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USMLE1 02
Cardiology 2
| Question | Answer |
|---|---|
| ECG: ST-segment depression | sign of subendocardial ischemia --> exertional angina |
| ECG: ST-segment elevation | Transmural ischemia --> prinz metal angina |
| ECG: U wave | hyPOK+ (positve wave AFTER the T wave) |
| ECG: Peaked T wave | hyPER K+ (accelerated repolarization of the cardiac muscle) |
| ECG: inverted T waves, ST elevation, new Q waves | MI |
| ECG: short PR interval + delta wave | WPW: bundle of Kent transmits electrical impulses from atria to ventr faster n w less regulation than AV node. Delta wave, a slurred upstroke in the QRS complex ass with a short PR interval. Never give these people digitalis (increases contractility). |
| when do your coronary arteries fill? | during diastole |
| formula for ejection fraction | EF = (stroke vol)/(end diastolic vol) |
| what determines diastolic BP? | the amount of blood in the arterioles while the heart is filling up in diastole <-- determined by constriction of peripheral arterioles |
| What is the main factor that controls TPR? | radius of the vessel. |
| Lung problems -- heart failure on which side? | L |
| Liver problems -- heart failure on which side? | R |
| Paroxysmal nocturnal dyspnea -- heart failure on which side? | L |
| L heart failure | Main sx: SOB. Forward failure. LV can fail: 1. Push against big afterload. 2. Xs vol to push out. 4. many infarcts -> contractility dec. End rslt: prob pushing blood out. End diast vol inc bc can't push blood out -> back up into lung -> pulm ed. |
| Chronic L heart failure | hemorrhage --> alveolar macrophages will phagocytose RBC's, rusty colored sputum, alveolar cytology see hear failure cells (alveolar macrophages that have phagocytosed RBC's --> broken down into hemosiderin) |
| R heart failure | Backward fail --> inc ven hydrostatic P --> neck vein dist, painful Hepmgly (nutmeg liver: inc P in vena cava -> hepatic vein --> P transmitted to liver's central vein --> red dots that look like nutmeg PLUS acites, pitting edema, neck vein distension. |
| What is the most common cause of congestive painful hepatomegaly? | R heart failure |
| Why do people with L heart failure have trouble sleeping? | While sleeping can absorb fluid from intersti into venous because no gravity --> extra blood going into R n L hrt. If LV fail, all that extra blood will -> pulm edema -> can't breathe lying down. Pillow orthopnea -- (decreases blood going to heart). |
| What is the best non-pharmocologic treatment for R or L heart failure? | Restrict water, restrict salt so that you don't tax the heart with extra volume it can't handle. |
| King of heart failure treatment: | Dec preld n aftld: ANGi's. Inc longev. Dec preld bc dec ANG II prod -> 1. dec prod of ald -> dec prod of ENaC chan -> dec salt absorp -> dec water reabs (follw Na) -> dec plas vol -> dec preld. 2. dec constric of renal art -> dec TPR -> dec aftld. |
| What is the best combo drug regimen for someone with CHF? | ACEi's + spironolactone. This is because eventually, aldosterone kicks in again (even though on ACEi's), so spironolactone (which also blocks the production of ENaC channels) make things a lot more effective. Increases longevity, decreased mortality. |
| Why does endotoxic shock cause high output heart failure? | endotoxic shock --> release ofC3a/C5a, NO --> peripheral resistance arterioles dilated --> inc venous return to R heart --> high output failure |
| What kind of heart failure does thiamine deficiency cause? | Thiam is cofactor for pyruvate dehyd (PD). [Pyruvate -(thiam + PD)-> AcetylCoA] --> dec prod of Acetyl CoA (lose 6 ATP per 1 molecule of Acetyl CoA NOT made --> Prob: lack of ATP. Sm musc nd ATP --> vasodil of art -> inc vol to hrt -> high output HF. |
| Why does Graves disease cause high output heart failure? | Thyroid hormone --> inc β receptors in the heart --> inc contractility --> dec end systolic volume --> inc ejection fraction [EF = SV/EDV = (EDV - ESV)/EDV] --> more blood being moved through system --> high output failure |
