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Rotation 2: IM Outpatient > Cardiac Portion > Flashcards

Flashcards in Cardiac Portion Deck (235):

myocardial ischemia


what is this and what is it caused by (3)? what determiens the severity? what are 3 contributatory factors? what how does it present as symptoms? what causes these symptoms in each?

temporary reduction of blood flow to an organ, potentially reversible, caused by mechanical, electrical, and valvular dysfunction

can be reversible or peremanent depending how long it has been happen for, can lead to infarction

this can cause angina when there is increased activity


Contributory factors: significant LVH, aortic stenosis, tachyarrythmias like afib/aflutter



1. angina pectoris 

1. O2 demand in the presence of fixed stenosis

- VASOSPAM and significant narrowing


1. prolonged decreaed O2=unstable angina or infarction

-acute thrombis likely present


sudden cardiac death in CHD


how soon does the pt die? what most likely causes it? when does this happen?

1. death within 1 hour after onset of symptoms usually within minutes

2. malignant arrhytmia commonly present 


common presenting manifestation of CHD, frequent end point in patients with CHD propr to MI and imparied LV function



why are women often misdiagnosed when they have CHD? (3)

1. atypical symptoms: pain radiating to right arm, arm pain along


2. many women produce false negative stress tests since single vessel disease more common


3. elderly or diabetic womeon complain of general malaise, loss of appetite, vague abdominal pain so if they have RF, GET EKG!!



stable angina pectoris


what does this pain feel like? is it reproducible? what are 3 things that make it better? what is the pattern? what are 6 things that can cause this? what are things you might see to clue you into this?

chest discomfort described as 

tightness, pressure, aching, choking that is often REPRODUCIBLE WITH ACTIVITY that resolve after cessation of activity, relaxation, or NTG


positive levine sign substernal to left sternum, with crescendo/decresendo pattern 1-5 mins, less likely to happen in AM (lower threshold)

can be brought on by: exertion, exercise, emotional stress,cold weather, cigarettes, sex


physical exam may be normal between episodes, may see xanthomas from hyperlidemia, AV nicking from HTN/DM, s4 gallop during angina, changes in BP




what are the 3 tests you can do to help identify stable pectoris for CAD? what do they show?

1. EKG: 

normal between episodes

ST segment depression/T wave change during angina then normalize after angina passes


2. Stress EKG: most helpful non invasive tool

-increase workload with meds or exercise, compare resing and stress EKG for ischemia, may consider adding image to make it more specific, ability to detect dermines the amoutn of vessel involvment


3. coronary angiography- Gold standard for CAD

-tells which vessels are involved, degree of stenosis, and LV function


what is the drug you give for acute angina pectoris? or for prophylaxsis if the pt is going to be doing exercise? 

sublingual NTG


reduces LV volume preload and decreasing O2 consumption


does this by causing venodilation, so that it decreases the amount of blood heading back to the heart, decreasing the volume and decreasing O2 demands


what are the 7 drugs you put someone on to help with chronic stable angina?

1. beta blockers ATENOLOL, METOROLOL: decreases HR, contractility, and BP improving exercise tolerance



2. long acting nitrates isosorbide dinitrate


****can develope nitrate tolerance so need to dose in intervals!!****


3. Non dihydropyridine calcium channel blockers dilate ARTERIES, decreasing afterload, decrease myocardial O2 consumption


4. dyhydropyridine calcium channel blockers  amlodipine, nifedipine dilate ARTERIES, decrease afterload and myocardial O2 consumption

***best used in combination with a BB, reduce risk of HYPOTENSION**


5. diltiazem and verapamil used with nitrates, dilates arterioles decreasing afterload, decrease HR, and O2 consumption

***don't use in HF patients!!***


6. ranolazine chronic angina that isn't controled with the above

**increase QT interval, but won't cause arrythmia**




what drug do you not want to use in CHD in a patient that has asthma/COPD because it can cause bronchospasm?

nonselective beta blockers


Use selective beta blocker!!


what two drugs decrease the mortality post MI and in HF patients?

Beta blockers

Atenolol and metoprolol


what 4 groups of patients with CHD qualitfy for revascularization?

1. patients with unacceptable symptoms controlled with meds


2. 3 vessel CAD with LV dysfunction OR left main coronary stenosis that compromises Left anterior descending (LAD) LEFT main artery consider CABG!!


3. patients post MI with ongoing ischemia


4. acute MI


when should percutaneous coronary revascularization/catherterization be used for CHD?

what are the rates of restenosis with angioplasty, stent, and drug eluting stent? what do you do to compensate for this?

angioplasty restenosis rate: 30-40%

angioplasty with stent placement: 15-20%

drug eluting stents restenosis: 5-8%


1. single or 2 vessel disease

2. 3 vessels disease in pt that doens't qualify for operative


drug eluting stents helped decrease rates of restenosis a lot, however probles with late thrombosis so requires intense anti-platelet RX of ASA and clopidogrel


coronary artery bypass for CHD


what happens during this procedure? which two vessels are most commonly used? which one is the best one to use and why? what two factors increase mortality rates? 

coronary arteries are bypassed using arteries or veins, low mortality if LV preserved


saphenous veins and mammary arteries most commonly used


internal mammary artery graft has highest patency rate over time**BEST OPTION WHEN POSSIBLE because arteries last longer than veins**


mortality increase with age and EF



coronary vasospasm

what can bring this on? what does the spasms cause? what will the pt feel and what will you see on the EKG? what can happen if this doesn't resolve?

can be in normal cornary arteries or superimposed o atherosclerotic ones, the spasms cause the artery to close


often induced by cold, emotional stress, meds, and cocaine


angina at rest with ST elevation


**can progress to MI if symptoms don't resolve**


prinzmetals angina


what is this caused by? when do you get symptoms? who is it more common int? what does arteriography show? what are the two treatment options?

coronary ishchemia from vasospasms


symptoms at rest, usually in AM

women> men


ateriography shows normal looking arteries


Tx: nitrates and calcium channel blockers (dihyrdopyridines)


what percent of people with unstable angina remain unstable and need revascularization?


what percent improve medically? and what do you need to do before allowing them to leave?

20% will remain unstable and need revascularization


80% will get better clinicallly and need to get stress test once stable, if they produce a positive test then it might be an indication for revascularization


unstable angina


what is this? what are you at high risk for? how do you differentiate between this and a NSTEMI? what are the two presentations of this? what are two things you do to diagnose this? what are the two things you need to do for tx and the three drugs they need to be on?

angina at rest with minimal activity >10 minutes

GET VERY CLOSE TO HAVING A MI BUT DONT, RIGHT AT THE BRINK OF CELL NECROSIS BUT TISSUE HASN'T DIED YET, high risk for developing MI in following days/weeks so much treat aggressively and quickly


VERY SIMULAR TO NSTEMI, except in unstable angina negative cardiac markers


new onset: angina

accerating or cresendo angina in pt with previously stable angina (gets worse doing less activity)





EKG: ST depression, T wave inversion




2. full anticoagulation and antiplatelet therapy


 prasurgrel/ticagrelor/clopidigrel OR glycoprotein IIb/IIIa

3. nitrates, Beta blockers, and Ca-blockers to decrease MVO2



what percent of people with unstable angina will have abnormal EKG?



so worry about the 50% that have a normal one, still might need to work them up


since the pathology of unstable angina and NSTEMI are the same....what is the only thing that you use to tell them apart?

cardiac enzymes


ck-creatine kinase




these indicate cell death and that the scale has tipped over the point of unstable angina and cell death is occuring, this is a myocardial infarction


non-stemi acute myocardial infarction


what is this caused by? what is this nickname for these? relate to morality? why must we treat aggressively? how do you differentiate between that and unstable angina?

infarcts caused by prolonged ischemia

CAD to plaque rupture to platelets to clotting to thrombus


small infarcts that are unstable and could go on to cause a bigger infarct so that is why we treat aggressively

"incomplete infarcts" with lower initial mortality but high risk of re-infarction with HIGH MORTALITY


DX: like unstable angine with POSITIVE CARDIAC ENZYMES


acute myocardial infarction



what is the cause of this? what does it lead to? what does patient complain of? what does this most likely occur? how does the patient appeare (3)? what often accompanies this? what are 6 signts of this? what are the 5 things you use to diagnose this?

prolonged ischemia resulting from inadequate tissue profusion leading to cell death and necrosis


total occulsion CAD to plaque to rupture to platelets to clotting, to occlusive thrombus

"elephant sitting on my chest and the worst pain I have felt in my life"


often early in the AM since coronary tone, SEVERE PAIN,  anxious, diaphoretic, and distress, LV dysfunction


variable pulse and BP, S4 gallop, apical mitral regurgitation, cold, cyanotic, low CO, ST elevation



1. Creatinine kinase (CK) ALWAYS ELEVATED!

check CK-MB, specific to damanged heart muscle

2. troponins cTnl represents muscle breakdown, sensitive to small infarcts

3. leukocytosis


5. echo left ventricular function, identify mitral regurge


what are the treatments for a  acute STEMI? (3)




1. percutaneous coronary intervention to reprofuse tissue (CATH)

- goal: open artery within 3 hours of onset of symptoms

goal: open atery within 90 mins presenting to hospital

***If within hour and a half of hospital that does this, consider transfer!!! Must also have CABG CAPABILITY****


2. thrombolytic (finbrinolytic) therapy: done if no access to cath lab, t-PA (altepase)

-done when ST elevation >1 mm in tow or more adjacent leads

50% reduction in mortality if given withint 1-3 hrs of symptoms


3. post thrombolytic management

a. ASA ongoing

b. heparin 24 hours


acute myocardial infarction



what is the cause of this? what does it lead to? what does patient complain of? what does this most likely occur? how does the patient appeare (3)? what often accompanies this? what are 6 signts of this? what are the 5 things you use to diagnose this?

prolonged ischemia resulting from inadequate tissue profusion leading to cell death and necrosis


total occulsion CAD to plaque to rupture to platelets to clotting, to occlusive thrombus

"elephant sitting on my chest and the worst pain I have felt in my life"


often early in the AM since coronary tone, SEVERE PAIN,  anxious, diaphoretic, and distress, LV dysfunction


variable pulse and BP, S4 gallop, apical mitral regurgitation, cold, cyanotic, low CO, ST elevation



1. Creatinine kinase (CK) ALWAYS ELEVATED!

check CK-MB, specific to damanged heart muscle

2. troponins cTnl represents muscle breakdown, sensitive to small infarcts

3. leukocytosis


5. echo left ventricular function, identify mitral regurge


what are the treatments for a  acute STEMI? (3)




1. percutaneous coronary intervention to reprofuse tissue (CATH)

- goal: open artery within 3 hours of onset of symptoms

goal: open atery within 90 mins presenting to hospital

***If within hour and a half of hospital that does this, consider transfer!!! Must also have CABG CAPABILITY****


2. thrombolytic (finbrinolytic) therapy: done if no access to cath lab, t-PA (altepase)

-done when ST elevation >1 mm in tow or more adjacent leads

50% reduction in mortality if given withint 1-3 hrs of symptoms


3. post thrombolytic management

a. ASA ongoing

b. heparin 24 hours


what are 3 drugs taht might be used to try to help in a actue MI early on pre hospital or in the ED?

