Cardio Flashcards
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
symptomatic:
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
- 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 4 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
*****REDUCE MORTALITY IN POST MI AND HF PATIENTS***
2. long acting nitrates isosorbide dinitrate
****DONT TAKE THIS WITH VIAGRA!!!!*****
****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 blockersamlodipine, 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**
7. antiplatelet drugs USED IN ALL PTS WITH CHD, PAD, AND CAROTID, DECREASES INCIDENCE OF CARDIAC DEATH AND MI, low dose asprin
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%
- single or 2 vessel disease
- 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)
DX:
NEGATIVE CARDIAC ENZYMES
EKG: ST depression, T wave inversion
Tx:
- HOSPITALIZE THEM!! BEDREST!!
- full anticoagulation and antiplatelet therapy
-HEPARIN +ASA+
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?
50%
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
MB
troponins
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
STEMI
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
DX:
- 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
4. EKG ELEVATED ST
5. echo left ventricular function, identify mitral regurge
what are the treatments for a acute STEMI? (3)
1
1
2
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?
- morphine sulfaste
- aspirin in ED
- nitro IV
acute myocardial infarction
STEMI
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
DX:
- 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
4. EKG ELEVATED ST
5. echo left ventricular function, identify mitral regurge
what are the treatments for a acute STEMI? (3)
1
1
2
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?
- morphine sulfaste
- aspirin in ED
- nitro IV
what are the contraindications (4) and realtive contraindications (1) for thromboltic therapy for a STEMI?
absolute contraindications:
- uncontrolled HTN
- stroke within 1 year
3. cerebral hemmorahage
4. recent head trauma
relative contraindications:
- abdominal or thoracic surgery within 3 weeks
what 5 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: i_mprove 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?
- full anticoagulation and antiplatelet therapy
-HEPARIN +ASA+
prasurgrel/ticagrelor/clopidigrel OR glycoprotein IIb/IIIa
- 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
sinus rythmn
rate?
rythmn?
p waves?
QRS?
rate 60-100
rythmn regular
p waves yes and upright
QRS narrow
sinus tachycardia
rate?
rythmn?
p waves?
QRS?
causes?
rate >100 bpm
rythmn regular
p waves yes
QRS narrow
causes:
1. normal, seen with exercise
2. changes in SA node firing seen with CHF, lung disease, hyperthyroidism in eldery
sinus bradycardia
rate?
rythmn?
p waves?
QRS?
causes?
rate?
rythmn? regular
p waves? yes
QRS? narrow
causes? common rythmn seen in early stage of acute MI
sinus arrythmia
rate?
rythmn?
p waves?
QRS?
causes?
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
rate?
rythmn?
p waves?
QRS?
other? 3
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
other?
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
atrial fib
rate?
rythmn?
p waves?
QRS?
other? 3
MULTIPLE REENTRANT CIRCUITS IN THE ATRIA
rate? 400-600 atrial contractions (blocked at AV by refractory period)
rythmn? irregullarly iregular supraventricular
p waves? NO!!! undulating baseline
QRS? narrow QRS
other:
- in new onset without med control: ventricular rate is very fast 120-180 bpm
- goal in ED: slow rate with meds
- Risk: BLOOD CLOT and stroke if they break off
atrial flutter
rate?
rythmn?
p waves?
QRS?
other? 4 things!
RENTRY CIRCUIT around annulus of tricuspid valve
250-350 flutter waves
regular
no p waves, flutter waves
QRS narrow
- most common presentation is 2:1 AV block with QRS ~150 bpm
- SAW TOOTH APPEARANCE in II, III, aVF
- after meds given to slow AV conduction given, most common form of block is 4:1 with ventricular rate ~75
- carotid masage can help slow VR down, allowing flutter waves to be seen
paroxysmal supraventricular tachycardia (PSVT)
rate?
rythmn?
p waves?
QRS?
who is it in? tx? 3 causes?
AV NODAL REENTRY!
abrupt onset and termination
carotid massage may help terminate
150-220
regular
not usually present
narrow QRS
- 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
- can be caused by coffee, alcohol, and excitement
in HF, how doese the body attempt to increase cardiac output?
- if cardiac output is low and can’t support normal circulatory function, body stimulates sympathetic stimulation to increase vasoconstriction and venous return
- causes increase in RA pressure and fluid retention at kidneys because of decreased filtration rates from decreased cardiact output
- cardiac output rises a little from fluid retention and increased venous return
- continue to increase right atrial pressure, fluid retention accelerates this causes overstretching of the heart of edema of the heart muscle
- cardiac output drastically decreases and the pt dies of DECOMPENSATION
junctional tachycardia
what is this chracterized by? what can it be confused with? what are two clinical connections?
very uncommon, but discussed for ACLS
NARROW QRS REGULAR TACHYCARDIA WITHOUT P WAVES
may be confused with PSVT but slower rate
clinical: digital toxicity, somtimes inferior wall MI
multifocal atrial tachycardia
what must be present?
rate?
rythmn?
cause?
what is it connected to?
