Term
| What are the three types of atrial septal defects? List them in order of highest to lowest in location in the septum |
|
Definition
-sinus venosus defects -ostium secundum (MC- in the region of the foramen ovale) -ostium primum (down syndrome pt's commonly and may be associated with a complete atrioventricular canal defect) |
|
|
Term
| What is eisenmenger's disease? |
|
Definition
| In CHD irreversible pulmonary HTN leads to reversal of shunt, HF, and cyanosis |
|
|
Term
| About 75% of patients with holt oram syndrome have what type of heart defect? |
|
Definition
|
|
Term
| What other genetic disorder is associated with ASD besides holt oram? |
|
Definition
|
|
Term
| What are two things seen on a CXR that would lead you to think coarctation of the aorta? |
|
Definition
Figure 3 appearance Notching of the ribs |
|
|
Term
| What should be given to an infant patient presenting with coarctation of the aorta and cardiac decompensation at first to try and restore blood flow? |
|
Definition
| Iv infusion of Prostaglandin E1 to chemically open the ductus arteriosus |
|
|
Term
| Most coarcted aortas are _________ in position |
|
Definition
|
|
Term
| Coarctation of the aorta is often accompanied by what two other heart defects |
|
Definition
-bicuspid aortic valve -VSD |
|
|
Term
| What is postcoarcectomy syndrome and what is done to prevent it? |
|
Definition
| Restoring pulsatile blood flow to the mess enteric arteries can cause mess enteric arteritis so feedings are usually delayed for 48 hours to prevent this |
|
|
Term
| In coarctation of the aorta there is a difference in what part of the heart looks hypertrophied on ECG and CXR depending on the age of the child... Explain |
|
Definition
Infants: RVH children: LVH |
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|
Term
| Describe the murmur heard with a PDA |
|
Definition
|
|
Term
| What class of drugs will close a PDA? What class of drugs will maintain a PDA? |
|
Definition
NSAIDs will close a PDA so pregnant women must avoid them
Prostaglandins will maintain a PDA |
|
|
Term
| What are the four typical features in tetralogy of fallot? What is the less common fifth that makes up the Pentad? |
|
Definition
-RVOTO -malaligned VSD -aorta that overrides the VSD -RVH 5th- ASD |
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|
Term
| Why do older pt's with tetralogy of fallot sometimes squat to ease the symptoms? |
|
Definition
| To increase peripheral vascular resistance which decreases the magnitude of the left to right shunt across the VSD |
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|
Term
| What is the characteristic CXR finding in a pt with tetralogy of fallot? |
|
Definition
|
|
Term
| In a pediatric pt with HTN what two classes of drugs are usually the first to be prescribed for treatment? |
|
Definition
-ACEI's: may be ESP beneficial in obese pt's since the likely mech is increased sodium retention and increased SNS activation- they also have beneficial effects in diabetes and dyslipidemia -CCB's *both classes are generally well tolerated and can be dosed once daily with a minimal side effect profile |
|
|
Term
| What two classes of hypertensive meds should be avoided in pediatric obese HTN patients? |
|
Definition
-diuretics: bc they can worsen insulin resistance and dyslipidemia, as well as increase SNS and renin activity -BBs: bc they can lead to weight gain, increased TG's, and decreased HDL levels |
|
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Term
|
Definition
| localized or diffuse dilation of an artery with diameter of at least 50% greater than the NL size of the artery |
|
|
Term
| what are the 3 layers of a blood vessel wall? |
|
Definition
|
|
Term
| What is the difference between a true aneurysm and a pseudo aneurysm? |
|
Definition
True= involves all three layers and is contained inside the endothelium False= involves only the outer layer and is contained by adventitia |
|
|
Term
| What are the two types of shapes of aneurysms? Which shape is characteristic of a true and which is characteristic of a false aneurysm? |
|
Definition
-saccular= false -fusiform= true |
|
|
Term
| what is the MC RF of a thoracic aortic aneurysm? What is the MC RF of a AAA? What is the MC RF of an aortic dissection |
|
Definition
atherosclerotic dz atherosclerotic dz HTN |
|
|
Term
| Name some commons RFs for TAA and AAAs |
|
Definition
| smoking, COPD, males, ATHEROSCLEROSIS, family hx, uni/bicuspid aortic valves, incr age, high BMI |
|
|
Term
| What is the indication for surgery with a thoracic aortic aneurysm? |
|
Definition
SIZE -ascending aorta: >5.5cm or 2x the diam of NL contiguous aorta -descending aorta: >6.5 cm |
|
|
Term
| what is the most commmon location of a AAA |
|
Definition
| infrarenal segment above the iliac bifurcation (95%) |
|
|
Term
| give the typical pt with a AAA |
|
Definition
| male >65 yo with peripheral vasc disease, who smokes (or did in the past) |
|
|
Term
| What is the most characteristic PE finding for a AAA |
|
Definition
| palpable pulsatile abd mass, but its found on <50% of patients |
|
|
Term
| What is the classic triad of a AAA rupture? |
|
Definition
