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196 Cards in this Set

  • Front
  • Back
What is the first heart sound due to?
The closing of the tricuspid and mitral valves in systole.
What is the second heart sound due to?
The closure of the aortic valve mostly but also the pulmonic valve.
What is the third heart sound due to?
S3 corresponds to rapid ventricular filling during early systole. This may be due to a regurg...is common in kids, but after age 40 is pathologic.

S3 gallop heard at the fourth intercostal space at the left parasternal border
What is the fourth heart sound due to?
occurs d/t reduced ventricular compliance during atrial contraction.
Common in people in their 40s and 50s.
What is the difference between low and high frequencies on an Echo?
Low frequencies have better tissue penetration

High frequencies have better image resolution.
What is the equation for ejection fracture calculation?
EF= (EDV-ESV/EDV)
What are the major limitations to Echos
- quality of images is sub-optimal due to poor penetration (adipose tissue and lungs and ribs get in the way)

- structures parallel to the beam may not be visible. must use multiple transducer posistions to avoid echo dropout
What is the main characteristic of Doppler echos?
-Measure velocity of blood ie speed and Direction of flow.

-can tell when there is regurg, stenosis.

-sample is depth dependent which limits max detectable velocity
What are the differences between TTE and TEE?
TTE- trans thoracic echo: standard approach in most pts, non-invasive and no side effects.

TEE- trans esophageal echo: offers superior image quality d/t shorter distance btwn transducer and heart.
-intubation and sedation comes with a slight risk.
= TEE is more sensitive for LA thrombus, valve vegetations and mitral regurg.
What is the normal area of the aortic valve?
3-4 cm
What are physical exam characteristics of aortic stenosis?
-systolic ejection murmur (peaks later in systole as the stenosis gets worse)

-delay in carotid pulse with a decrease in its volume

-enlarged and forceful PMI, but not displaced.

-increased CRP (labs)
What is the best imaging modality for A.S? What do all the other modalities show?
ECHO is the best- shows LVH, systolic ejection performance and aortic valve anatomy.

CXR- nondiagnostic

ECG- may show LVH
What is the tx for A.S.?
*Valve replacement tx- only proven effective tx.

-Valloon aortic valvotomy- relatively ineffective comparatively but used when comorbid factors prevent surgery.

-MED tx: antibiotic prophylaxis to prevent bacterial endocarditis.
-ACE-i not recommended for A.S.
What is the major cause of mitral stenisis?
Rheumatic disease

-also MS is three times more common in women.
What are the PE characteristics of MS?
-Loud S1
-S2 is followed by opening snap (occurs as the diastolic filling snaps open the mitral valve) The sooner the snap, the worse the dz (.12 normal vs .06 dz)
What is a Graham Steell's murmur?
in Mitral stenosis

Pulm HTN develops and a diastolic blowing murmur of pulmonic insufficiency.
How is MS prevented and treated either immediately or prophylactically?
Antibiotic treatment of beta-hemolytic strep infections.
What is the Tx for MS asymptomatic patients?
No therapy for asymptomatic pts.

-Diuretics alone can be given when dyspnea and orthopenea develop.
In MS patients who develop a-fib, what is the medicinal tx?
beta-blockers- slow down the heart rate to help with a-fib.
1.) give diltiazem or esmolol acutely
2.) chronically give beta-blocker, ca channel blocker or oral digoxin
What is the risk for pts with MS and A-fib? What do you give to prevent this?
Risk: systemic embolism!

-Tx: chronic anticoagulation with warfarin at an INR or 2.5-3.5.
What is the mechanical therapy recommendied for MS patients?
-Balloon valvotomy
-MS is fusion of the valve leaflets at the commisures.

