Cardio Flashcards
1
Q
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?
A
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
2
Q
sudden cardiac death in CHD
how soon does the pt die? what most likely causes it? when does this happen?
A
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
3
Q
why are women often misdiagnosed when they have CHD? (3)
A
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!!
4
Q
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?
A
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
5
Q
what are the 3 tests you can do to help identify stable pectoris for CAD? what do they show?
A
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
6
Q
what is the drug you give for acute angina pectoris? or for prophylaxsis if the pt is going to be doing exercise?
A
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
7
Q
what are the 7 drugs you put someone on to help with chronic stable angina?
A
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
8
Q
what drug do you not want to use in CHD in a patient that has asthma/COPD because it can cause bronchospasm?
A
nonselective beta blockers
Use selective beta blocker!!
9
Q
what two drugs decrease the mortality post MI and in HF patients?
A
Beta blockers
Atenolol and metoprolol
10
Q
what 4 groups of patients with CHD qualitfy for revascularization?
A
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
11
Q
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?
A
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
12
Q
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?
A
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
13
Q
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?
A
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**
14
Q
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?
A
coronary ishchemia from vasospasms
symptoms at rest, usually in AM
women> men
ateriography shows normal looking arteries
Tx: nitrates and calcium channel blockers (dihyrdopyridines)
15
Q
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?
A
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
16
Q
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?
A
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
17
Q
what percent of people with unstable angina will have abnormal EKG?
A
50%
so worry about the 50% that have a normal one, still might need to work them up
18
Q
since the pathology of unstable angina and NSTEMI are the same….what is the only thing that you use to tell them apart?
A
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
19
Q
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?
A
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
20
Q
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?
A
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
21
Q
what are the treatments for a acute STEMI? (3)
1
1
2
A
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
22
Q
what are 3 drugs taht might be used to try to help in a actue MI early on pre hospital or in the ED?
A
- morphine sulfaste
- aspirin in ED
- nitro IV
23
Q
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?
A
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
24
Q
what are the treatments for a acute STEMI? (3)
1
1
2
A
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
25
what are 3 drugs taht might be used to try to help in a actue MI early on pre hospital or in the ED?
1. morphine sulfaste
2. aspirin in ED
3. nitro IV
26
what are the contraindications (4) and realtive contraindications (1) for thromboltic therapy for a STEMI?
**absolute contraindications:**
1. uncontrolled HTN
2. **stroke within 1 year**
**3. cerebral hemmorahage**
**4. recent head trauma**
**relative contraindications:**
1. abdominal or thoracic surgery within 3 weeks
27
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**
28
what are the drugs that you use to treat unstable angina or NSTEMI?
1. full anticoagulation and antiplatelet therapy
**-HEPARIN +ASA+**
**prasurgrel/ticagrelor/clopidigrel _OR_ glycoprotein IIb/IIIa**
2. **nitrates**
**3. Beta blockers**
**4. Ca-blockers**
29
explain when the CK MB isoenzymes rise, peak, and fall?
rise: **4-6 hours**
peak: 1**6-24 hours**
fall: **2-3 days**
30
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
31
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**
32
sinus rythmn
## Footnote
rate?
rythmn?
p waves?
QRS?
rate 60-100
rythmn regular
p waves yes and upright
QRS narrow
33
sinus tachycardia
## Footnote
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**
34
sinus bradycardia
## Footnote
rate?
rythmn?
p waves?
QRS?
causes?
rate?
rythmn? **regular**
p waves? **yes**
QRS? **narrow**
causes? common rythmn seen in early stage of acute MI
35
sinus arrythmia
## Footnote
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_**
36
premature atrial contractions
## Footnote
rate?
rythmn?
p waves?
QRS?
other? 3
**ATRIAL RE-ENTRY or increase AUTOMATICITY, premature atrial depolarization**
## Footnote
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**
37
atrial fib
## Footnote
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:
1. **in new onset without med control: _ventricular rate is very fast 120-180 bpm_**
2. goal in ED: slow rate with meds
3. Risk: BLOOD CLOT and stroke if they break off
38
atrial flutter
## Footnote
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**
1. most common presentation is **2:1 AV block with QRS ~150 bpm**
2. SAW TOOTH APPEARANCE in **II, III, aVF**
3. after meds given to slow AV conduction given, most common form of block is **4:1 with ventricular rate ~75**
4. **carotid masage can help slow VR down, allowing flutter waves to be seen**
39
paroxysmal supraventricular tachycardia (PSVT)
## Footnote
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**
1. most in young healthy people without cardiac disease, can tell you the second it started and stopped. _cardiovert with adenosine 90-95% of the time if carotid massage doesn't work_
2. can be caused by coffee, alcohol, and excitement
40
in HF, how doese the body attempt to increase cardiac output?
1. if cardiac output is low and can't support normal circulatory function, body stimulates **sympathetic stimulation to increase vasoconstriction and venous return**
2. causes increase in **RA pressure and fluid retention at kidneys because of decreased filtration rates from decreased cardiact output**
3. cardiac output rises a little from fluid retention and increased venous return
4. continue to increase right atrial pressure, fluid retention accelerates this causes **overstretching of the heart of edema of the heart muscle**
5. cardiac output drastically decreases and the pt dies of DECOMPENSATION
41
junctional tachycardia
## Footnote
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
42
multifocal atrial tachycardia
## Footnote
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
43
junctional escape rythmn
## Footnote
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**
44
premature ventricular contractions (PVCs)
## Footnote
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**
45
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_
46
torsades de points
## Footnote
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_
47
ventricular fibrillation
## Footnote
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_**
48
mitral regurgitation
## Footnote
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**
49
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!
