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135 Cards in this Set
- Front
- Back
- 3rd side (hint)
Gold standard of diagnosis/follow-up of abdominal AA
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Abdominal U/S (nearly 100% sensitivity and specificity)
- may consider abdominal CT if can add valuable info when differential dx of patient's abdominal pain is broad (contraindicated in renal dz and has poor visualization of aortic branch origin) |
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Dilated cardiomyopathy due to alcohol - expected findings?
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Thrombocytopenia, macrocytosis, and elevated transaminases all suggestive of alcoholism
Total abstinence from alcohol is the mainstay of alcoholic cardiomyopathy management and it may reverse this condition if it is employed earlier in the course of the dz |
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transient ST elevations on ECG, chest pain that wakes one up during sleep
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Prinzmetal's angina
Greatest risk factor? epidemiology? tx? |
Greatest risk factor = smoking (often lack other cardiovascular risk factors
Other sx - young females Tx: nitrates or Ca channel blockade; avoid aspirin and non-selective beta blockers bc they can promote vasoconstriction |
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Indications for digoxin use
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1) increase contractility in pts with CHF
2) rate control agent in pts with afib or flutter |
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Good marker for hypovolemia
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Increased BUN/creatinine ratio (although not very specific)
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JVP distension and new-onset RBBB
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Massive PE (likely in a postoperative patient)
Also syncope (due to hypotension), tachycardia |
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ECG findings of MI
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ST elevations, T wave inversions, Q wave changes
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Which drugs have been shown to have a mortality benefit when given as secondary prevention?
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Aspirin, beta blockers, ACEi, lipid-lowering statin drugs
additionally, clopidogrel should be prescribed to all pts with unstable angina/non-ST elevation MI, as well as patients who are post PCI |
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Hypertensive urgency vs Hypertensive emergency
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Urgency: severe HTN (usually greater than or equal to 180/120) with no sx or acute end organ damage
Emergency: severe HTN with acute, life threatening end organ complications - malignant: severe HTN with retinal hemorrhages, exudates, or papilledema - hypertensive encephalopathy: severe HTN with cerebral edema and non-localizing neurologic sx and signs |
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severe N/V after returning from a party. Also complaining of CP more intense than any other previously experienced.
Exam reveals injected conjunctivae and bilateral dilated pupils. Pleural fluid has elevated amylase content. Dx? |
Esophageal Perforation - Boerhaave's syndrome (spontaneous esophageal rupture)
classic presentation is acute, severe chest or epigastric pain after an episode of retching. Fever and dyspnea are common (not hematemesis) pleural fluid will have high amylase concentration, low pH, and may contain particles of food |
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Digitalis (ie digoxin) toxicity
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1) increases ectopy - Atach
2) increases vagal tone and decrease conduction through AV node --> AV block - results in atrial tachycardia with AV block --> specific for digitalis toxicity |
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How to distinguish Atach vs Aflutter
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A tach --> slower atrial rate: 150-250 bpm as opposed to 250-350 bpm
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Characteristics of aortic stenosis murmur
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1) Harsh systolic murmur over right sternal edge
2) Only left sided heart murmurs increase on expiration 3) S4 due to left ventricular hypertrophy (forceful atrial contraction against thick, non-compliant ventricle) 4) radiation to carotids 5) tardus et parvus Indicators for surgery? |
symptomatic --> "SAD"
Syncope Angina Dyspnea |
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Complications of venous insufficiency
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Lower extremity edema,
stasis dermatidis ulceration |
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Amiodarone side effects
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check PFTs, LFTs, and TFTs
It's a K+ channel blocker - increase AP duration, increase ERP; used when other antiarrythmics fail; increase QT interval |
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Beta blockers such as metoprolol are relatively contraindicated in what patients?