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?
rate?
QRS?
p waves?
what can happen if sinus rate and AV rate are similar?
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?
most common ventricular rythmn
reentry more than automaticity
premature QRS complex that is wide and biazarre
no p waves
WIDE QRS >.12
irregularlly iregular, or regularly irregular (trigeminiy)
often followed by a pause
uniform or multiform
healthy and diseased hearts
bigeminy and trigeminy
ventricular tachycardia
what is this defined as?
what is sustained mean?
is the heart diseased?
hemodynamicaly stable?
what does it deteriorate into?
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?
“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
ventricular fibrillation
what is this? does it contain any waves?
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
DX:
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?
WHAT IS THE EXCEPTION OT THIS?!
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?
- decrease activity
- ACE INhibitors esp in HTN or HF, decrease preload and after load
- diuretics decrease preload
- 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?
- Holosystolic systolic murmer (heard throughout entire systole), 2. THRILL
- HIGH PITCHED
- BLOWING
- S3 gallop if severe
what are two random defomirites that are associated with mitral valve prolapse?
high arched palate
pectus excavatum!!
weird
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:
- familia hx, most common autosomal dominant (only get growth on valve)
- 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,
NOISE/MURMER SOFTENS WHEN SQUATTING KEY THIS MAKES HEART LARGER SO LEAFLETS FIT BETTER, OPPOSIT OF OTHER MURMERS
mitral valve prolapse
what are the 3 PE things you might find to indicate this?
- mid to late systolic click between s1 and s2 (tensing of chordae)
- high pitched late systolic murmer
- NOISE/MURMER SOFTENS WHEN SQUATTING KEY THIS MAKES HEART LARGER SO LEAFLETS FIT BETTER, OPPOSIT OF OTHER MURMERS
what are the 3 tx options for mitral valve prolapse?
- reassurance #1!!!!!
- Beta blocker if CP or arrythmia
- 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?
- LA DILATION, LV NORMAL WITH LVEDP NORMAL!! (just not getting blood)
- s1 and s2 loud
- opening snap after S2
- diastolic rumble low pitch from slow blood flow into LV
what are the 4 treatment options for mitral stenosis?
- decrease Na consumption, direutics
- control afib if present
- preferred intervention: precutaneous balloon vulvoplasty (alternative to surgery, first option for most patients)
- 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?
Males!
three main causes:
- born with bicuspid valve
- rheumatic fever
-
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?
- carotid pulses climb
- apex displaced
- s4 gallop
- systolic murmer with cresendo/decresendo
- sawing gratting sound during systole
- 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?
cath
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
- mild w/o symptoms: monitor, ACE, ARBS
- SURGERY!!! replacement with tissue or mechanical valve
- 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?
apex
left lateral debiscus position
tricuspid regurgitation
where do you hear it?
during what?
where does it radiate?
noise?
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
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
BATES:
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
SICK SINUS SYNDROME
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?
DX
TX
- 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
DX: ECG changes (SEE PICTURE)
TX:
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.
atherosclerosis
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?
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
- coronary heart disease (coronary artery disease)
- cartotid artery disease
- periphreal vascular disease
what are 9 risk factors for atherosclerosis?
which two are the most important?
- smoking
- diabetes mellitus
- dyslipidemia
- elevated CRP
- hypertension
- family hx in 1st degree relative
- males
- inactivity
in periphreal arterial disease, if you have a clot in these areas, where will the claudication symptoms radiate?
aorti-iliac
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?
- 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
- 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
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
RF: DIABETES MELLITUS, SMOKING, >60YRS
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
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?
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 extremity, loss of distal pulses
DX: doppler US (DO FIRST), ABI, angiography gold standard
Tx:
1. anticoagulation with heparin to prevent propogation of the thrombus
2. if severe: reprofusion
- embolectomy
- streptokinase, urokinase, tPA
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?
improves quality of life for pts with DISABLING CLAUDICATION ALREADY ON MAXIMUM THERAPY AND HAVE REST PAIN. PRESERVE LIMB VIATALITY AND PREVENTS AGAINST AMPUTATION
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
what are the symptoms that suggest an acute arterial occlusion is an emergency?
