Cardiology #2

zms2187's version from 2016-11-22 01:02


Question Answer
echo findings tamponade+ effusion, diastolic RV collapse, respiratory increase of inter-ventricular dependence, by doppler will see respiratory variations > 25% in mitral, aortic and/or tricuspid flow
Parvus et tardussmall and slow carotid upstroke- common with severe AS
Tamponade, explain respiratory changes and what happens to RVduring inspiration, the negative intra-thoracic pressure is transmitted to the cardiac chambers, creating a depression in the right ventricle and atrium which suctions the venous caval flow into the right atrium. The right ventricle expands while the left ventricle volume decreases. During expiration, the pressure in the thorax and in the pericardium are summed, superior to the pressure in the right chambers. The right ventricle is compressed. This consequence of ventricular inter-dependence can be assessed from parasternal long or short axis viewing both right and left ventricles. Mmode will allow the comparison of the right ventricle size between inspiration and expiration.
Why is Cardiac Index importantallows us to evaluate cardiac output among individuals of different sizes (CO/BSA) for standardization
Formula to calculate SVRbased on Ohms law where Q= P/R. R= P/Q so pressure is MAP - CVP and Q is CO
MAP = ?1/3 (Systolic aortic pressure) + 2/3 (Diastolic aortic pressure)
Frank Starling LawPreload for the ventricles is defined as amount of passive tension or stretch exerted on the ventricular walls (i.e. intraventricular pressure) just prior to the initiation of systole. This load determines end-diastolic sarcomere length and thus the force of contraction. The Frank–Starling law states that the passive length to which the myocardial cells are stretched at the end of diastole determines the active tension they develop when stimulated to contract. The Frank–Starling law is an intrinsic property of myocytes and is not dependent upon extrinsic nerves or hormones. The general principle is that increased preload causes increased force of contraction, which increases stroke volume and thus cardiac output. The Frank–Starling law (or mechanism) helps the heart match cardiac output to venous return.
Good LVH criteriaCornell criteria - R wave in aVL + S wave in V3 >28mm M and >20mm F
EKG criteria for RVHR axis deviation and dominant R wave w/secondary ST and/or T wave changes in V1/V2
Wide QRS, no P, rate 100-110accelerated idioventricular rhythm
Wide QRS, no P, rate 110-250VT or SVT w/aberrancy

Section 2

Question Answer
R axis deviation on EKG> 100 degrees. - in I and + in aVF
L axis deviation on EKGbetween -30 and -90. + in I and - in avF or II
Normal axis on EKGanywhere from 0 to 90, + in I and II or I and aVF
where are q waves common?small q waves (<0.03s) common in most leads EXCEPT V1-V3 and avR
Q wave criteria for MI?at least >1mm depth in 2 contiguous leads.
what is a U wavesmall (usually +) deflection after T wave. If faster HR U wave can be superimposed on preceding T wave. indicates afterpotentials of ventricular m vs repol of purkinje fibers
Pacemaker 4 letter code1st is chamber PACED (A, V, or dual), 2nd is chamber SENSED(A, V, or dual), 3rd is MODE (inhibit, triggered, dual), 4th is RATE RESPONSIVENESS
Meaning of VVIR pacer codepacemaker PACES the ventricle, SENSES the ventricle, INHIBITED by a sensed QRS complex, and is rate responsive
DDD pacer codePACES and SENSES the atria and ventricle. Dual mode indicates that sensed atrial activity will inhibit atrial output and trigger a ventricular output after a designated AV interval

temporary pacing

Question Answer
Indications for temp pacingacute hemodynam significant brady or asystole, termination of tachycardia via overdriving pacing (aflutter or SVT due to reentry), bridge to perm pacing, VT (brady-dependent VT or long QT), acute MI (new bifascicular block), acute AR (those who have brady and high LVEDP can improve hemodynamics)
Complications of transvenous pacingpneumothorax, RV perf, infection, bleeding, venous thrombosis
where do pads go for transq pacinganterior chest wall (inferior aspect of V3 or the palpable cardiac apex) and posterior (inferior edge of scapula or to the left or right of spine)
Transesophageal or transgastric pacingelectrode can be advanced to position behind LA to pace atrium, or into stomach to pace ventricle (though difficult to do 2/2 intolerable pain)
preferred site for transvenous pacerpreferred RIJ, if perm pacemaker planned then AVOID subclavian on the side of pacer placement. can also use femoral vein (preferred in cath lab) or EJ


Question Answer
Anatomical factors leading to afibLA fibrosis, pulmonary vein dilation, and reduced atrial contractility
cardiac surgery w/highest risk for post-op afibmitral valve surgery
Mechanism of afibfocal mechanism involving both increased automaticity and multiple reentrant wavelets usually occurring in the LA around the pulm vv.
Afib ekgabsent P waves. Atrial activity is chaotic, rate is usually 400-700bpm and ventricular response is usually 120-180bpm
TTE predictors of increased CVA riskmitral stenosis, LA enlargement, reduced LV systolic function, thrombus in LA appendage, decreased LA appendage emptying velocities
New afib, tests to orderTTE, consider ambulatory holter etc., TSH, renal function, LFTs
Goals of afib treatmentcontrol ventricular response, assess/manage stroke risk, restore/maintain sinus rhythm
Afib with evidence of pre-excitation on EKGgive procainamide. No calcium/beta blockers/lido/adenosine which can accelerate conduction down accessory pathway resulting in degeneration to ventricular rhythm
When to use dig for afibwhen beta/calcium blockers are contra-indicated (bronchospasm, hemodynamic instability). Dig is good at controlling resting HR but not great w/ventricular response.
Onset of digoxin action1-4 hours
Other drugs that promote maintenance of sinus rhythm, particularly in post-op period or post cardioversionACE inhibitors, statin
when to avoid anti-coagulation for afibthose w/contraindications to anticoag or those w/lone afib (age <65 with structurally normal heart)

Afib 2

Question Answer
historical factors lending highest risk of afibhx of thromboembolism (stroke, tia, systemic embolism), and rheumatic mitral stenosis
How long to continue anticoag post cardioversion to NSRat least 4 weeks (to allow for recovery of atrial transport mechanism and recurrence of AF). Post DCCV CO declines slightly along with atrial function
2 points for what factors in Chads and Chads-vasc?2 for hx of stroke/tia etc and age >75 in chads vasc only (1 point for age >65 in chadsvasc, 1 pt for age >75 in chads)
if afib >48 hours how long to wait before dccv?3 weeks, if cant wait then iv anti-coag or DOAC and do TEE before
what does literature show regarding efficacy of warfarin, asa, plavix for preventing stroke in afib?warfarin > asa (RR reduction 68% coumadin, 0-44% asa), asa similar to plavix for risk reduction, asa + plavix better together than on own. Warfarin > asa + plavix
PROTECT triallooked at Watchman device which was non-inferior to anticoagulation w/warfarin in terms of thromboembolic outcomes
AFFIRM trial?looked at whether its better to restore NSR in afib versus controlling ventricular rate/managing stroke risk only. both had similar outcomes w/survival and embolic outcomes.
which is more successful, DCCV or pharm cardioversion?DCCV works 80% of time and is better than pharm cardioversion

RV infarcts

Question Answer
why is RV less susceptible to infarction than LVRV uses less O2 (smaller muscle mass), coronary perfusion in RV occurs in both systole/diastole, more extensive collateral flow from L to R coronary aa.
most blood supply to RV via what artery ?RCA via RV marginal branches in R-dominant circulation (majority). 15% of cases caused by occlusion of L coronary circulation