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obstructive lung dz (ie asthma/COPD), but CAN be used in restrictive lung dz
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Explain the significance of S3
tx? |
low frequency diastolic sound -- associated with LV failure (can be normal in well-trained athletes and younger individuals)
Intravenous diuretics provide symptomatic benefits to patients with decompensated heart failure |
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Indicators of cocaine abuse
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EKG changes of myocardial ischemia: ST depression and T wave inversion
tx of cocaine related cardiac ischemia? |
Benzos - reduce anxiety and hypertension/tachycardia
Aspirin - retards thrombus formation Nitrates - being a vasodilator, will be beneficial for the cocaine-induced coronary artery vasoconstriction (pure alpha blockers and Ca channel blockers may be added if desired) - pure beta blockers would be contraindicated - may aggravate cocaine-mediated vasoconstriction |
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Young healthy patient develops CHF - name sx of CHF and what might have caused this?
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sx: PND, DOE, peripheral edema, hepatomegaly, cardiomegaly, bilateral pleural effusions, S3
likely due to myocarditis (viral infection, particularly Cocksackie B virus, is the most common cause |
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Clues of aortic dissection
Next best step in management? |
- Intense, retrosternal pain that radiates to the back of the chest, along with normal EKG = strongly suggestive; also presence of early diastolic murmur, characteristic of aortic regurg
- blood pressure may be different in both arms due to dissection - preferred diagnostic tool = TEE - can also use MRI and CT, but these are time consuming - |
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Indications for adenosine
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useful in initial diagnosis and management of pts with narrow-QRS-complex tachycardia
- slows the sinus rate, increases AV nodal conduction delay, or can cause transient block in AV node conduction. - useful in identifying P waves to clarify dx of Aflutter or Atach - can terminate paroxysmal SVT by interrupting the AV nodal reentry circuit - |
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SVT - what does this mean?
common sx? |
any tachycardia originating above the His-bundle
-includes sinus tach, multifocal Atach, Aflutter, Afib, AVNRT, AVRT, and junctional tachycardia sx: palpitations, dizziness, lightheadedness, SOB, diaphoresis, CP, presyncope, syncope |
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Indications for IV nitroglycerine
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- myocardial ischemia
- pulm edema - hypertensive urgency |
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Pt with systolic-diastolic abdominal bruit; hx of HTN and atherosclerosis
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strongly suggestive of renal artery stenosis (up to 85% of patients)
particularly if HTN is difficult to control despite use of multiple medications |
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Differential for blood pressure measured differently in both arms
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If with CP, consider aortic dissection
If greater in R arm than L - coarctation (if coarctation is proximal to left subclavian artery origin) Secondary to subclavian atherosclerotic dz |
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Signs of R ventricular infarction
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Signs of inferior MI - ST segment elevation in leads II, III, and aVF (inferior leads) and ST segment depression in leads I and aVL (left-most leads)
PE: hypotension, JVD, clear lung fields side: preload dependent and should be treated with IV FLUIDS, not preload reducing meds like nitrates and diuretics |
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Describe how diastolic dysfunction may lead to Afib? What is it commonly caused by?
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HTN is classic cause
Chronically elevated LV diastolic pressures cause LA dilatation, which in turn can lead to atrial fibrillation Tx = diuretics and BP control |
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Describe causes of high-output HF
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Anemia, hyperthyroidism, beriberi, Paget's dz, and AV fistulas
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When do you suspect hyperparathyroidism?
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uncommon cause of secondary HTN --> "stones, bones, abdominal moans, psychiatric groans"
look for muscle weakness, recurrent nephrolithiasis, neuropsychiatric sx, and hypercalcemia |
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Signs of coarctation of the aorta
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H/A, epistaxis, and blurred vision, elevated BP in upper extremities, possible "to-and-fro machinery murmur" over posterior chest, brachial femoral pulse delay on exam
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Hypothyroidism can cause _____
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HTN!
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Most important factors in improving pt survival?
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adequate bystander CPR
prompt rhythm analysis defibrillation |
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Causes of Afib
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Cardiac: HTN, acute ischemia, HF, myopericardial inflammation, valve dz, and surgery
Pulmonary: any acute lung dz (eg PNA), PE, and hypoxia Metabolic: catecholamine surges and hyperthyroidism Drugs: alcohol, cocaine, amphetamines, and theophylline |
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signs of Cushing's syndrome
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chronically elevated systemic corticosteroids
typical changes include: central obesity, DM, PROXIMAL MUSCLE WEAKNESS, psychosis, thin skin, and osteoporosis |
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Hypogonadism, arthropathy, DM, and hepatomegaly
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Hereditary hemachromatosis
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Three most common causes of aortic stenosis
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senile calcific aortic stenosis
bicuspid aortic valve (majority of patients under 70 yrs old) rheumatic heart dz |
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How to identify AR on exam and what is the primary medical therapy?
