CV2-Cardio Flashcards
what is predictive for a persons recovery/mortality from HF?
ejection fraction
what percent of people with HF die suddenly?
30-40%
what is the prognosis for HF once symptomatic?
if class 4 failure…what is the mortality in the first year?
pretty poor once symptomatic
if stage 4 the mortality is 40-50% if the first year alone…. :(
what can chronic elevation of catecholamines and sympathetic nervous system activity cause on the heart?
3 things
- progressive myocardial damage
- fibrosis (dysfunction)
- remodeling
what are the benefits and negatives of using a mechanical valve vs a tissue valve?
mechanical valve:
- last forever
- predispose pts for clot and stroke so must be put on a anticoagulant
tissue valve:
- don’t need anticoagulants
- can deteriorate over time
***tissue is the preferred method for those over 70!!**
what is another name for aortic regurgitation?
aortic insufficiency
aortic regurgitation
is this more common in m/f? what are four things that can cause this? what is the pathophys about what happens in this? what is important to note about the symptom onset??
75% in males
failure of the aortic valve to close all the way causing backflow into left ventricle
- rheumatic heart disease
- endocarditis on different valve
- bicuspid valve
- connective tissue disease
increase LVEDV, causing LV dilation leading to LV dysfunction with decrease EF and backs up to the lungs
- blood still flowing from the RA
- blood backing up from the aorta
*****LV failure often preceeds symptoms by 10-15 years so you MUST do serial echo/dopple to analyze to catch it before it is too late*****
aortic regurgitation
what are 5 interesting presentations that can occur at the arteries/pulses with aortic regurg?
- Water hammer pulse: rapid rising and collapsing of the pulse, bounds against finger
2. Quinke’s pulse: alternating flushing and paling at the skin at the root of the nail
3. pistole pulse over femoral artery
4. Derosiez’s sign to and from murmer over femoral artery
5. arterial pulse pressure widening: larger systolic and smaller diastolic so the difference is larger
aortic regurge
where do you hear it? what does it sound like? what can you feel? what happens with the apex?
- apex displaces laterally/inferiorlly
- diastolic thrill along left sternal border
- S3 with “blowing” diastolic decresendo murmer
- best heard with pt leaning foward 2-3rd LICS
what are the 3 test you use to dx a aortic regurg?
- EKG: LVH over time
2. echo: LV dysfunction later on, can see the aortic regurg jet detectable and semi quantifiable best!
- cath: tells regurg amount, LV dysfunction, intracardiac pressure (not usually need in young pt)
what are the 3 treatment options for aortic regurg?
- vasodilators: ACE/hyrdralizazide to decrease afterload
2. diruertics: decrease preload
3. Surgery with tissue or mechanical valve replacement
what is the most common cause of HF?
- *coronary heart disease**
- *aka MI/ischemia accounts for 75% of all HF cases!!!**
heart failure
explain the patho for this? what is the most commong cause of HF? what are the other 4 things that cause cause it? what is something important you want to remember about HF as a condition?
a physiologic state in which abnormal cardiac function prevents the heart from pumping blood at a rate necessary to meet the requirements of metabolizing tissues
to compensate you create abnormally elevated diastolic volume/pressure
this process causes a progressive weakening in the myocardium and the consequences are HEART FAILURE!!
- CHD: MIs/ischemia account for 75% MOST COMMON CAUSE
- primary pump failure
- valvular disease
- congenital heart disease
- longstanding uncontrolled HTN
***keep in mind HF is a dynamic state, so patients can enter and leave it when exposed to stimuli****
what must you remember about the tx of HF? why are the number of deaths increasing despite increase RX?
it must be individiualized for each patient!!!
there is an increase in the number of deaths despite improvements in Rx because
- the baby boomers are getting older and there are just more people with this condition
- increased salavage of people in strokes
explain:
systolic heart failure (2 causes)
diastolic heart failure (4 causes)
what do you need to remember about these?