50
what are the four tx options for mitral regurg? what must you consider regarding surgery?
1. decrease activity
2. ACE INhibitors **esp in HTN or HF, decrease preload and after load**
3. diuretics **decrease preload**
4. sugey!! **if decreased EF or LV dysfunction with progressive sxs**
\*\*\*the timing of sugery is really important because need to do it before you get left ventricular failure from response to stress, otherwise the valve only helps to much\*\*\*\*
repair better than replacement here
51
what are the five most important descriptors for mitral regurg?
1. Holosystolic systolic murmer (heard throughout entire systole), 2. THRILL
3. HIGH PITCHED
4. BLOWING
5. S3 gallop if severe
52
what are two random defomirites that are associated with _mitral valve prolapse?_
high arched palate
pectus excavatum!!
weird
53
mitral valve prolapse
## Footnote
What happens in this? what are the two causes of this? which is most common? and what two systemic conditions can cause this? what does this present with for symptoms? what else can be present? **what are the 3 key PE things you see?**
**abnormal connective tissue growth causing the leaflets to _buckle_**
caused by:
1. _familia hx, most common autosomal dominant_ (only get growth on valve)
2. systemic connective tissue disease **_MARFANS, EHLERS danlos_**
SXS: ususally asymptomatic but in women presents as _ATYPICAL CP thats "FLEETING" with palpitations_, Arrythmias present
mid to late systolic click between s1 and s2 (tensing of chordae), high pitched late systolic murmer,
**NOISE/MURMER SOFTENS WHEN SQUATTING KEY THIS MAKES HEART LARGER SO LEAFLETS FIT BETTER, _OPPOSIT OF OTHER MURMERS_**
54
mitral valve prolapse
what are the 3 PE things you might find to indicate this?
1. mid to late systolic click between s1 and s2 (tensing of chordae)
2. high pitched late systolic murmer
3. NOISE/MURMER SOFTENS WHEN SQUATTING KEY THIS MAKES HEART LARGER SO LEAFLETS FIT BETTER, OPPOSIT OF OTHER MURMERS
55
what are the 3 tx options for mitral valve prolapse?
1. reassurance #1!!!!!
## Footnote
2. Beta blocker if CP or arrythmia
3. surgery if MR severe (VERY RARE!!))
56
mitral stenosis
## Footnote
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
## Footnote
**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
57
what are the 4 PE findings for mitral stenosis?
1. LA DILATION, _LV NORMAL_ WITH LVEDP NORMAL!! (just not getting blood)
2. s1 and s2 loud
3. opening _snap_ after S2
4. _diastolic rumble low pitch_ from slow blood flow into LV
58
what are the 4 treatment options for mitral stenosis?
1. decrease Na consumption, direutics
2. control afib if present
3. preferred intervention: precutaneous balloon vulvoplasty (alternative to surgery, first option for most patients)
4. surgery if repair by #3 doesn't work/can't work
59
aortic stenosis
## Footnote
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:
1. born with **bicuspid valve**
2. **rheumatic fever**
3. _IDIPATHIC, wear and tear in eldery (_**sclerocacific**)_, MOST COMMON_
sx: DOE, **_angina pectoris, syncope with exercise ( periphreal vasodilation with decrease CO)_**
hallmark: left ventricular pressure higher than aortic pressure in systole, L sided heart failure, angina pectoralis (since heart has to work so hard to overcome increase in pressure, it requires more blood but the opening for coronary arteries is on the other side of this valve!)
carotid pulses climb, apex displaced, s4 gallop, _systolic murmer with cresendo/decresendo_, sawing gratting sound during systole, harsh low pitch
60
what are the 6 main things to remember about aortic stenosis sounds?
## Footnote
what two pt symptoms key?
1. _carotid pulses climb_
2. apex displaced
3. s4 gallop
4. _systolic murmer with cresendo/decresendo_
5. sawing gratting sound during systole
6. harsh low pitch
patient sxs: syncope, angina pectoris
61
what must you determine aortic stenosis from? what do you do to determine between the two?
aortic sclerosis
## Footnote
thickening/calcification _without fusing_, don't have symptoms
need to get echo to determine between the two?
62
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\*
63
what are the 3 surgery options for aortic stenosis?
if surgical candidate, get surgery
## Footnote
1. mild w/o symptoms: monitor, ACE, ARBS
2. SURGERY!!! replacement with tissue or mechanical valve
3. balloon valvuloplasty/transcather aortic valve implant- palliative for those who aren't surgical candidate...except in young adults
64
where do you hear aortic stenosis? what can help make it easier to hear?
2nd RICS
patient sitting leaning foward
65
what do you hear mitral stenosis and what can make it easier to hear?
apex
left lateral debiscus position
66
tricuspid regurgitation
## Footnote
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
67
pulmonic stenosis
## Footnote
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
68
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**
69
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**
70
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.