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high pitched, blowing descrescendo diastolic murmur best heard at 3rd rib, intensified with handgrip
Tx: afterload reduction with ACEi or Ca channel blockade (nifedipine) |
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Treatment for premature atrial beats
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benign and neither require any F/U or tx
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Best lifestyle interventions in patients newly diagnosed with stage I hypertension
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Obese patients: weight loss
Non-obese patients: diet high in fruits and veggies, followed by a low salt diet (smoking has little effect on blood pressure reduction, but significantly reduces CV dz) |
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What new heart sound may be appreciated following acute MI?
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S4 --> ischemic damage in setting of MI may lead to diastolic dysfunction and a stiffened LV, resulting in an atrial gallop
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Ascending aortic aneurysm vs Descending? Cause?
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Ascending: most often due to cystic medial necrosis or connective tissue disorders
Descending: usually due to atherosclerosis |
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What do you expect in HOCM PE and epidemiology?
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Syncope in a young patient with crescendo-decrescendo murmur at the lower left sternal border is most likely due to HOCM.
What is the inheritance pattern? |
Autosomal dominant
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Tx of pericarditis?
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NSAIDs
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Thiazide diuretics side effects (metabolic + electrolyte)
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Metabolic: hyperglycemia, increased LDL cholesterol, and plasma TG
Electrolytes: hyponatremia, hypoK, HyperCa |
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mechanism responsible for pain relief in pts with anginal pain tx with nitroglycerin
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dilation of veins and decrease in ventricular preload
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pathophysiologic mechanism responsible for vfib patients?
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reentrant ventricular arrythmia (ventricular fibrillation) -> most common cause of death in pts with acute MI
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HOCM murmur gets louder with what? autosomal dominant disorder
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located at hte left lower sternal border and is worsened by maneuvers that decrease preload (eg valsalva, standing)
Contrary to most murmurs, the murmur of HOCM increases as preload decreases since this lessens the size of the ventricular cavity and causes increased outflow obstruction |
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maneuvers that decrease/increase venous return
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Increase: Squatting, Recumbency, Leg raising
Decrease: Valsalva what about sustained handgrip? |
leads to increase in SVR and increased afterload!! -> leads to larger ventricular volume nad thus a decrease in outflow obstruction and quieter murmur
usually used to differentiate btw murmurs of aortic stenosis and mitral regurg where it causes a decrease and increase, respectively, in the severity of the murmur. |
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pharmacologic cardioversion for atrial fibrillation
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amiodarone and quinidine
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lidocains used for what?
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ventricular arrhythmias
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MR caused by what?
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myxomatous degeneration of the mitral valve leaflets and chordae and causes a mid-systolic click followed by a mid-to-late systolic murmur.
chronic severe MR causes what? |
left atrial and ventricular enlargement leading to Afib, LV dysfunction, and CHF
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tx for acute desponsated heart failure
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acute pulmonary edema, supplemental O2, assisted ventilation as needed, aggressive IV diuresis, and possible vasodilator therapy (nitroglycerine, nitroprusside)
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Chagas dz caused by what and characterized by what?
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chronic dz that can cause megaesophagus, megacolon, and/or cardiac dysfunction. Protozoan trypanosoma cruzi, endemic to Latin America, is responsible
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Afib -> what should be used pharmacologically?
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rate control better -> initially with beta blockers or Ca channel blockers.
immediate synchronized electrical cardioversion is indicated in hemodynamically unstable pts with rapid Afib |
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How to prevent ventricular remodeling in the weeks-months following MI?
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ventricular remodeling may lead to dilatation of the ventricle -> lessened by ACE inhibitors!
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how does arteriovenous fistula cause high-output cardiac failure?