6 p’s
- pain
- pallor
- 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
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?
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 morning, secondary skin changes ulcers above the ankle on medial aspect leads to stasis dermatitis with brownish pigmentation and stippling
Tx: ruduce swelling and prevent breakdown
- intermittent leg elevation
- compression stockings
- 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
DX:
- 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
- male
- smoker
- >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?
- watch it and monitor it
- >5cm: 20-40% over 5 years rupture, surgical to remove ELECTIVE SURGERY ADVISED!!
- >6cm: 15% risk it will rupture annually, ALWAYS SURGERY, REMOVE IT!!!!
Tx:
- open surgical repair (open with graft placement)
- endovascular (no surgical candidates, stents placed to reduce risk of rupture
prognosis of aortic aneursym is related to what two things?
- size of aneurysm
- CAD
what is the mortality rate of ruptured aortic aneurysm?
90%!!!!!
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
- rheumatic heart disease
- endocarditis on different valve
- bicuspid valve
- connective tissue disease
increase LVEDV, causing LV dilation leading to LV dysfunction with decrease EF and backs up to the lungs
- blood still flowing from the RA
- 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?
- 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?
- apex displaces laterally/inferiorlly
- diastolic thrill along left sternal border
- S3 with “blowing” diastolic decresendo murmer
- best heard with pt leaning foward 2-3rd LICS
what are the 3 test you use to dx a aortic regurg?
- EKG: LVH over time
2. echo: LV dysfunction later on, can see the aortic regurg jet detectable and semi quantifiable best!
- cath: tells regurg amount, LV dysfunction, intracardiac pressure (not usually need in young pt)
what are the 3 treatment options for aortic regurg?
- 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!!
- CHD: MIs/ischemia account for 75% MOST COMMON CAUSE
- primary pump failure
- valvular disease
- congenital heart disease
- 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
- the baby boomers are getting older and there are just more people with this condition
- increased salavage of people in strokes
explain:
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!*
explain:
- acute HF (1 cause, 4 symptoms)
- 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
explain:
- Left sided HF (leads to what? 2 causes)
- Right sided HF (associated with what? 2 causes)
what is the most common cause of right sided HF?
-
left sided heat failure: inadequate CO with pulmonary congestion
causes: post MI, aortic/mitral valve disease -
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:
- backward HF (where does the fluid go?)
- 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?
- 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
-maintains CO via STARLING MECHANISM
**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
- slight limitation of physical activitiy, some activities so SOB on exertion
- markled limitation of physical activities, like ADLS cause SOB
- 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)
- 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?
***THIS IS A MEDICAL EMERGENCY****
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?
- 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:
CARDIOMEGALY
KERLEY B LINES (DISTENSION OF PULMONARY VEINS)
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
>100 COMMON WITH HF
what are the 6 goals of treatment for HF?
- treat underlying cause
- reduction of cardiac workload (preload/postload)
- control excessive Na/water retention
- early initiation of ACEI/ARB (hydralazine in blacks)
- enhancement of cardiac contractility
what type of diet is reccomended for HF patients?
NO SALT ADDED.
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)
afterload:
- 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)
- what two things cause it cause as SE? what can it do? what does it decrease?
- what doesnt’t this cause?
- 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
sacubitil/valsartan
used for?
what does this do? what are 3 SE?
CONSIDER AS FIRST LINE TREATMENT FOR HF INSTEAD OF ACE OR ARB ALONE FOR HF!!!!!
- slowed HF progression better than a ACE alone
- 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?
indications:
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
- estrogen use increases RAAS
- intrinsic renal disease (any form of chronic renal parenchymal disease)
- renovascular HTN
- endocrine HTN
- 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?
genetics
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?
obesity
Na in diet
cigarette smoking increases NE
NSAIDS
excess alcohol
explain the ways in which HTN effect and contribute to end organ damage in:
- heart
- brain
- arteries
- renal
1. HEART
- RF for CHD
- LVH diastolic dysfunction POWERFUL PREDICTOR of morbidity and morality, in 50% of people with HTN
- HF over time
2. CEREBROVASCULAR
the major predisposing cause of STROKE
rupture of micro hemmorages from increase BP
correlate closely with SYSTOLIC BP
3. PVD
4. RENAL DISEASE
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
- SOB, DOE from LVH
- TIA, stroke, hemmorage
- 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 3 most important labs you want to check in a patient you are concerned about HTN?