| AV fistula | AVM -- art bld bypassing cap bed --> venous --> bld comes back faster. Mass is pulsatile, bruit there. If press on prox AVM, HR slows |
| Name the three types of angina | Exertional, Prinz Metal (vasospasm), Unstable (resting) |
| What is exertional angina? | subendocardium not getting enough blood, O2, and nutrients (furthest away from coronary arteries) --> reacts to this lack of O2 with pain and ST-elevation |
| Prinz metal more common in men or women? | women |
| What is vasospastic angina? | Vasospasm of coronary (TXA2 implicated) --> transmural ischemia --> ST elevation |
| What vessels used for CABG? | Saphenous vein (high tendency of fibrosing off after 10 years), internal thoracic (internal mammary) artery -- very good 10-year patency! |
| Name the 4 coronary arteries | R coronary artery (RCA); L coronary artery: Circumflex artery + L anterior descending artery (LAD) |
| What parts of the heart does the L anterior descending artery (LAD) supply? | 1. supplies the entire anterior of heart, 2. supplies anterior 2/3 of the interventricular septum |
| What parts of the heart does the R coronary artery supply? | 1. posterior heart, 2. posterior 1/3 of interventricular septum, 3. entire RV, 4. mitral valve postero-medial papillary muscles, 5. 95% of the AV node |
| Where are the conduction bundles of the heart located? | anterior 2/3 of the interventricular septum (this is supplied by the LAD) |
| Patient has a complete heart block that required pace maker – what was the most likely vessel that was thrombosed? | L anterior descending coronary artery |
| substernal chest pain, radiation down the L arm, into the jaw | acute MI due to LAD |
| older patient comes in complaining of severe GERD -- what should you rule out first? | MI with atypical sx's due to RCA occlusion (causes epigastric pain) |
| 3 or 4 days after pt has MI of the anterior heart, patient comes back to the ER complaining of chest pain. When you listen to the patient’s heart, you hear muffled heart sounds. You note that the patient’s neck veins are distended. What is the problem? | LAD thrombosis --> prior infarct of the anterior heart --> heart ruptures. Muffled heart sounds because there is blood in the pericardium due to the rupture. |
| What is a mural thrombus? | thrombus on the wall of the heart |
| Fetal circulation: which vessel has least amount of O2? | 2 umbilical arteries |
| Fetal circulation: which vessel has most amount of O2? | umbilical vein |
| How does the fetus get O2? | Chorionic villi -> dips into lake of blood fed by mom's spiral arterioles -> extr O2 -> HbF has hi affinity for O2-> comp in fetal circ w hypoxia --> inc release of EPO --> inc RBC prod --> polycythemia to comp for HbF not wanting to let go of O2. |
| Path of fetal blood | Syncytiotrophoblast --> cytotrophoblast --> chorionic villi --> umb vein --> liver (1. hepatic sinusoids -> hep vein -> IVC, 2. ductus venosus --> IVC-> RH --> foramen ovale --> L atrium --> aorta. SVC --> R heart --> tricuspid valve --> RV --> pulmonar |
| L to R shunt - what happens to the O2 saturation in the R heart? | O2 blood going into deO2 blood --> inc O2 sat in R heart (step up) |
| R to L shunt - what happens to the O2 saturation in the L heart? | deO2 blood joins O2 blood --> dec O2 sat in L heart (step down) |
| Ventricular Septal Defect -- what happens to O2 sat? | L heart is stronger than R heart, so blood will move LV to RV --> inc O2 sat in RV and in pulmonary arteries -- step up |
| Ventricular Septal Defect -- long term -- what are the consequences? | volume overloading RV --> pulmonary HTN --> RV hypertrophy --> RV becomes stronger than LV --> reversing the shunt -- R to L shunt (Isenmanger Syndrome) --> cyanosis tardive |
| What is Eisenmenger's Syndrome? | Eisenmenger's syndrome is defined as the process in which a left-to-right shunt in the heart causes increased flow through the pulmonary vasculature, causing pulmonary hypertension, which in turn, causes increased pressures in the right side of the heart |