1. morphine sulfaste

2. aspirin in ED

3. nitro IV



what are the contraindications (4) and realtive contraindications (1) for thromboltic therapy for a STEMI?

absolute contraindications:

1. uncontrolled HTN

2. stroke within 1 year

3. cerebral hemmorahage

4. recent head trauma


relative contraindications: 

1. abdominal or thoracic surgery within 3 weeks


what are 3 drugs taht might be used to try to help in a actue MI early on pre hospital or in the ED?

1. morphine sulfaste

2. aspirin in ED

3. nitro IV



what medications is a person who had a STEMI put on after intervention or thrombolytic therapy?

1. BETA BLOCKERS: decreases wall tension preventing MI complications, decreases morality!

2. nitrates

2.5 heparin

3. asprin/clopidigrel

4. ACE inhibitors: improve short and long term survival, decrease LV remodeling post MI, great for large infarcts


5. alosterone blockers 

6. statins LDL goal


what are the drugs that you use to treat unstable angina or NSTEMI?

1. full anticoagulation and antiplatelet therapy


 prasurgrel/ticagrelor/clopidigrel OR glycoprotein IIb/IIIa

2. nitrates

 3. Beta blockers

4. Ca-blockers 


explain when the CK MB isoenzymes rise, peak, and fall?

rise: 4-6 hours

peak: 16-24 hours

fall: 2-3 days


explain when the troponin cTnI rise, fall, and stay elevated? what is diagnostic? what is good about this test?

rise: 4-6 

peak: 8-12

remains elevated: 5-7 days

dianostic if >.1, abornal if >.05


This test is the most specific and sensitve, can test for small MI


in a failing heart you get________

so the body tries to compensate by increasing ______

in a failing heart you get decreased stroke volume

so the body tries to compensate the decreased cardiac output by increasing sympathetic control to increase contractility, but the volume it is pumping out still isn't as much as a normal heart

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in HF, how doese the body attempt to increase cardiac output? 

1. if cardiac output is low and can't support normal circulatory function, body stimulates sympathetic stimulation to increase vasoconstriction and venous return


2. causes increase in RA pressure and fluid retention at kidneys because of decreased filtration rates from decreased cardiact output


3. cardiac output rises a little from fluid retention and increased venous return


4. continue to increase right atrial pressure, fluid retention accelerates this causes overstretching of the heart of edema of the heart muscle


5. cardiac output drastically decreases and the pt dies of DECOMPENSATION


sinus rythmn 



p waves?


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rate 60-100

rythmn regular

p waves yes and upright

QRS narrow

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sinus tachycardia




p waves?



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rate >100 bpm

rythmn regular

p waves yes 

QRS narrow


1. normal, seen with exercise

2. changes in SA node firing seen with CHF, lung disease, hyperthyroidism in eldery


sinus bradycardia




p waves?



Q image thumb


rythmn? regular

p waves? yes

QRS? narrow

causes? common rythmn seen in early stage of acute MI


sinus arrythmia




p waves?



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rate? slight irregularity of sinus rythmn

rythmn? slightly irregular

p waves? yes

QRS? narrow


1. phasic speeding up with inspiration  and slowing down with expiration 

2. variation in vagal tone as result of herring breuer reflex


premature atrial contractions



p waves?


other? 3

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ATRIAL RE-ENTRY or increase AUTOMATICITY, premature atrial depolarization

rate? single beat

rythmn? premature complex

p waves? yes, but looks different than a regular p wave

QRS? narrow


1. if early coduction can be blocked at AV node

2. if there is no preceeding p wave then it is called junctional premature beat (only difference)

3. can appear as bigeminy, trigeminy

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atrial fib




p waves?


other? 3

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rate? 400-600 atrial contractions (blocked at AV by refractory period)

rythmn? irregullarly iregular supraventricular 

p waves? NO!!! undulating baseline

QRS? narrow QRS



1. in new onset without med control: ventricular rate is very fast 120-180 bpm

2. goal in ED: slow rate with meds

3. Risk: BLOOD CLOT and stroke if they break off


atrial flutter




p waves?


other? 4 things!

Q image thumb

RENTRY CIRCUIT around annulus of tricuspid valve


250-350 flutter waves


no p waves, flutter waves

QRS narrow

1. most common presentation is 2:1 AV block with QRS ~150 bpm


3. after meds given to slow AV conduction given, most common form of block is 4:1 with ventricular rate ~75

4. carotid masage can help slow VR down, allowing flutter waves to be seen


paroxysmal supraventricular tachycardia (PSVT)




p waves?


who is it in? tx? 3 causes?

Q image thumb


abrupt onset and termination

carotid massage may help terminate




not usually present

narrow QRS


1. most in young healthy people without cardiac disease, can tell you the second it started and stopped. cardiovert with adenosine 90-95% of the time if carotid massage doesn't work

2. can be caused by coffee, alcohol, and excitement



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multifocal atrial tachycardia


what must be present?




what is it connected to? 


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enhanced automaticity

3 or more p wave morphologies present, irregullarly irregular, >100 bpm


usually underlying pulmonary pathology present


junctional escape rythmn


what is this caused by? 

when can it happen? 



p waves?

what can happen if sinus rate and AV rate are similar?

Q image thumb

caused by the sinus slowing or sinus arrest so that the AV node takes over

**can occur during sleep due to increased vagal tone, if sinus rate slows during sleep, this takes over**


40-60 bpm

narrow QRS

no p waves usually seen

ususally well tolerated

may compete with sinus rythmn if rates similar


premature ventricular contractions (PVCs)


what is this the most common of? 

reentry or automaticity?

QRS? p waves? rythmn?  after? shape? what type of hearts? pattern? 

Q image thumb

most common ventricular rythmn

reentry more than automaticity


premature QRS complex that is wide and biazarre

no p waves


irregularlly iregular, or regularly irregular (trigeminiy)

often followed by a pause

uniform or multiform

healthy and diseased hearts

bigeminy and trigeminy

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junctional tachycardia


what is this chracterized by? what can it be confused with? what are two clinical connections? 

very uncommon, but discussed for ACLS




may be confused with PSVT but slower rate


clinical: digital toxicity, somtimes inferior wall MI


ventricular tachycardia

what is this defined as?

what is sustained mean?

is the heart diseased?

hemodynamicaly stable?

what does it deteriorate into?

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3 or more consective PVCs at rate >100


sustained: >30 seconds

more often uniform and regular, but can be irregular like torsades

seen in presence of structual cardiac pathology

rarely hemodynamically stable

deteriorates into vfib


torsades de points


what type of vtach is this?

what is it associated with?

what does it turn into?

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"twisting of the fingers"

polymorphic vtach, very fast, very dangerous, 200-300, pt unconcious


associated with prolonged QT interval


difficult to treat and turns into vfib

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ventricular fibrillation


what is this? does it contain any waves? 

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terminal arrhythmia associated with death

DEFIB ASAP (if you are outside the hospital pt will likely die but if happens at the hospital, the pt will likely live depending on how long it takes you to defib them)


UNDILATIONS ONLY, choatic oftren preceeded with vtach

rarely seen in pts with structually normal hearts


mitral regurgitation


what happens in the pathophys for this? what can you get? what are the common 3 symptoms patient presents with?  what are the five descriptors used to describe this? what are two things you might see on EKG? what will you see on echo? 

most common valvular condition


left ventricle backs up into left atria, both dilate overt time

increase in LA pressure, and LVEDV

backup causes pulmonary sxs


sx: DOE, orthopnea, symptoms of left HF and eventually right HF if backs all the way up through the lungs


Holosystolic systolic murmer (heard throughout entire systole), THRILL, HIGH PITCHED BLOWING, S3 gallop if severe


EKG: LA enlargement, often Afib!

echo: LA and LV dilation but decrease in function




In MOST murmers, what would you expect to see in results when squatting down and standing up quickly?



squatting down: increases the volume of the heart and venous return making the murmer WORSE


standing up: decreases the  venous return making the murmer less noticeable



mitral valve prolapse is opposit!! since large leaflets, making the heart bigger actually decreases the murmer (sqautting) because the leaflets fit better. Standing makes it worse because now you have the extra tissue!


what are the four tx options for mitral regurg? what must you consider regarding surgery?

1. decrease activity

2. ACE INhibitors esp in HTN or HF, decrease preload and after load


3. diuretics decrease preload

4. sugey!! if decreased EF or LV dysfunction with progressive sxs

***the timing of sugery is really important because need to do it before you get left ventricular failure from response to stress, otherwise the valve only helps to much****


repair better than replacement here


what are the five most important descriptors for mitral regurg?

1. Holosystolic systolic murmer (heard throughout entire systole), 2. THRILL



 5. S3 gallop if severe



what are two random defomirites that are associated with mitral valve prolapse?

high arched palate

pectus excavatum!! 




mitral valve prolapse


What happens in this? what are the two causes of this? which is most common? and what two systemic conditions can cause this? what does this present with for symptoms? what else can be present?  what are the 3 key PE things you see?

abnormal connective tissue growth causing the leaflets to buckle

caused by: 

1. familia hx, most common autosomal dominant (only get growth on valve)

2. systemic connective tissue disease MARFANS, EHLERS danlos



SXS: ususally asymptomatic but in women presents as ATYPICAL CP thats "FLEETING" with palpitations, Arrythmias present


mid to late systolic click between s1 and s2 (tensing of chordae), high pitched late systolic murmer, 



mitral valve prolapse 

what are the 3 PE things you might find to indicate this?