-this is in exact contrast to AS.
What makes a good candidate for balloon valvotomy?
-Pliable valves
-little valvular calcification
-little subvalvular apparatus involvement
-moderate or less mitral regurg present.
What occurs when a 'bad' candidate for balloon therapy is treated?
Surgery to open the commissurotomy or valve replacent is undertaken.
What must the patient have for appropriate diagnosis of pericarditis?
2 of the following:
-chest pain
-friction rub on auscultation
-ST elevation (caused by epicardial injury)
What are the physical findings in pericarditis?
-retrosternal chest pain, worse on inspiration
-friction rub
-increased JVP
What are ECG findings in pericarditis?
diffuse ST elevation w/out depression.
-PR depression in 2,3 avf
-PR elevation in avR
*with inverted QRS in avR
What is the best tx for pericarditis?
-NSAIDS for pain
-maybe prednisone in refractory cases
-colchicine if no response to NSAIDS
What are the common causes of chronic constrictive pericarditis?
-TB infection.
-post-radiotherapy
What is Kussmauls Sign?
inability to accomodate increased venous return in the RV d/t fixed constriction.
-results in a rise in JVP upon inspiration
What is the major cause of pericardial effusion?
most commonly exudative and either of viral or idiopathic etiology.
What are the S/S of pericardial effusion?
-Dyspnea, orthopnea
-JVD, Tachy, hypOtn if tamponade, hepatic enlargement
-muffled heart sounds on auscultation
What are the image/ecg findings of pericardial effusion?
ECG-Sinus tachy
CXR-globular heart
ECHO-size and location of effusion, evidence of tamponade, swinging of heart
How do you tell if pericardial effusion was acute or chronic?
Acute- rapid filling leads to critically acute intrapericardial pressure

chronic-gradual accum allows progressive stretching of pericardium-lots of volume with less intrapericardial pressure
What are epidemiologic factors of aortic aneurysms?
-abdominal more common than thoracic
-5-10x inc in men
-3% prevalence in ppl over 50
-of thoracic-ascending most common, desc are rare
What are the risk factors for Abdominal aortic aneurysms?
SMOKING
age
HTN
hyperlipidemia
What are risk factors for ascending thoracif aortic aneurysm?
-Marfan's
-CT diseases
-longstanding HTN
-bicuspid aortic valve
-family Hx
What are risk factors for descending thoracic aortic aneurysm?
Atherosclerosis
HTN
S/S of aortic aneurysms?
-hypogastrum or lowrer back pain
-steady gnawing quality that lasts
-rupture-hypOtn, pulsatile abd mass
-aortic insufficiency
-hemoptysis
-arterial thromboembolism
-cough, wheeze, dyspnea, hoarsness, pneumonia, dysphagia
What is the best diagnostic tool for AAA?
can use US, but CT is the best
-echo-good for screening aortic root but cannot visualize ddescending aorta.
What is the TX for AAA?
-BP control
- beta b do not reduce rate of growth!!
AAA>5.5cm=repair
AAA>4cm=monitor 6mo.
desc>6=repair
marfans or bicusp>5=repair
What recent tx is available for AAA? How does it fare?
Endovascular stent graft to place inside aneurysm.
-better short term outcome but similar mortality at 2 yrs.
-in co-morbit situations where surg is contraI, they fare just as well w/ conservative management that with stent.
What is the annual risk rate for aneurysm rupture?
AAA<4cm 0.3%
AAA 4-4.9 is a 1.5% risk
AAA 5-5.9 is 6.5% risk

upon rupture, 80% of people die
What is the best imaging technique for aortic dissection?
-TEE-quickest use if high degree of suspicion
-CT w/ contrast if suspicion is low, best d/t noninvasive
what are the stages of CHF?
A- risk factors without symptoms (HTN, obese, diabetes, atherosc, FHx)
B- heart disease but w/out CHF symptoms (MI, LVH, asympt valve dz, low EF)

C-Structural DZ w/ current symptoms of CHF (fatigue, short breath, reduce exercise)
How do ACE inhibitors aid in CHF tx?
-inhibit LVH
-inhibits conversion of AI to AII and thus decrease Na and h2o
-inhibit NS
-prevent vasoconstriction
What are the major side effects of ACE inhibitors?
ACE inhibitors reduce breakdown of bradyk and kininaseII
- COUGH and ANGIOEDEMA
What are the contraIndications for ACE inhibitors?
HypOtension and bilateral renal artery stenosis
When are ACE inhibitors indicated?
in ANY patient with systolic dysfunction.
What is the MOA of diruretics and how much should you dose?
Prevents resorption of Na in the renal tubule and enhances urinary excretion of Na and h2o

-perscribe as little as possible while still being effective
-excessive leads to electrolyte imbalances
What is the MOA of ARBs?
same pathway as ACE-Is but diff step.
-blocks binding of AII to the receptor.
Does ARB and ACE-Is side effect profile differ?
ARB- dont block bradyK and kininase breakdown, so no cough and less angioedema with them.