1. abd pain 2. hypotension 3. palpable pulsatile abd mass *present in 30-50% of cases |
|
|
Term
| what is the #1 radiological study to dx AAA |
|
Definition
|
|
Term
| What is the tx criteria for a unruptured AAA |
|
Definition
-quit smoking -aggressive HTN control (BBs) -incidental (<3 cm) no further follow up -3-4 cm= annual US to monitor change -4-4.5 cm= US Q6 months ->4.5 cm= referral to vasc surg |
|
|
Term
| describe the blood vessel wall in an aortic dissection |
|
Definition
| an intimal tear allows blood to escape and is contained in the media creating a true and false lumen |
|
|
Term
| What are the 3 points of fixation of the aorta that are often injured in traumatic circumstances |
|
Definition
-aortic root -at the attachment to the ligamentum arteriosum -diaphragmatic hiatus |
|
|
Term
| what are the stanford classifications for aortic dissections and what is the tx for each |
|
Definition
-type A- ascending, surg -type B- descending, med mngmnt |
|
|
Term
| what is the #1 RF for an aortic dissection |
|
Definition
|
|
Term
| name the three areas of the thorax where pain from different locations of an aortic dissection may occur? |
|
Definition
-ant chest/ mimicking acute MI= ascending -neck/jaw: arch, root -intrascap: descending |
|
|
Term
| what are good radiological exams for aortic dissection |
|
Definition
-CXR= widened mediastium >8 mm AP view -TEE= noninvasive and at bedside -CT for a hemodynamically stable pt |
|
|
Term
| What is the tx for an aortic dissection- immediate and surgical? |
|
Definition
immediate= IV bb to decr HR and diminish LV ejection force, Iv Na Nitroprusside to bring systolic below 120 type a= surg type b= med mngmnt |
|
|
Term
| what is the definition of cardiogenic shock? |
|
Definition
| decreased cardiac output and tissue hypoxia in the presence of adequate intravascular volume |
|
|
Term
| what is the leading cause of death in acute MI? |
|
Definition
|
|
Term
| what is the hallmark s/sx of cardiogenic shock |
|
Definition
| hypoperfusion without hypovolemia |
|
|
Term
| what is the most important initial thing to order on a pt who presents with possible cardiogenic shock? |
|
Definition
|
|
Term
| give the three paremeters that define cardiogenic shock in regards to systolic BP, cardiac index, and pulmonary capillary wedge pressure |
|
Definition
systolic <90 (diastolic <60, no a parameter though) cardiac index <2.2 PCW >15 mmHg |
|
|
Term
| what is the #1 pressor used in cardiogenic shock |
|
Definition
|
|
Term
| what are two blood thinning agents used in patients suffering from acute MI |
|
Definition
|
|
Term
| what is the cell life of a platelet? How does aspirin work? |
|
Definition
10 days-ish inhibits platelet cyclo-oxygenase and lasts for the life of the cell |
|
|
Term
| what are some major causes of hypovolemic shock? |
|
Definition
| GI bleed, major surg, extrav of plasma, trauma, burns |
|
|
Term
| what are some common causes of obstructive shock |
|
Definition
| Tension PTX, pericardial tamponade, obstructive valvular disease, PE |
|
|
Term
| what is the clinical definition of orthostatic hypotension |
|
Definition
| sustained drop in systolic BP (>20 mmHg) or diastolic (>10 mmHg) within 3 minutes of standing |
|
|
Term
| how do you differentiate neurogenic from non-neurogenic causes of orthostatic hypotension when measuring orthostatic BPs |
|
Definition
| non-neurogenic causes will have the drop in BP but accompanied by an increase of HR of >15 bpm |
|
|
Term
| name some meds that can cause orthostatic hypotension |
|
Definition
| antihypertensives, antidepressants, ETOH, narcotics, insulin, CCBs |
|
|
Term
| what is the criteria for SIRS? |
|
Definition
2 of these must be met -HR >90 -RR >20 or PaCO2 <32mmHg -Temp >100.4 or <96.8 -Wbc >12000 or <4000 |
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|
Term
|
Definition
| SIRS + a known source of infection |
|
|
Term
| what is designated as severe sepsis? |
|
Definition
| sepsis + end organ function |
|
|
Term
|
Definition
| state of acute ciruclatory failure characterized by persistent arterial hypotension despite adequate fluid resuscitation or by tissue hypoperfusion (lactate >4). unexplained by any other cause! |
|
|
Term
|
Definition
| viable bacteria within the liquid component of blood |
|
|
Term
| what is the number one drug used for a pt experiencing anaphylactic shock? What are the next two steps in medications? |
|
Definition
epinephrine -H1 and H2 blocker (diphenhydramine + ranitidine) -corticosteroids (prevent late phase anaphylaxis) |
|
|
Term
| what is neurogenic shock? |
|
Definition
| it occurs after a spinal cord injury. sympathetic outflow is disrupted resulting in unopposed vagal tone which leads to hypotension and bradycardia |
|
|
Term
| the anatomic level of injury impacts the severity of neurogenic shock, at what vertebral level is the entire sympathetic system likely to be disrupted |
|
Definition
above t1 from t1-L3 only partial sympathetic outflow may be disrupted |
|
|
Term
| what is used to maintain BP in neurogenic shock? reverse bradycardia? what can be given to prevent worsening of the neuro deficits |
|
Definition
crystalloid fluids, OR dopamine or dobutamine atropine methylprednisolone |