1. systolic heart failure: primary contraction abnormality
can get O2 to the tissues
causes: MIs, dilated cardiomyopathies
2. diastolic heart failure: impaired ventricular relaxation
elevation of ventricular filling pressures because if the ventricle can’t relax the heart has to work harder to fill it, backs up to the lungs
- causes: chronic HTN with LVH, hypertrophic cardiomyopathies, acute ischemia, restrictive cardiomyopathy*
- keep in mind these usually occur together!*
explain:
- acute HF (1 cause, 4 symptoms)
- chronic HF (3 causes, 2 symptoms)
what is something to keep in mind about the relationhip of the two?
1. ACUTE HF: caused by LARGE MI
sudden onset of symptoms, systolic failure, hypotension, and pulmonary edema
immediately the heart stops working correctly, everything gets backed up!!!
2. CHRONIC HF slow and gradual, cause by dilated cardiomyopathy, chronic valvular insufficiency, low EF
a. bp maintained till late
b. periphreal edema common
keep in mind an acute episode can superimpose on a chronic HF, exacerbation of HF
explain:
- Left sided HF (leads to what? 2 causes)
- Right sided HF (associated with what? 2 causes)
what is the most common cause of right sided HF?
-
left sided heat failure: inadequate CO with pulmonary congestion
causes: post MI, aortic/mitral valve disease -
right sided heart failure: associated with peripheral edema, hepatic congestion
causes: COPD/pulmonary HTN, pulmonic stenosis
most common cause of right sided HF is left sided heart failure!! backs it all up!!
explain the pathogenisis of:
- backward HF (where does the fluid go?)
- forward HF (what does this cause via what system?)
1. backward HF: inadequate ventricular emptying so the pressure in the atrium and venous system increase because the blood keeps coming and the ventricle is failing, causes transudation of fluid into interstitial spaces
2. forward HF: inadequate forward CO, causes Na and water retention since kidneys aren’t being profuses, mechanism: renin-angiotensin-aldosterone system
what are the bodys 2 main compensatory mechanisms if not getting enough blood profusion because of HF?
what are the two main mechanisms? how do they accomplush this? what is the consequences of these actions?
- redistribution of CO: blood flow goes to vital organs first like brain and heart with reduced flow to skin and muscle via adrenergic nervous system! aka sympathetic nervous system
2. Na and water retention since kidneys not profusing via renin-angiotensin system: accumulation of fluid and increasing venous return primarily from sympathetic nervous system with NE release
-maintains CO via STARLING MECHANISM
**consequence of this is volume overload and increase afterload that perpetuates the problem**keep in mind they are easy to turn on but hard to turn off….just like men.
explain how the bodies adrenergic nervous system is helpful and harmful in a pt who has HF?
Benefit of increased NE:
increase HR, contractility, and systemic vascular resistance helps to maintain arterial perfusion pressure
negatives of increased NE:
- elevated systemic vascular resistance increases burden or afterload and increases O2 requirement, making the heart have to work harder
- long term elevation of catecholamines** leads to progressive myocardial damage and fibrosis=**maladaptive remodeling or the shape of the ventricle changing from a cylinder to a sphere, perpetuates the problem
what is the most important/potent vasoconstrictor in the body? what specific thing does it constric?
angtiotensin II
causes arterioles to constrict increasing BP and SVR
what is aldosterone and what does it do in the body?
aldosterone is a mineralcorticoid hormone that causes increased renal Na and H2O** **reabsorption
what does long term activation of antgiotensin II and aldosterone lead to and why is this bad in HF patients?
what does it do to the mycardium and what structual changes does it cause?
leads to myocardial thinning and fibrosis aka maladaptive remodeling
this over time changes the shape of the ventricle from a cylander to a sphere making it able to pump less effectively, this mean its exacerbates the problem
***keep in mind the renin-angiotensin system is good, but but bad over time esp in HF patients because its activation long term causes deterioration of the heart function, decreasing CO, and prepetuating the renin system and making everything worse!***
what are the four stages for heart failure?
1. no limitation of physical activity
- slight limitation of physical activitiy, some activities so SOB on exertion
- markled limitation of physical activities, like ADLS cause SOB
- symptomatic at rest or with minimal activity, unable to enage in physical activity
what are the 7 presentations of a patient that would suggest they are experience HF?
