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DPAP Cardiology I

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Single largest killer of US men & women   CHD  
CHD causes what % of US deaths?   1 in 5  
___ % of pts experiencing an MI will die from it   41%  
Number US deaths/year from CHF   265,000  
Pts with CHF: prognosis   70% women & 80% of men under 65 will die within 8 years  
Increase in heart failure deaths in past decade   35%  
CHF effect on risk of sudden heart failure death:   increases risk x8  
lifetime risk devt of A-fib   1 in 4  
Inferior MI: EKG correlation   (II, III, aVF); RCA; left circumflex if left dominant  
Anterior MI: EKG correlation   (V2-V5); LAD  
Lateral MI: EKG correlation   (I, aVL, V5-V6); Left circumflex  
Inferolateral MI: EKG correlation   (II, III, aVF, I, aVL); Large RCA, or Left dominant Left circumflex  
Anterolateral MI: EKG correlation   (V4-V6, I, aVL); Left circumflex  
NYHA Class I:   No limitations or symptoms with normal activity  
NYHA Class II:   Slight limitations; normal activity (moderate exertion) results in symptoms.  
NYHA Class III:   Marked limitation; minimal activity/ exertion/ ADLs results in symptoms (none at rest)  
NYHA Class IV:   Symptoms present with minimal activity and at rest/nocturnally.  
Most common causes of heart failure:   Ischemic cardiomyopathy; Valvular cardiomyopathy; Hypertensive cardiomyopathy (diastolic non-compliant CHF more common in hypertension than Systolic (end stage hypertensive dz))  
Structural causes of heart dz   myocardial dz; pericardial dz  
Types of myocardial dz   Cardiomyopathy; myocarditis  
3 functional categories of cardiomyopathy   dilated; hypertrophic; restrictive  
3 types of myocarditis   infectious; toxic; idiopathic  
3 types of pericardial dz   Pericarditis; Pericardial effusion / tamponade; Pericardial constriction  
ACC/AHA CHF Guidelines: Stage A   At risk without known disease  
ACC/AHA CHF Guidelines: Stage B   Heart disease-asymptomatic  
ACC/AHA CHF Guidelines: Stage C   Prior or current symptoms  
ACC/AHA CHF Guidelines: Stage D   Advanced or refractory  
CHF risk factors   Age; Hypertension; Tobacco abuse; Diabetes mellitus; Obesity; ETOH/Substance abuse  
CHF precipitators   Coronary artery dz/MI; Valvular or congenital heart dz; Hypertension….diastolic dysfn; ETOH/substance abuse; Viral Infxns; PG; Idiopathic  
MI pathophysiology (4 steps)   1 plaque rupture; 2 plt activation aggregation; 3 fibrin generation; 4 thrombus formation  
2 pathways for ischemic heart dz progression   Progressive intraluminal narrowing; Sudden disruption/fissuring of plaques  
Progressive intraluminal narrowing tend to:   to produce collateral blood supply & more likely to cause worsening stable/unstable angina (>75%)  
Sudden disruption/fissuring of plaques likely to:   to rupture, causing ACS (Acute Coronary Syndrome) or Acute MI (25-75%)  
Tobacco: CAD risks   2x risk for 1/2 to 1 pack/day; 3x risk for > 1 pack/day; risk declines 50% after one year of tobacco cessation  
Most common causes of heart failure:   Ischemic cardiomyopathy; Valvular cardiomyopathy; Hypertensive cardiomyopathy  
Which type of non-compliant CHF is more common in HTN?   Diastolic more than Systolic (end stage hypertensive dz)  
What precipitates conduction system problems?   Coronary artery dz/MI (ischemia induced); congenital; anything that causes CHF  
CAD signs/symptoms   Chest pain/pressure/tightness; Jaw/ neck/ throat/scapular/ arm pain; SOB/ Dyspnea on exertion; N&V; Diaphoresis; Fatigue  
Deoxygenated blood draining from the heart itself enters the right atrium via:   the coronary sinus & thebesian veins  
Second most common cause of sudden death in young adults   Anomalous coronary arteries (4-15% of young people with sudden cardiac death); 1-2% of population  
Which valves do/do not have chordae/papillary mx?   AV valves do; semilunar valves do not  
period of ventricular contraction   systole  
period of ventricular relaxation   diastole  
