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137 Cards in this Set

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  • Back
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
-HTN > 140/90
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
You have an EKG of someone with angina. What do you see?
-ST depression
-T wave inversion
TX of Angina
-platelet inhibitors
H&P of MI
-radiating, substernal CP
-feeling of doom
What will you see on an EKG of someone having a MI?
-ST changes > 1mm in 2 consecutive leads
TX of MI
-monitor EKG, vitals, cardiac enzymes
What you find with a R sided MI
-usually with an inferior MI
-dec CO
-RV dilitation upon ECHO
TX of a right sided MI
-volume replacement (fluids)
-reperfusion (lytics)
-NO diuretics
Complications of MI
-V wall rupture
-V septal rupture
-Mitral dysfunction
Which chamber is most commonly affected with a myocardial contusion
Clinical presentation of myocardial contusion
-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
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
Clinical presentation of AS
-systolic murmur
-CO is fixed
-EKG shows LVH
-CXR shows large heart and calcification of valve
Tx of AS
-valve replacement
-NO afterload reduction
-hypotn (dec in CO)
-CHF/ Pulm edema
Physical exam of AR
-diastolic murmur
-water hammer pulse
-wide pulse pressure
TX of AR
-surgery (NO IABP)
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
-diastolic rumble
-EKG will show LAE and RVH
TX for MS
-B adrenergic blockers
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?
-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?
TX of hypertrophic cardiomyopathy
What are the most common causes of pericarditis?
What are some SXS and SNS of pericarditis?
-pleuretic CP/angina-like
-constitutional sxs
-friction rub/knock
-pulsus paradoxus
-ascites/leg edema
TX of pericarditis
Etiology of Pulm Edema
-LV failure
TX of Pulm Edema
Acute causes of MR
-papillary/tendinae ruptures
-abn leaflets
Chronic causes of MR
-infective endocarditis
-Rheumatic heart disease
-myxomatous disease
-marfan's disease
-Ehler's danlos syndrome
DX of MR
-can't hear a clear S1
-A fib on EKG
-look at diameter
TX of MR
-afterload reduction
Etiology of all tricuspid disease
-Carcinoid syndrome
DX of TS
-tall, sharp a waves
DX of TR
-JVD with y decent
-exacerbation of C wave
TX of tricuspid valve disease
-Na restriction
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
Epidemiology of Endocarditis (how you are affected)
-men >50 yo (70%)
-women <35 yo
Physical findings of endocarditis
-roth spots on retina
-friction rub
-splinter nail hemorrhages
-osler nodes
-janeway lesions
Key tests of endocarditis
-blood cultures
Tx of endocarditis
Most important test to do for Angina
-Stress test
CAD risk factors
-HTN >140/90
-high cholesterol
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
What is Prinzmetal's Angina
-angina due to coronary vasospasm
Tx of Prinzmetal Angina
Three types of PVD
-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
-swollen hands/feet
-strawberry mouth
TX of Kawasaki's disease
Tx of Coarctation of the aorta
the ______ BP is the most predictive of risk for vascular disease
optimal BP
- <115/75
risk is doubled with each increment of ______ above optimal BP
- 20/10
-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
-chronic renal disease
-renovascular disease
-cushing syndrome
-thyroid disease
-aortic coarctation
Labs for HTN
-fasting blood
-K, Na, creatinine, Ca
Tx of HTN
-wt reduction
-diet/physical activity
-alpha blockers
-particles that characterize how likely a plaque will form or not
what are some ApoB containing proteins?
-dietary TG
-hepatic TG
-short lived catabolic product of VLDL
-eventually becomes LDL
-cholesterol rich catabolic product
-lasts in your body for days
-optimally you want <100
-transfers excess cholesterol to liver
-vacuum cleaner of the body
Dx of hyperlipidemia
TX of hyperlipidemia
-Niacin if have cardiac risk factors
-Bile Acid Resins
Soluble fiber/ fish oils
-Non-HDL = TC - HDL
-represents the total of VLDL and LDL
-goal for nonHDL is 30 pts higher than the LDL goals
-TC = LDL + HDL + (TG/5)
-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
Physical findings of PAD
-smooth, shiny, hairless legs
-diminished pedal pulses
Labs for PAD
-ABI needs to be >1
Tx of PAD
-walking regimen
-stop smoking
-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
-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)
obesity in women (in of waist)
Dilated cardiomyopathy
-LV enlargement
-systolic dysfunction
causes of dilated cardiomyopathy
-ETOH (most common)
SNS and SXS of dilated cardiomyopathy
-low BP
-pitting edema
Tx of dilated cardiomyopathy
SNS and SXS of Hypertrophic Cardiomyopathy
Restrictive Cardiomyopathy
-deposition w/in heart muscle
-rigid, noncompliant V
-diastolic dysfunction
causes of restrictive cardiomyopathy
-sarcoidosis, amyloidosis, etc
SNS and SXS of restrictive cardiomyopathy
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
What type of heart failure is most common?
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
-orthopnea/ PND
-RUQ pain
-peripheral edema
-S3 (acute) S4 (diastolic)
TX of HF
-Na restriction
SXS of Pulm Edema
-severe dyspnea
-frothy pink sputum