1. mid to late systolic click between s1 and s2 (tensing of chordae)

 2. high pitched late systolic murmer 



what are the 3 tx options for mitral valve prolapse?

1. reassurance #1!!!!!

2. Beta blocker if CP or arrythmia

3. surgery if MR severe (VERY RARE!!))


mitral stenosis


what condition cases this? what happens to the valve..what is the nickname for this appearance? does it effect the lungs? how wide does the opening need to be? what becomes the issue? what are the symptoms? hat rythmn is common? what would echo show? what are the four PE findings for this? 

only caused by rheumatic fever

leaflets thicken and calcify narrowing the space cause "FISH MOUTH DEFORMITY"

can back up to the lungs

diastole becomes the issue because it can't fill

SXS: DYSPNEA, orthorpnea, pulmonary edema, AFib common

DX: eco: abnormal valve motion, LAE

LA DILATION, LV NORMAL WITH LVEDP NORMAL!! s1 and s2 loud, opening snap after S2, diastolic rumble low pitch from slow blood flow into LV


what are the 4 PE findings for mitral stenosis?

1. LA DILATION, LV NORMAL WITH LVEDP NORMAL!! (just not getting blood) 

2. s1 and s2 loud

 3. opening snap after S2

4. diastolic rumble low pitch from slow blood flow into LV


what are the 4 treatment options for mitral stenosis?

1. decrease Na consumption, direutics

2. control afib if present

3. preferred intervention: precutaneous balloon vulvoplasty (alternative to surgery, first option for most patients)

4. surgery if repair by #3 doesn't work/can't work


aortic stenosis



what are the 3 causes of this? which is most common? what the two many symptoms you see with this? what is the hallmark in pathology? what must it narrow to? what are the 6 characteristics of this condition?


three main causes:

1. born with bicuspid valve

2. rheumatic fever

3. IDIPATHIC, wear and tear in eldery (sclerocacific), MOST COMMON

sx: DOE, angina pectoris, syncope with exercise ( periphreal vasodilation with decrease CO)

hallmark: left ventricular pressure higher than aortic pressure in systole, L sided heart failure, angina pectoralis (since heart has to work so hard to overcome increase in pressure, it requires more blood but the opening for coronary arteries is on the other side of this valve!) 



carotid pulses climb, apex displaced, s4 gallop, systolic murmer with cresendo/decresendo, sawing gratting sound during systole, harsh low pitch


what are the 6 main things to remember about aortic stenosis sounds?


what two pt symptoms key?

1. carotid pulses climb

 2. apex displaced

3. s4 gallop

4. systolic murmer with cresendo/decresendo

5. sawing gratting sound during systole

6. harsh low pitch


patient sxs: syncope, angina pectoris


what must you determine aortic stenosis from? what do you do to determine between the two?

aortic sclerosis


thickening/calcification without fusing, don't have symptoms


need to get echo to determine between the two?


what do you need to do before surgery for aortic stenosis? what does this help you determine? 


identifies gradient between LV and aorta, and determines the presence/absence of CAD since these can opften go together.


**want to distinguish if pt gets angina pectoris from block in the coronary=CHD, or just no blood flow =aortic stenosis*


what are the 3 surgery options for aortic stenosis?

if surgical candidate, get surgery


1. mild w/o symptoms: monitor, ACE, ARBS


2. SURGERY!!! replacement with tissue or mechanical valve


3. balloon valvuloplasty/transcather aortic valve implant- palliative for those who aren't surgical candidate...except in young adults


where do you hear aortic stenosis? what can help make it easier to hear?

2nd RICS

patient sitting leaning foward


what do you hear mitral stenosis and what can make it easier to hear?



left lateral debiscus position


tricuspid regurgitation


where do you hear it? 

during what?

where does it radiate? 


whats often elevated?

what can it icnrease slightly with?


heard: lower left sternal border

holosystolic, pansystolic

radiates: right sternum to xifoid area

blowing noise

JVP often elevated

increases slightly with respiration



pulmonic stenosis


where do you hear this?

where does it radiate?

what might you hear?

when do you hear it? 

heard: 2-3rd left intercostal spaces


readiates to: left shoulder and neck


early pulmonic edjection sound heard


timing: systolic



WHat does it encompass?

who do we see it in? why?

what can cause it or it be a result from?

is it reversible?

what is it characterized by and what are the three types?

CLinical presentaiton?



  • encompasses physiologically inappropriate sinus bradycardia, sinus pause, sinus, arrest, or episodes of alternating sinus tachy and brady. 

most often in elderly: caused by scaring of the hearts conduction system

could occur in an infant who had heart surgery

  • may be causes of exacerbated by digitalis, calcium channel blockers, beta blockers... so on and so on. 
  • also could result from underlying collagen vascular or metatastic disease or surgical injury

REVERSIBLE if caused by digitlalis, quinidine, beat blockers , or aerosol propellants

  • AV block is characterized by refractory conduction of impulses from the atria to the ventricles through the AV node or bundle of HIS and divided into 1st degree, 2nd degree (Mobitz 1 or mobitz II) and complete 3rd block
    • FIRST degree heart block: all atrial beats conducted to the ventricles, PR interval is greater than 0.21 seconds
    • SECOND degree heart block: not all atrial beats are conducted to the ventricles 
      • Mobitz type 1 (wenckebach) is has lengthening of PR interval with shortening of RR interval. All atrial impulses will not be conducted to the ventricles. Typical pattern is repeated cycle of: normal PR interval, long PR, longer PR, even longer PR, and dropped beat. This is due to abnormal conduction in AV node
      • Mobitz type II: non conducted atrial beats. block within HIS bundle system. secondary to organic disease involving infra nodal system. can progress to complete heart block
    • ​THIRD degree heart block: (complete) complete dislocation between atria and ventricles. due to lesion distal to the HIS bundle

Clinical Prenenstation:

most asymptomatic, but may have syncope, dizziness, confusion, HF, palpitations, or decreased exercise tolerance

  • 1st degree AV conduction block usually asymptomatic. 
  • higher grade blocks may have weakness, fatigue, light headedness, syncope



permiinnant pacing

1st degree AV conduction block require no tx

  • only effective long term tx for other AV conduction disorders is permanent cardiac pacing
  • temporary transthoracic or transvenous pacing should be followed by permanent pacing when Mobitz type II or complete heart block dx.

A image thumb

sick sinus syndrome

sinus arrest with alternations of paroxysms or atrial tachycardia and bradyarrythmias


caused by sinoatrial disease


tx: permanent dual chamber pacer with auto ICD


chronic artieral insufficiency



1. intermittent claudication, progressing to pain at rest

2. PALE ON ELEVATION, DUSTY red when laid down

3. ulceration on the toes or points of trauma

4. COOL temp of limb

5. thin, shiny, atrophic skin, loss of hair on legs




what size arteries does this involve? what forms and where? what does this make and what is it made up of? what does it lead to? what are three example conditions that are caused by atherosclerosis?

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medium and large artery

gradual plaque formation on the intima of the medium/large vessels of ATERIES, material grows under the endothelia layer creating plaques: fat cholesterol and calcium


leads to:

gradual reduction in aterial lumen that prevents oxygen rish blood from geting to the tissues causing ischemia


the location of the arteries determines the name of the disease AKA

1. coronary heart disease (coronary artery disease)

2. cartotid artery disease

3. periphreal vascular disease


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what are 9 risk factors for atherosclerosis? 


which two are the most important? 

1. smoking

2. diabetes mellitus

3. dyslipidemia

4. elevated CRP

5. hypertension

6. family hx in 1st degree relative

7. males

8. inactivity


periphreal vascular disease


what is this condition? what type of involvment, occuring where? what is it the leading cause of? what are the 3 MOST IMPORTANT RF? what are the four must important symptoms, which one is most important? when does this come on and when does it stop and where does it occur? in sever disease, what are four things that can happen?

atherosclerosis of the extremities, segmental involvement often at branching points!!!!


leading cause of occludive arterial disease in pts over 40



claudication symptom most common (pain, aching, cramp, numbness or fatigue of muscle during exercise and relieved by rest!! claudication symptoms occur distal to stenosis), dimished distal pulses, hair loss with shiny skin appearance, with elevation of extremities get pallor of soles of feet and rubor (redness) in the leg, bruits in artery


in severe: pain at rest, ulceration, necrosis and gangrene from ischemia from lack of blood flow


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in periphreal arterial disease, if you have a clot in these areas, where will the claudication symptoms radiate?



femoral popliteal

aortoiliac: radiates to butt, hip, and thigh pain


femorapopliteal: radiates to calf 


claudication is.....

distal to the site of stenosis



Think about it. if you have a clot in your leg, your blocking the distal tissue from getting blood, so this is where the ishchemia happens and this is where the symptoms appear!


periphreal arterial disease

what are the three tests you can do to help diagnose it?

1. ankle/brachial index (higly sensitive and specific, compares systolic BP in brachial atery and posterior tibial artery) values less than .9 suggest PAD (ankle/arm) PRESSURE IN THE LEG DECREASES since isn't being profused with blood


2. duplex US, pulse wave doppler


3. contrast angiography **GOLD STANDARD** and definitive, done before endocasulcar or surgical revascularization


periphreal arterial disease


what are the 5 treatment options for PAD?

GOAL: prevent progression


1. lifestyle modification

-control glucose, BP, decrease BMI, stop smoking!!!


2. exercise: suprevised walking program

walk until pain comes on, stop, rest, and then begin again, creates collateral artery formation 30 mins 4x week PROVEN TO WORK BETTER THAN ANY DRUG!!


3. asprin/clopidigrel as secondary prevention to prevent against MI, STOKE, Death


4. cilostozol: only drug shown to help improve the symptoms of PAD other than a walking program, but not great, increased walking distance by 35%, this is PDE inhibitor, increases cAMP and prevent platelet aggregation and promotes flow by vasodilation


5. revascularization



how much can a supervised walking program increase pain free walking by?

