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210 Cards in this Set
- Front
- Back
Where does a fib usually originate? |
Entry to the R atrium
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How much does a coronary artery need to be occluded to require intervention? What is the exception?
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75% occlusion, except for the LAD at 50%
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Which coronary artery supplies the SA node?
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RC in 55% of people
Circ in 45% of people |
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Which coronary artery supplies the AV node?
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RC in 90% of people
Circ in 10% of people |
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Which tissue does the RCA supply? |
RA, RV, inferior and posterior wall of LV
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If there is an occlusion in the RCA, which infarct will be seen?
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Inferior or posterior MI
RV infarct |
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Which part of heart does LAD supply?
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Anterior 2/3 of septum
Anterior LV |
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Which conducting systems fed by LAD?
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LBB
RBB |
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What happens if there is an occlusion of the LAD
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Anterior wall MI
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What tissue does the cricumflex artery supply?
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Part of LA
Lateral wall |
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What MI occurs with circumflex artery ischemia?
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Lateral wall MI
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Formula for coronary perfusion pressure |
DBP-PAOP
Normal 60-80 |
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S1
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Closure of tricuspid and mitral valves right before systole
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S2
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Closure of the pulmonic and aortic valves right after systole
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What is the biggest problem with tachycardia?
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Increase O2 consumption
When HR increases, systole period stays the same but there is less time for diastole -Reduces ventricular filling -Reduces coronary perfusion |
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S3
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Kentucky
Where S1 is ken, S2 is tuc, and S3 is key S3 occurs in early diastole (whereas S1 is late diastole right before systole) |
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What causes S3?
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Rapid rush of blood into a dilated ventricle
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Who gets S3
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Mostly someone with HF
Could be due to fluid overload or mitral valve insufficiency Could be normal in teens or pregnancy |
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S4
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Tennessee,
Ten = S4 Nes = S1 See = S2 |
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Causes of S4 |
Late diastole before S1
Caused by blood pushing into non-compliant ventricle Due to MI, HTN, ventricular hypertrophy, aortic/pulmonic stenosis Always abnormal |
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Pericardial friction rub
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Inflammation of pericardium - pericarditis
Very common after MI or heart surgery |
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How do you hear a friction rub?
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Listen to 4-5th ICS at LSB with patient leaning forward
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Formula for CO
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CO = SV x HR
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What happens if preload is too high or too low? (e.g.hypovolemia, hypervolemia)
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If there is too much stretch on the myocardium, decreases contractility
If there is too little stretch on the myocardium, decreases contractility There is a window of adequate stretch to maximize CO |
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Preload =
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LVEDP
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PVR
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Pulmonary vascular resistance
Afterload of the R heart |
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SVR
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Systemic vascular resistance
Afterload of the L heart |
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Normal CI
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2.5-4
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What are the three determinants of SV?
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PAC
Preload, afterload, contractility |
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Pulsus alternans
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Alternating pulse waves (can be seen on a line tracing)
every other beat weaker Indicates LVF |
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Pulsus paradoxus
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Exaggerated response to inspiration, during inspiration pulse pressure changes > 10 mmHg.
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What does pulsus paradoxus indicate?
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Pericardial effusion
Constrictive pericarditis Severe lung disease CHF |
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PAD
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Pulm art diastolic
Can tell you about L ventricle function |
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Normal PAD
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8-12
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CVP waveform
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Normally lower pressure, small waves/squiggles
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RV waveform
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High amplitude
On systole pressure is very high, on diastole pressure is very low |
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PA waveform
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Not as much pressure difference a RV waveform, has dicrotic notch that represents pulmonary valve closure
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When would CVP not indicate right ventricular pressures accurately?
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In the case of tricuspid stenosis - this will make the atrial pressure unnaturally higher
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Normal PAS
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15-25
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Pulm HTN PAS
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>40
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Normal CVP
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2-12
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Indications for PA cath
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Cardiac surgery
Heart damage |
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Temperature specifications of PA cath CO measures
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Must be a 10 degree difference between patient temperature and injectate temperature
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Phlebostatic axis
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4th ICS and 1/2 anterior posterior diameter of chest
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Square wave test
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Determines ability of transducer to correctly read pressures
Flush line, should make a square then drop below baseline and then return to baseline |
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Abnormal square wave test
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After dropping below baseline, should not make a bunch of squiggles before returning to baseline
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Pre-hypertension
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120/80
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1st and 2nd choice drugs for HTN
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Diuretics first, then B block
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Which drug class works better than B blockers in black people?