1. dyspnea
2. orthopnea
3. paryoxysmal nocturnal dyspnea
4. abdominal symptoms
5. cerebral symptoms (decreased profusion to brain)
- unexplained weight gain from swelling in the legs
7. acute pulmonary edema ***MEDICAL EMERGENCY WORST POSSIBLE SITUATION….patient drowning in their own fluid backing into the alveoli!!!****
if you suspect pulmonary edema in a patient with HF, what test do you need to do STAT? what are the measurements that would cause you to be cocerned and confirm your dx?
***THIS IS A MEDICAL EMERGENCY****
pt is drowning from the inside out!!
pulmonary capillary wedge pressure via right heart cath
>20 mmHg: concerned with interstitial edema
>25 mmHg: concerned with pulmonary edema
what are the 7 physical findings that you could find in a pt suspected of HF?
- tachycardia common
2. crackers
3. S3 gallop low in pitch in early diastole (associated with HF)
4. increased JVP
5. hepato-jugular reflex (push on liver JVD goes up)
6. cardiac cachexia “wasted appearance”
7. pleura effusions with high levels of pulomary pressure!!
what are the three test you could do to diagnose HF and what would you excpect to find on each one?
which one is the best?
1. CXR:
CARDIOMEGALY
KERLEY B LINES (DISTENSION OF PULMONARY VEINS)
2. ECHO DOPPLER #1 best non invasive tool
3. BNP:
used for acute ventricular dysfunction or symptomatic heart failure, helps to distinguish SOB between cardiac and pulmonary cause
>100 COMMON WITH HF
what are the 6 goals of treatment for HF?
- treat underlying cause
- reduction of cardiac workload (preload/postload)
- control excessive Na/water retention
- early initiation of ACEI/ARB (hydralazine in blacks)
- enhancement of cardiac contractility
what type of diet is reccomended for HF patients?
<4 g Na diet or less
NO SALT ADDED.
what distinguishes a person as having end stage HF? what are the two options for a pt is this senario and what does it provide for the pt?
when patient no longer is responsible to any RX
1. LV assist devices (implantable pump device connected to external power supply)
- decreases cardiac workload to buy time for transplant
- can leave the hospital while waiting
- often used since not enough heart donors
- complications: thrombis formation, infection*
2. cardiac transplant
complications: rejection, infection, CHD in donor heart
what is the 5 year survival rate for a patient who has HF and recieves a cardiac transplant? how much does a transplant cost?
70%!!!!! thats pretty good
costs minimally $200,000
explain the drugs that are used to treat preload for HF? (2)
1. direutics
- loop dieurtics most potent (furosemide, torsemide)
- MUST monitor BUN, creatine, UA, and glucose
- can cause hyperurcemia and metabolic acidosis
- k sparing dieuretics
2. nitrates
explain the drug class that are used to treat afterload associated with HF? why is this important?
(not looking for specific drugs on this card)
afterload:
- always increase in HF bause of the neural and humoral influences that constrict PV and increase SVR
- increase in SVR decreases CO and causes back flow to lungs
treat with vasodilators:
decrease SVR
increase CO
decrease pulmonary capillary wedge pressure
decrease symptoms
decrease mortality
what are the three vasodilator drugs are typically used in treating the afterload in HF?
(3 drugs)
- what two things cause it cause as SE? what can it do? what does it decrease?
- what doesnt’t this cause?
- what does this inhibit? what does it do?
1. ACE inhiborts
-caution hypotension, dry cough
decrease mortality by >25%
decrease remodeling (fibrosis, wall thinning, cell death)
2. angiotensin II receptor blockers
less protection against remodeling than ACE but don’t cause cough
3. sacubitril
neprilysin inhibitor
degrades vasoactive peptides
what is the new drug combination
sacubitil/valsartan
used for?
what does this do? what are 3 SE?
CONSIDER AS FIRST LINE TREATMENT FOR HF INSTEAD OF ACE OR ARB ALONE FOR HF!!!!!