150%....most important because it has shown to work better than any drugs!!


periphreal arterial disease


explain in extreme cases what the two options are for revascularization? Who is it  appropriate for? 



1. endovascular revascularization: angioplasty with a stent to restore blood flow, decreased complications over surgery


2. surgery to bypass: fancy plumbing, anticoagulation with heparin to prevent propogration of the thrombus





acute aterial occlusion


what is this caused by and why is it acute? what are the 5 common causes of this? what are the four risk factors that you want to control? what are the 5 symptoms? what are the three things you use to diagnose it and which is the gold standard?  what is the treatment option? and what are the 2 tx options if it is severe?

Q image thumb

 caused by embolism since happens quickly, something travels and blocks the artery , thrombus in situ


most common causes: afib, ventricular aneurysm, anterior MI, prostetic valve, thrombis at site of stenosis


RF: smoking, control of DM, HTN, hyperlipidemia so NEED TO CONTROL THESE!!!


rapid onset of pain, parenthesia, numbness, coldness in involed extremityloss of distal pulses


DX: doppler US (DO FIRST), ABI, angiography gold standard



1. anticoagulation with heparin to prevent propogation of the thrombus

2. if severe: reprofusion 


-streptokinase, urokinase, tPA

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what are the symptoms that suggest an acute arterial occlusion is an emergency?

6 p's

1. pain

2. pallor

3. pulselessness

4. parenthesia

5. poikilothemia

6. paraylysis


these indicate tissue could die and threatens limb vitality so what to get vascular on board stat to hopefully prevent amputation

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chronic venous insufficiency


what does this most commonly come from? what four other things can cause it? what are the 2 contributing factors to this? what are the 6 symptoms/exam findings you will see? when is it the worse? what can it lead to? what are the three tx options?

Q image thumb

can result as consequence of both DVT (75% of the time)  and superficial venous insufficiency


other causes: varicose veins, trauma, neoplastic venous obstruction


veins become functionally inadequate due to damage of the valves which results in bidirecitonal flow, and loss of venous wall tension that results in stasis


gradual progression of leg edema from ANKLE TO CALF!! OFTEN PAINFUL!!! NORMAL LIMB TEMP! pools at the bottom. shiny skin, skin ulcers, cyanotic aching when standing, edema worse at the end of the day, and best in the morningsecondary skin changes ulcers above the ankle on medial aspect leads to stasis dermatitis with brownish pigmentation and stippling


Tx: ruduce swelling and prevent breakdown

1. intermittent leg elevation

2. compression stockings

3. calf exercise


if chronic venous insufficiency transitions into stasis dermatitis, how do you treat it?

wet compresses

hydrocortisone cream

possibly zinc if chronic


aortic aneurysm


what is the problem with this condition? what is the pathophys? what are three things that can cause it? what are the four symptoms you see? what are the two diagnostics you wanna do, which is the one of choice?

dilation of a segment of blood vessel,  thoracic or abdominal


most are asymptomatic until they rupture which is the issue, so goal is to identify them before they get to this point

weakness in vessel wall and subsequent dilation of vessel caused by genetics, atherosclerosis, medial cystic necrosis or damnage to intima


suddent onset, "ripping or tearing" abdominal, flank (abdominal), or back pain (thoracic), hypotension, shock, pulsatile mass



1. abdominal US **study of choice**

2. CT angiography or MRA (magnetic resonance angiography) prior to intervention  OR for thoracic



who is important to screen for aortic aneurysm? 3

1. male

2. smoker

3. >6o years old with PAD and family history of AAA


explain the risk of rupture for aortic aneurysm based on the size and what are the tx reccomendations at each stage?

1. watch it and monitor it 


2. >5cm: 20-40% over 5 years rupture, surgical to remove ELECTIVE SURGERY ADVISED!!


3. >6cm: 15% risk it will rupture annually, ALWAYS SURGERY, REMOVE IT!!!!




1. open surgical repair (open with graft placement)

2. endovascular (no surgical candidates, stents placed to reduce risk of rupture


prognosis of aortic aneursym is related to what two things?

1. size of aneurysm

2. CAD


what is the mortality rate of ruptured aortic aneurysm?



thats why its important to try to monitor it and find it early!!!!


aortic regurgitation


is this more common in m/f? what are four things that can cause this? what is the pathophys about what happens in this? what is important to note about the symptom onset??

75% in males

failure of the aortic valve to close all the way causing backflow into left ventricle


1. rheumatic heart disease

2. endocarditis on different valve

3. bicuspid valve

4. connective tissue disease


increase LVEDV, causing LV dilation leading to LV dysfunction with decrease EF and backs up to the lungs

1. blood still flowing from the RA

2. blood backing up from the aorta


*****LV failure often preceeds symptoms by 10-15 years so you MUST do serial echo/dopple to analyze to catch it before it is too late*****


aortic regurgitation


what are 5 interesting presentations that can occur at the arteries/pulses with aortic regurg?

1. Water hammer pulse: rapid rising and collapsing of the pulse, bounds against finger


2. Quinke's pulse:  alternating flushing and paling at the skin at the root of the nail


3. pistole pulse over femoral artery


4. Derosiez's sign to and from murmer over femoral artery


5. arterial pulse pressure widening: larger systolic and smaller diastolic so the difference is larger


aortic regurge


where do you hear it? what does it sound like? what can you feel? what happens with the apex?


1. apex displaces laterally/inferiorlly

2. diastolic thrill along left sternal border

3. S3 with "blowing" diastolic decresendo murmer

4. best heard with pt leaning foward 2-3rd LICS


what are the 3 test you use to dx a aortic regurg?

1. EKG: LVH over time


2. echo: LV dysfunction later on, can see the aortic regurg jet detectable and semi quantifiable best!


3. cath: tells regurg amount, LV dysfunction, intracardiac pressure (not usually need in young pt)


what are the 3 treatment options for aortic regurg?

1. vasodilators: ACE/hyrdralizazide to decrease afterload


2. diruertics: decrease preload


3. Surgery with tissue or mechanical valve replacement


what is the most common cause of HF?

coronary heart disease
 aka MI/ischemia accounts for 75% of all HF cases!!!




heart failure


explain the patho for this? what is the most commong cause of HF? what are the other 4 things that cause cause it? what is something important you want to remember about HF as a condition?

a physiologic state in which abnormal cardiac function prevents the heart from pumping blood at a rate necessary to meet the requirements of metabolizing tissues

to compensate you create abnormally elevated diastolic volume/pressure


this process causes a progressive weakening in the myocardium and the consequences are HEART FAILURE!!


1. CHD: MIs/ischemia account for 75% MOST COMMON CAUSE

2. primary pump failure

3.  valvular disease

4. congenital heart disease

5. longstanding uncontrolled HTN


***keep in mind HF is a dynamic state, so patients can enter and leave it when exposed to stimuli****


what must you remember about the tx of HF? why are the number of deaths increasing despite increase RX?

it must be individiualized for each patient!!!


there is an increase in the number of deaths despite improvements in Rx because

1. the baby boomers are getting older and there are just more people with this condition

2. increased salavage of people in strokes



systolic heart failure (2 causes)

diastolic heart failure (4 causes)


what do you need to remember about these?

1. systolic heart failure: primary contraction abnormality

can get O2 to the tissues

causes: MIs, dilated cardiomyopathies


2. diastolic heart failure: impaired ventricular relaxation

elevation of ventricular filling pressures because if the ventricle can’t relax the heart has to work harder to fill it, backs up to the lungs


causes: chronic HTN with LVH, hypertrophic cardiomyopathies, acute ischemia, restrictive cardiomyopathy


keep in mind these usually occur together!



1. acute HF (1 cause, 4 symptoms)

2. chronic HF (3 causes, 2 symptoms)



what is something to keep in mind about the relationhip of the two?

1. ACUTE HF: caused by LARGE MI

sudden onset of symptoms, systolic failure, hypotension, and pulmonary edema

immediately the heart stops working correctly, everything gets backed up!!!

2. CHRONIC HF slow and gradual, cause by dilated cardiomyopathy, chronic valvular insufficiency, low EF

a. bp maintained till late

b. periphreal edema common



keep in mind an acute episode can superimpose on a chronic HF, exacerbation of HF






1. Left sided HF (leads to what? 2 causes)

2. Right sided HF (associated with what? 2 causes)


what is the most common cause of right sided HF?

1. left sided heat failure: inadequate CO with pulmonary congestion    

causes: post MI, aortic/mitral valve disease


2. right sided heart failure: associated with peripheral edema, hepatic congestion   

causes: COPD/pulmonary HTN, pulmonic stenosis



most common cause of right sided HF is left sided heart failure!! backs it all up!!


explain the pathogenisis of:

1. backward HF (where does the fluid go?)

2. forward HF (what does this cause via what system?)

1. backward HF: inadequate ventricular emptying so the pressure in the atrium and venous system increase because the blood keeps coming and the ventricle is failing, causes transudation of fluid into interstitial spaces


2. forward HF: inadequate forward CO, causes Na and water retention since kidneys aren’t being profuses, mechanism: renin-angiotensin-aldosterone system


what are the bodys 2 main compensatory mechanisms if not getting enough blood profusion because of HF?

what are the two main mechanisms? how do they accomplush this? what is the consequences of these actions?

1. redistribution of CO: blood flow goes to vital organs first like brain and heart with reduced flow to skin and muscle via adrenergic nervous system! aka sympathetic nervous system


2. Na and water retention since kidneys not profusing via renin-angiotensin system: accumulation of fluid and increasing venous return primarily from sympathetic nervous system with NE release




**consequence of this is volume overload and increase afterload that perpetuates the problem**keep in mind they are easy to turn on but hard to turn off....just like men.


explain how the bodies adrenergic nervous system is helpful and harmful in a pt who has HF?