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Ca channel blockers
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Maze procedure
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Ablation of a-fib generating tissue, creates a designated pathway for signal
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Mechanical valve care
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Anyone with mechanical valve needs coumadin
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Transverse aortic aneurysm symptoms
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Dyspnea, stirdor, HOARSENESS, chest pain
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Descending aortic aneurysm symptoms
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back/chest pain, tearing sudden pain
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Complication after d/c IABP
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Reperfusion injury may occur and cause compartment syndrome
Requires surgical intervention |
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IABP positioning
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Leg of insertion must be kept straight so as not to kink balloon
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Number one contraindication for IABP
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Aortic valve insufficiency
Because if that balloon inflates and the aortic valve don't close good, it's going to push pressure back into the heart and cause damage |
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Most common complication after cardiac transplant
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Graft atherosclerosis
Remember that if bradycardia occurs, person must be paced |
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Alpha receptor control
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Vascular vasoconstriction
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B2 receptor control
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Bronchial tree vasodilation on sympathetic stimulation
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How does the vagus nerve affect HR?
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Vagus nerve innervates sinus node - increased parasympathetic output causes bradycardia
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Inotrope of choice for HF
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Milrinone
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DA cardiac dose
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5-10 mcg
Acts at B receptors Increases contractility, HR, |
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Alpha dose of DA
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10-20 mg
Affects alpha receptors - vasculature to cause vasoconstriction |
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How does dobutamine differ from DA?
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Affects B only, no alpha effects
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Dobutamine dosing
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2-10 mcg, don't exceed 20
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Review: which receptors do the following drugs affect:
Epi DA NE Neo Dobuatmine |
Epi - alpha, B1, B2
DA - renal, B, alpha NE - mostly alpha, little B Neo - pure alpha |
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Who cannot get a B blocker?
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Anyone with severe asthma
Will cause bronchoconstriction |
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Which B blocker affects only B1, so shouldn't affect the lungs?
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Metoprolol
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Two common alpha blockers
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Nipride
Hydralazine Decrease SVR |
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What is the only drug to block parasympathetic effects on the heart?
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Atropine
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SVT rate
How do you know it's SVT |
150-250
The sinus node can't fire that fast |
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Where does adenosine work?
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On the AV node only
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Difference between cardioversion and defibrillation
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Cardioversio is synched to the R wave, lower voltage
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Treatment of SVT
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Vagal stimulation
Adenosine 6 mg rapid push, then 12 mg rapid push x 2 if necessary Calcium channel blockers: diltiazem B blockers: lopressor Cardioversion if all else fails |
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RVR
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Rapid response in ventricles to a fib
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RVR presentation
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pale and poofy
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Effects of a fib
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Decreased CO, UOP, BP, fatigue
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A fib and clots
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21 days after onset, 40% have stroke if untreated
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Treatment of a fib
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Metoprolol - rate control
Diltiazem - rate control Amiodarone - convert Sotolol (Beta) - convert |
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What is special about the QT interval?
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Ventricles are refractory during this period
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Why is it dangerous to have a prolonged QT interval?
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Second half of the T wave is relative refractory, meaning that if a PAC occurred overtop it could capture the tissue excitability and cause Vtach
Torsade de point is a type of vtach |
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Drugs that cause QT prolongation:
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Quinolones (levaquin)
Antidepressants Haldol (gets more attention because accumulates faster) |
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Electrolyte imbalance that will cause PVCs/vtach
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Hypokalemia
Hypomagnesemia |
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Medical treatment for vtach if pulse present:
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Amiodarone 150 mg bolus over 10 min, then 1 mg/min drip
Lidocaine 1 mg/kg Then lido drip |
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Treatment for v fib
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Epi 1 mg or vasopressin 40 units
Amiodarone 300 mg Procainamide 17 mg/kg Mag 2g m Shock |
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Leads that look at the inferior wall
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II, III, aVF
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Leads that look at the anterior wall
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V2, V3, V4
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Leads that look at the lateral wall
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I, aVL, V5, V6
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Acute coronary syndrome
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Plaque rupture
Will result in unstable angina, NSTEMI, or STEMI |
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What happens after plaque ruptures?