- creatine, BUN
- electrolytes Na and K (want to check K cause you will likely put them on a dieuretic and this can cause hypokalemia)
- 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
- ACE
- 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 are the physical exam findings that can suggest a patient has HTN since it is mostly asymptomatic? 6
- narrowing of the arterioles A/V
- A-V nicking (arteriosclerosis where artery looks like it is crossing the vein)
- silver or copper wired appearance
- hemorrhages or exudates
- papilledema
- bruits
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?
SYSTOLIC BP!
what are four non pharm ways to decrease HTN?
diet
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?
- 1st line therapy and should be included in ANY drug therapy
- more potent in blacks, elderly, obese
- avoid in patiens with hyponaturemia and gout
- LOW DOSAGE
- 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
- decreases CO
- helpful in pts with other comorbid disorders like:
- angina pectoris, post MI, migrain headaches, essential tremors - 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)
losartan
like ACE but no cough!
renoprotective in diabetics
direct renin inhibitor for HTN
aliskren
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!
- 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
- 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 - second drug would be BB, ACEI, or Ca blocker Exception:
ii. if BP is >160/90 can start dual Rx at the same time - 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
- continuous
what are the 3 reasons you would want ambulatory monitoring of a patients cardiac symptoms?
- arrythmia detection and correlating it with patient symptoms
- evaluation of syncope
- arrythmia tx effectiveness
what are 5 reasons you would want to do a stress test on a patient?
- CP/angina pectoris
- functional ability in CHD
- screening of high risk individuals with atypical symptoms
- response to intervention (cath, CABG), check them before they are released
- screening for patients with certain occupation requirements
low pretest probability (Stress test)
what two population characteristics fall into this category? do you do a stress test in them?
- asymptomatic men and women of all ages
- 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?
- men of all ages with atypical chest pain
- women >50 with atypical chest pain
- 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?
- men >40 with typical CP
- 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?
- evidence of ishchemia with ST depression of T wave inversion
- achieve target HR of 85-90% of predicted maximal HR (220-age)
- dangerous arrythmia
- 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?
- adenosine
- dipyridamole
- regadenoson
- 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 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
- substernal?
- brought on by exertion?
- relieved by NTG?
what do you need to keep in mind about women and stress tests? (3)
- high incidence of false positivites in young healthy women w/o risk factors and atypical CP
- decreased sensitivitiy in women with CHD because they are more likely to have 1 vessel disease
- ORDER STRESS WITH IMAGING FOR THESE PEOPLE! young without RF or atypical CP
what are the 4 things that make it so you can’t read an EKG that make it useless to do a stress EKG??
- LVH
- LBBB
- Digoxin
- WPW abnormality!!
**DON’T READ THEM, YOU’LL LOOK DUMB!!!**
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 would you see on a stress test that indicates a positives test?
downward or horizontal sloping ST depression or T wave inversion
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
explain the cardiac enzyme testing for:
CK MB
Troponin
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!!!
what are the 2 qualifications for ischemia on the EKG?
what do you compare? what two other things can cause this?
>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
what are the three phases you see the EKG go through if someone is having an MI?
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
“injury”
3. Q wave formation >.04 seconds wide and >1/3 the height of the R wave
“death”
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?
- ischemia but NOT dianostic for MI
- first couple hours then they invert
- “hyperacute T waves”
- potentially reversible if blood flow is returned, T wave will return to normal
stage 2 MI:
ST segement
- when does this occur?
- 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?
- occurs after a couple hours
- ST elevation at the J point >1 mm in two or more contigious leads
- can be in limb or precordial
- 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?
- some people have regullarly elevated ST segment
- common in young healthy individuals
- ST returns to baseline during exercise
How to differentiate from MI:
- t wave remains an independent waveform, aka the ST segment doesn’t blend with T wave
- in MI: ST merges with T wave
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?
- occurs 2-3 days later
- >.04 seconds wide and >1/3 height of R wave
- “death” has occured, not reversible
- diagnostic of MI
- by the point Q waves develop, ST returns to baseline
- persist for lifetime of pt
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**
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!!****
where do you see the lead changes for a inferior MI?
II, aVF, III
reciprocal if present in lateral leads! I and aVL
left lateral MI
what artery would be blocked?
where do you see the changes?
where might you see reciprocal changes?
left lateral circumflex artery
changes: I, aVL, V5, V6 (lateral leads)
reciprocal in: inferior leads!
what leads would you see changes if you were suspecting a lateral wall MI?
changes: aVL, I, V5, V6
reciprocal changes in inferior leads!
anterior MI
what artery would be blocked?
where do you see the changes?
where might you see reciprocal changes?
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
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!
what does this show you?
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??
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
- 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
- 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
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!
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?
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?
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
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
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
DX:
- do echo
- EKG, nonspecific changes
Tx:
- no alcohol
- underlying cause should be treated
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
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?