- slowed HF progression better than a ACE alone
- se: hypotension, angioedema, hyperkalemia
when are biventricular pacers indicated in HF?
what does this do for a HF pateint?
if QRS >.12 and severe refractory CHF
improves symptoms and quality of life and EF
this is called “cardiac resynchronization therapy
what is are the primary and secondary indications for a ICD?
indications:
secondary: resuscitated cardiac arrest/vfib or hemodynamically unstable Vtach
primary: EF <.35 with mild to moderate HF sym,ptoms
by controlling someones HTN, how much do you decrease their stroke incidence?
30-40%
by controlling someones HTN, how much do you decrease their new onset HF?
50%
by controlling someones HTN how much do you decrease their incidence of MI?
20-25%
infective endocarditis
what is this and what will you see on the vavlue? whare are 4 physical locations on the body that are portal of entry for the bacteria? what are 3 ways it can get into the blood? what is the most common causative organism? what are the three most common organisms that can cause it? what are 4 long term complications it can lead to?
bacteria cause infection on a cardiac valve or an endocardial surface and cause a VEGETATION “small growth” that moves with the valve
-skin, oral cavity, GI, upper respiratory
-dental work, flossing, cleaning, central lines
**most are due to bacterial infections, however some are fungal***
organisms: staph aureus most common, virdians group D streptococci, enteroccocus faecaslis
can lead to permanent damage including:
- valve damage
- HF (usually left sided)
- strokes from emboli to the brain
- damage elsewhere from emboli
what percent of people that get infective endocarditis have a underlying valve abnormality?
50% of people
provides are source of turbulent flow that makes it easier for the bacteria to pool there ex: IV drug user
do CABG and permanent pacemakers predispose pt for infective endocarditis?
NOPE!!
what happens when prostetic valves get infected with infective endocarditis? what are 4 common concuring conditions with infective endocaridits?
usualy a DISASTER!
- rheumatic valve disease
- aortic stenosis/sclerosis/regurg
- mitral stenosis/regurge/prolapse
- congenital heart defect
what are the two most common valves involved in infective endocarditis?
what do you see on them and where are they growing? what are they made of?
aortic valve and mitral valve
vegetation occurs on the low pressure side of the valve
- mitral it occurs on the atrial side
- aortic it occurs on ventricular side
vegetation made of: platelets, fibrin, colonies of bacteria
in right ventricular infective endocarditis, which valve is involved? what is the only way you get this? what is the causative agent?
tricuspid involvement in 85% of cases
pulmonary valve in 15%
only in the setting of IV drug use!
causitive agent usually STAPH aureus
what are the 8 clinical findings you would expect to see in a patient with
infective endocarditis
- febrile
- symptoms of infectious emboli spreading elsewhere
- petechiae on palate or conjunctive (from micro emboli)
- subungal “splinter” hemmorages
5. olsers nodes-painful raished lesions on fingers and toes
6. janeway lesions: painless red lesions on palms or soles
7. roth spots-exudative lesions in retina
NEW OR CHANGING REGURGITANT MURMERS
what are the two test you can order to confirm infective endocarditis?
1. Blood cultures 3 sets 1 hour apart
- TEE-90% sensitive
explain the differences between acute and subacute presentations for infective endocarditits? which organisms are likely to cause each?
1. acute
staph aureus and other virlulent organisms
acute with rapid progressing destruction and infection
early emboli
2. subacute
virdans streptococci, enterococcus
gradular valvular destruction
what are the Duke major and minor requirements for infective endocarditis?
Major: 3
Minor: 5
What combinations do you get a definite dx?
Major:
- 2+ blood cultures
- abnormal TEE
- new/changing regurgitant murmer
Minor:
- IV drug use
- prior valve abnormality
- fever
- systemic emboli
- immunologic lesions (janeway, olsens, roth)
Definite DX:
2 major
1 major 3 minor
5 minor
what are the new guidelines for abx prophylaxis for infective endocarditis?
prosthetic heart valve
prior episode of endocarditis
complex cyanotic congenital heart disease
other valvular lesions whether congenital or acquired do not require endocarditis prophylaxis before procedures
for dental procedure use amoxicillin 2 grams 30-60 mins before surgery
what is the treatment for infective endocarditis?
and if empiric tx? (2)
viridans streptococci: penicillin G x 4 hours q 4 weeks
empiric tx while awaiting culture results: vancomycin and ceftriaxone IV
how many americans are effected by hypertension? what percent of those are adequately controlled?