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shunt blood from arterial to venous side, thereby increasing cardiac preload.
pt develops heart failure despite maintaining a nl or high CO bc the circulation is unable to meet the O2 demand of the peripheral tissues |
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describe reinin-angiotensin-aldosterone system in understanding HTN
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renin produced by JGA cells of kidney in response to hypoperfusion.
renin cleaves angiotensinogen into angiotensin I. angiotensin I is converted to angiotensin II by ACE in lung angiotensin II is a potent vasoconstrictor. also promotes vasopressin (ADH) release from pituitary and aldosterone production in the adrenal cortex. |
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three major mechanical rupture due to MI
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mitral regurg due to papillary muscle rupture
left ventricle wall rupture interventricular septum rupture (all 3 can result in hTN) |
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medications that improve mortality in CHF pts
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ACEi, beta blocker, ARB, spironolactone
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digoxin in CHF
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improves symptoms but no mortality benefit (is that true? also reduces hospitalizations
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cardiac stress testing: which meds should be withheld for at least 48 hrs
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beta blockers, ca channel blockers, and nitrates (antianginal agents)
however, should be continued in pts with known CAD undergoing stress testing to assess efficacy of antianginal therapy |
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strongest predictors of AAA expansion and rupture
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strongest predictors: large aneurysm diameter, rapid rate of expansion, and current cig smoking
What are current indications for operative/endovascular repair? |
large aneurysm diameter (>5.5cm), rapid rate of expansion (>1cm/yr), and presence of sx (abdominal, back or flank pain; limb ischemia) regardless of aneurysm size
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Aortic dissection with sx of lower extremity weakness. Mechanism?
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dissection extending into the spinal arteries causing spinal cord ischemia
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most useful lab test for assessment of re-occlusion after MI
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CK-MB because it typically returns to nl levels within 1-2 days. Troponin takes 10 days to return to nl
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most common causes of AR
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bicuspid aortic valve in young adults in developed countries
rheumatic heart dz in developing countries |
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First line medical therapy for HOCM?
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either beta blockers or cardiac acting Ca channel blockers (dilt) since they promote DIASTOLIC RELAXATION (ie beta blockers increase time to refill ventricle during diastole)
differentiate murmur of HOCM vs aortic stenosis |
HOCM: left sternal border
aortic stenosis: R sternal border |
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symptomatic bradycardia treated with what?
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IV atropine, followed by transcutaneous pacing. Meds that slow the HR should be replaced with alternative therapeutic regimens. If bradycardia doesn't resolve, permanent pacemaker may be necessary
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role of IV adenosine
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causes temporary AV block, which is useful in identifying, and sometimes terminating, SVT.
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common cause of endocarditis a/w nosocomial UTI
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Enterococcus
what about healthcare-associated and community-acquired? |
healthcare-associated: staphylococcal
community acquired: streptococcal |
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Mitral stenosis - how is it connected with Afib and hemoptytis?
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Mitral stenosis results in LA dilation and a risk of Afib and cardiac emboli. The pressure is also transmitted to the pulmonary vasculature, which can result in dyspnea, cough, and hemoptysis
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niacin causing flushing and pruritis. mechanism?
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side effect explained by prostaglandin-induced peripheral vasodilatation that can be reduced with low dose ASA
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CHADS2 score
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0 - no anticoagulation (preferred) or ASA
1 - anticoagulation (preferred) or ASA 2-6 - anticoagulation CHF HTN Age>75 DM Prior stroke or TIA |
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Most frequent origin for ectopic foci causing Afib?
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pulmonary veins
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chostochondritis
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chest pain that is reproducible with palpation suggest MSK etiology -> sharp, focal, lasts for hours, worsens with inspiration and movement all suggests musculoskeletal etiology
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primary hyperaldosteronism (conn's syndrome) causes what findings?
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HTN, mild hypernatremia, hypoK, and metabolic alkalosis
dx suggested by low renin and elevated aldosterone levels |
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Constrictive pericarditis can cause what?
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CO compromised and venous pressures become chronically elevated -> increased JVP, severe ascites and hepatic congestion, dyspnea and weakness.
how is dx made and tx? |
calcified pericardium on CXR, thickened pericardium on CT or MRI,, pressures during cardiac cath; sharp x and y descents are characteristically seen on central venous tracing
tx: diuretics or pericardiectomy |
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Most common causes of pericarditis?