the load that stretches the cardiac muscle prior to contraction   preload  
the resistance against which the left ventricle must contract   afterload  
ability of cardiac muscle to shorten, when given a load   myocardial contractility  
myocardial contractility is increased by:   sympathetic stimulation/action  
myocardial contractility is decreased by:   myocardial injury  
afterload comprises:   blood volume/viscosity; resistance in aorta & other peripheral vessels  
Preload is increased by:   inspiration or increasing venous return to right heart)  
Amount of blood remaining after ejection:   end systolic volume  
In diastole, _____% of ventricular filling occurs before atrial contraction   80  
SV=   EDV (end diastolic volume) – ESV (end systolic volume)  
CO =   HR x SV (normal about 5 L/min)  
Adult normal cardiac blood volumes:   SV=70ml, EDV=135ml, ESV=65ml, CO=5L total blood  
volume of blood ejected from each ventricle during one minute   Cardiac output  
volume of blood ejected with each heartbeat   Stroke volume  
Starling’s Law:   SV increases as the EDV increases  
Ejection Fraction formula:   EF% = SV/EDV  
A quantitative measure of contractility   Ejection Fraction  
Normal EF   67% (at DUMC: >55%)  
Annulus:   fibrous ring surrounding each of the 4 cardiac valves; fn: to provide structural support to the heart  
narrowing or obstruction to forward flow while valve is open   Stenosis  
backward leakage during time when valve is closed   Regurgitation / Insufficiency  
S1 = _____ valve closing   Mitral (Systole)  
S2 = _____ valve closing   Aortic valve closing (diastole)  
S3 may indicate:   CHF (sounds like: Ken-Tuc-Key)  
S4 may indicate:   HTN or CAD (sounds like: Tenn-es-see)  
Which heart sound is always pathological?   S4  
Left & right coronary arteries arise from what part of the aortic root?   Sinuses of Valsalva  
Branches off the left main coronary artery   LAD; Left circumflex  
Right Dominant: Septum supplied by:   Distal branches from RCA (supply the septum 70%)  
Left Dominant: Septum supplied by:   Distal branches from LCx (supply the septum 20%)  
SA Node is supplied by:   RCA 60% of the time & by LCX 40% of the time  
AV node supplied by:   dominant artery (RCA or LCx)  
small vascular channels that interconnect the normal coronary arteries   Collateral Vessels  
Function of collateral vessels in normal myocardium   Nonfunctional because no pressure gradient is present  
S/S of conduction problems   palpitations; dizziness; presyncope/ syncope  
Myocardial dz categories   Cardiomyopathy; Myocarditis  
MI Pathophysiology steps   1. Plaque rupture; 2. Plt activation/aggregation; 3. Fibrin generation; 4. Thrombus formation  
Cardiac ischemia risk factors   Age; Gender ? FH; Sedentary Lifestyle; Tobacco; HTN; DM/insulin resistance; Hyperlipidemia  
DM increases risk/incidence of:   Diffuse dz; small vessel dz; CHF & death rates post MI; death or MI post CABG & PCI  
Recommended for sedentary lifestyle   Devoted exercise 30 min/day, 5 d/wk; initially under med supervision  
Causes of coronary ischemia leading to chest pain   Atherosclerosis; Vasospastic disorders; stenosis or HCM; Coronary thrombosis/ embolization; Acute aortic dissection  
Causes of noncardiac CP   Pericarditis; myocarditis; MVP; chostocondritis; C- or T-spine dz/thoracic outlet; GI/gall bladder; PE; pneumonia; pneumothorax  
JNC7: Normal   SBP <120; DBP <80  
JNC7: Pre-HTN   SBP 120-139; DBP 80-89  
JNC7: HTN, Stage I   SBP 140-159; DBP 90-99  
JNC7: HTN, Stage II   SBP >160; DBP >100  
ATP III: High total Chol =   >200 mg/dl  
ATP III: Hypertriglyceridemia   >150 mg/dl  
ATP III: Low HDL Cholesterol   < 40 mg/dl  
ATP III: High LDL (& known CAD)   > 100 mg/dl  
ATP III: High LDL (> 2 Risk Factors)   > 130 mg/dl  
ATP III: High LDL (< 2 Risk Factors)   > 160 mg/dl  
Before a dx of CAD, diabetics risk of MI =   risk of non-diabetic with prior MI  
Almost all MI’s result from:   coronary atherosclerosis & superimposed coronary thrombosis  


   





 
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