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Platelets are activated
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What happens after platelets activated?
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Aggregation - stick together and to the plaque, will eventually form occlusion
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How do ASA and plavix act?
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Antiplatelet
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What does t wave inversion mean?
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Ischemia
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What does ST elevation mean?
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Injury
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What do a q wave mean?
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Infarction
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ST segment
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End of the S wave to the beginning of the T wave
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Cardiac Markers
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Myoglobin peaks in 8 hours, gone by 24
CKMB and troponin peaks at 24, diminishes by 72 |
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Unstable angina and cardiac enzymes
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Negative enzymes in USA
If enzymes elevated, means there was a STEMI/NSTEMI |
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Which leads will show EKG changes if left main is affected?
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V1-V6, Lead I, AVL
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Complications s/p anterior wall MI
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BBB, 2nd degree AV type II, CHB
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Complications s/p inferior wall MI
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1st degree block, 2nd degree block type I, bradycardias
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Inferior wall MI complications
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Primarily rate problems since RCA supplies both nodes in most people
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Treatment for right ventricular MI
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Optimize right ventricular preload by giving fluids
Avoid increasing RV afterload (be good to the lungs - don't make them tight) Give inotropes if fluids don't work |
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Antithrombin drugs
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Heparin
LMWH (lovenox) |
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Nitrates MOA
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Decreases preload and afterload via vasodilation
Give IV for STEMI |
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Absolute contraindications for B blockers
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Severe CHF
PE Asthma 2nd/3rd HB |
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When to use a Ca channel blocker during ischemia?
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When B blocker not doing the job
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Contraindication for Ca channel blocker
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LV dysfunction
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ACE inhibitors use s/p MI
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Prevents LV remodeling s/p MI
Lowers SVR Thereby reducing mortality |
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Pacemaker QRS
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If person is v-paced, QRS will always be wide
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Failure to sense
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Heart does not need pacing spike, but the pacer fails to sense that
There will be pacer spikes where there ought not be |
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Failure to capture
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Pacer spikes present, no QRS to follow
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IHSS
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Idiopathic hypertrophic subaortic stenosis
No room for the ventricles to fill - too much overgrown tissue |
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Why avoid dehydration with HF?
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Dehydration will activate renin AA sytem, resulting in vasoconstriction, making the heart work harder
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How to counteract high SVR in HF?
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Vasodilate
Use ACEI to prevent RAA effects Also, nitro, ARB |
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BNP as a marker for HF
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Mild, BNP < 500
Moderate, BNP 500-1000 Severe, BNP > 1500 |
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PAOP and BNP in relationship to HF treatment
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Diuretics and vasodilators will decrease PAOP and BNP
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What are the goals of treating HF?
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Reduce LV filling pressure
Reduce afterload Increase contractility |
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Treatment modalities for CHF
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Nitro, morphine, lasix, ACEI, ARBs (losartan)
Fluid and sodium restriction |
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Three positive inotropes
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Dobutamine - B stimulator
Milrinone - stimulates and also vasodilates Digoxin |
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CI in cardiogenic shock
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Less than 2
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Trend of PAOP, PAP, CVP, MAP, BP in cardiogenic shock
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PAOP, PAP, CVP increased
BP MAP decreased |
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Isovolumentric contraction
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The portion of systole where the ventricles contract and have to raise enough pressure to overcome the afterload
Uses majority of cardiac O2 |
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Initial treatment for PEA
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CPR and epi
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Posterior wall MI lead changes
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II, III, aVF
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Posterior wall MI reciprocal changes
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V1, V2
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Most prominent edema in a R HF patient on bedrest
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Sacrum and scapulas
Not legs/feet because this is dependent-edema |
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Inferior wall MI EKG changes
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II, III aVF
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Inferior wall MI EKG reciprocal changes
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I, aVL
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What does it mean when the PAD is >5 greater than the PAOP?
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Pulmonary HTN present
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Pressure values with PE
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1. Low sats
2. PAOP normal 3. Elevated PAP 4. Elevated RAP Basically, normal L side pressures, elevated R side pressures, O2 sats affected |
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Nitroprusside MOA
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Mixed vasodilator
Reduces afterload by causing vasodilation primarily in arteries |
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Hydralazine MOA
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Decreases afterload by causing peripheral artery vasodilation
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Which drug effectively reduces preload more than afterload?