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US: idiopathic or viral pericarditis (>40%, rads therapy, cardiac surgery, and connective tissue disorders (less than 10%)
In developing countries, TB! |
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distinguishing tricuspid regurg on exam
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augmentation of intensity of holosystolic murmur with inspiration (100% sensitivity and 88% specificity in differentiating R sided systolic murmurs from all others
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How to treat stable vs unstable SVT
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stable: initially with vagal maneuvers followed by adenosine and AV nodal blockers.
unstable: DC cardioversion |
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tx for third degree heart block
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characterized by complete independence of P waves and QRS complexes, both of which contract at completely separate rates.
tx is expeditious pacemaker placement, as the rhythm can degenerate into Vtach or Vfib |
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causes of restrictive cardiomyopathy
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sarcoid, amyloid, postradiation fibrosis, endocardial fibroelastosis, loffler's syndrome (endomyocardial fibrosis with a prominent eosinophilic infiltrate) and hemochromatosis (dilated cardiomyopathy can also occur)
common causes of amyloidosis? |
multiple myeloma and chronic inflammatory dz such as RA
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S4 causes
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a-stiff-heart
restrictive cardiomyopathy or LV hypertrophy from prolonged HTN S4 corresponds with atrial contraction and is believed to result from the sound of blood striking a stiffened LV |
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tx of first degree AV nodal block
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nl QRS: due to delayed AV nodal conduction and require no further evaluation
widened QRS: likely conduction delay below the AV node and should have electrophysiology testing to determine its nature |
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ICU patient requiring aggressive vasopressors to maintain BP develops cool, dusky fingertips.
What happened? |
pressors such as NE can cause ischemia of the distal fingers and toes 2/2 vasospasm. dx suggested by symmetric duskiness and coolness of all fingertips.
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nl JVP
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3cm above sternum when bed at 45 degrees
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hypoK + HTN
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look up!
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adverse effects of digoxin
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N/V, diarrhea, vision changes, arrhythmias
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Prinzmetal's angina characteristics
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vasospastic disorder that typically occurs in young female smokers. Chest pain usually occurs in the middle of the night, and episodes are a/w transient ST elevations on EKG
most a/w what condition? |
Raynaud phenomenon
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patient with MI who develops cold leg and no distant pulses. Next step?
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ECHO to r/o thrombus in LV
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Physical exam finding a/w aortic dissection
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tearing CP radiating to the back and neck.
AORTIC REGURG is complication and p/w early diastolic murmur |
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premature atrial complexes tx
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asymptomatic: tobacco and alcohol are reversible risk factors for PACs (also caffeine and stress)
symptomatic: beta blockade |
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ARDS criteria
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bilateral lung opacities on imaging c/w pulm edema, no signs of cardiac failure or fluid overload (PCWP < 18), PaO2/FiO2 < 300 mmHg and PEEP > 5cm H20
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characteristics of second degree heart block
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prolongation of PR interval with occasional dropped beats
Mobitz I: PR interval gradually lengthens until beat is dropped --> due to AV NODE CONDUCTION IMPAIRMENT tx = Mobitz II: PR intervals are of constant length before dropped beat, below level of AV node block Prognosis better for type I |
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approach to wide complex tachy
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pic
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EKG findings with pericardial effusion
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electrical alternans: amplitudes of QRS complexes vary from beat to beat. Fairly specific for pericardial effusion.
Enlargement of cardiac silhoutte can be seen on CXR. Echo for definitive dx |
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orthostatic hypotension
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drop in 20mmHg systolic or 10mmHg diastolic when moving from lying down to standing.
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reasons for increased susceptibility to orthostatic hTN in elderly
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progressively decreasing baroreceptor sensitivity, arterial stiffness, decreased NE content of sympathetic nerve endings, and reduced sensitivity of the myocardium to sympathetic stimulation
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objective findings of cardiogenic shock?
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reduced cardiac index and elevated pulm capillary wedge pressures (>12) d/t ventricular pump failure.
SVR is typically increased to maintain adequate tissue perfusion pressure. |
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Aortic regurgitation causes what realizations in the patient?