|
|
Term
| What is infective endocarditis? |
|
Definition
| an infection of the endocardium (innermost surface of the heart) usually involving the cusps of the valves |
|
|
Term
| What are some of the MC pts that would present with an infective endocarditis? |
|
Definition
| pts with structural cardiac defects (acfquired stenosis or regurgitation) or pts that have had a valve replacement. also IV drug users and hx of indwelling pulm catheter or central venous catheter |
|
|
Term
| if a patient presents with an unexplained fever and a new onset of a heart murmur, what should always be on the differential? |
|
Definition
|
|
Term
| what valve is MC associated with infective endocarditis? which valves are MC affected after? What valve is MC affected in IV drug users? |
|
Definition
-mitral, aortic, mitral +aortic, tricuspid, rarely pulmonic -tricuspid in IV drug users (MC cause of R sided IE) |
|
|
Term
| Some common signs of infective endocarditis are splinter hemorrhages, osler nodes, roth spots, and janeway lesions. describe what each of these is |
|
Definition
-splinter hemorrhages: linear red marks on the nail bed -osler nodes: painful raised lesions on the fingers and toes) -roth spots: lesions on the retina with small, clear centers -janeway lesions: painless red lesions on the palms or soles |
|
|
Term
| what is the MC causative agent in acute endocarditis (native valve) |
|
Definition
|
|
Term
| what is the MC causative agent in subacute native valve IE |
|
Definition
|
|
Term
| acute pericarditis is an inflammation of the pericardium characterized by what three things? |
|
Definition
| chest pain, pericardial friction rub, and EKG changes |
|
|
Term
| describe the chest pain associated with acute pericarditis |
|
Definition
| sharp, substernal or pericordial and pleuritic. radiating sometimes to the trapezius, relieved by sitting forward and upright but WORSENED when lying down, with inspiration/swallowing, and with certain body movements |
|
|
Term
| What is the mainstay of tx for acute pericarditis? how about acute pericarditis due to a recent MI? |
|
Definition
NSAIDs use Aspirin with post MI bc NSAIDs delay ventricular healing |
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|
Term
| Are corticosteroids indicated for tx of acute pericarditis? |
|
Definition
| not usually, they rarely tx it fully and it usually returns. use nsaids |
|
|
Term
| the pericardium usually contains how much fluid? it can expand to hold how much fluid? what happens when this is exceeded? |
|
Definition
20-50 mL 90-120 mL capacity of atria and ventricle to fill is compromised which increases pericardial pressure, leading to decr stroke volume, decr CO, and hypotension |
|
|
Term
| what is cardiac tamponade? |
|
Definition
| a medical emergency caused by fluid in the pericardial space, resulting in decreased ventricular filling and subsequent hemodynamic compromise |
|
|
Term
| what is the MCC of pericardial effusion leading to cardiac tamponade? |
|
Definition
|
|
Term
| WHat is beck's triad? what is it the classic presentation of? |
|
Definition
cardiac tamponade! 1. hypotension 2. narrow pulse pressure 3. quiet heart sounds |
|
|
Term
| What are the three most common findings in a patient with cardiac tamponade |
|
Definition
dyspnea jugular venous distention tachycardia |
|
|
Term
| what is pulsus paradoxis? what is it pathognomic for? |
|
Definition
pericardial effusion! -an abnormally large decrease in systolic pressure during inspiration. normal fall in pressure is <10 mmHg |
|
|
Term
|
Definition
| during inspiration venous return to the heart should increased and any neck vein distention should diminish. when there is an absence of collapse or a paradoxical rise in the jugular column--- this is kussmauls sign |
|
|
Term
| cardiac tamponade is completely reliant on the ________ of fluid accumulation |
|
Definition
|
|
Term
| during pericardial effusion, if fluid accumulates rapidly how much fluid does it take to cause in incr in pericardial pressure and a decr in CO? if it accumulates slowly, over time, how much fluid can theoretically accumulate before any hemodynamic compromise? |
|
Definition
|
|
Term
| what should all patients with cardaic tamponade receive initally for tx? what is the gold standard of tx? |
|
Definition
-O2, vol expansion with fluids, bed rest with leg elevation, inotropic drugs (dobutamine) -pericardiocentesis! |
|
|
Term
| what are the 4 different kinds of pericardial effusions? |
|
Definition
1. exudates (leaky capillaries: infection, malignancy, trauma) 2. transudates (incr. hydrostatic or decr. oncotic pressures: CHF, atelectasis, renal or liver dz) 3. empyema: infection in pleural space 4. hemothorax: trauma or malignancy |
|
|
Term
| what is the gold standard for dx of a pericardial effusion |
|
Definition
| thoracocentesis and the fluid is sent for eval |
|
|
Term
| what is acute coronary syndrome |
|
Definition
| spectrum of clinical presentations seen in a range from unstable angina to NSTEMI to STEMI |
|
|
Term
| What is the primary cause of acute coronary syndrome? |
|
Definition
|
|
Term
| Low levels of what to cations can cause cardiac arrhytmias? these should always be checked in a patient with any cardiac complaint |