50 million americans
only 25% are adequately controlled
what is the definition of HTN?
what about elderly?
whats idea?
HTN >140/90
eldery: >150/90
ideal <120/80
what are the two types of categories of HTN and which is most common?
what are five things that can cause the second?
essential hypertension:
aka idiopathic/primary 95% of cases, etiology unknown
secondary hypertension: 5% of cases
- estrogen use increases RAAS
- intrinsic renal disease (any form of chronic renal parenchymal disease)
- renovascular HTN
- endocrine HTN
- pregnancy
secondary HTN:
due to renovasular disease
what is this and how does it work? what are the two types and who do you find them in?
2 types of renal artery stenosis that increase the production of renin, cause decreased BF to the kidneys increasing BP
1. fibromuscular hyperplasia (FMH)
- young adults
- BP increases renal function preserved
tx: angioplasty to increase BF to kidney
2. atherosclerosis of renal artery
- older patients
- elevated BP not responsive to meds
- renal function impaired, intervention may or may not help
what are the 7 things that can influence/cause HTN?
genetics
environmental factors
sympathetic nervous system hyperactivity
renin-angiotensin-aldosterone system
defect in natriuresis (getting rid of Na in the body)
intracellular Na and Ca
insulin resistance
what are 5 exacerbating factors for HTN that can make it worse?
obesity
Na in diet
cigarette smoking increases NE
NSAIDS
excess alcohol
explain the ways in which HTN effect and contribute to end organ damage in:
- heart
- brain
- arteries
- renal
1. HEART
- RF for CHD
- LVH diastolic dysfunction POWERFUL PREDICTOR of morbidity and morality, in 50% of people with HTN
- HF over time
2. CEREBROVASCULAR
the major predisposing cause of STROKE
rupture of micro hemmorages from increase BP
correlate closely with SYSTOLIC BP
3. PVD
4. RENAL DISEASE
nephrosclerosis: narrows kidney arterioles causing glomerular damage and decreased function, HTN accelerates this procress, common in Blacks
since HTN is usually asymptomatic, what symptoms let on a pt might have it? 8
- SOB, DOE from LVH
- TIA, stroke, hemmorage
- MI, angina, HF
at what point to do you treat HTN in people and the elderly?
BP >140/90 requires tx in those <60, including those with DM or CKD
BP >150/90 >60 year old, a little more liberal with the elderly
what are the physical exam findings that can suggest a patient has HTN since it is mostly asymptomatic? 6
- narrowing of the arterioles A/V <5.
- A-V nicking (arteriosclerosis where artery looks like it is crossing the vein)
- silver or copper wired appearance
- hemorrhages or exudates
- papilledema
- bruits
what are the 3 most important labs you want to check in a patient you are concerned about HTN?
- creatine, BUN
- electrolytes Na and K (want to check K cause you will likely put them on a dieuretic and this can cause hypokalemia)
- lipid levels: TC, LDL, HDL, triglycerides
what drugs will you typically use to treat HTN in
black populations
thiazide and/or CCB
what drugs will you typically use to treat HTN in
pts >18 with CKD
- ACE
- ARB if can’t tolerate ACE
use these regardless of race or diabetes status if they have CKD!!!!!!! big hint there!!
what drugs will you typically use to treat HTN in
post MI patient
combine BB with ACE/ARB
BB are no longer reccomended for HTN but they can help in adjunct in patients post MI even though it doesn’t actually help treat the HTN
what drugs will you typically use to treat HTN in
diabetes
almost always require 3 drug regimen
- ACE (or ARB if can’t tolerate)
WITH
- thiazide OR CCB
what is the goal of treating HTN? what are you trying to reduce risk of? what should you focus on? what should you look for a in a drug?
decrease endpoints including MI, Stroke, LVH, PAD, all cause cardiac mortality, HF, and renal failure
try to find drugs that treat more that one co-morbidity
focus on SYSTOLIC BP as the most important aspect for reducing morbidity and mortality
which number should you focus on when trying to reduce morbidity and mortality?