71
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
1. coronary heart disease (coronary artery disease)
2. cartotid artery disease
3. periphreal vascular disease
72
what are 9 risk factors for atherosclerosis?
which two are the most important?
1. smoking
2. diabetes mellitus
3. dyslipidemia
4. elevated CRP
5. hypertension
6. family hx in 1st degree relative
7. males
8. inactivity
73
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
74
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!
75
periphreal arterial disease
what are the three tests you can do to help diagnose it?
1. **ankle/brachial index** (higly sensitive and specific, compares systolic BP in brachial atery and posterior tibial artery) **values less than .9 suggest PAD (ankle/arm) PRESSURE IN THE LEG DECREASES since isn't being profused with blood**
**2. duplex US, pulse wave doppler**
**3. contrast angiography \*\*GOLD STANDARD\*\* and definitive, done before endocasulcar or surgical revascularization**
76
periphreal arterial disease
## Footnote
what are the 5 treatment options for PAD?
**GOAL: prevent progression**
**1. lifestyle modification**
-**_control glucose, BP, decrease BMI, stop smoking_!!!**
**2. exercise: suprevised walking program**
walk until pain comes on, stop, rest, and then begin again, *creates collateral artery formation* _30 mins 4x week PROVEN TO WORK BETTER THAN ANY DRUG!!_
**3. asprin/clopidigrel as _secondary prevention_ to prevent against MI, STOKE, Death**
4. **cilostozol:** only drug shown to help improve the symptoms of PAD other than a walking program, but not great, increased walking distance by 35%, this is *PDE inhibitor, increases cAMP and prevent platelet aggregation and promotes flow by vasodilation*
***5.*** **revascularization**
77
periphreal vascular disease
## Footnote
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**
78
acute aterial occlusion
## Footnote
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
79
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!!
80
periphreal arterial disease
## Footnote
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
81
what are the symptoms that suggest an acute arterial occlusion is an emergency?
6 p's
1. pain
2. pallor
3. _pulselessness_
_4. parenthesia_
_5. poikilothemia_
_6. paraylysis_
_these indicate tissue could die and threatens limb vitality so what to get vascular on board stat to hopefully prevent amputation_
82
chronic venous insufficiency
## Footnote
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
1. intermittent leg elevation
2. compression stockings
3. calf exercise
83
if chronic venous insufficiency transitions into stasis dermatitis, how do you treat it?
wet compresses
hydrocortisone cream
possibly zinc if chronic
84
aortic aneurysm
## Footnote
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:
1. **abdominal US \*\*study of choice\*\***
**2. CT angiography or MRA (**magnetic resonance angiography) prior to intervention OR for thoracic
85
who is important to screen for aortic aneurysm? 3
1. male
2. smoker
3. \>6o years old with PAD and family history of AAA
86
explain the risk of rupture for aortic aneurysm based on the size and what are the tx reccomendations at each stage?
1. **watch it and monitor it**
2. **\>5cm:** 20-40% over 5 years rupture, surgical to remove _ELECTIVE SURGERY ADVISED!!_
3. **\>6cm: 15% risk it will rupture annually**, _ALWAYS SURGERY,_ _REMOVE IT!!!!_
Tx:
1. open surgical repair (open with graft placement)
2. endovascular (no surgical candidates, stents placed to reduce risk of rupture
87
prognosis of aortic aneursym is related to what two things?
1. size of aneurysm
2. CAD
88
what is the mortality rate of ruptured aortic aneurysm?
**90%!!!!!**
**thats why its important to try to monitor it and find it early!!!!**
89
aortic regurgitation
## Footnote
is this more common in m/f? what are four things that can cause this? what is the pathophys about what happens in this? what is important to note about the symptom onset??
75% in males
failure of the aortic valve to close all the way causing backflow into left ventricle
1. rheumatic heart disease
2. endocarditis on different valve
3. bicuspid valve
4. connective tissue disease
**increase LVEDV, causing LV dilation leading to LV dysfunction with decrease EF and backs up to the lungs**
1. blood still flowing from the RA
2. blood backing up from the aorta
\*\*\*\*\***LV failure often preceeds symptoms by 10-15 years so you MUST do serial echo/dopple to analyze to catch it before it is too late\*\*\*\*\***
90
aortic regurgitation
## Footnote
what are 5 interesting presentations that can occur at the arteries/pulses with aortic regurg?
1. **Water hammer pulse:** rapid rising and collapsing of the pulse, bounds against finger
**2. Quinke's pulse:** alternating flushing and paling at the skin at the root of the nail
**3. pistole pulse over femoral artery**
**4. Derosiez's sign** to and from murmer over femoral artery
**5. arterial pulse pressure widening**: larger systolic and smaller diastolic so the difference is larger
91
aortic regurge
## Footnote
where do you hear it? what does it sound like? what can you feel? what happens with the apex?
1. apex displaces laterally/inferiorlly
2. diastolic thrill along left sternal border
3. S3 with "blowing" diastolic _decresendo_ murmer
4. best heard with pt leaning foward 2-3rd LICS
92
what are the 3 test you use to dx a aortic regurg?
1. EKG: LVH over time
**2. echo:** LV dysfunction later on, can see the aortic regurg jet detectable and semi quantifiable **best!**
3. cath: tells regurg amount, LV dysfunction, intracardiac pressure (not usually need in young pt)
93
what are the 3 treatment options for aortic regurg?
