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72 Cards in this Set
- Front
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W/ re to treatment of CHF, ______ are the most effective means of providing symptomatic relief to patients with moderate to severe CHF.
A. ACE inhibitors B. ARBs C. Beta-blockers D. Diuretics E. Hydralazine and isosorbide dinitrates F. Spironolactone |
D. Diuretics !!
W/ re to treatment of CHF, DIURETICS are the most effective means of providing symptomatic relief to patients with moderate to severe CHF. **Diuretics have not been shown to reduce mortality or improve prognosis but are excellent for symptom control. Goal is relief of signs and symptoms of volume overload (dyspnea, peripheral edema). *** Diuretics used: furosemide (Lasix) is most potent and is a loop diuretic. Hydrochlorothiazide is a thiazide that has moderate potency and is often used too. |
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The combo of what two meds should be hte initial treatment in most symptomatic CHF patients?
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diuretic and an ACE inhibitor
beta blocker also is very useful p. 19 of Step UP |
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Most common cause of death from CHF is ....
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sudden death from ventricular arrhytmias. p. 20
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Beta blockers are proven to decrease mortality in patients with post-MI heart failure. They are reported to improve symptoms of CHF as they may slow progression of heart failure by slowing down tissue remodeling. Decrease in HR leads to decrease dO2 consumption. Beta blockers also have antiarrhythmic and antiischemic effect. But not all beta-blockers are equal. There is only evidence for what three?
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Metoprolol, Carvedilol, bisoprolol
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This is useful for patients with low EF who continue to have symptoms despite optimal therapy (with ACEi, beta blocker, aldo antagonist, diuretic). This med is useful in patients with EF < ______ , severe ______, or severe a-fib. It is a positive inotropic agent that has short-term symptomatic relief but has NOT been shown to improve mortality.
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DIGITALIS!
40% , CHF |
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At what stage do you start the followings drugs?
1. Mild CHF 2. Mild to Moderate CHF 3. Moderate to Severe CHF A. Start ACEi B. Start beta-blocker C. Start digoxin D. Start loop diuretic |
1. Mild CHF: A. Start ACEi, restrict sodium intake
D. Start loop diuretic IF volume overload or pulmonary congestion is present 2. Mild to Moderate CHF: B. Start beta-blocker 3. Moderate to Severe CHF: C. Start digoxin |
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How do you diagnose atrial fibrillation?
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ECG findings of irregularly irregular rhythm.
Mulitple foci in atria fire continuously in chaotic pattern, causing irregular rapid ventricular rate. Atria is quivering continuously instead of contracting distinctly. Atrial rate is over 300 bpm but impulses are blocked at AV node so ventricular rate ranges from 75-175. |
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What is the treatment for a-fibrillation in
A. a hemodynamically UNSTABLE patient? B. a hemodynamically stable patient? |
A. if hemodynamically UNSTABLE, do immediate electrical cardioversion to sinus rhythm
B. if hemodynamically STABLE, control rate first with beta blocker to 60-100. Then cardioversion to sinus rhythm. . Then anticoagulate to prevent embolic CVA. If AFib present > 48 hours or uknown period of time, risk of embolization during cardioversion is signif. Anticoagulate patient for 3 weeks before and 4 weeks after cardioversion. To avoid waiting 3 weeks, get a transesophageal echocardiogram to image L atrium . If no thrombus present, start IV hep and perform cardioversion in 24 hours. |
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For chronic afib, with what med class is rate control and anticoagulation achieved?
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rate control with beta blocker or calcium channel blocker
anticoagulate with warfarin; though note that with patients with olne AFib, undera age 60, no anticoag needed as these are at low risk for embolization. p25 |
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[ Atrial fibrillation / Atrial flutter ] is one irritable automaticity focus in the atria that fires very close to 300 bpm and fives rise to regular atrial contractions. [ Atrial fibrillation / Atrial flutter ] is multiple foci in the atria firing continuously in chaotic patter causing very irregular, rapid ventircular rate. Atrial rate is over 400 bpm but ventricular rate is at 75-175.