BELOW AV NODE IN BUNDLE OF HIS
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,
CAN HAVE MORE THAN ONE IN A ROW
What are two really unique things that can cause a person to be in 3rd degree complete heart block?
- lyme disease…so check titers
- 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
mobitz type I, second degree AV block
aka WENCHEBACH
where does it occur and what is it characterized?
WITHIN the AV node
usually benign and rarely goes on to third degree HB
NEVER SEE MORE THAN ONE DROPPED BEAT IN A ROW, IF YOU SEE THIS THEN IT IS A MOBITZ TYPE 2
lengthening of PR interval and then p wave without QRS
third degree AV block
what is this called?
what happens in this?
what should you look for in the rates?
“complete heart block” MEDICAL EMERGENCY!!!! ALWAYS NEED PACEMAKER
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
THEY MARCH OUT INDEPENDENTLY!!
right bundle branch block
what are the two qualifying characteristics?
where do you see the reciprocal changes? what are the changes and why?
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
left bundle branch block
what are the two qualifications for this?
what will you always have?
where do you see the reciprocal changes?
1. >.12 QRS
2. Broad/notched QRS in V5/V6
ALWAYS WILL HAVE DOWNWARD Q or RS in V1
reciprocal in: V1/V2 with wide deep S wave
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)
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?
occurs on the left bundle branch!!
MOST COMMON HEMIBLOCK IN NORMAL AND DISEASED HEARTS!
1. NARROW QRS
2. left axis deviation > (-30)
3. NO OTHER CAUSES OF LAD
STEPS:
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
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?
SICK HEARTS ONLY
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
WHAT IS THE MOST COMMON HEMIBLOCK?
LEFT ANTERIOR FASICLE HEMIBLOCK
why are women often misdiagnosed when they have CHD? (3)
1. atypical symptoms: pain radiating to right arm, arm pain along
- 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
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
DX:
echo!!! may need endomyocardial biopsy
tx: diuretics and cardiac transplant in extreme
explain the relationship between lipids and athlerosclerosis?
(both LDL and HDL)
- vascular injury like smoking DM facilitates the uptake of lipoproteins
- increase in LDL (oxidized) directly leads to vascular damage and premature atherosclerosis
- LDL oxidation is nessacary for endothelia damage
- HDL: cardioprotective and prevents the oxidation of LDL, reverse transporter of cholesterol
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
- DIABETES MELLITUS
- nephrotic syndrome
- Chronic renal failure
- hypothyroidism
those who have athlerosclerosis commonly have….
dyslipidemia
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
what are four things you might find if a patient that has hyperlipidemia?
- athlerosclerosis disease like PVD, CHD
- eruptive xanthomas: can be seen on the buttocks with extremely high levels of triglycerides
- tendinous xanthomas: very high LDL, nodules on tendons most commonly on achilles, back of hand, and patella
- xanthelasma: yellow plaque on the skin around the eyes
explain the four treatment groups and what type of statin therapy they would recieve?
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
ABI
**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!**
familia dyslipidemia
what is defective in these individuals?
what are the levels for heter/homozygotes?
what are three things you might find on PE?
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
hypertriglyceridemia
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
TX:
- very sensitive to diet, weight reduction and exercise
- fibrinic acid or niacin
what are the 5 lifestyle adjustments you can make to decrease dyslipidemia?
- smoking cessation
- decrease intake of saturated fats
- decrease total calories
- increase physical activity
- 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
- low dose gives you the most bang for your buck, increasing dose you see less effective
- can cause chemical diabetes but the benefits outweigh the risks
- myalgia
4. myositis and rhabdomyolysis
what is the critial difference in the treatment between pericarditis and myocarditis?
pericarditis: NSAIDS…respond within a couple hours NORMAL LV FUNCTION and SIZE
myocarditis: NO NSAIDS EVER….MAKE IT WORSE DECREASE IN LV FUNCTION AND INCREASE SIZE
***must do a echo to look for the presense of myocarditis….
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?
tx?
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
Tx:
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
Dx:
Ekg
echo (to check for heart abnormalities)
throid function test (hyperthroidism can cause afib)
TX:
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
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
DX:
EKG: might show LVH
echo: key!! show LVH, asymmetrical septal hypetrophy and small left ventricle, and diastolic dysfunction
tx:
- Beta blockers, calcium channel blockers
- ablation
- defib, pacers and mitral valve replacements as needed
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?