SYSTOLIC BP!
what are four non pharm ways to decrease HTN?
diet
weight reduction, aerobic activity
decrease alcohol, Na intake DASH DIET
smoking cessation
what is the reccomended 1st choice for the majority of patients when treating HTN?
thaizide dieuretic
thiazide dieuretics for HTN
who are these most potent in 3? which patients should you avoid these in? what is the doseage? what can they cause 4?
- 1st line therapy and should be included in ANY drug therapy
- more potent in blacks, elderly, obese
- avoid in patiens with hyponaturemia and gout
- LOW DOSAGE
- can cause hypokalemia, hyperurcemia, hyperglycemia, abnormalities of lipids
beta blockers in tx of HTN
what do they decreaes? who are they helpful in 4? what are the 4 SE you need to be aware of if prescribing to a pt?
used as a 2nd or 3rd line drug because of increased risk for stroke
- decreases CO
- helpful in pts with other comorbid disorders like:
- angina pectoris, post MI, migrain headaches, essential tremors - SE: exacerbation of bronchospasms in nonselective, bradycardia, worse acute HF, masks signs of hypoglycemia in diabetics!!
ACE inhibitors
who is this the DOC in 4? what does it prevent? what does it have a synnergistic relationship with ? what does it inhibit? what are 2 negative SE?
inhibits bradykinin degradation
significant efficacy improvement when combined with diuretic SYNERGISTIC RELATIONSHIP
ANTI-HTN DOC in diabetics, CKD, LV dysfunction, HF and prevents remodeling!!
SE: dry cough in 20%, angiodema
angiotensin II receptor blocker (ARBS)
losartan
like ACE but no cough!
renoprotective in diabetics
direct renin inhibitor for HTN
aliskren
i. binds with renin, stopping it from working and blocking the initiation of RAAS
ii. increased cost vs ACE but similar in efficacy
calcium channel blockers for HTN
what are the two types? what are the 3 SE of the first class? what are the second class used for and who don’t you use them in? what can they cause and what shouldn’t you combine them with?
preferrable in blacks and elderly
1. dihydropyridine
reflex tachycardia, headaches, periphreal edema
2. nondihydropyridines
used for arrythmias
can exacerabte HF so don’t use in HF patients, bradycardia, don’t use with BB
alpha receptor blockers
what can it cause 2? who else can it be helpful in? what can happen if you take it too long?
relax smooth muscle and decrease SVR
tachyphylaxis common with prazosin
SE: postural hypotension and syncope following 1st dose, palpitations, headache
useful in BPH (prostatic hypertrophy)
centrally acting agents
what is the MOA? what can it cuase? what is one benefit to increase compliance?
methyldopa, clonidine
stimulate CNS presynaptic alpha-2 receptors reducing efferent peripheral sympathetic flow
postural hypotension but benefits they come in a patch and are effective for 7 days
what is the initial TX for HTN and what is the exception to this?
initial tx: thiazide dieuretic
exception: diabetic, move right to the ACE and add dieuretic later, multiple agents are often needed here
what are the guidelines for txing HTN?
this is a lot of info so probs just read through it!
- Initial rx: thiazide diuretic with some exceptions
if diabetic start on ACE then use thiazide diuretic later, multiple agents often needed
2 . initial low dose and follow up in 4-6 weeks
- titrate up to moderate/high dose before adding a second agent exception:
i. if the first drug is a thiazide, low dose is sufficient and shouldn’t increase the dose so add the second med instead of increasing the dose - second drug would be BB, ACEI, or Ca blocker Exception:
ii. if BP is >160/90 can start dual Rx at the same time - most patients will be controlled with 2 drugs, but if need three, usually diuretic, ACE and CCB
what are the 3 types of ambulatory monitoring you can do and what are the benefits of each one?
aka how long do they record? which ones are commonly used? when do you use them?