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Arial flutter = one irritable automaticity focus
Atrial fib = multiple foci |
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Name the tachycardia that is characteristics of the description:
A. saw-tooth baseline B. No P waves identified, no QRS complexes identified. There is very irregular rhythm. C. irregularly irregular D. narrow QRS complexes E. wide, bizzare QRS complexes |
A. saw-tooth baseline = atrial flutter (best seen in II, III and aVF)
B. No P waves identified, no WRS complexes identified. There is very irregular rhythm. = ventricular tachycardia C. irregularly irregular = atrail fibrilation D. narrow QRS complexes = paroxysmal supreventricular tachycardia E. wide, bizzare QRS complexes = ventricular tachycardia |
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This tachyarrythmia has ECG findings of:
variable P wave morphology and variable PR and RR intervals. At least three different P wave morphologies are required to make an accurate diagnosis. A. Atrial-fibrillation B. Atrial flutter C. Multifocal atrial tachycardia D. Paroxysmal supraventricular tachycardia E. Wolff-Parkinson-White Syndrome F. Ventricular tachycardia G. Ventricular fibrillation |
C. Multifocal atrial tachycardia
Other notes about MAT: - usually occurs in patients with severe pulmonary dz - thus, treatment involves improving oxygenation and ventilation - dx of "wandering atrial pacemaker" is identical except that the HR is NOT tachycardic p.27 |
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This tachyarrythmia has ECG findings of:
Irregularly irregular rhythm (irregular RR intervals and excessively rapid series of tiny, erratic spikes on ECG with a wavy baseline and no identifiable P waves) A. Atrial-fibrillation B. Atrial flutter C. Multifocal atrial tachycardia D. Paroxysmal supraventricular tachycardia E. Wolff-Parkinson-White Syndrome F. Ventricular tachycardia G. Ventricular fibrillation |
A. Atrial-fibrillation
Multiple foci in the atria fire continuously in a chaotic pattern, causing a totally irregular rapid ventricular rate. Treat with rate control first (beta blockers), then possibly cardioversion to sinus rhythm. Also anticoagulate. p.24 |
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This tachyarrythmia has ECG findings of:
a QRS complex appearing after every second or third "tooth" (P wave) best seen on inferior leads II, III, aVF A. Atrial-fibrillation B. Atrial flutter C. Multifocal atrial tachycardia D. Paroxysmal supraventricular tachycardia E. Wolff-Parkinson-White Syndrome F. Ventricular tachycardia G. Ventricular fibrillation |
Described is a saw-tooth baseline. Thus, it is B. Atrial flutter.
One irritably automaticity focus in the atria is the culprit |
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This tachyarrythmia has ECG findings of:
NARROW QRS complexes sans discernible P waves (P waves are buried within the QRS complex) OR with P waves which may or may not be discernible, depending on the rate A. Atrial-fibrillation B. Atrial flutter C. Multifocal atrial tachycardia D. Paroxysmal supraventricular tachycardia E. Wolff-Parkinson-White Syndrome F. Ventricular tachycardia G. Ventricular fibrillation |
D. Paroxysmal supraventricular tachycardia
as a rule of thumb, NARROW QRS complexes suggest arrhythmia originates at or above the level of the AV node whereas WIDE QRS complexes suggest that arrhythmia originates outside the normal conducting system or there is a supraventricular arrhythmia with coexisting His-Purkinje system abnormality. Treatment: stimulate the vagus delay (Valsalva, carotid snus massage, breath holding, cold water head immersion), or pharmacologic therapy (IV adenosine). Prevention: digoxin or catheter ablation of the accessory pathway. p27 |
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This tachyarrhythmia has ECG findings of:
Narrow complex tachycardia, short P-R interval, and a delta wave (upward deflection seen before the QRS complex) A. Atrial-fibrillation B. Atrial flutter C. Multifocal atrial tachycardia D. Paroxysmal supraventricular tachycardia E. Wolff-Parkinson-White Syndrome F. Ventricular tachycardia G. Ventricular fibrillation |
E. Wolff-Parkinson-White Syndrome
an accessory conduction pathway from atria to ventricles thru the bundle of Kent causes premature ventricular excitation because it lacks the delay seen in the AV node. p29 |