- rythmn control
- 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
- DC cardioversion after being on antiarrythmic: 90% successful
- if recurrence: DEFINITIVE RX: ABLATION VIA CATH (eliminates Pacs that initiate afib)
drugs to maintain SR once cardioverted
- Type IC fleocainide
- type III amiodarone
50% WILL HAVE RECURRANCE RATE
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
PLUS
LIFE LONG ANTICOAGULATION WITH WARFARIN TO PREVENT EMBOLISM, use ASA in elderly
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)
DX:
echo!!! may need endomyocardial biopsy
see LV wall thickening
decreased diastolic relaxation
tx: diuretics and cardiac transplant in extreme, CCB might help with symptoms
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
what are the 6 causes of restrictive cardiomyopathy?
Amyloidosis
Hemochromatosis
Fabry Disease
Gaucher Disease
Endomyocardial Fibrosis-Loeffler Endocarditis-hypereosinofilia syndrome
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 (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
DX:
EKG: might show LVH
echo: key!! show LVH, asymmetrical septal hypetrophy and small left ventricle, and diastolic dysfunction
tx:
- Beta blockers, calcium channel blockers (verapamil)
- myomectomy (to remove extra septal muscle)
- ablation, ICD, dual chamber 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
metabolic syndrome
qualifications
Major contributor to coronary disease
Three or more of the following:
Abdominal obesity
Tri >150
HDL <40 M, <50 W
Fasting glucose over 110
HTN
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
raynauds
what is this caused by? what does it look like? what is it associated with? what is the treatment?
“VASOMOTOR DISORDER”
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
hypertriglyceridemia
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
TX:
- very sensitive to diet, weight reduction and exercise
- fibrinic acid or niacin
varicose veins
what is this caused by? what does this look like? what makes this better, what makes this worse? what are 4 RF? what are the two main influencing factors for this? what is the two most common treatments for this? what about three surgical interventions?
superficial venous insufficiency and valvular incompetency
tortuous veins green blue “spider veins”, dilated in lower extermity
worsened with prolonged standing and relieved with elevation, can be related to valves or vein walls
RF: women who are pregnant, obescity, family, prolonged sitting or standing
- intrinsic weakness of vein wall and increase intraluminal pressure leads to reversal blood flow
- exposure to high pressures cause superficial veins to dilate bceause superficial veins lack support and thing walled compared to deep veins
tx: elastic stockings, leg elevation
can do laser ablation, sclerotherapy, surgical stripping
varicose veins
which vein is most common?
what are 5 things that can happen as result of having varicose veins? what test can you do?
most common is great saphenous vein
- chronic edema
- abnormal pigmentation
- fibrosis
- atrophy
- skin ulceration
brodie-tendelenburg tests: differentiates saphenofemoral valve incompetence from perforator vein incompetence (the ones that communicate between deep and superficial system)
thrombophlebitis
what is this? which vein is this most common in? what might you feel? what is the triad that puts you at higher risk for this? what is trousseaus sigh you nwa to be aware of? how do you dx? what is the TX?
partial or complete occlusion of vein and inflammatory changes“inflammatory reaction with thrombus of a being under the skin” in deep or superficial veins
most occur in saphenous vein, cord may be palpable following resolution of acute symptoms, dull pain, tenderness, asymptomatic
VIRCHOWS TRIAT (predisposes pt to this):
- stasis: >4 hrs immobolized
- vascular injury: trauma, infection, inflammation
- hypercoagubility: Factor V lieden, OCP, pregnancy
trousseau’s sign: migratory thrombophlebitis ususally associated with malignancy and vasculitis
DX: venous duplex ultrasonography (noncompressible vein with clot and vein wall thickening)
tx: supportive! elevation, rest, compression stockings, NSAIDS
giant cell arteritis
what is this an inflammation of? what two types of people does it most commonly effect? what does it frequently involve, what might this cause? what might happen in 15% of patients? what are the 5 symptoms a pt might complain of? what two labs and test do you want to do? what is the two tx and when should they begin?
medium and large vessels inflammation
>50 years old, often with polymyalgia rheumatica, 50% experience shoulder and pelvic girdle pain who have this
frequently involves temporal artery, if not treated aggressively wil cause blindness, in larger arteries can cause thoracic aortic aneurysm in 15% of pts
pts complain of: unilateral temporal headache, scalp tenderness, jaw claudication, diplopia
dx: increased ESR, CRP, but do temporal artery biopsy to confirm
tx: high dose prednisone 1-2 months and low dose aspirin, BEGIN TX IMMEDIATELY!!!!!!!
pericardial effusion
what is this? what are 5 things that can cause it?
what can it limit if large enough?
how do you dx?
what are the tx options? (5 total)
accumulation of fluid in the pericardial cavity from inflamatory or infectious process that includes pericarditis >50ml
also from:
- neoplasms
- cardiac surgery
- trauma
small pericardial effusions: can be asymptomatic
sudden acclumination of 200mL may raise intracardiac pressure enough to signiciantly limit venous return to the heart
DX: echo
Tx: depends on extent
- diuretics, NSAIDS, colchicine or corticosteroids to help minimze fluid accumulation
- pericardiocentesis, initial tx of choice for large pericardial effusion
cardiac tamponade
what is this?
what are 5 things that can cause this?
what are two things this reduces?