Benefit of increased  NE:

increase HR, contractility, and systemic vascular resistance helps to maintain arterial perfusion pressure


negatives of increased NE:

-elevated systemic vascular resistance increases burden or afterload and increases O2 requirement, making the heart have to work harder

-long term elevation of catecholamines leads to progressive myocardial damage and fibrosis=maladaptive remodeling or the shape of the ventricle changing from a cylinder to a sphere, perpetuates the problem


what is the most important/potent vasoconstrictor in the body? what specific thing does it constric?

angtiotensin II


causes arterioles to constrict increasing BP and SVR


what is aldosterone and what does it do in the body?

aldosterone is a mineralcorticoid hormone that causes increased renal Na and H2O reabsorption


what does long term activation of antgiotensin II and aldosterone lead to and why is this bad in HF patients?

what does it do to the mycardium and what structual changes does it cause?

leads to myocardial thinning and fibrosis aka maladaptive remodeling


this over time changes the shape of the ventricle from a cylander to a sphere making it able to pump less effectively, this mean its exacerbates the problem


***keep in mind the renin-angiotensin system is good, but but bad over time esp in HF patients because its activation long term causes deterioration of the heart function, decreasing CO, and prepetuating the renin system and making everything worse!***


what are the four stages for heart failure?

1. no limitation of physical activity

2. slight limitation of physical activitiy, some activities so SOB on exertion

3. markled limitation of physical activities, like ADLS cause SOB

4. symptomatic at rest or with minimal activity, unable to enage in physical activity


what are the 7 presentations of a patient that would suggest they are experience HF?

1. dyspnea

2. orthopnea

3. paryoxysmal nocturnal dyspnea

4. abdominal symptoms

5. cerebral symptoms (decreased profusion to brain)

6. unexplained weight gain from swelling in the legs

7. acute pulmonary edema ***MEDICAL EMERGENCY WORST POSSIBLE SITUATION....patient drowning in their own fluid backing into the alveoli!!!****


if you suspect pulmonary edema in a patient with HF, what test do you need to do STAT? what are the measurements that would cause you to be cocerned and confirm your dx?


pt is drowning from the inside out!!


pulmonary capillary wedge pressure via right heart cath

>20 mmHg: concerned with interstitial edema

>25 mmHg: concerned with pulmonary edema


what are the 7 physical findings that you could find in a pt suspected of HF? 

1. tachycardia common

2. crackers

3. S3 gallop low in pitch in early diastole (associated with HF)

4. increased JVP

5. hepato-jugular reflex (push on liver JVD goes up)

6. cardiac cachexia "wasted appearance"

7. pleura effusions with high levels of pulomary pressure!!




what are the three test you could do to diagnose HF and what would you excpect to find on each one? 


which one is the best? 

1. CXR:




2. ECHO DOPPLER #1 best non invasive tool


3. BNP:

used for acute ventricular dysfunction or symptomatic heart failure, helps to distinguish SOB between cardiac and pulmonary cause



what are the 6 goals of treatment for HF?

2. treat underlying cause

3. reduction of cardiac workload (preload/postload)

4. control excessive Na/water retention

5. early initiation of ACEI/ARB (hydralazine in blacks)

6. enhancement of cardiac contractility


what type of diet is reccomended for HF patients? 



what distinguishes a person as having end stage HF? what are the two options for a pt is this senario and what does it provide for the pt? 

when patient no longer is responsible to any RX


1. LV assist devices (implantable pump device connected to external power supply)

-decreases cardiac workload to buy time for transplant

-can leave the hospital while waiting

-often used since not enough heart donors

complications: thrombis formation, infection


2. cardiac transplant

complications: rejection, infection, CHD in donor heart


explain the drugs that are used to treat preload for HF? (2)

1. direutics 

-loop dieurtics most potent (furosemide, torsemide)

-MUST monitor BUN, creatine, UA, and glucose

-can cause hyperurcemia and metabolic acidosis

-k sparing dieuretics


2. nitrates


explain the drug class that are used to treat afterload associated with HF? why is this important?


(not looking for specific drugs on this card)


-always increase in HF bause of the neural and humoral influences that constrict PV and increase SVR

-increase in SVR decreases CO and causes back flow to lungs


treat with vasodilators:

decrease SVR

increase CO

decrease pulmonary capillary wedge pressure

decrease symptoms

decrease mortality


what are the three vasodilator drugs are typically used in treating the afterload in HF?


(3 drugs)

1. what two things cause it cause as SE? what can it do? what does it decrease?

2. what doesnt't this cause? 

3.what does this inhibit? what does it do?

1. ACE inhiborts

-caution hypotension, dry cough

decrease mortality by >25%

decrease remodeling (fibrosis, wall thinning, cell death)


2. angiotensin II receptor blockers

less protection against remodeling than ACE but don't cause cough


3. sacubitril

neprilysin inhibitor

degrades vasoactive peptides


what is the new drug combination


used for? 


what does this do? what are 3 SE?



1. slowed HF progression better than a ACE alone

2. se: hypotension, angioedema, hyperkalemia



when are biventricular pacers indicated in HF?

 what does this do for a HF pateint?

if QRS >.12 and severe refractory CHF


improves symptoms and quality of life and EF


this is called "cardiac resynchronization therapy


what is are the primary and secondary indications for a ICD?


secondary: resuscitated cardiac arrest/vfib or hemodynamically unstable Vtach

primary: EF


what are the two types of categories of HTN and which is most common?


what are five things that can cause the second?

essential hypertension:

aka idiopathic/primary 95% of cases, etiology unknown


secondary hypertension: 5% of cases

1. estrogen use increases RAAS

2. intrinsic renal disease (any form of chronic renal parenchymal disease)

3. renovascular HTN

4. endocrine HTN

5. pregnancy



secondary HTN:

due to renovasular disease


what is this and how does it work? what are the two types and who do you find them in? 

2 types of renal artery stenosis that increase the production of renin, cause decreased BF to the kidneys increasing BP


1. fibromuscular hyperplasia (FMH)

-young adults

-BP increases renal function preserved

tx: angioplasty to increase BF to kidney


2. atherosclerosis of renal artery

-older patients

-elevated BP not responsive to meds

-renal function impaired, intervention may or may not help


what are the 7 things that can influence/cause HTN?


environmental factors

sympathetic nervous system hyperactivity

renin-angiotensin-aldosterone system

defect in natriuresis (getting rid of Na in the body)

intracellular Na and Ca

insulin resistance


what are 5 exacerbating factors for HTN that can make it worse?


Na in diet

cigarette smoking increases NE


excess alcohol


explain the ways in which HTN effect and contribute to end organ damage in:


1. heart

2. brain 

3. arteries

4. renal


-RF for CHD

-LVH diastolic dysfunction POWERFUL PREDICTOR of morbidity and morality, in 50% of people with HTN

-HF over time



the major predisposing cause of STROKE

rupture of micro hemmorages from increase BP

correlate closely with SYSTOLIC BP


3. PVD



nephrosclerosis: narrows kidney arterioles causing glomerular damage and decreased function, HTN accelerates this procress, common in Blacks



since HTN is usually asymptomatic, what symptoms let on a pt might have it? 8

1. SOB, DOE from LVH


2. TIA, stroke, hemmorage


3. MI, angina, HF


at what point to do you treat HTN in people and the elderly?

BP >140/90 requires tx in those , including those with DM or CKD


BP >150/90 >60 year old, a little more liberal with the elderly


what are the physical exam findings that can suggest a patient has HTN since it is mostly asymptomatic? 6 

1. narrowing of the arterioles A/V

2. A-V nicking (arteriosclerosis where artery looks like it is crossing the vein)

3. silver or copper wired appearance

4. hemorrhages or exudates

5. papilledema

6. bruits

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what are the 3 most important labs you want to check in a patient you are concerned about HTN?

1. creatine, BUN


2. electrolytes Na and K (want to check K cause you will likely put them on a dieuretic and this can cause hypokalemia)


3. lipid levels: TC, LDL, HDL, triglycerides


what drugs will you typically use to treat HTN in


black populations

thiazide and/or CCB


what drugs will you typically use to treat HTN in


pts >18 with CKD

1. ACE

2. ARB if can't tolerate ACE


use these regardless of race or diabetes status if they have CKD!!!!!!! big hint there!!


what drugs will you typically use to treat HTN in


post MI patient

combine BB with ACE/ARB



BB are no longer reccomended for HTN but they can help in adjunct in patients post MI even though it doesn't actually help treat the HTN


what is the goal of treating HTN? what are you trying to reduce risk of? what should you focus on? what should you look for a in a drug?

decrease endpoints including MI, Stroke, LVH, PAD, all cause cardiac mortality, HF, and renal failure


try to find drugs that treat more that one co-morbidity



focus on SYSTOLIC BP as the most important aspect for reducing morbidity and mortality


which number should you focus on when trying to reduce morbidity and mortality?



what are four non pharm ways to decrease HTN?


weight reduction, aerobic activity

decrease alcohol, Na intake DASH DIET

smoking cessation


what is the reccomended 1st choice for the majority of patients when treating HTN?

thaizide dieuretic


thiazide dieuretics for HTN


who are these most potent in 3? which patients should you avoid these in? what is the doseage? what can they cause 4? 

1. 1st line therapy and should be included in ANY drug therapy


2. more potent in blacks, elderly, obese

3. avoid in patiens with hyponaturemia and gout


5. can cause hypokalemia, hyperurcemia,  hyperglycemia, abnormalities of lipids


beta blockers in tx of HTN


what do they decreaes? who are they helpful in 4? what are the 4 SE you need to be aware of if prescribing to a pt?

used as a 2nd or 3rd line drug because of increased risk for stroke


1. decreases CO

2. helpful in pts with other comorbid disorders like:

-angina pectoris, post MI, migrain headaches, essential tremors


3. SE: exacerbation of bronchospasms in nonselective, bradycardia, worse acute HF, masks signs of hypoglycemia in diabetics!!


ACE inhibitors


who is this the DOC in 4? what does it prevent? what does it have a synnergistic relationship with ? what does it inhibit? what are 2 negative SE?

inhibits bradykinin degradation


significant efficacy improvement when combined with diuretic SYNERGISTIC RELATIONSHIP


ANTI-HTN DOC in diabetics, CKD, LV dysfunction, HF and prevents remodeling!!