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Nitroglycerin first causes venous dilation, reducing preload
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Symptoms of aortic aneurysm dissection
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Ripping pain
Radiating to back BP uneven in arms Aortic regurg murmur |
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Why is IABP contraindicated with aortic regurgitation?
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IABP will increase the regurgitation
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What is the PAOP like with PE?
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Normal or decreased
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At what dose is nitro a venous dilator to decrease preload?
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Less than 1 mcg/kg/min
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Between PAOP and CI, which is better to estimate L ventricular function?
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PAOP, because as long as the function is good, PAOP will be normal (except with aortic stenosis)
CI on the other hand can be affected by P, A, and C |
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Exercise teaching for CHF patients
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1. Avoid isometric exercise (e.g. weight lifting - causes valsalva maneuver), isotonic exercise ok
2. Avoid exercise in temp extremes 3. Avoid exercise after meals |
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Occlusion of RCA will cause STEMI of what leads?
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II, III, aVF
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Indications for ventricular septal repair:
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STEMI V1-V4
S3 Crackles in lung bases, dyspnea Holosystolic murmur at lower left sternal border |
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If person gets electrical cardioversion for a fib, and then goes into vtach, then what?
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Turn sync off and regular defib
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Aortic dissection BP differences between arms
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>25
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CK washout
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Earlier and higher CK peks
Indication of successful reperfusion |
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Which two paramaters are best to determine whether or not to d/c IABP?
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CI and SVR
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Signs of ventricular septal rupture
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MI V1-V4
Holosystolic murmur at lower left sternal border Sudden onset of chest pain, hypotension |
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Ashman's phenomenon
|
?
Associated with a fib |
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Cause of a wide, notched P wave
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Mitral stenosis - because cases atrial enlargement
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Why reduce fever in endocarditis?
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To decrease O2 consumption
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Normal SVR
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Don't know
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What drug of choice for someone with increased PAOP and increased SVR?
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Nitroprusside - mixed vasodilator
Will dilate veins to decrease preload and dilate arteries to decrease afterlaod |
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Why would nitroprusside be given in cardiogenic shock? Along with what other drug?
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In cardiogenic shock, preload is increased by pump failure and afterlaod is increase by compensation - Nitroprusside tx
Along with dobutamine |
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Hypertrophic cardiomyopathy aka
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Idiopathic hypertrophic subaortic stenosis
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Why no nitrates for hypertrophic cardiomyopathy?
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Venous dilation will decrease venous return back to the heart, thereby decreasing preload
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Normal ABI
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Greater than 1
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Where is S1 heard best?
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Mitral area
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Complications of mitral valve regurgitation
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Pulmonary congestion and pulm HTN
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Why recommend no added salt for someone with heart problems?
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No added salt instruction gets better compliance than a 2gm Na restriction
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Three electrolyte imbalances that increase likelihood of dig toxicity
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Hypokalemia, hypercalcemia, hypomagnesemia
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Common drug treatment after PCI
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Nitrates - as antispasmodics
Anticoags/platelet inhibitors to prevent re-occlusion PCI damages the coronary intima layer and increases release of clotting mediators |
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Heart sound heard only on inspiration and at the pulmonic area
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S4
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How does myoglobin r/o MI
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Negative myoglobin in the first 4 hours after cx pain will r/o MI
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Drugs to treat hypertrphic cardiomyopathy
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B blockers
Ca channel blockers Nitro to reduce preload |
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Mobitz I vs. Mobitz II
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Mobitz I - PR interval gets longer and longer and then drops
Mobitz II - PR interval consistent and then drops |
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Most common sign of myocardial contusion
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Usually R ventricle affected
Signs of right failure JVD common |
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Strain pattern
|
Occurs with hypertrphic cardiomyopathy:
Right ventricle: asymetric T wave inversion in V1/V2 Left ventricle: asymetric T wave inversion in V5/V6 |
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Anterolateral EKG changes
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I, aVL, V3-V6
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How are S3/S4 best heard and why?
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Best heard with bell of stethoscope b/c they are low pitched
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Where are most extra heart sounds heard best?
