
-EKG will show LAE and RVH - TX for MS
-
-digoxin
-B adrenergic blockers
-valvuloplasty
-anticoagulation - What is dressler's syndrome?
-
-pericarditis that is post MI due to autoimmune rxn to neo-Ag
-commonly seen in an anterior infarction - What does the dressler's pt present with?
-
-low grade fever
-2-10 wks after MI
-CXR shows enlargement
-pericardial friction rub - T/F: Younger victims of a MI do better than older ones bc they are more healthy.
- F: older victims do better bc they have more collaterals
- How does the heart compensate during distress?
-
-tach
-vasoconstriction
-SV modification (positive inotope) - What is the most useful test for dx of a MI?
- -coronary angiography
- What is hypertrophic cardiomyopathy?
-
-heart is enlarged from some pathology and doesn't function or fill effectively
-caused by genes or HTN - What is the etiology of hypertrophic cardiomyopathy?
-
-genetics
-AS
-HTN - TX of hypertrophic cardiomyopathy
-
-BB
-CCB
-myomectomy - What are the most common causes of pericarditis?
-
-MI
-CA
-viral
-myxedema
-radiation/drugs
-surgery - What are some SXS and SNS of pericarditis?
-
-pleuretic CP/angina-like
-constitutional sxs
-friction rub/knock
-pulsus paradoxus
-ascites/leg edema
-hypotn - TX of pericarditis
-
-NSAIDS
-ASA
-Indomethacin
-pericardiocentesis - Etiology of Pulm Edema
-
-HTN
-LVH
-LV failure - TX of Pulm Edema
-
-O2
-diuretics
-morphine - Acute causes of MR
-
-endocarditis
-papillary/tendinae ruptures
-abn leaflets - Chronic causes of MR
-
-infective endocarditis
-Rheumatic heart disease
-scleroderma
-myxomatous disease
-marfan's disease
-Ehler's danlos syndrome
-pseudoxanthoma
-congenital - DX of MR
-
-can't hear a clear S1
-A fib on EKG
-look at diameter - TX of MR
-
-afterload reduction
-digoxin
-anticoagulation
-valvuloplasty - Etiology of all tricuspid disease
-
-RF
-Carcinoid syndrome
-Marfan's
-Ebstein's - DX of TS
-
-tall, sharp a waves
-S4 - DX of TR
-
-JVD with y decent
-exacerbation of C wave - TX of tricuspid valve disease
-
-Na restriction
-valvuloplasty - Labs of Pericarditis
-
-ESR elevated/ WBC elevated
-neg cardiac monitors
-diffuse ST elevations/PR depression
-SMA 8 if due to thyroid
-silhouette on CXR - Etiology of Endocarditis
-
-Strep viridans
-Coag neg staph
-enterococcus - Epidemiology of Endocarditis (how you are affected)
-
-men >50 yo (70%)
-women <35 yo
-nosocomial
-congenital - Physical findings of endocarditis
-
-roth spots on retina
-murmurs
-friction rub
-rales
-splinter nail hemorrhages
-osler nodes
-janeway lesions
-arthritis - Key tests of endocarditis
-
-blood cultures
-ECHO - Tx of endocarditis
-
-PCN
-ceftriaxone
-vancomycin - Most important test to do for Angina
- -Stress test
- CAD risk factors
-
-HTN >140/90
-tobacco
-high cholesterol
-obesity
-HDL<40
-DM
-male
-stress - Peripartum Cardiomyopathy
-
-can occur from last month of pregnancy to 5 mos post partum
-occurs in AA females, multiparity, obesity
-sxs: SOB - SXS and SNS of Cardiac Tamponade
-
-Beck's triad
-tach - What is Prinzmetal's Angina
- -angina due to coronary vasospasm
- Tx of Prinzmetal Angina
-
-NTG
-BB - Three types of PVD
-
-takayasu
-kawasaki
-coarctation of aorta - Takayasu's arteritis
-
-most common in females 20-40
-narrowing of vessels causing ischemia
-sxs: fatigue, night sweats, diminished pulses, bruits - Kawasaki's disease
-
-subQ lymph node syndrome in children <5 yo
-causes vasculitis of the coronary arteries - SXS of Kawasaki's disease
-
-persistent fever
-rash
-swollen hands/feet
-strawberry mouth - TX of Kawasaki's disease
-
-ASA
-immunoglobulin - Tx of Coarctation of the aorta
-
-prostaglandins
-surgery - the ______ BP is the most predictive of risk for vascular disease
- -systolic
- optimal BP
- - <115/75
- risk is doubled with each increment of ______ above optimal BP
- - 20/10
- preHTN
-
-120-139/ 80-89
-can either be diastolic or systolic change - you tx HTN with two agents when...