SE: dry cough in 20%, angiodema


angiotensin II receptor blocker (ARBS)



like ACE but no cough!

renoprotective in diabetics


direct renin inhibitor for HTN



i. binds with renin, stopping it from working and blocking the initiation of RAAS

        ii. increased cost vs ACE but similar in efficacy


calcium channel blockers for HTN


what are the two types? what are the 3 SE of the first class? what are the second class used for and who don't you use them in? what can they cause and what shouldn't you combine them with?

preferrable in blacks and elderly

1. dihydropyridine

reflex tachycardia, headaches, periphreal edema


2. nondihydropyridines

used for arrythmias

can exacerabte HF so don't use in HF patients, bradycardia, don't use with BB 


alpha receptor blockers


what can it cause 2? who else can it be helpful in? what can happen if you take it too long?

relax smooth muscle and decrease SVR

tachyphylaxis common with prazosin


SE: postural hypotension and syncope following 1st dose, palpitations, headache

useful in BPH (prostatic hypertrophy)


centrally acting agents


what is the MOA? what can it cuase? what is one benefit to increase compliance? 

methyldopa, clonidine


stimulate CNS presynaptic alpha-2 receptors reducing efferent peripheral sympathetic flow


postural hypotension but benefits they come in a patch and are effective for 7 days


what is the initial TX for HTN and what is the exception to this?

initial tx: thiazide dieuretic


exception: diabetic, move right to the ACE and add dieuretic later, multiple agents are often needed here


what are the guidelines for txing HTN?


this is a lot of info so probs just read through it!

1. Initial rx: thiazide diuretic with some exceptions

if diabetic start on ACE then use thiazide diuretic later, multiple agents often needed


2 .    initial low dose and follow up in 4-6 weeks


3.       titrate up to moderate/high dose before adding a second agent exception:

           i.     if the first drug is a thiazide, low dose is sufficient and shouldn’t increase the dose so add the second med instead of increasing the dose


 4. second drug would be BB, ACEI, or Ca blocker Exception:

           ii.     if BP is >160/90 can start dual Rx at the same time


5.  most patients will be controlled with 2 drugs, but if need three, usually diuretic, ACE and CCB



what are the 3 types of ambulatory monitoring you can do and what are the benefits of each one?


aka how long do they record? which ones are commonly used? when do you use them?

1. Holter monitor

-2 lead EKG

-24 hours


         2. external event monitor

            - most patients use this now

   -allows for monitoring for weeks or more

     -helpful when the experiences are spread out and infrequent symptoms

        -when patient has symptoms they push a button and it stores the information


          3. implantable loop recorders

     -monitoring for up to 3 years

           -hold up to the phone and the receiver the cardiologist has interprets it



what are the 3 reasons you would want ambulatory monitoring of a patients cardiac symptoms?

1. arrythmia detection and correlating it with patient symptoms

2. evaluation of syncope

3. arrythmia tx effectiveness


what are 5 reasons you would want to do a stress test on a patient?

1. CP/angina pectoris


2. functional ability in CHD


3. screening of high risk individuals with atypical symptoms


4. response to intervention (cath, CABG), check them before they are released


5.screening for patients with certain occupation requirements


what are the 3 qualities you used to deteremines a patients pretest probability for CHD?


what are the three questions you want to ask them about their type of CP?

age, gender, characteristic of CP


1. substernal?

2. brought on by exertion?

3. relieved by NTG?

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low pretest probability (Stress test)


what two population characteristics fall into this category? do you do a stress test in them?

1. asymptomatic men and women of all ages

2. women


avoid stress testing in this group!! high rate of false positives and then you are stuck with the results and have to work them up!


intermediate pretest probability for stress test (10-90%)


what are the 3 population characterstics for this group? should you do a stress test in this population?

1. men of all ages with atypical chest pain

2. women >50 with atypical chest pain

3. women 30-60 with typical CP



stress tests warrented in this group for DX of CAD!


high pretest probability (90%) for stress in CAD


what are the two population characteristics of this group? what might this provide? what might you want to consider as testing for this group instead?

1. men >40 with typical CP

2. women >60 with typical CP



might provide prognostic value in this group, may want to consider coronary angiograph instead because high risk!


what are the four indications to STOP a stress test?

1. evidence of ishchemia with ST depression of T wave inversion


2. achieve target HR of 85-90% of predicted maximal HR (220-age)


3. dangerous arrythmia


4. decreasing BP! STOP!


what is the one absolute thing you much achieve in order to intrepret a stress test as negative?

must achieve 85-90% of maximal predicted HR!!! otherwise you can't say the test was negative!!


explain what these four meds do in pharmocologic stress tests and which ones they are used in?

1. adenosine

2. dipyridamole

3. regadenoson

4. dubutamine

1. adenosine: dilates coronary arteries used in nuclear imaging


2. dypyridamole: dilates coronary arteries used in nuclear imaging


3. regadenoson dilates the coronary arteries ***MOST COMMONLY USED***give bolus injection  works like adenosine


4. dubutamine: increases HR and contractility used in echo!



what would you see on a stress test that indicates a positives test?

downward  or horizontal sloping ST depression or T wave inversion

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what do you need to keep in mind about women and stress tests? (3)

1. high incidence of false positivites in young healthy women w/o risk factors and atypical CP


2. decreased sensitivitiy in women with CHD because they are more likely to have 1 vessel disease




what are the 4 things that make it so you can't read an EKG that make it useless to do a stress EKG??

1. LVH


3. Digoxin

4. WPW abnormality!!




what is the gold standard for cornary imaging? who is it warranted in?

left heart cath to do coronary angiography


do in: high risk individuals with classic ischemia symptoms


what do you need to keep in mind about ordering cardiac enzymes when a patient comes in to the ED with chest pain?

rise 4-6 hours after MI, so when pt is in the ED with symptoms and ST elevation, it is expected the first set would be negative, keep this in mind, if taken 4-6 hours post MI then you will see these as positive


what are the 2 qualifications for ischemia on the EKG?


what do you compare? what two other things can cause this?

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>1mm ST depression that is horizontal or downward sloping that persists for .08 sec past J point


**only needs to be in 1 lead!!**


compare the PR segment and the ST segment using the J point


2 other causes: hypokalemia, digoxin

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what are the three phases you see the EKG go through if someone is having an MI?

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1. T wave peaking followed by T wave inversion first couple hours  "ischemia"


2. ST elevation at the J point in two or more contigious leads >1mm after a couple hours



3. Q wave formation >.04 seconds wide and >1/3 the height of the R wave


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explain the cardiac enzyme testing for:





1. CK MB

rises in 6 hours after infarct


2. troponin (cTn)

rises 2-3 hours earlier than CK-MB so slighty better


which lead should you NOT look at when interpreting Q waves?

aVR these Q waves are never significant!!!


stage 1 of MI:

T wave peaking and T wave inversion


what does this suggest?

when does this happen?

what is this nicknamed?

is this reversible?

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1. ischemia but NOT dianostic for MI

2. first couple hours then they invert

3. "hyperacute T waves"

4. potentially reversible if blood flow is returned, T wave will return to normal



stage 2 MI:

ST segement


1. when does this occur?

2. what is the qualification for it to be called ST elevation?

what leads can it be in?

what does it indicate?

does it go away?


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1. occurs after a couple hours

2. ST elevation at the J point >1 mm in two or more contigious leads

3. can be in limb or precordial

4. INJURY beyond ischemia!!! occurs in acute MI but can return to normal if blood flow returned tells you that a true infarction has occured and that it will evolve into death unless there is immediate intervention


explain what early depolarization is?

how is this different than ST elevation?

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1. some people have regullarly elevated ST segment

2. common in young healthy individuals

3. ST returns to baseline during exercise


How to differentiate from MI:

1. t wave remains an independent waveform, aka the ST segment doesn't blend with T wave

2. in MI: ST merges with T wave

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stage 3 of MI:

formation of new Q waves


when does this occur?

what are the qualifications for this?

what does this indicate? reverisble?

what is this diagnostic for?

is there still ST elevation?

how long does it last?

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1. occurs 2-3 days later

2. >.04 seconds wide and >1/3 height of R wave

3. "death" has occured, not reversible

4. diagnostic of MI

5. by the point Q waves develop, ST returns to baseline

6. persist for lifetime of pt

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inferior MI


what artery would be blocked?

where do you see the changes?

where might you see reciprocal changes?

what other MI location might this commonly be paired with?

***what is something important you need to keep in mind when looking at change in V1-V3**

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right coronary artery


changes in inferior leads II, aVF, III


reciprocal: lateral leads I and aVL


***If there are changes in V1-V3 as well where the R is super tall consider this person is having a posterior MI as welll since the right coronary arter also feeds the posterior wall!! DONT CONSIDER THESE RECIPROCAL CHANGES!!****

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where do you see the lead changes for a inferior MI?



reciprocal if present in lateral leads! I and aVL

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left lateral MI



what artery would be blocked?

where do you see the changes?

where might you see reciprocal changes?

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left lateral circumflex artery


changes: I, aVL, V5, V6 (lateral leads)


reciprocal in: inferior leads!

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what leads would you see changes if you were suspecting a lateral wall MI?

changes: aVL, I, V5, V6


reciprocal changes in inferior leads!

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anterior MI

what artery would be blocked?

where do you see the changes?

where might you see reciprocal changes?

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left anterior descending artery


changes: any precordials esp V1-V4

this can be easy to pick out with poor R wave progression


reciprocal: inferior leads

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anterolateral MI



what artery would be blocked?

where do you see the changes?

where might you see reciprocal changes?

left main coronary artery


changes: I, aVL, all precordials


reciprocal changes: inferior leads



**think about it....the left main coronary supplies both the anterior and the lateral branches so therefore it makes sense you would have changes in both of these!

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what does this show you?


Q image thumb

anterior infarction

V1-V4 shows anterior heart


posterior MI


what artery is the most common cause of this?

where do you need to look for the changes and why?

what are two important things you MUST remember about this??



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90% of patients are supplied by right coronary artery


changes: instead of ST elevation you see ST DEPRESSION and TALL R WAVE IN V1,

this is a mirror image of anterior infarcts because you don't have leads that overly the posterior back


1. must distinguish between this and right axis deviation because in RAD you will also have tall R wave so need to check V6 for large S wave

2. often occurs with INFERIOR MI because they are from the same blood supply of the right cornary artery


in the pic...note tall R waves in V1, to rule our RAD, look at V6, there are tall R instead of deep S so this is posterior MI

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what does a posterior MI often occur with?

often occurs with inferior MI because they are from the same blood supply of the right coronary artery


what are the two types of SA dysfunction and what happens in each? who is this common in and what can it cause? can you distinguish between these on an EKG? what might  a person need if they aren't able to compensate or are symptomatic? what 3 drugs can cause this?

most common in ELDERLY

the pause followed these can cause syncope, dizziness


Sinus Arrest: SA node doesn't fire


Sinus block: SA node fires but the signal is blocked so it doesn't cause atrial depolarization, usually caused by scar tissue


***you can't determine between these on a EKG have to insert a cath to distinguish between the presense of an impuslse and the lack of impulse***


drug causes: bb, NCCBs


person might need a pacemaker!