-both also have hypOtn, hypEr Kalemia, renal effects
Which population of CHF patients can get ARBs and ACE-Is?
Stage C pts.
-also get Beta blockers

-can also give aldosterone INSTEAD of ARB but in the same combo of 3 drugs.
How do Beta blockers aid in CHF?
-block NS effects
*inhibits vasoconstriction
*inhibits Na retention
*decreases pre-load and afterload

*** use them whenever systolic dysfunction is present
What are the contraIndications for beta blockers?
-Asthma
-2nd or 3rd degree AV block
-during an episode of acue decompensated HF
-HR below 60 or systolic pressure below 90
What is the MOA for aldosterone antagonists?
Second hormone in the renin-angioT-aldosterone cascade
-antagonists: inhibit Na retention and hypOkalemia
-prevents myocardial fibrosis
ACT to SAVE K+
Which aldosterone antagonist is used often in conjunction with ACE-Is in the hospital setting?
Spironolactone- side effect is gynecomastia

also can use Eplerone
What are contraIndications of Aldosterone antagonists?
-K+ greater than 5mmol/L

-Creatinine greater than 2.5 mg/dL
-other signs of renal failure
SE:
-Hyperkalemia and uremia
What is the MOA of Digoxin?
Inhibits Na/K pump.
-thereby increases intrAcellular Calcium
-increases contractility
What are the benefits of Digoxin?
Introduces Sinus rhythm.
-Use in A Fib if beta blockers dont work!!
-use after ACE,BB,AR< diuretics and CCB havent worked
What are the side effects of Digoxin?
anorexia, nausea, arrhythmias, confusion and visual disturbances.

-HypOkalemia increases SE susceptibility
What causes caution w/ Digoxin dosing?
-low therapeutic window.

-Loading dos of 10-15ug/kg lean body weight (divided into 3 six hour doses)
-maint. doses at 1/4 of loading dose
How do hydralazine and isosorbide dinitrate function in CHF tx?
-direct acting vasodilators
-generally ACE-Is are better
BUT- africans respond better to nitrates and hydralazine
When do you use isosorbide dinitrate and hydralazine in CHF?
in african american patients

in pts who are intolerant of both ACE-Is and ARBs
What are co-morbid conditions with CHF?
Angina
A-Fib
-Asthma and COPD (can still use a BB with the later)
-DM
-Abnormal TSH
-Gout-d/t diuretics (prevent w/ allopurinol, tx w/ colchicene)
-renal dysfunction
-anemia
Which patients should be considered for ICD (implantable cardioverter Defib)
-class II or III HF
-LVEF below 30%
and
-no other conditions greatly limiting life expectancy
Which patients should be considered for CRT (cardiac re-synchronization therapy)
it is a bi-ventricular device
-pts w/ prolonged QRS (>120msec)
*this causes dyssynchronous contraction, decreased LVEF and mitral regurg.
Which drug acts as a direct renin inhibitor?
Aliskiren
-approved for HTN reduction
-lowers BP in a dose dependent fashion

SE: hyperkalemia, teratogenesis, renal failure, gout and kidney stones
Which class of drugs are known as the -prils?
ACE inhibitors are the -prils
What is the MOA of the -pril drugs and what are their side effects?
-prils are ACE inhibitors
SE: cough and angioedema, kyperkalemia, renal failure, teratogenesis.
What class of drugs are known as the -Sartans?
ARBs.
Their MOA is to block the AT1 receptor for ATII, thus works on a different part of the RAAS pathway than the ACE-I.

-no cough or angioedema
S/S: teratogen, hyperkalemia,
What family of drugs are the
-ones?
Aldosterone antagonists.
Spironolactone, eplerenone.
-block the final step in the RAAS
Which drug is related to BNP and is given in hospital settings for acute decompensated heart failure?
What does it do?
Nesiritide. (recompinant BNP) given only in the ER.