| Atrial Septal Defect -- what happens to O2 sat? | Patent foramen ovale. Pressures in LA greater than pressures in RA --> O2 blood from LA joins deO2 blood in RA --> inc O2 sat in RA, RV, pulm arteries - step up |
| What is the difference in O2 sat between a ventricular septal defect and an atrial septal defect? | In atrial septal defect, you have an increase in RA O2 sat, which does not occur in VSD. Run risk of Eisenmenger's Syndrome as well as paradoxical embolization. |
| What is paradoxical embolization? | A paradoxical embolus is a blood clot that originates in the venous circulation, but actually ends up on the arterial side. Blood clot in veins --> VC --> RA --> ATRIAL SEPTAL DEFECT or VENTRICULAR SEPTAL DEFECT --> LA or LV --> aorta --> clot now in art |
| Teratogen that most likely causes patent foramen ovale (atrial septal defect) | EtOH - Fetal Alcohol Syndrome. |
| In a newborn, what drug would you give to maintain a patent ductus arteriosus? | PGE2 (a vasodilator) |
| Patent ductus arteriosus -- what happens to O2 sat? | Aortic pressures greater than pulmonic pressures --> O2 blood from aorta flows into pulmonary arteries --> increases O2 sat in pulmonary arteries (step up, only O2 sat) --> volume overloads pulmonary circulation --> pulmonary HTN |
| Patent ductus arteriosus -- long term -- what are the consequences? | pulmonary HTN --> volume backs up into RV --> RV hypertrophy --> pulmonic pressures become greater than aortic pressures --> deO2 blood from pulmonary arteries goes directly through patent ductus arteriosus into aorta --> enters aorta distal to the subcla |
| In PE, what sound would you hear with a patent ductus arteriosus? | Machinery murmur heard between the scapulas on the patient's back |
| Infection that causes patent ductus arteriosus | Congenital rubella |
| Patent ductus arteriosus -- how would you close it non-surgically? | Indomethacin - NSAID --> blocks COX --> decreased production of PGH2 --> decreased PGE2 --> block vasodilation --> ductus arteriosis closes |
| Tetrology of Fallot -- name the 4 defects | 1. overriding aorta, 2. pulmonic stenosis, 3. ventral septal defect, 4. RV hypertrophy |
| What determines how cyanotic a patient with Tetralogy of Fallot is? | Degree of pulmonic stenosis determines how much blood gets into the lungs to pick up O2 |
| What shunts are cardio-protective in a patient with Tetralogy of Fallot? | 1. atrial septal defect, and 2. patent ductus arteriosus. This is because since the L heart pressures are greater than R heart, they will push the O2 blood from the L heart into the R heart and get more blood into the lungs to pick up O2 |
| What is transposition of the great arteries? | Pulmonary artery and aorta switch positions so that the RV is drained by the aorta and the LV is drained by the pulmonary artery |
| What shunts are cardio-protective in a patient with transposition of the great arteries? | ASD and VSD. These shunts are actually required for life because without them, the systemic circulation has no way of getting oxygenated blood. |
| What is situs inversus? | a congenital condition in which the major visceral organs are reversed or mirrored from their normal positions |
| Kartagener syndrome | Primary ciliary dyskinesia (PCD). rare autos recess, causes defect in cilia lining resp tract and fallopian tube. reduced mucus clearance from lungs, n susceptibility to chronic recurrent resp infxn. Can cause defective organ placement n situs inversus. |
| Dry Beri Beri, Wet Beri Beri | ThiamineDef- DryBeriBeri: Myelin needs ATP --> peripheral neuropathy. Wet Beri Beri: Heart needs ATP --> L heart failure --> R heart failure --> dependent pitting edema, congestive cardiomyopathy --> biventricular enlargement (both sides of heart fail). |
| Branham Sign | (branham sign -- sign of AV fistula, bradycardia produced by digital closure of an artery proximal to an arteriovenous fistula). |
Created by:
christinapham
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