|
Definition
|
|
Term
| Initial tx for an acute coronary event is MONA, what does this stand for (include dosages) |
|
Definition
M- morphine 2-5 mg IV Q5-30min PRN (can sub Fentanyl) O- oxygen 4 L/min via nasal cannula N- nitroglycerin 0.4 mg SL Q5min MAX 3 tab A- aspirin 165-325, sub clopidogrel 300-600mg loading dose if allergic to ASA |
|
|
Term
| what do ST elevations represent in a pt with ACS (acute coronary syndrome) |
|
Definition
| active and ongoing transmural myocardial injury |
|
|
Term
| NSTEMI can be differentiated from unstable angina, how? |
|
Definition
| presence of cardiac enzymes |
|
|
Term
| the posterior descending artery arises from the RCA or the LCA? |
|
Definition
| can arise from either, but most often arises from the RCA |
|
|
Term
| obstruction of the right coronary artery commonly affects what pacing node in the heart? how does the manifest physically? |
|
Definition
| SA node and the AV node and a bradycardia may be present with or without heart block |
|
|
Term
| What are the 5 cardiac risk factors? |
|
Definition
HTN DM Smoking FAmily Hx Hyperlipidemia |
|
|
Term
| What is Dresslers syndrome? |
|
Definition
| a post MI syndrome that includes pericarditis, fever, leukocytosis, and pericardial or pleural effusions |
|
|
Term
| Which cardiac enzymes are elevated 3-12 hrs after injury, are peaked at 24 hours, and return to normal at 5-14 days? |
|
Definition
|
|
Term
| which cardiac enzymes are elevated 3-12 hours after initial injury, peak at 24 hours, and return to normal at 48-72 hours |
|
Definition
|
|
Term
| what is the absolute first thing you should order on anyone with chest pain? |
|
Definition
|
|
Term
| differentiate stable vs unstable vs prinzmetal angina |
|
Definition
Stable- exacerbated with activity and relieves with rest unstable- increasing intensity in a resting pt prinzetal- vasospasm at rest with preservation of ability to do physical activity |
|
|
Term
| differentiate stable vs unstable vs prinzmetal angina |
|
Definition
Stable- exacerbated with activity and relieves with rest unstable- increasing intensity in a resting pt prinzetal- vasospasm at rest with preservation of ability to do physical activity |
|
|
Term
| What is the MC type of cardiomyopathy? also, the MCC of heart transplant, and the 3rd MCC of heart failure... |
|
Definition
|
|
Term
| What are the most common causes of dilated cardiomyopathy? |
|
Definition
-usually an insult to the cells -Ischemia, d/t CAD and prior MI -ETOH abuse -infection |
|
|
Term
| Is dilated cardiomyopathy a diastolic or systolic problem? Describe the pathophysiology. |
|
Definition
| Its a diastolic issue. There is decreased LV function and decreased strength of contraction which leads to dilation of the LV, this dilation leads to further dysfunction of contractility and heart failure ensues. |
|
|
Term
| What two murmurs are associated with dilated cardiomyopathy, why? |
|
Definition
| tricuspid and mitral regurgitation can occur due to the progressive dilation |
|
|
Term
| What is the most common presenting symptom of dilated cardiomyopathy? What do the signs and symptoms generally mimic? |
|
Definition
-Dyspnea -CHF (both L and R sided!)--> fatigue, DOE, SOB, orthopnea, paroxysmal nocturnal dyspnea, incr edema, incr weight, and incr abd girth |
|
|
Term
| What type of extra heart sound is associated with dilated cardiomyopathy? |
|
Definition
|
|
Term
| What will an echo of dilated cardiomyopathy pt show? |
|
Definition
| LV dilation and dysfunction with high diastolic pressure and decreased cardiac output. The LV wall is usually NL though |
|
|
Term
| What are the three points of tx for dilated cardiomyopathy |
|
Definition
-remove offending agent if possible (like ETOH) -tx like CHF: diuretics, ACEI/ARBs, BBs, etc -Anticoagulation should be considered since these pts are at high risk for embolization |
|
|
Term
| What are most cases of hypertrophic cardiomyopathy caused by? |
|
Definition
| most are inherited as an autosomal dominant trait, but some are due to spontaneous mutations |
|
|
Term
| Is the main issue in hypertrophic cardiomyopathy diastolic or systolic dysfunction? Explain pathophys |
|
Definition
| Diastolic. The ventricles become stiff and hypertrophied, causing increased diastolic filling pressures. There is no issue with systolic function. Also these pts often have an outflow obstruction that exacerbates the issues. The diastolic pressures increase further with things that incr HR and contractility (exercise) or decr L ventricular filling (valsalva) |
|
|
Term
| What are some sx of hypertrophic cardiomyopathy |
|
Definition
| -sx: DOE, angina, dizziness or syncope after exertion, palpitations, SUDDEN DEATH |
|
|
Term
| What are some signs of hypertrophic cardiomyopathy? What extra heart sound is associated? |
|
Definition
-S4 (due to blood from the atria hitting a noncomplaint ventricle) -SEM -bisiferous pulse -elevated diastolic BP -sustained PMI |
|
|
Term
| Where is the SEM of hypertrophic cardiomyopathy best heard? |
|
Definition
| Left lower sternal border |
|
|
Term
| What factors increase the SEM of hypertrophic cardiomyopathy and what decr it? |