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At apex of heart - using bell
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When does ruptured papillary muscle occur?
|
During the healting perior after an inferior MI affects the posterior leaflet of the mitral valve
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Signs of ruptured papillary muscle
|
Recent MI
Hypoxia Lung crackles Holosystolic murmur (mitral regurg from bad valve) |
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Which lead is best for looking at changes in the R ventricle?
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V4R
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Murmur at lower left sternal border
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Tricuspid murmur
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What is the best medication treatment for high BP
|
To decrease afterload, which is SVR
|
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Big contraindication to percutaneous angioplasty
|
Left main CAD
Why? Because inflating a balloon to mash the plaque down may cause too much ischemia Can only do this when there is a CABG around the L main |
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Chest pain soon after PCI, what do you think?
|
Re-occlusion of the newly opened vessel, get back to the lab
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What does the pulm art cath show with ventricular septal rupture
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Increased SVO2 - because oxygenated blood reenters the right heart from the rupture.
Increased CO based on pulm art cath readings - because this reads from the right ventricle However - if you look at the L ventricle CO via vigeleo, CO is decreased |
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Plum artery catheter CO
|
Measures the CO in the right ventricle only
|
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Naseritide MOA
|
Vasodilator with diuretic effects
|
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Procardia MOA
|
Ca channel blocker that decreases preload/afterload by dilating arteries and veins, decreases myocardial O2 consumption
Decreases vasospasm |
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How does procardia differ from diltiazem and verapamil?
|
Does not decrease contractility
|
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What changes occur for someone with mitral regurg if the afterload decreases
|
V waves get smaller on PAOP because with lower SVR, ventricle able to pump out better so there is less regurg (which is reflected by v waves)
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Which type of dysfunction are inotropes used for and which are they not used for?
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Used for systolic dysfunction, not diastolic dysfunction
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Aortic regurgitation and pulse pressure
|
Creates a widened pulse pressure (Sys-dias)
|
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Lidocain use with MI
|
Only used if there are dysrhythmias, not prophylactically
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When you hear Mobitz I, think:
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R coronary artery, inferior wall MI
Leads I, III, aVF |
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Things to avoid when you have a pacemaker:
|
MRI
Close proximity to running engine Radio transmitters TENS May interefere with pacer |
|
Goal cholesterol level
|
Less than 200
|
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Goal LDL
|
Less than 130
|
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EKG changes with procainamide
|
May increase the QT interval by 50%
|
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Why no diuretics and vasodilators for hypertrophic cardiomyopathy?
|
They decrease venous return, so there's not adequate preload
|
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Symptoms of pericarditis
|
Pleural friction rub
Pleuritic chest pain Fever |
|
Pleuritic chest pain
|
Sharp pain accentuated with inspiration
|
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B blocker regimen in HF
|
Start at low dose and titrate up so as not to suddenly inhibit a sick heart
|
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Dobutamine and lasix use in HF
|
Remove fluid to reduce preload to reduce workload, then increase contractility efforts with dobutamine
|
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Drugs used after PCI
|
Anticoags, platelet inhibitors,
Nitrates for anti-spasmodics |
|
Complications of endocarditis
|
Emboli - of the bacteria vegitations on valves
|
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Which lab value is most specific to identifying MI?
|
Troponin
|
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Wolf Parkinson White syndrome
|
An accessory pathway around the AV node, causes a loss in the AV node delay (which is bad because the delay allows for the atria to contract during ventricular diastole)
|
|
What abnormal will be seen with WPW?
|
SVT
|
|
Only permanent treatment for WPW
|
Ablation
|
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EKG determinant of ventricular hypertrophy
|
Add the height of the s wave in v1/v2 to the height of the r wave in v5/v6, if it's >35 there is ventricular hypertrophy
|
|
What is the maintenance dose of natrecor for a HF patient?
|
0.01 mcg/kg/min
After a 2 mcg/kg bolus |
|
Which leads help differentiate vtach from SVT with aberrancy
|
V1 and V6
|
|
Another drug besides amiodarone used to convert a fib to NSR
|
Ibutilide (Corvert)
|
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What makes hypertensive emergency different from hypertensive urgency?
|
Presence of target organ involvement
|
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J point
|
Where QRS ends and ST segment begins
|
|
Which part of the T wave is the danger zone?
|
The later half
|
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What do leads V8 and V9 look for?
|
Posterior wall MI
|