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This tachyarryhthmia has ECG findings of:
rapid and repetitive firing of 3+ PVCs in a row at a rate of 100-250 bpm, sinus P waves continue with their cycle unaffected by the tachycardia A. Atrial-fibrillation B. Atrial flutter C. Multifocal atrial tachycardia D. Paroxysmal supraventricular tachycardia E. Wolff-Parkinson-White Syndrome F. Ventricular tachycardia G. Ventricular fibrillation |
F. Ventricular tachycardia
Originates belo the bundle of His. Can be sustained VT (persists in absence of intervention for longer than 30 seconds and is almost always symptomatic thus is life threatening and can progress to VFib if untreated!) or nonsustained VT (brief, limited, usually asymptomatic BUT when CAD and LV dysfunction are present, it is an independent risk factor for sudden death). |
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This tachyarrythmia has ECG findings of:
No atrial P waves can be identified, no QRS complexes can be identified, there is a very irregular rhythm A. Atrial-fibrillation B. Atrial flutter C. Multifocal atrial tachycardia D. Paroxysmal supraventricular tachycardia E. Wolff-Parkinson-White Syndrome F. Ventricular tachycardia G. Ventricular fibrillation |
G. Ventricular fibrillation
MEDICAL EMERGENCY - immediate defibrillation and CPR are warranted! Multiple foci in the ventricles fire rapidly, leading to a chaotic quivering of the ventricles and no cardiac output. If refractory, continue CPR, give an epinephrine bolus, defibrilate 1 minute after epi bolus, then administer IV amiodarone (second lin agents are lidocaine, magnesium, procainamide). Continue IV infusion of the effective antiarrhythmic agent. p31 |
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What are ECG patterns of premature atrial complexes and premature ventricular complexes?
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PACs: early P waves that differ in morphology from normal sinus P wave (since these P waves originate within the atria and not the sinus node). QRS complexes are normal. PACs can be normal in a heart but can be a precursor of ischemia in a dzed heart.
PVCs: since conduction is NOT thru normal conduction pathways, it is slower than normal, causing a WIDE QRS. Wide, bizarre QRS complexes followed by a compensatory pause; P waves are not usually seen because it is "buried" within the QRS complex. Naming: Couplet = two successive PVCs, bigeminy = sinus beat followed by a PVC, trigeminy = 2 sinus beats followed by a PVC. p22 |
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What is sinus bradycardia (rate less than ____ bpm) and what drug can elevate sinus rate by blocking vagal stimulation to the SA node?
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sinus bradycardia < 60 bpm (though clinically actually significant when rate is persistently < 45 bpm); atropine p32
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What is sick sinus syndrome?
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Sinus node dysfunction characterized by persistent spontaneous sinus bradycardia. Symptoms include: dizziness, confusion, syncope, fatigue, and CHF. Pacemaker implantation might be required. p32
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What are the different levels/types of AV block? Which require pacemaker implantation?
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1. FIRST DEGREE AV BLOCK
- PR interval is prolonged (>0.20 seconds) - QRS complex follows each P wave like normally; delay is usually in the AV node - benign condition that doesn't require treatment 2. SECOND DEGREE AV BLOCK, MOBITZ TYPE 1 - Progressive prolongation of PR interval until P wave fails to conduct 3. SECOND DEGREE AV BLOCK, MOBITZ TYPE 2 - P wave fails to conduct suddenly, without a preceding PR interval prolongation, thus QRS drops suddenly - often progresses to complete heart block thus pacemaker implantation is necessary 4. THIRD DEGREE (COMPLETE) HEART BLOCK - absence of conduction of atrial impulses to the ventricles, no correspondence between P waves and QRS complexes - ventricular escape rhythm pacemaker rate of 25-40 bpm - pacemaker implantation necessary p33 |
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_________, the most common type of cardiomyopathy, is characterized by [ diastolic / systolic / both ] dysfunction.