|
Definition
-Increased: with valsalva and standing (decr L ventricular size and therefore decr filling) -Decreased: sustained handgrip (incr systemic resistance decr the pressure gradient across the aortic valve), squatting or lying down (incr LV filling) |
|
|
Term
| What does and echo of a hypertrophic cardiomyopathy pt show? |
|
Definition
| LVH, asymmetric septal hypertrophy, small LV and diastolic dysfxn |
|
|
Term
| What is the tx FOR ALL PTS with hypertrophic cardiomyopathy |
|
Definition
| AVOID STRENUOUS ACTIVITY! |
|
|
Term
| What is the tx for a sx-atic pt with hypertrophic cardiomyopathy |
|
Definition
BBs, CCBs if no relief from BBs diuretics if fluid retention |
|
|
Term
| What is the surgical option for hypertrophic cardiomyopathy patients |
|
Definition
| myomectomy by excising part of the myocardial septum, or mitral valve replacement |
|
|
Term
| What is the least common type of the 3 types of cardiomyopathy? |
|
Definition
|
|
Term
| Is restrictive cardiomyopathy a systolic or diastolic problem? explain pathophys |
|
Definition
| diastolic, restricted ventricular filling dt decreased ventricular compliance. The systolic function and ventricular wall thickness are normal |
|
|
Term
| What are some causes of restrictive cardiomyopathy |
|
Definition
| amyloidosis, sarcoidosis, hemochromatosis, scleroderma, idiopathic |
|
|
Term
| What are the s/sx of restrictive cardiomyopathy |
|
Definition
| -elevated filling pressures cause signs of L heart failure (dyspnea and exercise intolerance) and R heart failure (peripheral edema, ascites) |
|
|
Term
| What does an echo of a pt with restrictive cardiomyopathy show |
|
Definition
| Thickened myocardium and possible systolic ventricular dysfxn. Incr r and L atrium size with NL LV and RV size. |
|
|
Term
| In a pt with amyloidosis and restrictive cardiomyopathy what does the myocardium appear as on echo |
|
Definition
| brighter than usual or with a speckled appearance |
|
|
Term
| How is restrictive cardiomyopathy tx? |
|
Definition
-tx underlying cause: hemo (phlebotomy or deferoxamine), sarcoidosis (glucocorticoids), amyloidosis (possibly chemo) -other CHF treatments as needed |
|
|
Term
| How is restrictive cardiomyopathy tx? |
|
Definition
-tx underlying cause: hemo (phlebotomy or deferoxamine), sarcoidosis (glucocorticoids), amyloidosis (possibly chemo) -other CHF treatments as needed |
|
|
Term
| In AFib, what is the typical atrial rate? Ventricular rate? |
|
Definition
-atrial: >400 -ventricular: 75-175 |
|
|
Term
| What are the three main goals of tx of AFib? |
|
Definition
-Ventricular Rate control (of greater importance than rhythm control!) - Restore NSR -Assess need for anticoagulation |
|
|
Term
| What are some common drugs used for controlling ventricular rate in AFib? |
|
Definition
-CCBs: Diltiazem (Cardizem) -Beta Blockers: Carvedilol, esmolol -Digoxin (rarely ever used alone), Amiodarone (if refractory to other tx) |
|
|
Term
| What is the rule for cardioverting new onset Afib-- If its been present for less than 48 hours? Greater than 48 hours? |
|
Definition
-less than 48 hours, okay to cardiovert -greater than 48 hours: either need to anticoagulate for 3 weeks then cardiovert, or get a TEE and r/o atrial thrombus and immediately cardiovert |
|
|
Term
| How long should a patient with new onset AFib be anticoagulated after cardioversion... assuming they will not need lifelong cardioversion ? |
|
Definition
|
|
Term
| In a hemodynamically UNSTABLE patient with AFib, what are the parameters for cardioversion? |
|
Definition
| Always immediately cardiovert, regardless of how long AFib has been going on |
|
|
Term
| What is the CHADS2 score? What are the parameters? What score requires anticoagulation chronically? |
|
Definition
-clinical prediction for the risk of stroke in patients with non-valvular AF -CHF, HTN, age >75, DM, Previous stroke or TIA -all are worth one point -a score >2 should be started on OAC, unless contraindicated |
|
|
Term
| What is the pathognomonic description of AFib's rhythm? |
|
Definition
|
|
Term
| What is the pathognomonic description of a rhythm strip of a flutter? |
|
Definition
|
|
Term
| What is the most common cause of atrial flutter? |
|
Definition
|
|
Term
| What is an AV block? How many different types are there? |
|
Definition
It is a refractory conduction of impulses from the atria to the ventricles through the AV Node or the Bundle of His. -There is first degree, Second degree type 1 (wenkebach) and second degree type 2 (Mobitz), and third degree (total) AV Block |
|
|
Term
| What is a first degree AV block-- what will be seen on EKG? What must be the same in every cycle for it to be considered first degree? |
|
Definition
-on EKG you will see a QRS that is greater than 0.2 seconds (or one large box on the EKG). -The PR interval must be prolonged the same amount of time each cycle, and the P-QRS-T sequence is normal in every cycle also |
|
|
Term
| Where exactly is the delay in a first degree AV BLock? |
|
Definition
|
|
Term
| What is the tx for a first degree AV block? |
|
Definition
| it's a benign condition, no tx necessary |
|
|
Term