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first degree AV block


what is this classified by?

what do you want to think of it as?

what causes this?

what type of heart do you find it in?

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PR interval >.2 seconds!


want to look at the limb leads for this, think of it like a "delay"rather than a block


can be in normal or dieased hearts caused by prolonged delay at AV node or bundle of HIS causing a longer PR interval


sick sinus syndrome


what is this a combination of?

what is not work?

what percent will have AV node dysfunction?

what are the two presentations you might see?

how DX?

how to TX?

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sinus arrest with alternations of paroxysms or atrial tachycardia and bradyarrythmias and clearly related to sinus node dysfunction (hence the name, duh)


"SA node dysfunction with symptoms"..most commonly cause by aging


40% will have AV node dysfunction


1. afib: controled or slow rate in the absence of meds

2. brady-tachy synddrome: artial tachyarrythmias and symptomatic bradycardia


DX: 24 hour holter monitor


tx: permanent dual chamber pacer with auto ICD


in sinus arrest or sinus block, what are the two rythmns and their characterstics that can kick in to compensate?

Junctional escape rythmn: Narrow QRS 40-60 bpm


ventricular rythmn: Narrow QRS with 30-45 bpm


mobitz type I, second degree AV block



where does it occur and what is it characterized?

WITHIN the AV node

usually benign and rarely goes on to third degree HB



lengthening of PR interval and then p wave without QRS

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third degree AV block


what is this called? 

what happens in this?

what should you look for in the rates?




no atrial impulses make it through to stimulate the ventricles each are beating INDEPENDENTLY!! the block prevents the atria and ventricles from communicating

**QRS are wide and bizarre looking almost like PVCs since they are from ventricular origin**


AV dissociation where the ventricular rate is slower than the atrial rate

atria: 60-100

junctional: 40-60

ventricular: 30-45


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second degree AV block general


what happens in this type of block?

what do you have more of?

what are the two types?

not every atrial impulse is able to pass through the AV node into the ventricles


more QRS than P waves since not all of them make it through


Mobitze Type 1 second degree block: Wenchebach

Mobitz Type II second degree block


mobitz type II second degree AV block


where does this occur?

what is this defined as?

is this benign? what does pt usually need? 



dangerous and pt usually needs a pacemaker, can progress to third degree AV block

presence of a dropped beat WITHOUT lengthening of the PR interval, RANDOM dropped QRS,



What are two really unique things that can cause a person to be in 3rd degree complete heart block?

1. lyme check titers


2. congenital heart block, they are born with it where their junction rythmn has been sufficient to supply blood so they are asymptomatic


what is the LEADING cause of COMPLETE HEART BLOCK?

degenerative disease of the conduction system


right bundle branch block


what are the two qualifying characteristics?

where do you see the reciprocal changes? what are the changes and why?

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1. QRS >.12

2. V1 and V2 have R-S-R' with rabbit ear appearance

reciprocal changes in lateral leads with DEEP S wave!



Handlers explaination: in RBBB, the left bundle branch still works so the conduction runs down the left side, usually on a EKG you only see the left ventricle contraction which gives you the R wave, however, in RBBB the left ventrcile is reponsible for causing the right ventricle to depolarize so the conduction goes from the left side over to the right cell by cell which is why depolarization has a longer duration and a R’ spike in V1 and V2, the R’ is the right ventricle depolarizing. this process is a left to right depolarization

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left bundle branch block


what are the two qualifications for this?

what will you always have?

where do you see the reciprocal changes?

Q image thumb

1. >.12 QRS

2. Broad/notched QRS in V5/V6



reciprocal in: V1/V2 with wide deep S wave

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hemiblocks general


how do these occur?

what is this branch made up of? 

what do they cause? what is normal?

what must you do to prove a hemiblock?

the left bundle branch is made up of two fasicles, so either of these can become individually blocked

1. left anterior fasicle

2. left posterior fasicle


they cause axis devation

they have NORMAL QRS, and must rule out other reasons for axis deviation (aka LVH, RVH)

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left anterior hemiblock


where does this occur? 

what are the qualifications? (3)

what are the steps to determine if this qualifies?

explain the direction of the vector and depolarization?

Q image thumb

occurs on the left bundle branch!! 




2. left axis deviation > (-30)




1. determina LAD via I and aVF

2. should also be negative in II (headed away and more neg)


rushes down the posterior fascile and swoops down and up traveling in a inferior superior, and right to left direction!! think about it

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Left posterior fasicle


what type of hearts do yo usee this in? 

what are the 3 qualifiations? 

what is the direction and depoliarzation vector?

where do you see the R waves and S waves?

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1. narrow QRS

2. RAD

3. no other reason for RAD (like RVH)

4. tall R waves inferiouraly, deep S waves laterally


runs down the anterior fasicle traveling superior to inferiorly and left to right depolarization

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dilated cardiomyopathy


who is this most common in? what does this reduce? what part of the heart does this effect? what is the biggest hint to this? what are two things you might hear? what might you see on examinatin of the neck? what are four causes of this? what do you do to diagnose? tx?

MOST commony type of cardiomyopathy, esp in black men


reduced strength of ventricular contraction, causing dilation of left ventricle, left or biventricular failure causing dyspnea, s3 gallop, pulmonary crackles, increase JVP


causes: genetic abnormalities (25-30%), alcohol consumption, postpartum, idiopathic



-do echo

-EKG, nonspecific changes



-no alcohol

-underlying cause should be treated





why are women often misdiagnosed when they have CHD? (3)

1. atypical symptoms: pain radiating to right arm, arm pain along


2. many women produce false negative stress tests since single vessel disease more common


3. elderly or diabetic womeon complain of general malaise, loss of appetite, vague abdominal pain so if they have RF, GET EKG!!



explain the role of LDL and HDL?

LDL: carries lipid to the arteries after being oxidized


HDL: removes lipids from the arteries


**together these contribute the the managing of atherosclerosis**


role of tryglycerides is unknown


what is the major source of endogenously derived cholesterol?


what about exogenously?

liver and intestines


exogenously: diet


what is the rate limiting step in the liver in cholesterol biosynthesis?


what happens when you increase your dietary cholesterol?

converting HMG CoA to mevalonic acid by HMG CoA reductase


**this is where statins work**


when you increase intake of dietary cholesterol: down regulation of LDL receptors and elevation of LDL cholesterol


what are the goals for LDL lowering?

TRICK QUESTION...there are no goal levels anymore, it is based on intensity of statin therapy!!!


what was the main point from the PROVE-IT-TIMI 22 test?

lower we can lower the LDL the better we are at preventing ASCVD and progression


get it down and keep it down


explain the relationship between lipids and athlerosclerosis?


(both LDL and HDL)

1. vascular injury like smoking DM facilitates the uptake of lipoproteins


2. increase in LDL (oxidized) directly leads to vascular damage and premature atherosclerosis


3. LDL oxidation is nessacary for endothelia damage


4. HDL: cardioprotective and prevents the oxidation of LDL, reverse transporter of cholesterol


what are four things you might find if a patient that has hyperlipidemia?

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1. athlerosclerosis disease like PVD, CHD


2. eruptive xanthomas: can be seen on the buttocks with extremely high levels of triglycerides


3. tendinous xanthomasvery high LDL, nodules on tendons most commonly on achilles, back of hand, and patella


4. xanthelasma: yellow plaque on the skin around the eyes

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dyslipidemia in adults is heavilly influenced by what three things? 

how is it usually detected?


what are four conditions that make people more apt to get dyslipidemia? 


diet, lifestyle and genetics


often detected in asymptomatic adults during routine blood screening



2. nephrotic syndrome

3. Chronic renal failure

4. hypothyroidism


those who have athlerosclerosis commonly have....



explain the four treatment groups and what type of statin therapy they would recieve?

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what is the difference between

primary prevention

seconday prevention


for dyslipidemia?

primary prevetion: lowering cholesterol/LDL will prevent NEW ONSET CHD, they don’t have it yet and you want to prevent them from getting it!


secondary prevention: lowering cholesterol/LDL will prevent recurring coronary events, they already have it so you want to prevent progression

goal:  decrease total mortality in presences of existing disease


familia dyslipidemia


what is defective in these individuals?

what are the levels for heter/homozygotes?

what are three things you might find on PE?

Q image thumb

lack LDL receptors or they are defective so the LDL isn't taken up by the liver to be degraded


heterozygotes: have total cholesterol at birth >350 with high LDL


homoxygotes: have total chonesterol >700 with high LDL


PE: tendon xanthomas, xanthelasma, cutaneous xanthomas

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if someone doesn't fit into one of the categories indicated for statin therapy...what are 4 other considerations that would make you more likely to Rx them anyway?

family hx of premature ASCVD

high sensitivity CRP >2

Coronary calcium score >300



**you need to use clinical judgement!!**


how much can you expect high intensity statins to lower LDL?

what are the two drugs?

lowers LDL by 50%

atorvastatin, rousuvastatin


how much can you expect a moderate intensity statin to lower LDL?


what are the drugs?

 lowers LDL by 30-50%

      simvastatin, pravastatin, lovastatin or lower dose of atorvastatin, rousuvastatin


what should you always use first in the treatment of elevated LDL?

***always use statins first unless for some reason the pt can’t tolerate them!**





are you at risk for developing CAD?

what is this associated with?

why do you treat? when?

what are 3 things it is associated with for dxs?

what are the 2 tx options?

risk for developing CAD is controversial, however, may play a role when LDL is also elevated


associated with Very low density lipoprotein (triglycerides)

inverse relationship between VLDL and HDL….so therefore treat hypertriglyceridemia >200 


associated with obesity, T2DM, metabolic syndrome



1. very sensitive to diet, weight reduction and exercise

2. fibrinic acid or niacin


what are the 5 lifestyle adjustments you can make to decrease dyslipidemia?