1. Holter monitor
- 2 lead EKG
- 24 hours
2. external event monitor
- most patients use this now
- allows for monitoring for weeks or more
- helpful when the experiences are spread out and infrequent symptoms
- when patient has symptoms they push a button and it stores the information
3. implantable loop recorders
- monitoring for up to 3 years
- hold up to the phone and the receiver the cardiologist has interprets it
- continuous
what are the 3 reasons you would want ambulatory monitoring of a patients cardiac symptoms?
- arrythmia detection and correlating it with patient symptoms
- evaluation of syncope
- arrythmia tx effectiveness
what are 5 reasons you would want to do a stress test on a patient?
- CP/angina pectoris
- functional ability in CHD
- screening of high risk individuals with atypical symptoms
- response to intervention (cath, CABG), check them before they are released
- screening for patients with certain occupation requirements
what are the 3 qualities you used to deteremines a patients pretest probability for CHD?
what are the three questions you want to ask them about their type of CP?
age, gender, characteristic of CP
- substernal?
- brought on by exertion?
- relieved by NTG?
low pretest probability (Stress test)
what two population characteristics fall into this category? do you do a stress test in them?
- asymptomatic men and women of all ages
- women <50 with atypical CP
avoid stress testing in this group!! high rate of false positives and then you are stuck with the results and have to work them up!
intermediate pretest probability for stress test (10-90%)
what are the 3 population characterstics for this group? should you do a stress test in this population?
- men of all ages with atypical chest pain
- women >50 with atypical chest pain
- women 30-60 with typical CP
stress tests warrented in this group for DX of CAD!
high pretest probability (90%) for stress in CAD
what are the two population characteristics of this group? what might this provide? what might you want to consider as testing for this group instead?
- men >40 with typical CP
- women >60 with typical CP
might provide prognostic value in this group, may want to consider coronary angiograph instead because high risk!
what are the four indications to STOP a stress test?
- evidence of ishchemia with ST depression of T wave inversion
- achieve target HR of 85-90% of predicted maximal HR (220-age)
- dangerous arrythmia
- decreasing BP! STOP!
what is the one absolute thing you much achieve in order to intrepret a stress test as negative?
must achieve 85-90% of maximal predicted HR!!! otherwise you can’t say the test was negative!!
explain what these four meds do in pharmocologic stress tests and which ones they are used in?
- adenosine
- dipyridamole
- regadenoson
- dubutamine
1. adenosine: dilates coronary arteries used in nuclear imaging
2. dypyridamole: dilates coronary arteries used in nuclear imaging
3. regadenoson dilates the coronary arteries ***MOST COMMONLY USED***give bolus injection works like adenosine
4. dubutamine: increases HR and contractility used in echo!
realistically, what is it always best to do when doing a stress test?
combine both imaging and EKG
increases specificity to 90%
downside: cost
what is the most commonly used test for accessing the heart for CAD/angina?
treadmill stress test!
what would you see on a stress test that indicates a positives test?
downward or horizontal sloping ST depression or T wave inversion
what do you need to keep in mind about women and stress tests? (3)
- high incidence of false positivites in young healthy women w/o risk factors and atypical CP
- decreased sensitivitiy in women with CHD because they are more likely to have 1 vessel disease
- ORDER STRESS WITH IMAGING FOR THESE PEOPLE! young without RF or atypical CP
echo + EKG stress tests
what would you expect to see in ischemic hearts (2)? in healthy hearts?
aka, what happens to the size of the heart and EF?
- ischemic hearts: decreased or absent contraction seen on echo
if large ischemia get large heart with decreased EF
in normal hearts: contracts normally, heart gets smaller with exercise and EF increases!
nuclear stress test and EKG
what two substances can be used in this test? what does this testing system rely on in the heart? what do active and inactive areas appeare as? what do you need to compare and what are you looking for?
thallium or TC99 SESTAMbib
distributes these to heart via blood flow and then through Na/k pump, active areas light up, inactive show defect
compare resting and stress images for areas of reversible ischemia aka lit up area originally that then turns dark
what are the 4 things that make it so you can’t read an EKG that make it useless to do a stress EKG??
- LVH
- LBBB
- Digoxin
- WPW abnormality!!