| What is the difference between the specific area that is blocked in the two types of second degree blocks? |
|
Definition
-In a Wenckebach (type 1), there is block of the AV node -In a Mobitz (type 2), there is block of the purkinje fiber bundles (His Bundle or Bundle Branches) |
|
|
Term
| Describe what is seen on an EKG of a 2nd degree Mobitz block? |
|
Definition
| -there is progressive lengthening of the PR interval until finally the AV node is totally blocked and a QRS is dropped. There is usually a consistent pattern of P:QRS ratio too, such as 3:2 (always one more P than QRS) |
|
|
Term
| Does a 2nd degree Mobitz AV block require tx? |
|
Definition
| No, it's benign and no tx is necessary |
|
|
Term
| Describe what a 2nd degree Mobitz (type 2) AV block looks like on an EKG? The ratio of P to QRS? |
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Definition
-you will see a number of totally blocked paced atrial depolarizations before conduction to the ventricles is successful. -the ratio of P:QRS is often something like 3:1, or even higher |
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Term
| What is the treatment of a 2nd Degree Mobitz (Type 2) AV block |
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Definition
| this is a serious condition that can lead to a complete heart block, a pacemaker is often necessary |
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Term
| Just by looking at an EKG, how can one differentiate between a Wenckebach and Mobitz AV block, if they're both 2:1 ratio |
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Definition
-since Wenckebach originates in the AV node, you will see a lengthened PR interval -since Mobtiz originates below the AV node (His Bundle or Bundle Branches) you will see a widened QRS with a normal PR interval |
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Term
| How can one use vagal maneuvers on a pt to determine the difference between a Wenckebach and a Mobitz if they are both 2:1 and hard to differentiate on EKG? |
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Definition
-The AV node is richly supplied with parasympathetic innervation, so vagal maneuvers inhibit the AV node, making it more refractory -Since Wenkebach's originate in the AV node, the vagal maneuver will increase the parasympathetic innervation of the AV node, increasing the number of cycles/series to produce a 3:2 or 4:3 wenkebach -in the Mobitz, the block is in the ventricular conduction, so a vagal maneuver will either eliminate the block or have no effect |
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Term
| what is a complete 3rd degree AV block? |
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Definition
| it is total block of conduction to the ventricles, so atrial depolarizations are not conducted. The ventricles take over and start pacing at their inherent rate of 25-40 bpm |
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Term
| What is the tx of a complete 3rd degree AV block |
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Definition
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Term
| What is a bundle branch block? What will be seen on EKG (specifically, how wide will the QRS be?) |
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Definition
-its a delay in conduction to either the Left or the Right bundle branch -on EKG you will see a widened QRS with two peaks -the QRS should be wider greater than .12 seconds (three small squares), bc simultaneous depolarization of the ventricles typically occurs in less than .12 seconds |
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Term
| What leads will you see a Right bundle branch block in? Left? |
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Definition
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Term
| What is considered an incomplete Bundle branch block? |
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Definition
| when you see the two peaked R's of a BBB in a QRS of normal duration |
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Term
| which type of Bundle Branch block is thought of to be more severe (telling of a more serious underlying disease) |
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Definition
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Term
| What is the tx for a symptomatic BBB? |
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Definition
pacemaker possibly cardiac resynchronization tx |
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Term
| What two types of rhythms are bundled under the term 'supraventricular tachycardia'? |
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Definition
-paroxysmal atria tachycardia and paroxysmal junctional tachycardia -because they both originate above the ventricles |
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Term
| What is the difference between paroxysmal atrial tachycardia and paroxysmal junctional tachycardia in terms of where they occur |
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Definition
-They both are paced at rates of 150-250 bpm -PAT occurs from an irritable focus in the atria -PJT occurs from an irritable focus in the AV junction |