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dilated cardiomyopathy; systolic : an insult ( ischemia, infection, alcohol, medication) causes dysfunction of the L ventricular contractility.
basically leads to signs and symptoms of L and R sided CHF (S3, S4 and murmurs of mitral or tricuspid infsufficiency), cardiomegaly, coexisiting arrhythmias, SUDDEN DEATH p34 |
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Hypertrophic cardiomyopathy is a [ diastolic / systolic / both ] dysfunction due to ...
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diastolic dysfunction due to a stiff hypertrophied ventricle with elevated diastolic filling pressures. Thus, pressures increase further with factors that increase HR and contractility (such as exercise) or decrease L ventricular filling (Valsalva maneuver). Sudden death possible. p34
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Restrictive cardiomyopathy is a [ diastolic/ systolic / both] dysfunction due to....
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both diastolic and systolic! Infiltraiton fo the myocardium results in impaired diastolic ventricular filling due to decreased ventricualr compliance. Systolic dysfunction is variable and usually occurs in advanced disease. Causes: amyloidosis, sarcoidosis, scleroderma, chemo.p35
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What is myocarditis?
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Inflammation of the myocardium. Can be asymptomatic or present with fever, fatigue, chest pain, pericarditis, CHF, arrhythmia or even death.
Causes: viral (Coxsackie, Parvo), bacteria (Group A/rheumatic fever, Lyme dz), SLE, medications (sulfonamides) Look for elevations in cardiac enzyme levels and erythrocyte sedimentation rate. Treatment is supportive. |
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If an ECG shows diffuse S-T elevation and PR depression, and patient has pleuritic chest pain, fever and leukocytosis and gives a preceding hx of symptoms of a viral illness sucha s nonproductive cough or diarrhea, the patient likely has...
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pericarditis
p.37 |
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What is the imaging of choice for imaging a pepricardial effusion and cardiac tamponade?
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Echocardiogram!
p36 |
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Pericardial effusions are associated with things like ascites, and salt and water retentions states such as...
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CHF, cirrhosis, nephrotic syndrome
p39 |
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Cardiac tamponade is defined as accumulation of pericardial fluid.
TRUE OR FALSE: It is the rate of fluid accumulation that is important, not the amount. |
TRUE!. 200 mL that develops rapidly can cause cardiac tamponade. 2L of fluid can accumulate slowly before cardiac tamponade occurs. When fluid accumulates slowly, pericardium has opportunity to stretch and adapt to the increased volume. p40
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Almost all cases of this valvular heart disease are due to rheumatic heart disease.
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Mitral stenosis
MS results in elevated L atrial adn pulmonary vernous pressure leading to pulmonary congestion. SOUNDS LIKE: S2 is followed by an opening snap (the closer the two the more severe the stenosis). The murmur is often followed by a loud S1. Other: "fishmouth" orifice |
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This valvular heart disease is characterized by a harsh crescendo-decrescendo systolic murmur and radiates to the carotid arteries. Can have a soft S2.
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Aortic stenosis p42
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This valvular heart disease yields widened pulse pressures and is a diastolic decrescendo murmur best heard at left sternal border.
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Aortic regurgitation/ insufficiency p44
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This valvular heart disease is characterized by a holosystolic murmur at the apex and a-fib is a common finding.
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Mitral regurgitation. Afterload reduction with vasodilators is recommended for symptomatic patients only; they are NOT recommended in most asympomatic patients as they can mask progression of the disease. 45
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This valvular heart disease is usually secondary to RV dilation or IV drug users. Characterized by blowing holosystolic murmur.
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Tricuspid regurgitation.
Usually asymptomatic unless patient develops symptoms of RHF/pulmonary HTN. 46 |
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This valvular heart disease is common in pts with genetic connective tissue disorders and is a midsystolic or late systolic click plus mid to late systolic murmur.