-causes naturiuresis, diuresis and mild vasodilation
What are the only two ARBs that are FDA approved for HF?
Valsartan and Candesartan
What are the characteristics of Vaslsartan?
-1/2 life of 6 hours
-30/70 renal/hepatic metab
oral bioavailability of 23%
39% of market shares
What are the characteristics of candesartan?
-1/2 life of 5-9 hours
-approved for HF!
-60/40 rehal/hepation metab
3% of market shares
Which class of drugs are known as the -kirens?
Renin inhibitors.
-Aliskiren: avoids ACE inhibitor side effects.
Which ACE-I is given as IV only form?
Enalaprilat
Which two ACE-Is have very short halflives but are tight binging to ACE?
Ramapril and Quinapril
Which ARB has a short halflife in general?
Losartan
What is the general sequence of drugs given for CHF?
-diuretic
-ACE-inhibitor
-ARB
-Aldosterone Antagonist
-Nitrates and hyro- (Afr. Amer)

-BB need to be given somewhere in here but not acutely.
What is the MOA for nitrates?
increase cGMP
-cuases dephosphorylation of myosin light chains, preventing myosin and actin from linking.
-causes vascular smooth muscle relaxation
What is the sequence of Nitrate vasodilation?
Veins, arterioles then arteries
What are the most common side effects of nitrates?
Headache then hypotension
reflex responses:tachycardia, water and sodium retention

-hypotension, tachycardia, carcinogen, headaches and Tolerance (tachyphylaxis)
How do nitrates affect platelets?
They stimulate guanylyl cyclase activity which functionally decreases platelet aggregation
What are the overall benefits of NO?
Decreased:
-venous return
-blood volume
-blood pressure
-intraventricular pressure
-left ventricle volume
What is the most common use for Nitrates?
Unstable angina

-sublingual is most common
-transdermal is for chronic use
What are contraindications for NO?
-obstructive hypertrophic cardiomyopathy
-hypovolemia
-anemia
-increased intracranial pressure
-cardiac tamponade
What is the most common Nitrate drug?
Isosorbide dinitrate
-100% bioavailable
Oral
T1/2=5 hours
What class of drugs are known as the ipines?
Ca channel blockers
How do Ca channel blockers help in HF?
decrease intracellular Ca stores, which would normally activate myosin light chain kinases.
-relaxes vascular smooth musc
-decreased bp
reduced contractility
What are the three major drugs from the -ipine class?
-Amlodipine-long T1/2,HTN, Angina. SE: Edema

-Nifedipine:HTN, Angina, HEART FAILURE.
SE: flushing, edema headache

-Nimodipine:Selective for Cerebral arteries.
What are the two drugs in the second class of Ca channel blockers?

What are their general SEs?
Verapamil and Diltiazem

SE: bradycardia, heartblock, hypOtension, constipation
The SA and AV nodes are very sensitive to which drug?
Verapamil
-great to increase contractility and reduce heart rate
T1/2= 6-8 hrs.
limits emergens of cancer from cells by blocking p-glycoprotein
What is Ranolazine used for?
new drug, not FDA approved
inhibits FA oxidation and shifts energy source to glucose, which uses less O2 to produce the same amt of ATP.

CYP3A4 metabolized: contrain
(ketoconazole, verapamil, rifampin)
-prolongs QT interval
What are the only two beta blockers approved for CHF and what are their SEs?
Carvedilol- immediate and long acting

metoprolol succinate-only long acting

SE: fatigue, bradycardia, heart block.
Contra-i: asthma, hypoglycemia
How does the pancreas change with old age?
No change in size, but the main pancreatic duct and its branches wide.
increase in fibrous tissue and fatty deposition with acinar cell atrophy; however, the large reserve of the organ results in no significant physiologic changes. The functional reserve of the pancreas may be reduced, although this can occur as a result of delayed gastric emptying rather than pancreatic changes.
What is the MOA of digitalis?
Blocks Na/K pump
-improves myocardial concractility d/t an increase in Na intracellularly and a reduction of Ca efflux
What are the electrical effects of digoxin at low doses?
-Slows sinus and AV nodes
-Increased PR interval
-Decreased QT interval

High doses: dysrhythmias and asystole
What are the common uses for digoxin?
Atrial fibrillation and heart failure

-used when diuretics and ACEIs are not sufficient
Which class of drugs are known as -ide?
Diuretics.
-Feurosamide
-hydrochlorothiozide
What are the stages of HTN (4)
Class Systolic Diastolic
Norm <120 <80
PreHTN 120-139 80-89
St. 1 140-159 90-99
St.2 >160 >100
What are syndromes which lead to secondary HTN?
-Renal HTN (GFR<60 and albumin-creatinine ratio>30)
-coarctation of the aorta
-primary aldosteronism
-cushings
-pheochromocytoma
Which diuretics are better used for HTN?
Thiazides
-long half lives, often used with a fixed combo of ace inhibitor for uncomplicated hypertension.
What drug is the shorter acting diuretic and when is it indicated for HTN?
Chlorthalidone
-shorter half life
-used for resistant hypertension
-pts w/ chronic kidney disease or HF.