1. **vasodilators: ACE/hyrdralizazide to decrease afterload**
**2. diruertics: decrease preload**
**3. Surgery with tissue or mechanical valve replacement**
94
what is the most common cause of HF?
* *coronary heart disease**
* *aka MI/ischemia accounts for _75% of all HF cases!!!_**
95
heart failure
## Footnote
explain the patho for this? **what is the most commong cause of HF**? what are the other 4 things that cause cause it? what is something important you want to remember about HF as a condition?
a physiologic state in which _abnormal cardiac function_ _prevents the heart from pumping blood at a rate necessary to meet the requirements_ of metabolizing tissues
to compensate you create **abnormally elevated diastolic volume/pressure**
**_this process causes a progressive weakening in the myocardium and the consequences are HEART FAILURE!!_**
1. **CHD: MIs/ischemia account for 75% MOST COMMON CAUSE**
2. primary pump failure
3. valvular disease
4. congenital heart disease
5. longstanding uncontrolled HTN
\*\*\*keep in mind HF is a dynamic state, so patients can enter and leave it when exposed to stimuli\*\*\*\*
96
what must you remember about the tx of HF? why are the number of deaths increasing despite increase RX?
it must be individiualized for each patient!!!
**there is an increase in the number of deaths despite improvements in Rx because**
1. the baby boomers are getting older and there are just more people with this condition
2. increased salavage of people in strokes
97
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!*
98
explain:
1. acute HF (1 cause, 4 symptoms)
2. chronic HF (3 causes, 2 symptoms)
what is something to keep in mind about the relationhip of the two?
**1. ACUTE HF: caused by _LARGE MI_**
**sudden onset of symptoms, systolic failure, hypotension, and pulmonary edema**
*immediately the heart stops working correctly, everything gets backed up!!!*
**2. CHRONIC HF** **slow and gradual, cause by dilated cardiomyopathy, chronic valvular insufficiency, low EF**
**a. bp maintained till late**
**b. periphreal edema common**
keep in mind an acute episode can superimpose on a chronic HF, exacerbation of HF
99
explain:
1. Left sided HF (leads to what? 2 causes)
2. Right sided HF (associated with what? 2 causes)
what is the most common cause of right sided HF?
1. **left sided heat failure:** inadequate CO with _pulmonary congestion_
causes: post MI, aortic/mitral valve disease
2. **right sided heart failure:** associated with _peripheral edema, hepatic congestion_
causes: COPD/pulmonary HTN, pulmonic stenosis
most common cause of right sided HF is left sided heart failure!! backs it all up!!
100
explain the pathogenisis of:
1. backward HF (where does the fluid go?)
2. forward HF (what does this cause via what system?)
**1. backward HF:** inadequate ventricular emptying so the pressure in the atrium and venous system increase because the blood keeps coming and the ventricle is failing, _causes transudation of fluid into interstitial spaces_
**2. forward HF:** inadequate forward CO, causes _Na and water retention since kidneys aren’t being profuses, mechanism: renin-angiotensin-aldosterone system_
101
what are the bodys 2 main compensatory mechanisms if not getting enough blood profusion because of HF?
## Footnote
what are the two main mechanisms? how do they accomplush this? what is the _consequences of these actions?_
1. **redistribution of CO:** blood flow goes to vital organs first like brain and heart with reduced flow to skin and muscle via _adrenergic nervous system! aka sympathetic nervous system_
**2. Na and water retention since kidneys not profusing via renin-angiotensin system:** accumulation of fluid and increasing venous return primarily from _sympathetic nervous system with NE release_
-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.
102
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_
103
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_**
104
what is aldosterone and what does it do in the body?
aldosterone is a **mineralcorticoid** hormone that causes **increased renal _Na and H2O**_ _**reabsorption_**
105
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_
## Footnote
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!\*\*\*
106
what are the four stages for heart failure?
**1.** no limitation of physical activity
2. slight limitation of physical activitiy, some activities so **SOB on exertion**
3. markled limitation of physical activities, like **ADLS cause SOB**
4. symptomatic at rest or with minimal activity, **unable to enage in physical activity**
107
what are the 7 presentations of a patient that would suggest they are experience HF?
**1. dyspnea**
**2. orthopnea**
**3. paryoxysmal nocturnal dyspnea**
**4. abdominal symptoms**
5**. cerebral symptoms** (decreased profusion to brain)
6. **unexplained weight gain from swelling in the legs**
**7. acute pulmonary edema \*\*\*MEDICAL EMERGENCY WORST POSSIBLE SITUATION....patient drowning in their own fluid backing into the alveoli!!!\*\*\*\***
108
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**
109
what are the 7 physical findings that you could find in a pt suspected of HF?
1. _tachycardia common_
_2. crackers_
_3. S3 gallop low in pitch in early diastole (associated with HF)_
_4. increased JVP_
_5. hepato-jugular reflex_ (push on liver JVD goes up)
_6. cardiac cachexia "wasted appearance"_
_7. pleura effusions with high levels of pulomary pressure!!_
110
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**
111
what are the 6 goals of treatment for HF?
2. treat underlying cause
3. reduction of cardiac workload (preload/postload)
4. control excessive Na/water retention
5. early initiation of ACEI/ARB (hydralazine in blacks)
6. enhancement of cardiac contractility
112
what type of diet is reccomended for HF patients?