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Mitral valve prolapse. 46
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This congenital heart condition is usually asymptomatic until middle age (~ 40yrs). Transesophagus echocardiogram (TEE) with bubble study is diagnostic.
A. Atrial septal defect B. Coarctation of the Aorta C. Patent Ductus Arteriosus D. Ventricular septal defect E. Tetralogy of Fallot |
A. Atrial septal defect
Pulmonary HTN is common though also doesn't occur until later in life (a few decades out). R heart failure can occur too. Unless they are very large, most defects do not require closure. Surgical repari when pulmonary to systemic blood flow ratio is greater than 2:1 or if patient is symptomatic. p 49 |
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This congenital heart condition is the most common congenital cardiac malformation. On CXR, enlargement of the pulmonary artery and cardiac silhouette occurs. An echo shows the defect well. Complications include endocarditis, progressive aortic regurg, HF, pulmonary HTN and Eisenmenger's.
A. Atrial septal defect B. Coarctation of the Aorta C. Patent Ductus Arteriosus D. Ventricular septal defect E. Tetralogy of Fallot |
D. Ventricular septal defect
p50 |
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This congenital heart condition sounds harsh and is a blowing holosystolic murmur with thrill. Can often be heard best at fourth left intercostal space. Murmur decreases with Valsalva and handgrip. The smaller the defect, the louder the holosystolic murmur.
A. Atrial septal defect B. Coarctation of the Aorta C. Patent Ductus Arteriosus D. Ventricular septal defect E. Tetralogy of Fallot |
D. Ventricular septal defect
p50 |
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Clinical features of this congenital heart condition include: HTN in upper extremities with hypotension in loewr extremities. Well-developed upper body with underdeveloped leowr half. Midsystolic murmur heard over back. Symtpoms include HA, cold extremities, claudication with exercise, and leg fatigue. Delayed femoral pulses compared to radial pulses. Prevalence increased in Turner's syndrome. CXR shows notching of ribs and "figure 3" appearance.
A. Atrial septal defect B. Coarctation of the Aorta C. Patent Ductus Arteriosus D. Ventricular septal defect E. Tetralogy of Fallot |
B. Coarctation of the Aorta
p51 |
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Associated with congenital rubella syndrome, high altitude and premature births. The shunting pattenr results in volume overload, pulmonary HTN (loud P2) and R sided heart failure. Continuous "machinery murmur" at L second intercostal space (both systolic and diastolic components)
A. Atrial septal defect B. Coarctation of the Aorta C. Patent Ductus Arteriosus D. Ventricular septal defect E. Tetralogy of Fallot |
C. Patent Ductus Arteriosus
p52 |
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Adults with this congenital heart condition usually expire due to heart failure and/or infective endocarditis.
A. Atrial septal defect B. Coarctation of the Aorta C. Patent Ductus Arteriosus D. Ventricular septal defect E. Tetralogy of Fallot |
C. Patent Ductus Arteriosus
p52 |
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Clinical features of this congenital heart condition include: signs of heart failure, loud P2 (sign of pulmonary HTN), R ventricular hypertrophy secondary to pulmonary HTN, continuous machinery murmur at L second intercostal space, wide pulse pressur eand bounding peripheral pulses, lower extremity clubbing (toes more likely than fingers to be cyanotic).
A. Atrial septal defect B. Coarctation of the Aorta C. Patent Ductus Arteriosus D. Ventricular septal defect E. Tetralogy of Fallot |
C. Patent Ductus Arteriosus
p52 |
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This congenital heart condition is characterized by a triad of cardiac abnormalities: ventricular septal defect, R ventricular hypertrophy, pulmonary artery stenosis, and overriding aorta.
A. Atrial septal defect B. Coarctation of the Aorta C. Patent Ductus Arteriosus D. Ventricular septal defect E. Tetralogy of Fallot |
E. Tetralogy of Fallot p52
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When is correction of the patent ductus arteriosus contraindicated?
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If severe pulmonary HTN or R to L shunt is present, do NOT correct PDA!!! Surgery is contraindicated then! If pulmonary vascular dz is absent, then do surgical ligation.