-furosemide-6 hr half life
-torsemide-longer half life
What drugs are eplerenone and spironolactone? How do they help with primary hypertension?
They are aldosterone inhibitors
-inhibit aldosterone from acting in the renal tubule and prevent Na and H2O resorb
When does CVD risk double in regard to BP ranges?
starting at 115/75
risk double with each increment of 20/10
What are the percent benefits of lowering BP on stroke, MI and HF?
Stroke 35-40%
MI 20-25%
HF 50%
What components make up the 'metabolic syndrome'?
-HTN
-Obesity (BMI over 30)
-Dyslipidemia
DM
What is the BP goal of therapy for patients with DM and chronic kidney disease?
DM- <140/90

CKD ,130/80

Definately get Systolic goal in persons over 50 yoa.
What are the top three lifestyle modifications which will reduce Systolic BP?
-Weight reduction-10kg in weight and 5-20 in mmHg

-DASH diet (fruits and veggies, low sodium) 8-14mmHg

-exercise 4-9mmHg
What is the drug tx for stage 1 htn w/out compelling indications?
Thiazide diuretics

-may consider a second drug for combo: ACEI, ARB, CCB, BB
What is the drug tx for stage 2 htn w/out compelling indications?
2 drug combo therapy
-thiazide diuretic
AND
-ACEI, ARB, CCB OR BB
What is the drug tx for HTN WITH compelling indications?
-Diuretic as a loop diuretic (clorthalidone)

Other combo may be added as needed.
How often should serum K and Creatinine be monitored for HTN patients?
1-2 x per year.
How often are follow up visits in general for HTN pts once they've reached their goal?
3-6 month intervals

-more frequent visits and monitoring is recommended for stage 2 HTN patients
Which types of drugs should be used for pregnant women with HTN?
Methyldopa and BBs with vasodilarots are preferred for fetus safety.

**ACEI and ARBs are contraindicated for pregnancy
What is atrial flutter?
Non-focal source of atrial arrhythmia.

-most common circuit rotates in a counterclockwise direction in the R. atrium round the tricuspid annulus. 80%
What is the pattern of the most common flutter?
-sawtoothed pattern in II and III and aVF.

-the ventricular response varies making the QRS and heart rate change. This has nothing to do with the flutter atrial rate.
What are the atrial and ventricular rates in atrial Flutter?
Atrial rate = 260-300 bpm
Ventricular = 150 bmp or 2:1

Ventricular rate of 150 is atrial flutter with a 2:1 block until proven otherwise.
What is the TX for atrial flutter?
-Direct Cardioversion
-50-100 J to restore normal rhythm
-risk of thromboembolic events is high! *anticoag tx
-risk for developing HF d/t LVH, tachy is high. controlling w/ CCB, BB and digoxin may help.
Which drugs are used for both atrial flutter and fibrillation to attempt conversion?
-Porcainamide
-amiodarone
-ibulitide
What does this ECG show?
Atrial Flutter with a 2:1 heart block

-atrial rate around 300
-vent rate of around 150
Why are isoproterenol and nitro used in the table tild test?
How are they administered?
Used to provoke syncopal episodes by vasodialtion.
-Isoproterenol: 1-3mg/min will inc HR to 25% inc
-NO: fixed dose of 400mg spray sublingual
When is table tilt test indicated?
recurrent syncope, high risk pts w/ a single episode but lacks structural heart disease evidence.
What is first line therapy for patients with documented PACs and PVCs?
Beta Blockers (metoprolol or atenolol)
What is the difference between Mobitz type I and type II blocks? Which may be associated with pathologic syncope?
Mobitz are AV blocks
1: no wide QRS
2: widened QRS with progression to complete heart block.
ECG shows: Prolonged PR interval with dissociation of PR and QRS.
What are the characteristic findings of acute pericarditis on ECG?
-Depression of the PR interval
-ST segment elevation
What ECG findings are in brugada's syndrome?
Incomplete RBBB
St elevation in v1 or v2
-palpitations
What indicates ventricular dysplasia on ECG findings?
an epsilon wave:
-incomplete RBBB
-inverted T wave in V1
how does ventricular tachycardia reperesent on ECG?
Fusion beats or av dissociation during a wide QRS complex tachycardia
Which drug is used in narrowing the DD of tachycardia? How?
Adenosine (IV bolus of 6mg)
or carotid massage