**NO SALT ADDED.**
113
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*
114
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**
115
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**
116
what are the three vasodilator drugs are typically used in treating the afterload in HF?
(3 drugs)
1. what two things cause it cause as SE? what can it do? what does it decrease?
2. what doesnt't this cause?
3. what does this inhibit? what does it do?
**1. ACE inhiborts**
-caution *hypotension, dry cough*
**decrease mortality by \>25%**
**decrease remodeling (fibrosis, wall thinning, cell death)**
**2. angiotensin II receptor blockers**
less protection against remodeling than ACE but don't cause cough
**3. sacubitril**
_neprilysin inhibitor_
degrades vasoactive peptides
117
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!!!!!**
1. slowed HF progression better than a ACE alone
2. se: hypotension, angioedema, hyperkalemia
118
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
119
what is are the primary and secondary indications for a ICD?
indications:
_secondary:_ **resuscitated cardiac arrest/vfib or hemodynamically unstable Vtach**
_primary:_ **EF**
120
what are the two types of categories of HTN and which is most common?
what are five things that can cause the second?
**essential hypertension:**
aka idiopathic/primary 95% of cases, etiology unknown
**secondary hypertension:** 5% of cases
1. estrogen use increases RAAS
2. intrinsic renal disease (any form of chronic renal parenchymal disease)
3. renovascular HTN
4. endocrine HTN
5. pregnancy
121
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
122
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
123
what are 5 exacerbating factors for HTN that can make it worse?
obesity
Na in diet
cigarette smoking increases NE
NSAIDS
excess alcohol
124
explain the ways in which HTN effect and contribute to end organ damage in:
1. heart
2. brain
3. arteries
4. 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_
125
since HTN is usually asymptomatic, what symptoms let on a pt might have it? 8
1. SOB, DOE from LVH
2. TIA, stroke, hemmorage
3. MI, angina, HF
126
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
127
what are the 3 most important labs you want to check in a patient you are concerned about HTN?
1. _creatine, BUN_
2. electrolytes Na and _K_ (want to check K cause you will likely put them on a dieuretic and this can cause hypokalemia)
3. lipid levels: TC, LDL, HDL, triglycerides
128
what drugs will you typically use to treat HTN in
**black populations**
thiazide and/or CCB
129
what drugs will you typically use to treat HTN in
**pts \>18 with CKD**
1. ACE
2. ARB if can't tolerate ACE
_use these regardless of race or diabetes status if they have CKD!!!!!!! big hint there!!_
130
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
131
what are the physical exam findings that can suggest a patient has HTN since it is mostly asymptomatic? 6
1. narrowing of the arterioles _A/V_
2. _A-V nicking_ (arteriosclerosis where artery looks like it is crossing the vein)
3. **silver or copper wired appearance**
4. hemorrhages or exudates
5. **papilledema**
6. bruits
132
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_**
133
which number should you focus on when trying to reduce morbidity and mortality?
SYSTOLIC BP!
134
what are four non pharm ways to decrease HTN?
diet
weight reduction, aerobic activity
decrease alcohol, Na intake DASH DIET
smoking cessation
135
what is the reccomended 1st choice for the majority of patients when treating HTN?
thaizide dieuretic
136
thiazide dieuretics for HTN
## Footnote
who are these most potent in 3? which patients should you avoid these in? what is the doseage? what can they cause 4?
1. 1st line therapy and should be included in ANY drug therapy
2. more potent in _blacks, elderly, obese_
3. avoid in patiens with _hyponaturemia and gout_
4. _LOW DOSAGE_
5. can cause _hypokalemia, hyperurcemia,_ _hyperglycemia, abnormalities of lipids_
137
beta blockers in tx of HTN
## Footnote
what do they decreaes? who are they helpful in 4? what are the 4 SE you need to be aware of if prescribing to a pt?
used as a 2nd or 3rd line drug because of increased risk for _stroke_
1. decreases CO
2. helpful in pts with other comorbid disorders like:
- angina pectoris, post MI, migrain headaches, essential tremors
3. SE: _exacerbation of bronchospasms in nonselective, bradycardia, worse acute HF, masks signs of hypoglycemia in diabetics!!_
138
ACE inhibitors
## Footnote
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_
139
angiotensin II receptor blocker (ARBS)
losartan
like ACE but no cough!
renoprotective in diabetics
140
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
141
calcium channel blockers for HTN
## Footnote
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_
142
alpha receptor blockers
## Footnote
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)_
143
centrally acting agents
## Footnote
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
144
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
145
what are the guidelines for txing HTN?
this is a lot of info so probs just read through it!
1. Initial rx: thiazide diuretic with some exceptions
if diabetic start on ACE then use thiazide diuretic later, multiple agents often needed
2 . initial low dose and follow up in 4-6 weeks
3. titrate up to moderate/high dose before adding a second agent exception:
i. if the first drug is a thiazide, low dose is sufficient and shouldn’t increase the dose so add the second med instead of increasing the dose
4. second drug would be BB, ACEI, or Ca blocker Exception:
ii. if **BP is \>160/90 can start dual Rx** at the same time
5. most patients will be controlled with 2 drugs, but if need three, usually diuretic, ACE and CCB
146
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
147
what are the 3 reasons you would want ambulatory monitoring of a patients cardiac symptoms?