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Term
| What will PAT look like on EKG? |
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Definition
-the p waves will not look like normal sinus p waves. -there will be a P for every QRS -150-250 bpm |
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Term
| What will PJT look like on EKG? |
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Definition
| no discernable P waves, usually, and paced at a rate of 150-250 bpm |
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Term
| When you see PAT with an AV Block at a 2:1 P:QRS ratio, what should be the first thing that comes to mind? What is the tx? |
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Definition
-Digitalis toxicity -Occurs more often in pt's with low K, so can carefully give IV K |
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Term
| Why might one see inverted P waves randomly in PJT? |
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Definition
| Because a rapidly pacing junctional focus may also depolarize the atria from below in a retrograde fashion |
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Term
| What are some tx options for PSVT? |
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Definition
-Valsalva, carotid massage, cough, holding breath, head immersion in cold water -IV adenosine is first choice -Back up choices are IV verapamil and IV esmolol |
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Term
| What are the side effects of adenosine |
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Definition
| -headache, flushing, SOB, chest pressure, nausea |
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Term
| Why does digitalis cause the PAT with 2:1 AV BLock? |
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Definition
| Because excess digoxin can provoke an atrial focus into such an irritable state that it suddenly paces rapidly. BUT it markedly inhibits the AV node so that only every second stimulus conducts to the ventricles |
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Term
| What is the definition of a premature atrial contraction (PAC)? What will it look like on EKG |
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Definition
| early beat arising from an automaticity focus in the atria. On EKG will see an early p wave that looks different in morphology than the normal sinus P wave, but the QRS should be normal |
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Term
| What is the tx for symptomatic PACs? |
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Definition
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Term
| What are some causes of PACs? |
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Definition
| Adrenergic excess, alcohol, drugs, infection, electrolyte imbalances, dig toxicity |
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Term
| What is a PVC? Look like on EKG? |
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Definition
| A beat arising from an automaticity focus in one ventricle, that slowly spreads to the other. On EKG you will see a large, wide QRS complex with a compensatory pause afterword, and usually no p wave. The reason the QRS complex is so wide is it's paced by a ventricular focus that paces at an inherently slower rate than the SA node |
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Term
| What is the most lethal cause of PVC? |
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Definition
| hypoxic myocardial tissue |
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Term
| What does a couplet, bigeminy, and trigeminy mean in terms of PVCs? |
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Definition
| -couplet is two successive PVCs, bigeminy is a sinus beat followed by a PVC, trigeminy is a sinus beat followed by two PVCs |
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Term
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Definition
| nothing unless symptomatic. BBs if symptomatic. Russ Dailey also mentioned lidocaine? |
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Term
| What is the definition of ventricular tachycardia? Where does it originate-- are p waves still present/atria still functioning? |
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Definition
| the rapid firing of three or more PVCs in a row, at a rate between 100 and 250 bpm. AV dissociation is present, so the atria are steal beating at their inherent rate (not affected by the tachy), the problem is distal to the bundle of His (otherwise it would be a supraventricular tachycardia!) |
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Term
| What are two of the MCCs of PVC? Name some others... |
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Definition
-CAD with hx of MI -Electrolyte disturbances: hypoK, hypoCa, and hypoMg -prolonged QT, drug toxicity, congenital defects |
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Term
| What are Cannon A Waves? Why is it seen in V Tach? |
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Definition