-slow conduction through the av node, thus, if tachy ends with either maneuver, they are likely to involve the AV node in the re-entrant circuit
How do holter monitors, event monitors and loop recorders differ?
-Holter: 24-48 hour constant monitor

-Event: only triggered to record at start of event

-Loop: worn for a month, implantable
What is IE and what are the four groups associated with it?
IE: an infection of the heart's endocardial surface
Groups:
1 Native Valve
2 Prosthetic Valve
3 IV drub abuse
4 Nosocomial IE
How do acute and subacute IE differ?
Acute: affects normal valves, rapidly destructive, metastatic, commonly caused by staph, fatal if untreated in 6 wks.

Subacute: affects damaged valves, indolent nature, fatal by 1 year if not treated
What proportion of IV drug use is associated with IE?
25% of US cases from IVDU
-5:1 male:female
What are the S/S associated with acute IE?
-High fever and chills
-arthralgia/myalgia
-abdominal pain
-back pain
-pleuritic chest pain
Signs: murmur, petechiae, splinter hemorrhages, clubbing, splenomegaly, osler's nodes, roth spots
What are the S/S of subacute IE?
-low fever
-anorexia
-weight loss
-fatigue
-arthralgias/myalgias
What are the essential blood tests for IE?
-Minimum of three seperate venipuncture sites
-typical organisms present in at least 2 of those sites
-strep infections
-no need to test for anarobics
0Drwa CBC+diff, electrolytes, renal fx, urinalysis also
Imaging techniques to use in IE?
TTE and or TEE is first line
-CXR can help in calcification or vegitation imaging
-Ekg: no very useful, maybe can see tiny MIs.
What are the four major groups of complications arising from IE?
-Valvular damage
-empoli
-immunologic phenomena
-metastatic infections (septic)
What are the treatment options to the two most common agents in IE?
-Strep viridans:
*penecillin
*Gentamicin and vancomycin if pen allergy

-Staph aureus
*nafcillin
*vancomycin
*gentamicin
*Daptomycin
*Cefazolin
What is the proportion of people with bicuspid aortic valves? What are the complications and when do they occur?
1% with bicuspid valves
Complications:
-1/3 become stenotic
-1/3 become regurgitant
1/3 do nothing

Stenosis develops in 40-60 yoa
What is the process of tricuspid aortic stenosis?
Inflammatory process 60-80yoa.
1-lesion similar to plaque of CAD
2 HTN and hyperlipidemia
3 correlation btwn calc coronaries and aortic Ca.
4 increased CRP levels
What are the demographics of pts symptoms of Angina and aortic stenosis?
35% of people with aortic stenosis have CC of Angina

-50% will die in 5 years
What are the demographics of pts symptoms of Syncope and aortic stenosis?
15% of people with aortic stenosis will have CC syncope

-50% will die in 3 years
What are the statistics of pts symptosm of CHF and Aortic Stenosis?
50% of people with aortic stenosis will have CC of CHF

-50% will die in 2 years

Overall only 25% pts With symptoms survive within 3 years without valve replacement.
What is the normal aortic valve area and when will they begin symptoms?
area is 3-4 cm.

symptoms occur when it is 1/3 normal size.
What are physical exam results in a patient with aortic stenosis?
-systolic ejection murmur (peak of murmur depends on dz progression. mild dz peak early, bad dz, peak later)

-delay in carotid pulse and volume

S1-may be followed by a click if A.S. is congenital

S2- splitting
S4-gallop
Which diagnostic tests are useful and which are contraindicated for Aortic Stenosis?
-EKG = LVH
-CXR- may see pulm HTN in end stage disease
-ECHO- leaflet Ca and thickening, LVH

-Stress test is contraindicated for symptomatic patients, causes hypOtn.
What is the Tx for aortic stenosis?
Valve replacement.
-under 40, no coronary angiogram

-above 40, do angiogram to rule out CAD and need for CABG simultaneously
What is medication therapy for aortic stenosis?
Diuretics and nitrates to relieve HF symptoms before surgery.