- -BP is more than 20/10 above the goal
- Stage 1 HTN
-
-140-159 systolic
-90-99 diastolic - STage 2 HTN
-
-160 systolic
-100 or above diastolic - causes of HTN
-
-sleep apnea
-drugs/alchohol
-chronic renal disease
-renovascular disease
-hyperaldosteronism
-cushing syndrome
-pheochromocytoma
-thyroid disease
-aortic coarctation - Labs for HTN
-
-EKG
-Urinalysis
-fasting blood
-Hct
-K, Na, creatinine, Ca - Tx of HTN
-
-prevention
-wt reduction
-diet/physical activity
-diuretic
-alpha blockers
-BB
-ACEI
-ARB
-CCB - ApoB
- -particles that characterize how likely a plaque will form or not
- what are some ApoB containing proteins?
-
-VLDL
-IDL
-LDL
-Chylomicrons - Chylomicrons
- -dietary TG
- VLDL
- -hepatic TG
- IDL
-
-short lived catabolic product of VLDL
-eventually becomes LDL - LDL
-
-cholesterol rich catabolic product
-lasts in your body for days
-optimally you want <100 - HDL
-
-transfers excess cholesterol to liver
-vacuum cleaner of the body - Dx of hyperlipidemia
-
-amylase
-lipase
-LFTs
-WBC - TX of hyperlipidemia
-
-Statins
-Niacin if have cardiac risk factors
-Ezetimibe
-Fibrates
-Bile Acid Resins
Soluble fiber/ fish oils - Non-HDL
-
-Non-HDL = TC - HDL
-represents the total of VLDL and LDL
-goal for nonHDL is 30 pts higher than the LDL goals - TC
- -TC = LDL + HDL + (TG/5)
- TG
-
-not very atherogenic
-<150 is NL
-200-400 is very hight - risk factors of metabolic syndrome
-
-bp >130/>85
-fasting glucose >110
-TG >150
-HDL <40 for men
-abd waist span of 40 " - risk factors for PAD
-
-smoking
-CAD
-claudication - Physical findings of PAD
-
-smooth, shiny, hairless legs
-diminished pedal pulses
-bruits - Labs for PAD
-
-ABI needs to be >1
-ultrasound
-angiography - Tx of PAD
-
-walking regimen
-stop smoking
-PCI
-surgical revascularization - SXS and SNS of Bueger's disease
-
-associated with smoking
-lesions seen in larger vessels
-presents with pain at rest
-gangrene and ulcerations occur
-tx: stop smoking - What is the most common hyperlipoproteinemia seen?
- -type II (overproduction of LDL)
- How much of your cholesterol is exogenous? endogenous?
-
-exo: 1/3
-endo: 2/3 - corneal arcus
-
-lipid deposit in the cornea
-no vision change - xanthelasma
- -cholesterol deposit of inner eye
- HDL levels
-
-<40 is low
->60 is high - levels of TG
-
-<150 is low
-150-199 is borderline
-200-499 is high
->500 is very high - LDL levels
-
-<100 is optimal
-130-159 is borderline high
-160-189 is high
->190 is very high - obesity in men (in of waist)
- ->40
- obesity in women (in of waist)
- ->35
- Dilated cardiomyopathy
-
-LV enlargement
-systolic dysfunction - causes of dilated cardiomyopathy
-
-genes
-viral
-drugs
-ETOH (most common) - SNS and SXS of dilated cardiomyopathy
-
-dyspnea
-tach
-low BP
-JVD
-S3
-pitting edema - Tx of dilated cardiomyopathy
-
-diuretics
-digoxin - SNS and SXS of Hypertrophic Cardiomyopathy
-
-CPOE
-DOE
-murmur
-syncope - Restrictive Cardiomyopathy
-
-rare
-deposition w/in heart muscle
-rigid, noncompliant V
-diastolic dysfunction - causes of restrictive cardiomyopathy
-
-toxins
-sarcoidosis, amyloidosis, etc - SNS and SXS of restrictive cardiomyopathy
-
-dyspnea
-JVD
-S4 - Tx of restrictive cardiomyopathy
- -tx the underlying cause
- T/F: plaques with a large lipid cap over them are more likely to rupture
- F: less likely to tear open
- T/F: antioxidants, folic acid, and HRT are effective therapies to prevent plaque formation
- false
- What type of heart failure is most common?
- -systolic
- Systolic dysfunction
-
-due to ischemia or previous MI
-ventricle may be dilated - diastolic dysfunction
-
-stiff ventricle
-does not dilate properly
-due to HTN - Stage A of HF
- -risk factors are present, but there is no structural or functional abn
- Stage B of HF
- -structural abn but no sxs of HF
- Stage C of HF
- -structural abn with sxs of HF
- Stage D of HF
- -advanced structural disease with sxs despite therapies
- SXS of HF
-
-DOE
-orthopnea/ PND
-cough
-nocturia
-RUQ pain
-peripheral edema - SNS of HF
-
-tach
-JVD
-rales
-hepatosplenomegaly
-S3 (acute) S4 (diastolic) - TX of HF
-
-Na restriction
-diuretics
-ACEI
-ARB
-Digitalis
-BB
-Spironolactone
-vasodilators - SXS of Pulm Edema
-
-severe dyspnea
-frothy pink sputum
-hypoxia