5 symptoms, which is most important?
how does the patient appeare?
what makes the problem worse?
compression on the heart due to the acccumulation of fluid or blood in the pericardial sac LIFE THREATENING
- trauma
- rupture of the heart post MI
- complication from a cath
- aortic dissection
- PERICARDIAL EFFUSION
increased intracardial pressure limits ventricular filling and reduces stroke volume and cardiac output **heart doesn’t fill properlly with blood**
elevated venous pressure, increase JVP, fall in systolic BP, narrowed pulse pressure, circulatory shock, **pulsus paradox** (drop >10 mmHg in the systolic BP during Insppiration this occurs because the left ventricle is more compressed because of fluid inthe sac so left ventricle has signifcantly less filling and stroke volume)
**appeare acutely ill**
since less blood getting ot the body, the sympathetic system is stimulated which prepetuates the problem
cardiac tamponade
what do you use to dx? (3)
what is the tx?
DX:
primarly echo
can add computed tomography and MRI as adjunct
TX:
closed pericardiocentesis
myocarditis
what is this?
what is the most common cause of this (3)?
what are the 8 causes of this?
a primary inflammatory process of the myocardium, most often caused by infectious agent
viral origin most common: coxsackievirus B, A, HIV, CMV etc
bacterial
fungal: aspergillos, candidiasis
parasitic: trypanosoma cruzi “changas”
Rickettsial
tx:
supportive
antimicrobial if identified agent biopsy guided
AVOID NSAIDS, can make it worse!
myocarditis
what might you see before this?
what might be the initial presentation?
what are 3 symptoms?
what are two ways you can dx this?
PRODOMAL VIRAL SYNDROME followed by symptoms of mycarditis (CP, dyspnea)
HF MAY BE THE INITIAL PRESENTATION!!!
Tachycardia, muffled heart sounds, elevated temp
DX:
difficult to confirm diagnosis
viral titer
endomyocardial biopsy may isolate virus (rare) or show characteristic pathology of myositis-inflammatory infiltrate
pericardial effusion without cardiac compression
what can this occur with?
what symptsom might you have?
what is important to see on EKG?
what is the best techique used to identify TAMPONADE?
can occur with pericarditis
symptoms if present: hiccups, nasues, coup, chest pressure
CXR: cardiomegaly >250 ml
EKG: decreased WRS voltage
echo: best technique to identify TAMPONADE
Tx: depends on if pt is hemodynamically stable or not
pericardial effusion with compression of the heart causes
temponade
pericardial effusion with compression of the heart
TAMONADE
what happens in this?
what are TWO things that are limited here?
fatal?
what happens to the pressures in RV and LV and CO?
What is the IMPORTANT THING YOU SEE?!?!!?
increasing pericardial fluid raises intrapericardial pressure resulting in compression of the heart
limits ventricular fillling and reduces stroke volume
FATAL IF NOT RECOGNIZED EARLY
causes CARDIAC TAMPONADE, compression of the heart:
1. equilibration of LV and RV diastolic pressure
2. marked decrease in CO
- BECKS TRIAD: decline in arterial pressure, elevation of venous pressure, quiet heart
what might you see on a EKG of someone with pericarditis??
what is the major sign of this?
ST elevation in all leads with the exception of aVR and V1 sometimes aVL
*****big hint here….people don’t infarct their whole heart like this!! they would be completely dead and it just doens’t happen….so if alive and you see this entire ST elevation….you see it throughout!!!! they also have a different type of chest main******
explain the concept or pulsus parodoxus?
what do you see this in?
during normal inspiration venous return increas and thre is a slight incres in RV volume this normally causes a slight right to left shift of the heart and compressing the left ventricle and decreasing LV output by a normal 2-3%
Pulsus paradoxus: marked exageration of this process increase in intrapericardial pressure so RV and LV volumes are decreased. inspiration causes a marked decrease in LV volume resulting in a systolic BP drop >10
TAMPONADE with pericardial effusion
constrictive pericarditis
explain the pathophys of this?