-ACE-Is NOT recommended b/c cause vasoD but do not increase C.O. cause syncope

-Antibiotic prophylaxis to prevent endocarditis during valve replacement surgery.
What are the surgical options and risks for A.S valve replacement?
-mechanical: must be on anticoags for rest of life

-bioprosthetic: only platelet inhibitors for life, but may breakdown over time

-balloon valvotomy: recommended only when co-morbid prevents surgery.
What are the epidemiological factors of mitral stenosis?
Almost all from Rheumatic HD
-3x more in women
-usually in 40-50s
What is the pathobiology behind mitral stenosis?
-normally diastole causes = pressures btwn the LA and LV.
-MS causes pressure gradient to develop.
-causes LA and Pulm A and RV pressure inc. causes RVH!
-CO decreases
Why is hemoptysis common in Mitral Stenosis?
LA pressure increases causing Pulm HTN, causes small bronchial veins to rupture.
-cough up blood
What is Ortner's syndrome and how does it occur?
-Hoarsness
caused by large LA in Mitral stenosis which impinges on the the recurrent laryngeal nerve. also may get dysphagia from esophagus impingement
What is the significance of the opening snap? What about its timing?
-Opening snap occurs in diastole at some point after S2
-the shorter the time interval between S2 and the Snap indicates severity of M.S.
-Normal is .12 msec, .06msec indicated bad level of stenosis
What is the Graham Steells murmur? what causes it?
It is a low blowing diastolic murmur of pulmonary insufficiency which causes backflow into the right Vent.
-occurs due to pulm HTN
What are the non-invasive imaging techniques for M.S?
EKG- shows Left Atrial enlarg, atrial fibrillation, and RVH is pulm htn is present

CXR- see straightening of left heart border, d/t LAH, pulm venous htn causes Kerley B lines

-ECHO-can measure leaflet thickness and pulm a pressure
Describe the stages of mitral leaflet stenosis with severity
Normal 4-5 cm
Mild 1.75
*Symptoms btwn 2-1.75
moderate 1.75-1.25
mod/sev 1.25-1.0
Severe less than 1.0 cm
What types of medicinal tx are indicated for pts w/ M.S?
1- Diuretics (decrease volume and increase breathing)
2. short acting BB or Ca blockers such as esmolol or diltiazem
(pts develop afib and will decompensate d/t inc HR and RA pressure and dec CO, thus need to act fast)
What is the major long term risk associated with a fib M.S patients?
Thromboembolism!
TX w/warfarin to INR 2.5-3.5 to prevent clot formation.
-convert back to sinus rhythm after anticoag is therapeutic.
What mechanical intervention is indicated for M.S.?
-balloon valvectomy
(b/c cross bridging of valves occurs in MS and not in AS)
What factors consider a candidate good for balloon valvectomy in MS?
1 pliable valves
2 little valvular calcification
3 sub-valv apparatus not involv
4 less than mod mitral regurg

-must do echo first to tell
What does the EKG of MS show?
-RAD consistent w/ RVH (- in I and + in aVF)
-R waves present in V1
-biphasic P waves (indicate Left atrial abnormality)
What are the common etiologies for Mitral Regurg?
Any abnormal MV anatomy:
-MVP most common 2/3
-MI- causes papillary dysf or infarct and improper fx of chordae (1/4)
-inf. endocarditis
-myxomatous degeneration
-RH
-weigh loss drugs used to be a cause but were pulled
What are the classic symptoms of mitral regurg on physical exam?
-pulses: brisk (sharp upstroke, normal volume)

-increased splitting of S2

-holosystolic murmur loudest at apex w/ radiation to the axilla
What is the pathologic progression of mitral Regurg?
1-LVH
2-LAH
3- pulm htn
4- eventually LVH dysfunction d/t ischemia
-5 causes dilation and deformed anatomy (regurg gets worse) and LV contractile dysfunction
What imaging technique is best for mitral regurg?
Echo- TTE
-asesses LVH size and systolic functionality
-etiology of the regurg
What are the medicinal tx indicated for mitral regurg?
---SURGERY!
Severe acute- artery vasoD (BB, alpha ant and nitro.