1. arrythmia detection and correlating it with patient symptoms
2. evaluation of syncope
3. arrythmia tx effectiveness
148
what are 5 reasons you would want to do a stress test on a patient?
1. _CP/angina pectoris_
2. functional ability in _CHD_
3. screening of _high risk_ individuals with atypical symptoms
4. response to intervention (cath, CABG), check them before they are released
5. screening for patients with certain occupation requirements
149
low pretest probability (Stress test)
## Footnote
what two population characteristics fall into this category? do you do a stress test in them?
1. _asymptomatic_ men and women of all ages
2. _women_
avoid stress testing in this group!! high rate of false positives and then you are stuck with the results and have to work them up!
150
intermediate pretest probability for stress test (10-90%)
## Footnote
what are the 3 population characterstics for this group? should you do a stress test in this population?
1. men of all ages with _atypical chest pain_
2. women _\>50 with atypical chest pain_
3. women _30-60 with typical CP_
stress tests warrented in this group for DX of CAD!
151
high pretest probability (90%) for stress in CAD
## Footnote
what are the two population characteristics of this group? what might this provide? what might you want to consider as testing for this group instead?
1. men \>40 with typical CP
2. women \>60 with typical CP
might provide _prognostic value_ in this group, may want to consider _coronary angiograph instead because high risk!_
152
what are the four indications to STOP a stress test?
1. evidence of _ishchemia with ST depression of T wave inversion_
2. achieve target _HR of 85-90%_ of predicted maximal HR (220-age)
3. dangerous _arrythmia_
4. _decreasing BP! STOP!_
153
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!!
154
explain what these four meds do in pharmocologic stress tests and which ones they are used in?
## Footnote
1. adenosine
2. dipyridamole
3. regadenoson
4. dubutamine
**1. _adenosine_**: dilates coronary arteries used in _nuclear imaging_
**_2. dypyridamole:_** dilates coronary arteries used in _nuclear imaging_
**_3. regadenoson_** dilates the coronary arteries \*\*\*MOST COMMONLY USED\*\*\*give _bolus injection_ works like adenosine
**_4. dubutamine:_** increases HR and contractility used in _echo!_
155
what are the 3 qualities you used to deteremines a patients _pretest probability for CHD?_
what are the three questions you want to ask them about their type of CP?
age, gender, characteristic of CP
1. substernal?
2. brought on by exertion?
3. relieved by NTG?
156
what do you need to keep in mind about women and stress tests? (3)
1. high incidence of _false positivites_ in young healthy women w/o risk factors and atypical CP
## Footnote
2. decreased sensitivitiy in women with CHD because they are more likely to have 1 vessel disease
3. _ORDER STRESS WITH IMAGING FOR THESE PEOPLE!_ young without RF or atypical CP
157
what are the _4 things that make it so you can't read an EKG that make it useless to do a stress EKG??_
1. LVH
2. LBBB
3. Digoxin
4. WPW abnormality!!
\*\*DON'T READ THEM, YOU'LL LOOK DUMB!!!\*\*
158
what is the gold standard for cornary imaging? who is it warranted in?
left heart cath to do coronary angiography
## Footnote
do in: high risk individuals with classic ischemia symptoms
159
what would you see on a stress test that indicates a positives test?
downward or horizontal sloping ST depression or T wave inversion
160
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
161
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
162
which lead should you NOT look at when interpreting Q waves?
aVR these Q waves are never significant!!!
163
what are the 2 qualifications for ischemia on the EKG?
## Footnote
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_
## Footnote
\*\*only needs to be in 1 lead!!\*\*
compare the PR segment and the ST segment using the J point
**2 other causes:** hypokalemia, digoxin
164
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"
165
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?
1. ischemia but NOT dianostic for MI
2. first couple hours then they invert
3. "hyperacute T waves"
4. potentially reversible if blood flow is returned, T wave will return to normal
166
stage 2 MI:
ST segement
1. when does this occur?
2. what is the qualification for it to be called ST elevation?
what leads can it be in?
what does it indicate?
does it go away?
1. occurs after a couple hours
2. _ST elevation at the J point \>1 mm in two or more **contigious** leads_
3. can be in limb or precordial
4. INJURY beyond ischemia!!! occurs in acute MI but can return to normal if blood flow returned tells you that a true infarction has occured and that it will evolve into death unless there is immediate intervention
167
explain what early depolarization is?
how is this different than ST elevation?
1. some people have regullarly elevated ST segment
2. common in young healthy individuals
3. ST returns to baseline during exercise
How to differentiate from MI:
1. _t wave remains an independent waveform, aka the ST segment doesn't blend with T wave_
2. _in MI: ST merges with T wave_
168
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?
1. occurs 2-3 days later
2. _\>.04 seconds wide and \>1/3 height of R wave_
3. "death" has occured, not reversible
4. diagnostic of MI
5. by the point Q waves develop, ST returns to baseline
6. persist for lifetime of pt
169
inferior MI
## Footnote
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!!\*\*\*\***
170
where do you see the lead changes for a inferior MI?
II, aVF, III
reciprocal if present in lateral leads! I and aVL
171
left lateral MI
## Footnote
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!**
172
what leads would you see changes if you were suspecting a lateral wall MI?
changes: aVL, I, V5, V6
reciprocal changes in inferior leads!