5 causes
initial episode of pericarditis transitions to a chronic stage with fibrosis and calcification and THICKENING of the pericardium RESTRICTION OF FILLING
failure of blood to get into the heart because of the contricted pericarditis
obliteration of the pericardial space with fusion of pericardium to the epicardium
picture the outside of you heart wrapped in ductape that you havd such stiffening of the walls that it is unable to relax properally so you get elevation of diastolic pressures in all cardiac chambers, decrease stroke volume, get less blood to the body
activates the RAAS exacerbating the probelm and appeares like right sided heart failure
causes:
radiation, TB, uremia, neoplastic, postpericardotomy (post heart surgery)
constrictive pericarditis
what do you see on PE?
5 things on PE
what do you see on CXR?
what do you see on ECHO?
- pedal edema
- abdominal ascites
- hepatomegaly
- elevated JVP KUSSMAULS SIGN (distension of neck veins during inspiration)
- KNOCK HEARD ALONG left sternal border: diastolic sound that is the sudden cessation of ventricular filling
CXR: calcification 50%
EKG: low QRS voltage
echo: pericardium densely thickened, immobile, dilation of hepatic veins
constrictive pericarditis
supportive other than pericardiectomy
infective endocarditis
what is this and what will you see on the vavlue? whare are 4 physical locations on the body that are portal of entry for the bacteria? what are 3 ways it can get into the blood? what is the most common causative organism? what are the three most common organisms that can cause it? what are 4 long term complications it can lead to?
bacteria cause infection on a cardiac valve or an endocardial surface and cause a VEGETATION “small growth” that moves with the valve
-skin, oral cavity, GI, upper respiratory
-dental work, flossing, cleaning, central lines
**most are due to bacterial infections, however some are fungal***
organisms: staph aureus most common, virdians group D streptococci, enteroccocus faecaslis
can lead to permanent damage including:
- valve damage
- HF (usually left sided)
- strokes from emboli to the brain
- damage elsewhere from emboli
what happens when prostetic valves get infected with infective endocarditis? what are 4 common concuring conditions with infective endocaridits?
usualy a DISASTER!
- rheumatic valve disease
- aortic stenosis/sclerosis/regurg
- mitral stenosis/regurge/prolapse
- congenital heart defect
what are the two most common valves involved in infective endocarditis?
what do you see on them and where are they growing? what are they made of?
aortic valve and mitral valve
vegetation occurs on the low pressure side of the valve
- mitral it occurs on the atrial side
- aortic it occurs on ventricular side
vegetation made of: platelets, fibrin, colonies of bacteria
in right ventricular infective endocarditis, which valve is involved? what is the only way you get this? what is the causative agent?
tricuspid involvement in 85% of cases
pulmonary valve in 15%
only in the setting of IV drug use!
causitive agent usually STAPH aureus
what are the 8 clinical findings you would expect to see in a patient with
infective endocarditis
- febrile
- symptoms of infectious emboli spreading elsewhere
- petechiae on palate or conjunctive (from micro emboli)
- subungal “splinter” hemmorages
5. olsers nodes-painful raished lesions on fingers and toes
6. janeway lesions: painless red lesions on palms or soles
7. roth spots-exudative lesions in retina
NEW OR CHANGING REGURGITANT MURMERS
what are the two test you can order to confirm infective endocarditis?
1. Blood cultures 3 sets 1 hour apart
- TEE-90% sensitive
explain the differences between acute and subacute presentations for infective endocarditits? which organisms are likely to cause each?
1. acute
staph aureus and other virlulent organisms
acute with rapid progressing destruction and infection
early emboli
2. subacute
virdans streptococci, enterococcus
gradular valvular destruction
what are the Duke major and minor requirements for infective endocarditis?
Major: 3
Minor: 5
What combinations do you get a definite dx?
Major:
- 2+ blood cultures
- abnormal TEE
- new/changing regurgitant murmer
Minor:
- IV drug use
- prior valve abnormality
- fever
- systemic emboli
- immunologic lesions (janeway, olsens, roth)
Definite DX:
2 major
1 major 3 minor
5 minor
what are the new guidelines for abx prophylaxis for infective endocarditis?
prosthetic heart valve
prior episode of endocarditis
complex cyanotic congenital heart disease
other valvular lesions whether congenital or acquired do not require endocarditis prophylaxis before procedures
for dental procedure use amoxicillin 2 grams 30-60 mins before surgery
what is the treatment for infective endocarditis?
and if empiric tx? (2)
viridans streptococci: penicillin G x 4 hours q 4 weeks
empiric tx while awaiting culture results: vancomycin and ceftriaxone IV