Chronic symptomatic: use ACE-I to dec. LV volume

Chronic not symptomatic:
no drugs, dont use ACEI b/c they would decrease bv but since asymptomatic, don't have any after-load yet.
Describe the timing of surgery for mitral Regurg.
-Asympt an elderly: NO surger

-Asympt and w/LV dysfunct: surgery w/ REPAIR only, do before LVH occurs. dont replace b/c asympt & replace would cause LV dysf which would make them worse than they are now.

-Sympt: Do surgery. orthopnea, fatigue, dyspnea
Why is repair better than replace in mitral regurg?
-restores competence
-maintains LV function (improved post-op vent fx and survival)
-avoids prosthesis
Which factors make replacement of mitral valve difficult?
-posterior chordal rupture
-anterior involvement
-rheumatic dz
What is good about MV replacements verses repairs?
guarantees valve compentence.
-but the apparatus connections to LV are destroyed resulting in decreased LV fx and LVEF
What are the physical exam characteristics of aortic regurgitation?
-bounding pulses
-S3 present
-to and fro pulses
-wide pulse pressure btwn systole and diastole
-Decrescendo murmur
What is DeMussets sign?
occurs in aortic regurg:
-head bobbing
What is Corrigan's Water Hammer Pulse?
occurs in aortic regurg: abrupt rise with rapid collapse of the pulse
What is Quincke's pulse?
occurs in aortic regurc:
capillary pulsations noted in the nail bed.
What is Bisferin's pulse?
occurs in aortic regurg: bifed pulse on palpation.
What is an Austin-Flint murmur?
occurs in aortic regurg:
functional diastolic rumble which mimics mitral stenosis. Does not have opening snap.
What are the numerical considerationf for people with aortic regurg for valve replacement?
-LVEF less than 50%

-LV end diastolic dimension greater than 7.5cm

-LV end systolic dimension is greater than 5.5cm
What valve dz may pre-dispose one to aortic regurg?
-Rheumatic DZ
-endocarditis
-trauma
-CT disease
-dilation of aortic root d/t HTN
-aortic dissection
-syphilitic aortitis
-cystic medionecrosis
How does tricuspid regurg manifest?
-commonly d/t RV dilation, not from valve deformity itself.
ex: copd
what is the most common cause of tricuspid regurg?
-infective endocarditis of IV drug users.

Staph aureus
What are the s/s of tricuspid regurg?
ascites
edema
JVD
larve V wave
What Tx is availabe for tricuspid regurg?
get down to main cause:
-LVH-LAH-RVH-regurg? tx LVH

-if just d/t regurg, use diuretics
-surgery for valve alone is not entertained, must need CABG or some other surgery too.
not all that well tolerated.
what is carvallo's sign
murmur intensity increases with inspiration. (tricuspid murmur)
What medicinal tx are there for aortic regurg?
For Asymptomatic pts:
-ACE-I (decrease after-load)
-hydralazine

symptomatic:
surgery ASAP, short term stabilization is as above.
What is an A wave?
occurs in the jugular vein in concordance with right atrial contraction.

caused by either:
-decreased right ventricular compliance (pulm stenosis, COPD, pulm regurg, pulm htn)
-tricuspid stenosis
What is a C wave?
occurs in concordance with the carotid pulse, it is a positive upstroke in the jugular

Caused by tricuspid regurg
What is a V wave?
occurs in the jugular in concordance with systole.
What are the limitations to ECHO?
-sub-optimal image quality d/t poor tissue penetration (fat, lung tissue in the way)

-drop-out of structures that are parallel to the beam
*prevent by using multiple image planes
What is the first line tx for people with PACs and PVCs?
beta blockers (metoprolol or atenolol)
What is the formula for LVEF?
LVEF= (EDV-ESV/EDV
When is provocative testing indicated for angina?
-exercise w/ ekg is most recommended
-dont do w/ anything acute such as acute MI, arrhythmias, aortic stenosis, AA dissection, PE, pericarditis, AV block
-dobutamine, dipyrimadole or adenosine are provokers.
-looking for ST shifts
what is tx for angina?
-control risk factors:bp, smoking, weight, diet and exer
-Drugs:
Aspirin
Platelet inhibitor:
*Clopidogrel- inhibits ADP rec
*dipyridanole-not recomm
ACE-I: all pts w/ CAD + DM or LVsystolic dysf.
-BB

CABG or PCI: to prevent MI (2-3 vessel block)
*CABG if LAD involved or has diabetes
*PCI only if ischemia is present