Note: Indomethacin indicated for closure; prostaglandin E1 can be used to keep the PDA open (ex. if transposition of the great vessels is present). p52 |
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Cyanosis is the most common symptom. Degree of clinical symptoms depends largely on degree of R ventricular outflow obstruction. Pts experience Tet spells (they squat after exertion such as exercise or crying spell. This increases SVR, which helps shunt blood from RV to the lungs instead of the aorta. Oxygen, morphine and beta blockers might also be needed if pt continues to be cyanotic. Murmur is a crescendo decrescendo and heard best at L upper sternal border.
A. Atrial septal defect B. Coarctation of the Aorta C. Patent Ductus Arteriosus D. Ventricular septal defect E. Tetralogy of Fallot |
E. Tetralogy of Fallot p52
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CXR classically shows a "boot shaped" heart.
A. Atrial septal defect B. Coarctation of the Aorta C. Patent Ductus Arteriosus D. Ventricular septal defect E. Tetralogy of Fallot |
E. Tetralogy of Fallot p52
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Treatment is surgical. Most patients have surgery within the first year of life. Twenty year survival rates after surgery are above 80%. The most common causes of death are sudden cardiac death and heart failure.
A. Atrial septal defect B. Coarctation of the Aorta C. Patent Ductus Arteriosus D. Ventricular septal defect E. Tetralogy of Fallot |
E. Tetralogy of Fallot p52
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Match each characteristic CXR to its condition:
1. boot shaped heart 2. "figure 3" appearance 3. notching of the ribs A. Atrial septal defect B. Coarctation of the Aorta C. Patent Ductus Arteriosus D. Ventricular septal defect E. Tetralogy of Fallot |
1. boot shaped heart = E. Tetralogy of Fallot
2. "figure 3" appearance = Coarctation of the Aorta 3. notching of the ribs = Coarctation of the Aorta |
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Differentiate between hypertensive emergency and hypertensive urgency.
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Hypertensive emergency = BP > 220/120 + end organ damage.
Hypertensive urgency = the above without end organ damage. End organ damage systems to assess: - eyes (papilledema) - CNS (altered mental status, intracranial hemorrhage, HTN encephalopathy) - kidneys (renal failure or hematuria) - heart (unstable angina, MI, CHF with pulmonary edema, aortic dissection) - lungs (pulmonary edema) p53 |
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Hypertensive emergency can lead to ____________________ (PRES), a radiographic condition which is thought to be caused by autoregulatory failure of cerebral vessels as well as endothelial dysfunction. What are the symptoms of PRES and the classic radiogrpahic finding?
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Posterior reversible encephalopathy syndrome (PRES).
Note: may or may not be reversible. Elevated BP overwhelm the autoregulatory mechanisms of the cerebral vessels, leading to arteriolar dilation and extravasation of fluid into the brain. Symptoms include: insidious onset of HA, altered level of consciousness, visual changes, seizures. Classic radiographic (MRI usually) finding is posterior cerebral white matter edema. p53 |
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What are some causes of hypertensive emergency? (11)
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- noncompliance with antihypertensive therapy
- Cushing's syndrome - Drugs like cocaine, LSD, methamphetamines - hyperaldosteronism - eclampsia - vasculitis - alcohol withdrawal - pheo - noncompliance with dialysis - renal artery stenosis (atherosclerosis or fibromscular dysplasia) - polycystic kidney disease |
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What is the treatment for hypertensive emergencies?
1. reduce mean arterial pressure by ___% in 1-2 hours. 2. If severe (diastolic >130), or if hypertensive encephalopathy is present, IV agents like what (5) are appropriate? 3. In patients in less immediate danger, oral agents like what 5 are appropriate? |
1. reduce mean arterial pressure by 25% in 1-2 hours.
2. If severe (diastolic >130), or if hypertensive encephalopathy is present, IV agents like what (5) are appropriate: hydralazine, esmolol, nitroprusside, labetalol, nitroglycerin 3. In patients in less immediate danger, oral agents like what 5 are appropriate: captopril, clonidine, labetalol, nifedipine, diazoxide p54 |
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Differentiate between a Type A and a Type B aortic dissection.