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widening of pulse pressure can be felt as a "water hammer" pulse
lying down and turning to the left brings the heart closer to the chest wall and can make the pt more aware of the forceful heartbeat |
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peripheral edema in someone taking BP meds
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dihydropyridine Ca channel antagonists such as AMLODIPINE should always be considered in differential dx, along with other causes of peripheral edema such as heart failure, renal dz and venous insufficiency
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what can occur as a complication of aortic dissection?
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cardiac tamponade with rupture of the aorta and rapid accumulation of blood in the pericardial space.
-> increased pericardial pressure causes compression of cardiac chambers and limits diastolic filling of the R sided chambers. |
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s/e of amiodarone
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indicated for ventricular arrhythmias. also used for rhythm control in pts with atrial fib and underlying left ventricular systolic dysfunction
a/w broad range of adverse effects, including hypo and hyperthyroidism, hepatotoxicity, pneumonitis, corneal deposits, and skin changes (blue gray skin discoloration) |
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vasovagal syncope workup
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usually a clinical dx and needs no further testing. if hx and physical exam point strongly toward diagnosis and resting ECG is nl.
upright tilt table test may be used to establish dx! patient passively moves pt from different positions and if there are signs of unconsciousness, the test is positive > limited sensitivity/specificity |
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PVCs following MI
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3829
common in pts post MI and can be recognized by their widened QRS (>120msec), bizarre morphology, and compensatory pause. even though they may indicate a worse prognosis, tx NOT INDICATED unless pt is symptomatic. if symptomatic, beta blockers |
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which murmurs should always be investigated using echo?
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diastolic and continuous murmurs as well as loud systolic murmurs.
midsystolic soft murmurs (grade 1-II/VI) in an asymptomatic young pt are usually benign and need no further workup |
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WPW mgmt
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those who develop afib with RVR should be treated with cardioversion or antiarrhythmics like procacinamide
AV nodal blockers like beta blockers, ca channel blockers, digoxin, and adenosine should be avoided bc they can increase conductance through the accessory pathway. |
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young pt with severe symptomatic HTN with HA, epistaxis, and e/o L ventricular hypertrophy on ECG
dx? |
probably coarctationo f hte aorta -> simultaneous palpation of hte brachial and femoral pulses to assess for brachial-femoral delay.
also have supine bilateral brachial and popliteal blood pressures measured to assess for differential pressures |
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flecainide
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typically used to treat ventricular arrhythmias or SVT such as Afib. class 1c antiarrhythmic med that blocks sodium channels.
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when should renovascular htn be suspected
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all pts with resistant HTN and diffuse atherosclerosis, asymmetric kidney size, recurrent flash pulm edema, or elevation in serum creatinine > 30% from baselineafter starting ACEi or ARB.
prsence of continuous abdominal bruit has a high specificity for hte presence of renovascular HTN |
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beck's triad
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hypotension, distended neck veins, and muffled heart sounds -> indicative of cardiac tamponade.
reduction of LV preload, stroke volume and CO! |
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necessary adjunct to tx of MI if pulmonary edema is present
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diuretics such as furosemide
aka flash pulmonary edema |
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OCP use and hypertension
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OCP can be a potential cause of elevated BP and hypertension, and discontinuing its use can correct the problem in most pts
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pulsus paradoxus
pulsus parvus et tardus |
fall in systemic arterial pressure by more than 10mmHg during inspiration, and is often a/w cardiac tamponade
- may also occur in conditions w/o pericardial effusion such as severe asthma or COPD pulsus parvus et tardus: decreased pulse amplitude and delayed pulse upstroke: a/w aortic stenosis |
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procainimide, lidocaine, quinidine
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procainimide: treats atrial and ventricular arrhythmias
lidocaine: used to treat ventricular arrhythmias quinidine: used to treat atrial arrhythmias |
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what do pericardial effusions appear as on cxr?
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enlarged, watter bottle shaped cardiac silhouttes on cxr
PE of pericardial effusions without cardiac tamponade include diminished heart sounds on auscultation and a difficult to palpate PMI. 4445 |
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young person with heart failure. suspect what? and what do you expct on echo
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dilated cardiomyopathy, particularly after coxsackievirus B infxn. dx made by echo, which typically shows dilated ventricles and diffuse hypokinesia resulting in systolic dysfunction (low EF).
tx largely supportive, involving mainly the mgmt of CHF sx |
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cardiac index, TPR, and LVEDV in heart failure?