| venous pulsations that occur secondary to the right atrium contracting against a closed tricuspid valve. Since the atria are contracting at a normal rate and the ventricles are dissociated, the atria will inevitably at some points be contracting against closed valves. |
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Term
| What is the tx for VTach in a pt with sustained who is hemodynamically stable, and those who are unstable? |
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Definition
-Stable: IV procainamide, amiodarone, or Solatol -Unstable: immediate cardioversion then IV amiodarone to hold the NSR |
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Term
| What is the tx for a stable pt in nonsustained v tach who has no underlying cardiac dz and is asymptomatic? how about those with underlying cardiac disease? |
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Definition
-no tx, they are not at increased risk of sudden death -electrophysiologic studies to determine need for ICD and amiodarone is the best antiarhythmic drug |
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Term
| What is torsades de pointes and what causes it? |
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Definition
-V Tach in which the QRS complexes are twisting around the baseline -Caused spontaneously, 'lyte disturbances, or due to Long QT syndrome |
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Term
| What is long QT syndrome? |
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Definition
| a congenital or acquired DO that is characterized by recurrent syncope, a QT interval .5-.7 sec long, Ventricular arrhthmyias and occasionally sudden death |
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Term
| What is Brugada syndrome? |
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Definition
| a congenital DO more common in asian men that causes syncope, v fib, and sudden death |
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Term
| What is the MCC of Vfib? other causes (2)? |
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Definition
-ischemic heart disease -antiarrythmics that cause Long QT syndrome -AFib with RVR in a pt with WPW syndrome |
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Term
| What will be seen on an EKG of VFib? |
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Definition
| Bag of worms, no discernible waves, very irregular rhythm |
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Term
| Give the steps for ACLS of a pt in VFib... |
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Definition
-CPR and defibrillation x 2, start epi at 1 mg bolus then Q3-5 min, defib again -After 3rd shock, start amiodarone 300 mg (may repeat once in 5 min a dose of 150 mg) |
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Term
| What is the tx for torsades de pointes? |
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Definition
| defibrillation and IV Magnesium |
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Term
| 95% of HTN cases are due to essential HTN with no identifiable cause. What are some lifestyle choices that exacerbate essential HTN? |
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Definition
| -ETOH, tobacco, high salt intake, lack of exercise, NSAIDs, and low K intake |
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Term
| What is the MCC of secondary htn overall? in young women? other causes? |
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Definition
-renal artery stenosis -OCP use -sleep apnea, coarctation of aorta, chronic steroid tx, cushing's, thyroid and parathyroid disease, primary hyperaldosteronism |
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Term
| What is a normal BP, pre HTN, HTN? HTN urgency vs. malignant htn (htn emergency)? |
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Definition
-120/80 and below -121-139/81-89 -140/90 and above ->180/>120 and the difference is emergency has signs of end organ damage |
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Term
| What are two of the most common initial pharm tx for HTN? in diabetics? mechanism of actions... |
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Definition
-Thiazide diuretic (acts on distal renal tubule to increase excretion of sodium and chloride--these pt's should have a K supplement) and BB's (decr. HR and CO and decr renin release) -ACE Inhibitor (inhibits renin-angiotensin system and inhibits bradykinin degradation--bradykinin dilates BVs, so inhibiting it's degradation helps to keep BP low) |
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Term
| What is the difference between the inital tx for a pt with stage 1 and stage 2 htn. |
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Definition
-stage 1 (140-159/90-99) Lifestyle mods and 1 drug -stage 2 (>160/>100) lifestyle mods and 2 drugs |
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Term
| What is an added bonus of thiazide diuretics, and part of the reason why they should always be first or second line in HTN tx? |
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Definition
| bc they increase the effectiveness of all other HTN meds |
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