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Type A (proximal): involves the ascending aorta (includes retrograde extension from descending aorta).
Type B (distal): is limited to the descending aorta (distal to the take-off of the subclavian artery). p54 |
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Diagnosis of an aortic dissection involves which of the following?
A. CXR showing widened mediastinum (> 8 mm on AP view) B. TEE C. Aortic angiography |
Though you can do all of these, the best is the TEE. CXR can be incidental. Aortic angiography you do if you are going to fix with surgery (Type A).
Treatment is to: 1. Initiate IV beta-blockers to lower heart rate and diminish force of L ventricular ejection 2. Initiate IV sodium nitroprusside to lower systolic BP below 120 mmHg then 3. If type A --> surgery ; If type B --> medical management with pain control |
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What are symptoms suggesting exapnsion and impending rupture of an abdominal aortic aneurysm? Then, what is the triad for a ruptured AAA? What is the diagnostic test of choice?
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- Sudden onset of severe pain int he back or lower abdomen, radiating to the groin, buttocks or legs.
- Grey Turner's sign (ecchymoses on back and flanks) - Cullen's sign (ecchymoses around umbilicus). If RUPTURED: abdominal pain, hypotension, and palpable pulsatile abdominal mass. EMERGENT LAPAROTOMY INDICATED! Diagnostic test of choice is an ultrasound! If pt is hemodynamically stable, then for preoperative planning, CT is the choice test. p56 |
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Management of AAA largely depends on the size of the aneurysm. If the aneurysm is greater than ____cm then surgical resection with synthestic graft placement is recommended. This can be done endovascularly by accessign the femoral artery.
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> 5cm
(normal is ~ 2 cm) p56 |
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Peripheral vascular disease is an occlusive atherosclerotic disease of the lower extremities. What are the common:
A. sites of occlusion/stenosis (3) B. Risk factors (3) C. clinical features |
A. sites of occlusion/stenosis : superficial femoral artery, popliteal artery, aortoiliac occlusive dz
B. Risk factors: smoking, CAD, hyperlipidemia, HTN, diabetes C. clinical features : intermittent claudication (crampy leg pain reproduced by same walking distance, relieved with rest), rest pain (continuous, often prominent at night), diminished or absent pulses, muscular atrophy, decreased hair growth, thick toenails, and decreased skin temp p57 |
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What is the ankle to brachial index used for? And what is it?
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Ratio of systolic BP at ankle: systolic BP at arm
Normal = 0.9-1.3 AB > 1.3 is due to noncompressible vessels . Claudication ABI , 0.7, rest pain ABI < 0.4. |
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What are the six P's regarding clinical features of an acute arterial occulsion? (pain, pallor, ....)
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pain
pallor polar (cold) paralysis parasthesias pulselessness p58 |
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When it comes to acute arterial occlusion, the main goal is to assess viability of tissues to salvage the limb. Skeletal muscle can tolerate how many hours of ischemia?
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6 hours! Perfusion should be reestablished within this time frame.
Then immediately anticoagulate with IV heparin, Thrombolytics can also be infused intraarterially. Treat any complications such as compartment syndrome, that may occur. p59 |
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DVTs are caused by Virchow's triad which is....
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Virchow's triad: endothelial injury, venous stasis, hypercoaguability. Altogether, these give rise ot venous thrombosis.
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Chronic venous insufficiency patients usually have a history of DVT. This makes sense because DVT causes destruction of venous valves in the deep venous system thus gravity leads to the blood column to be transmitted to the ankles. Valves in the perforator veins are also damaged ...why?
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Valves in the perforator veins are also damaged secondary to the chronically elevated deep venous pressure inhibiting transmission of blood from superficial to deep, as normally occurs.