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decreased CI (decreased cardiac output), increased TPR, and increased LVEDV
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three clinical findings characteristic of aortic dissection
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abrupt onset "tearing" pain in the chest or back, variation in the blood pressure between right and left arms, and widened mediastinum on CXR.
when two or more of these findings are present, the incidence of dissection exceeds 80% |
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pt with wide complex Vtach following IV furosemide (h/o heart failure)
next step? |
measure serum electrolytes --> loop diuretics cause hypoK and hypoMg -> can cause ventricular tachy, adn also potentiates the side effects of digoxin
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property of dipyrimidole in the use of myocardial perfusion scanning
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reveals areas of restricted myocardial perfusion
the redistribution of coronary blood flow to nondiseased segments induced by this drug is called coronary steal phenomenon dipyridamole and adenosine are coronary vasodilators |
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differentiating between cardiac adn liver related causes of lower extremity edema?
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hepatojugular reflux
pts with peripheral edema d/t heart failure have elevated JVP and positive hepatojugular reflux. those with peripheral edema from primary hepatic dz and cirrhosis have reduced or nl JVP and negative hepatojugular reflux |
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acute aortic dissection: when to do surgery vs medical mgmt
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type A (ascending aorta): medical therapy and surgery
type B (descending aorta): medical therapy alone -> beta blockers! |
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electrical alternans and sinus tachycardia
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identify on 4390
highly specific sign for large pericardial effusion. due to swinging motion of the heart in the pericardial cavity causing a beat to beat variation in QRS axis and amplictude. emergency pericardiocentesis! |
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acute limb ischemia
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angio typically shows an abrupt cutoff of arterial blood flow. IV heparin should be started immediatley upon suspicion.
definitive treatment is surgical embolectomy or intra-arterial fibrinolysis/mechanical embolectomy via interventional radiology |
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middle or older age male with prostatic hypertrophy who loses consciousness after awakening to void at night
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situtional syncope
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paroxysmal supraventricular tachycardia (PSVT)
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most commonly results from accessory conduction pathways through the AV node.
vagal maneuvers and meds that decrease conduction through the AV node often resolve the PSVT |
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hemodynamic monitoring in septic shock, cardiogenic shock
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septic: low pulmonary capillary wedge pressure, low SVR, increased CO, and high mixed venous oxygen saturation
cardiogenic: low CO, elevated PCWP!, increased SVR. decreased CO decreases tissue perfusion which signals tissue to extract more O2 from the blood and decrease MVO2 |
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important cause of hypertension in elderly patients
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isolated systolic hypertension. caused by decreased elasticity of the arterial wall.
should always be treated due to increased risk for cardiovascular events. initial therapy involves monotherapy with low dose thiazide, ACEi, or long acting ca channel blocker |
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when are nitrates contraindicated?
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aortic stenosis, recent PDEi use, or RV infarction!!!!
When right ventricular SV decreases, CO is impaired. Therefore, any medication that reduces preload (nitrates or diuretics) will exacerbate rather than improve sx. First step in tx of RV MI is generally IV fluid resuscitation to increase the RV stroke volume and enhance LV filling. |
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hyperthyroidism related tachysystolic afib -> next step in mgmt?
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beta blocker!
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first line therapies for improving exercise tolerance in pts with stable angina pectoris
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beta blockers! (in addition to ASA and sublingual nitroglycerin prn)
ca channel or long acting nitrates if beta blockers contraindicated or can be used in combination |
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sudden onset of syncope without warning signs, presence of structural heart disease, and frequent ectopic beats
likely cause of syncope? |
arrythmia
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edema in CHF
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multifactorial
most important contributor is increased renal sodium retention, resulting from activation of the RAAS system. activation of this system is a reuslt of renal hypoperfusion 2/2 decreased cardiac output |
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vascular and immunologic manifestations of infective endocarditis
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4668
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new conduction abnormality in pt with infective endocarditis
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perivalvular abscess with extension in the adjacent cardiac conduction tissue!
aortic valve endocarditis and IVDU are both independently a/w increased risk of periannular extension of native valve endocarditis |
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