1. smoking cessation

2. decrease intake of saturated fats

3. decrease total calories

4. increase physical activity

5. decrease sodium intake


HMG CoA inhibitos


what do these do?

what is important about the dosing?

what can it cause 

what are two SE?

rate limiting step in cholesterol synthesis; up regulates LDL receptors


1. low dose gives you the most bang for your buck, increasing dose you see less effective

2. can cause chemical diabetes but the benefits outweigh the risks

3. myalgia

4. myositis and rhabdomyolysis


restrictive cardiomyopathies


what is this caused by? what three things might you see this in? how does the pt present and what else do they often have? what is the Dx and what might you need to get? what is the tx?

fibrosis/infiltration of the ventricular wall because of collagen defects like amyloidosis, diabetes, endomyocardial fibrosis


pts present with dereased exercise tolerance, in sever get right sided HF,  pulomary hypertension usually present



echo!!! may need endomyocardial biopsy


tx: diuretics and cardiac transplant in extreme


what are the two side effects you need to be aware of with HMG-CoA inhibitors?

myalgia:  : most common and benign, have then stop taking measure CK, usually normal and can usually start again at a lower dose


myositis/rhabdomyolysis: rare but life threatening, muscle pain/weakness with increased CK >10x the normal limit causing the kidneys to block up and can lead to death DC THE DRUG!!!


atrial fib


is this in healthy people?

what are 3 things that can cause this in healthy people?

what percent of people have this attributed to cardiac or pulmonary disease?

what do you do if hemodynamicaly unstable? how to test?

what are three things that can be caused by excessive ventricular rate?

can be in healthy individuals without heart disease caused by emotional stress, post surgery, ETOH "holiday heart"


can be "lone" without any precipitating factors


95% in presence of cardiac or pulmonary disease


first goal: access hemodynamic stablilty by pulse ...if not stable DC cardioversion


excessive ventricular rate can cause hypotension, pulmonary congestion,  CP


how long do you need to have afib to be at risk for thromboemboli?

48-72 hours


lone atrial fibrillation



what is this characteristics of this?

what happens in this?

what is the natural progression of this?


electrical disturbance in the absence of cardiac or systemic disease


paroxysmal episodes of symptomatic afib that revert to NSR spontaneously with brief course of meds


natural history: increased frequency of episodes over time and becomes harder to maintain NSR with meds




dependent of frequency of episodes


evaluation and Tx 

new onset afib


what are 3 things you should look for?

3 tests? 

rapid control in ED?

drug for recent onset? 

if these don't work?

look for underlying cardiac, pulmonary, and systemic disease




echo (to check for heart abnormalities)

throid function test (hyperthroidism can cause afib)



1. first goal: acute/rapid rate control in ED is initial goal: IV diltiazem or Beta blockers

2. ibutilitde Type III for recent onset **THIS IS A PHARM CARDIOVERTER***

3. if these don't work than proceed to CARDIOVERSION


if pt has been in afib >72 hours what do you need to do before cardioversion? 2 drugs

anticoag for 3 weeks before cardioversion with

coumadin, dabigatran


*****if the patient can't tell you exactly when it started you MUST DO THIS AND DELAY CARDIOVERSION!!!! don't put them on a BB just put them on a anticoagulation......the only way to get around this is to do a TEE to check for a clot if the person needs to be converted sooner****** 


what are the two management strategies for Afib?


are they both ok to use?


1. rythmn control

2. rate control




****both rythmn control and rate control are acceptable long term strategies to prevent morality, stroke, and quality of life, choice of tx strategy is based on SYMPTOMS!! risk of bleeding, and side effects of the anti-arrhymics***


rythmn control method for 

chronic/recurrent Afib


what is the goal of this method?

what are benefits/negatives?

if you can't cardiovert via meds, what are your next two options?

what two meds do you use to prevent afib recurrance?

what percent will have afib reocurrance?

goal: cardiovert to NSR and use drug to maintain SR (often young people so that way they have no limitations)


benefits: increase cardiac output/function

negatives: side effects of meds and reccurances


if you can't cardiovert with med

1. DC cardioversion after being on antiarrythmic: 90% successful

2. if recurrence: DEFINITIVE RX: ABLATION VIA CATH (eliminates Pacs that initiate afib)


drugs to maintain SR once cardioverted

1. Type IC fleocainide

2. type III amiodarone



rate control approach for chronic/reccurent afib


what is the goal of this?

benefit? negatives?

what are the 3 drugs you can accomplish this with and what DO THEY NEED TO BE ON???


goal: leave in afib and anticoagulate with warfarin


benefit: no cardioversion

bad: increase risk of bleeding from anticoagulant


chronic rate control with drugs

1. diltiazem

2. beta blockers

3. digoxin in eldery/sendentary



hypertrophic cardiomyopathy


what does the patient present with? what might be the first presentation? what are four things you might find on exam?  what are the two DX and what is most important?  what are the four treatment options?

Q image thumb

massive hypertrophy, **usually of septum (assymetric septal hypertrophy)**, left ventricle

unrelated to pressure overload, present at birth, diastolic dysfunction, suddent death in athletes! (small left ventricle so can't get enough blood and the leaflet blocks the outflow tract)


OFTEN ASYMPTOMATIC IN CHILDREN patients present with dyspnea and angina, syncope and arrythmia like Afib that can lead to sudden decompensation and sudden death may be the first presentation in young athletes during strenous activity!!!!!


on exam: sustained PMI, loud s4 and S3, loud harsh aortic outflow murmer cresendo-decreshendo is charactericstic (INCREASED MURMER WITH VALSALVA AND STAND, DECREASED SQUATTING!!!) KEY!! variable systolic murmer, jugular venous pulsations bisferiens pulse with double/triple pulse because the ventricle is contracting against the obstuction of the aorta by MV leaflet



EKG: might show LVH

echo: key!! show LVH, asymmetrical septal hypetrophy and small left ventricle, and diastolic dysfunction



1. Beta blockers, calcium channel blockers (verapamil)

2. myomectomy (to remove extra septal muscle)

3. ablation, ICD, dual chamber pacers and mitral valve replacements as needed


hypertrophic cardiomyopathy


what does the patient present with? what might be the first presentation? what are four things you might find on exam?  what are the two DX and what is most important?  what are the four treatment options?

massive hypertrophy, usually of septum, left ventricle


patients present with dyspnea and angina, syncope and arrythmias common, sudden death may be the first presentation


on exam: sustained PMI, loud s4, variable systolic murmer, jugular venous pulsations



EKG: might show LVH

echo: key!! show LVH, asymmetrical septal hypetrophy and small left ventricle, and diastolic dysfunction



1. Beta blockers, calcium channel blockers

2. ablation

3. defib, pacers and mitral valve replacements as needed


hypertrophic cardiomyopathy

explain what is going on on in the heart?



"handler: the area right below the aorta outflow tract narrorws because the intraventricular septum grows and it closes off, so the mitral valve leaflets move abnormally towrads the intraventricular septum and blocks this area so the blood can't get out of the left ventricle, this is dynamic meand the amount of blocking depends on the activity you are doing" 


obstruction: MV moves abnormally towards the intraventricular septum obstructing the Left ventricular outflow tract 


myocardial fiber hypertrophy and disarray

mitral valve often thickens causing abnormal  movement blocks the blood getting out of the heart

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hypertrophic cardiomyopathy

how are 50% of these cases started?

what is the inheritance?

what must you do for the family?

what is essential?

Genetically transmitted in >50% of cases.

Autosomal dominant with high penetrance


Must perform echocardiography on all siblings and offspring of a patient with HCM.


Genetic counseling is essential


restrictive cardiomyopathies


what is this caused by? what three things might you see this in? how does the pt present and what else do they often have? what is the Dx and what might you need to get? what is the tx?

fibrosis/infiltration of the ventricular wall because of collagen defects like causing the ridgid walls to prevent diastolic filling

characteristic: abnormal diastolic function


pts present with dereased exercise tolerance, in sever get right sided HF,  pulomary hypertension usually present, jugula venous distension, S3/S4, inspiratory increase in venous pressure (KUSSMALS SIGN)



echo!!! may need endomyocardial biopsy

see LV wall thickening

decreased diastolic relaxation


tx: diuretics and cardiac transplant in extreme, CCB might help with symptoms


what are the 6 causes of restrictive cardiomyopathy?



Fabry Disease

Gaucher Disease

Endomyocardial Fibrosis-Loeffler Endocarditis-hypereosinofilia syndrome


metabolic syndrome



Major contributor to coronary disease

Three or more of the following:

Abdominal obesity

Tri >150

HDL <40 M, <50 W

Fasting glucose over 110



what is cor pulmonale?

what is an acute cause?

what are two chronic causes?

what are the two treatments

right ventricular hypertension that leads to right sided heart failure, commonly seen with pulmonary hypertension when the increased fluid backs up


acute causes: PE, rapid increase in pulm arterial pressure, RV overload, dysfunction/fail

Chronic causes: COPD, PAH progressive hypertrophy and forced dilation of RV over months, dysfunction/failure


**you literally get every symptom ever,  treat with diuretics to decrease volume of fluid and give continuous long term O2 which improves life expectancy**


superficial thrombophlebitits


what is this and what do you do about it?

requires termination of the IV line at the site of infection and use of warm comrpesses




what is this caused by? what does it look like? what is it associated with? what is the treatment?


spasm of the digital arteries to a variety of stimulus including cold weather


 paroxysmal palor and cyanosis folowed by rubor


progressive and symmetric dz

 associated with autoimmune like CREST



Tx: calcium channel blockers






are you at risk for developing CAD?

what is this associated with?

why do you treat? when?

what are 3 things it is associated with for dxs?

what are the 2 tx options?

risk for developing CAD is controversial, however, may play a role when LDL is also elevated


associated with Very low density lipoprotein (triglycerides)

inverse relationship between VLDL and HDL….so therefore treat hypertriglyceridemia >200 


associated with obesity, T2DM, metabolic syndrome



1. very sensitive to diet, weight reduction and exercise

2. fibrinic acid or niacin