Thus leads to ambulatory venous HTN, which results in interstitial fluid accumulation (edema), and extravasation of plasma proteins and RBCs into subcutaneous tissues, resulting in brawny induration adn pigmentation (a brown-black color) of skin. This leads to eventual reduced capillary blood flow and hypoxia of tissues such that even mild trauma can precipitate tissue death and ulcer formation. p 62 |
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What are chronic changes that occur due to chronic venous insufficiency? (2)
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Skin changes: becomes thin, atrophic, shiny, cyanotic. Brawny induration develops with chronicity
Venous ulcers: less painful than ulcers associated with arterial insufficiency, usually located just above the medial malleolus, often rapidly recur. p62 |
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What is superficial thrombophlebitis and what is the treatment?
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Superficial thrombophlebitis is just pain tenderness, induration and erythema along the course of a superficial vein. In upper extremities it is at the site of an IV infection. In lower extremities, it is usually associated with varicose veins (secondary to static blood flow in these veins).
No anticoag is required as rarely causes PE. Mild analgesic like aspirin is usually all that is required. Continued activity is recommended. If severe thrombophlebitis (with pain and cellulitis), then bed rest, elevation and hot compresses are advised. Only if septic or suppurative are antibiotics indicated. p.53 |
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Cardiac primary tumors are rare. Usually cardiac neoplasms are metastases from other primary tumors such as ... (6)
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breast, lung, lymphomas, kidneys, Kapos's sarcoma in AIDS patients, skin
p.63 |
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What are the signs of SHOCK?
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hypotension, oliguia, tachycardia, altered mental status!
p63 |
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What is the Cardiac Output, systemic vascular resistance, and pulmonary capillary wedge pressure for each of the following types of shock?
A. Cardiogenic B. Hypovolemic C. Neurogenic D. Septic |
A. Cardiogenic: CO low, SVR high, PCWP high
B. Hypovolemic: CO low, SVR high, PCWP low C. Neurogenic: CO low, SVR low, PCWP low D. Septic: CO high, SVR low, PCWP low p64 |
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What are the initial steps to a patient in shock? (Basically, stabilize the patient hemodynamically and determine the cause of shock by...)
1. Establishing [what type of lines] 2. Administering a [what type of] bolus (in most cases, except for cardiogenic and sometimes neurogenic) 3. Draw blood: [what 4 tests] 4. ECG, CXR 5. Continous pulse oximetry 6. [what medication/types ] if the patient remains hypotensive despite fluids 7. Pulmonary artery catheter and/or echo can also help if the above are still not clear |
1. Establishing two large-bore venous catheters, a central line and an arterial line.
2. Administering a fluid bolus (in most cases) 3. Draw blood: CBC, electrolytes, renal function, PT/PTT 4. ECG, CXR 5. Continous pulse oximetry 6. Vasopressors dopamine or NE if the patient remains hypotensive despite fluids 7. Pulmonary artery catheter and/or echo can also help if the above are still not clear p64 |
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What kind of shock is associated with
A. severe peripheral vasodilation (flushing, warm skin) B. peripheral vasoconstriction (cool skin) |
A. severe peripheral vasodilation (flushing, warm skin): septic shock
B. peripheral vasoconstriction (cool skin): hypovolemic shock p67 |
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In septic shock:
A. signs of SIRS will be present. What are the SIRS signs? B. Signs of shock will be present. (BP?, urine output?, lactic acidosis) C. Will patient have fever or hypothermia? |
A. SIRS: two of the following: fever, tachypnea, tachycardic, increased WBC
B. hypotensive, oliguria, lactic acidosis C. can be either feverish or hypothermic Diagnosis of septic shock is essentially clinical. Can be confirmed by postivei blood cultures but negative cultures ar ecommon. A source of infection can aid in diagnosis. |
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Neurogenic shock results from a failure of the sympathetic nervous system to maintain adequate vascular tone (sympathetic denervation). This can occur due to what types of injuries and is characterized by what type of vasculature (constriction vs dilation; SVR status)?
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Injuries like: spinal cord injury, severe head injury, spinal anesthesia, pharmacologic sympathetic blockade
Characterized by peripheral vasodilation with decreased SVR. 68 |