173
anterior MI
## Footnote
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**
174
anterolateral MI
## Footnote
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!
175
what does this show you?
anterior infarction
V1-V4 shows anterior heart
176
posterior MI
## Footnote
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
1. must distinguish between this and right axis deviation because in RAD you will also have tall R wave so need to check V6 for large S wave
2. often occurs with INFERIOR MI because they are from the same blood supply of the right cornary artery
in the pic...note tall R waves in V1, to rule our RAD, look at V6, there are tall R instead of deep S so this is posterior MI
177
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!
178
first degree AV block
## Footnote
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_
179
sick sinus syndrome
## Footnote
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**
180
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
181
dilated cardiomyopathy
## Footnote
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
182
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
183
second degree AV block general
## Footnote
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**
184
mobitz type II second degree AV block
## Footnote
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_**
185
What are two really unique things that can cause a person to be in 3rd degree complete heart block?
1. lyme disease...so check titers
## Footnote
2. congenital heart block, they are born with it where their junction rythmn has been sufficient to supply blood so they are asymptomatic
186
what is the LEADING cause of COMPLETE HEART BLOCK?
degenerative disease of the conduction system
187
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_**
188
third degree AV block
## Footnote
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!!
189
right bundle branch block
## Footnote
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_
190
left bundle branch block
## Footnote
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
191
hemiblocks general
## Footnote
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)
192
left anterior hemiblock
## Footnote
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
193
Left posterior fasicle
## Footnote
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
194
WHAT IS THE MOST COMMON HEMIBLOCK?
LEFT ANTERIOR FASICLE HEMIBLOCK
195
why are women often misdiagnosed when they have CHD? (3)
**1. atypical symptoms: pain radiating to _right arm_**, _arm pain along_
2. many women produce false negative stress tests since single vessel disease more common
**3. elderly or diabetic womeon complain of general malaise, loss of appetite, vague abdominal pain** so if they have RF, GET EKG!!
196
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
197
what is the major source of endogenously derived cholesterol?
what about exogenously?
liver and intestines
exogenously: diet
198
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_
199
what are the goals for LDL lowering?
TRICK QUESTION...there are no goal levels anymore, it is based on _intensity of statin therapy!!!_
200
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
201
restrictive cardiomyopathies
## Footnote
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
202
explain the relationship between lipids and athlerosclerosis?
(both LDL and HDL)
1. vascular injury like smoking DM facilitates the uptake of lipoproteins
2. increase in LDL (oxidized) directly leads to vascular damage and premature atherosclerosis
3. LDL oxidation is nessacary for endothelia damage
4. _HDL_: cardioprotective and prevents the oxidation of LDL, reverse transporter of cholesterol
203
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_
1. DIABETES MELLITUS
2. nephrotic syndrome
3. Chronic renal failure
4. hypothyroidism
204
those who have athlerosclerosis commonly have....
dyslipidemia
205
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_
206
what are four things you might find if a patient that has hyperlipidemia?
1. **_athlerosclerosis_** disease like PVD, CHD
2. **_eruptive xanthomas_:** can be seen on the buttocks with extremely high levels of triglycerides
3. **_tendinous xanthomas_:** very high LDL, nodules on tendons most commonly on achilles, back of hand, and patella
4. **_xanthelasma_**: yellow plaque on the skin around the eyes
207
explain the four treatment groups and what type of statin therapy they would recieve?
208
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!!\*\*
209
how much can you expect high intensity statins to lower LDL?
what are the two drugs?
lowers LDL by 50%
atorvastatin, rousuvastatin
210
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
211
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!\*\*
212
familia dyslipidemia
## Footnote
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_
213
hypertriglyceridemia
## Footnote
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:
1. **very sensitive to diet, weight reduction and exercise**
2. **fibrinic acid or niacin**
214
what are the 5 lifestyle adjustments you can make to decrease dyslipidemia?
1. smoking cessation
2. decrease intake of saturated fats
3. decrease total calories
4. increase physical activity
5. decrease sodium intake
215
HMG CoA inhibitos
## Footnote
what do these do?
what is important about the dosing?
what can it cause
what are two SE?
rate limiting step in cholesterol synthesis; up regulates LDL receptors
1. low dose gives you the most bang for your buck, increasing dose you see less effective
2. can cause _chemical diabetes_ but the benefits outweigh the risks
3. _myalgia_
_4. myositis and rhabdomyolysis_
216
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....
217
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!!!
218
atrial fib
## Footnote
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_
219
how long do you need to have afib to be at risk for thromboemboli?
48-72 hours
220
lone atrial fibrillation
## Footnote
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
221
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**
222
hypertrophic cardiomyopathy
## Footnote
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:**
1. Beta blockers, calcium channel blockers
2. ablation
3. defib, pacers and mitral valve replacements as needed
223
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\*\*\*\*\*\*
224
what are the two management strategies for Afib?
are they both ok to use?
1. rythmn control
2. rate control
\*\*\*\*both rythmn control and rate control are acceptable long term strategies to prevent morality, stroke, and quality of life, choice of tx strategy is based on SYMPTOMS!! risk of bleeding, and side effects of the anti-arrhymics\*\*\*
225
rythmn control method for
chronic/recurrent Afib
what is the goal of this method?
what are benefits/negatives?
if you can't cardiovert via meds, what are your next two options?
what two meds do you use to prevent afib recurrance?
what percent will have afib reocurrance?
goal: _cardiovert to NSR and use drug to maintain SR_ (often young people so that way they have no limitations)
benefits: increase cardiac output/function
negatives: side effects of meds and reccurances
if you can't cardiovert with med
1. **_DC cardioversion after being on antiarrythmic_**: 90% successful
2. if recurrence: **_DEFINITIVE RX: ABLATION VIA CATH_** (eliminates Pacs that initiate afib)
_drugs to maintain SR once cardioverted_
1. Type IC fleocainide
2. type III **_amiodarone_**
50% WILL HAVE RECURRANCE RATE
226
_rate control_ approach for chronic/reccurent afib
## Footnote
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
227
restrictive cardiomyopathies
## Footnote
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
228
hypertrophic cardiomyopathy
## Footnote
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
229
what are the 6 causes of restrictive cardiomyopathy?
Amyloidosis
Hemochromatosis
Fabry Disease
Gaucher Disease
Endomyocardial Fibrosis-Loeffler Endocarditis-hypereosinofilia syndrome
230
hypertrophic cardiomyopathy
## Footnote
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:**
1. **_Beta blockers,_** **_calcium channel blockers (verapamil)_**
2. **_myomectomy_** (to remove extra septal muscle)
3. **_ablation_**, **_ICD_**, **_dual chamber pacers_** and mitral valve replacements as needed
231
hypertrophic cardiomyopathy
## Footnote
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_**
232
metabolic syndrome
## Footnote
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_**
233
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\*\****
234
superficial thrombophlebitits
## Footnote
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
235
raynauds
## Footnote
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
236
hypertriglyceridemia
## Footnote
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:
1. **very sensitive to diet, weight reduction and exercise**
2. **fibrinic acid or niacin**
237
varicose veins
## Footnote
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
1. intrinsic _weakness_ of vein wall and _increase intraluminal pressure_ leads to **reversal blood flow**
2. 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
238
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**
1. chronic edema
2. abnormal pigmentation
3. fibrosis
4. atrophy
5. skin ulceration
**brodie-tendelenburg tests: differentiates saphenofemoral valve incompetence from perforator vein incompetence** (the ones that communicate between deep and superficial system)
239
thrombophlebitis
## Footnote
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):_
1. stasis: \>4 hrs immobolized
2. vascular injury: trauma, infection, inflammation
3. 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
240
giant cell arteritis
## Footnote
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!!!!!!!
241
pericardial effusion
## Footnote
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:
1. neoplasms
2. cardiac surgery
3. 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
1. **diuretics, NSAIDS, colchicine or corticosteroids** to help minimze fluid accumulation
2. **pericardiocentesis, initial _tx of choice for large pericardial effusion_**
242
cardiac tamponade
## Footnote
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**
1. trauma
2. rupture of the heart post MI
3. complication from a cath
4. aortic dissection
5. 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
243
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
244
myocarditis
## Footnote
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!_
245
myocarditis
## Footnote
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**
246
pericardial effusion without cardiac compression
## Footnote
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
247
pericardial effusion with compression of the heart causes
temponade
248
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**
3. **_BECKS TRIAD: decline in arterial pressure, elevation of venous pressure, quiet heart_**
249
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_**\*\*\*\*\*\*
250
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_**
251
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)**
252
constrictive pericarditis
what do you see on PE?
5 things on PE
what do you see on CXR?
what do you see on **ECHO**?
1. pedal edema
2. abdominal ascites
3. hepatomegaly
4. **_elevated JVP KUSSMAULS SIGN (distension of neck veins during inspiration_**)
5. _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_**
253
constrictive pericarditis
supportive other than pericardiectomy
254
infective endocarditis
## Footnote
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:
1. valve damage
2. HF (usually left sided)
3. strokes from emboli to the brain
4. damage elsewhere from emboli
255
what happens when prostetic valves get infected with infective endocarditis? what are 4 common concuring conditions with infective endocaridits?
usualy a DISASTER!
1. rheumatic valve disease
2. aortic stenosis/sclerosis/regurg
3. mitral stenosis/regurge/prolapse
4. congenital heart defect
256
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
1. mitral it occurs on the atrial side
2. aortic it occurs on ventricular side
vegetation made of: **platelets, fibrin, colonies of bacteria**
257
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_**
258
what are the **_8_** clinical findings you would expect to see in a patient with
## Footnote
**infective endocarditis**
1. febrile
2. symptoms of infectious emboli spreading elsewhere
3. _petechiae on palate or conjunctive_ (from micro emboli)
4. _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_**
260
what are the two test you can order to confirm infective endocarditis?
**1. Blood cultures 3 sets 1 hour apart**
2. **TEE-90% sensitive**
261
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
262
what are the Duke major and minor requirements for infective endocarditis?
Major: 3
Minor: 5
What combinations do you get a definite dx?
Major:
1. 2+ blood cultures
2. abnormal TEE
3. new/changing regurgitant murmer
Minor:
1. IV drug use
2. prior valve abnormality
3. fever
4. systemic emboli
5. immunologic lesions (janeway, olsens, roth)
**_Definite DX:_**
**2 major**
**1 major 3 minor**
**5 minor**
263
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
264
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_