**DON’T READ THEM, YOU’LL LOOK DUMB!!!**
echocardiography
what type of test is this? what are the two options? what are the 8 things it can help you look for?
noninvasive 2D tests with doppler
options: transthoracic echo or TEE
Tells about:
- LV function and EF
2. hypertrophy, dilation
3. endocarditis via TEE
4. HF, valvular insufficiency/stenosis
5. effusion
right heart catherization
what type of vasculature do you enter? what is the pathway if follows? who do you use this in? what are two things it can record? what are 4 complications?
- enters central vein
- right atrium, right ventricle, pulmonary artery, pulmonary capillary wedge
invasive monitoring for critically ill patients
records: pressure and oximetry
complications: pneumothorax, arterial puncture, infection, thrombis
left heart catheterization
what vasculature does this enter? what is the pathway? what can be done from this approach? what do you look for? what are four complications?
- enters artery
- aorta, aortic valve, LV, LA
CORONARY IMAGING DONE FROM THIS SIDE!!!!
- contrast injected into coronary arteries to identify stenosis/occlusions
complications: death, stroke, bleeding, thrombis/emboli
what is the gold standard for cornary imaging? who is it warranted in?
left heart cath to do coronary angiography
do in: high risk individuals with classic ischemia symptoms
CT coronary angiography
what type of test is this? what is it less effective then? what are the 3 indications for this?
3D imaging of coronary arteries using contrast dye
lacks sensitivity and specificity compared with contrast coronary angiography
indications:
- intermediate risk for CHD
- atypical CP with low to moderate risk
- unclear/inconclusive stress test
what is the most common type of heart attack? what is the two mechanisms by which this can happen?
complete occlusion of the coronary artery
- progressive narrowing via atherosclerosis
- sudden occlusion via ruputure, erosion, fissuring of plaque with superimposed thrombosis
what are the three things you want to consider when diagnosing a MI?
- history and physical
- cardiac enzymes
- EKG
what do you need to keep in mind about ordering cardiac enzymes when a patient comes in to the ED with chest pain?
rise 4-6 hours after MI, so when pt is in the ED with symptoms and ST elevation, it is expected the first set would be negative, keep this in mind, if taken 4-6 hours post MI then you will see these as positive
explain the cardiac enzyme testing for:
CK MB
Troponin
1. CK MB
rises in 6 hours after infarct
2. troponin (cTn)
rises 2-3 hours earlier than CK-MB so slighty better
what are the 2 qualifications for ischemia on the EKG?
what do you compare? what two other things can cause this?
>1mm ST depression that is horizontal or downward sloping that persists for .08 sec past J point
**only needs to be in 1 lead!!**
compare the PR segment and the ST segment using the J point
2 other causes: hypokalemia, digoxin
what is the J point?
The end of the QRS and the begining of the ST segment
what are the 4 things a that prevent you from being able to read ischemia on a EKG?
- LVH
- LBBB
- digoxin
- WPW
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”
which lead should you NOT look at when interpreting Q waves?
aVR these Q waves are never significant!!!
stage 1 of MI:
T wave peaking and T wave inversion
what does this suggest?
when does this happen?
what is this nicknamed?
is this reversible?
- ischemia but NOT dianostic for MI
- first couple hours then they invert
- “hyperacute T waves”
- potentially reversible if blood flow is returned, T wave will return to normal
stage 2 MI:
ST segement
- when does this occur?
- what is the qualification for it to be called ST elevation?
what leads can it be in?
what does it indicate?
does it go away?
- occurs after a couple hours
- ST elevation at the J point >1 mm in two or more contigious leads
- can be in limb or precordial
- INJURY beyond ischemia!!! occurs in acute MI but can return to normal if blood flow returned tells you that a true infarction has occured and that it will evolve into death unless there is immediate intervention
what can persistent ST elevation indicate?
ventricular aneurysm
explain what early depolarization is?
how is this different than ST elevation?
- some people have regullarly elevated ST segment
- common in young healthy individuals
- ST returns to baseline during exercise
How to differentiate from MI:
- t wave remains an independent waveform, aka the ST segment doesn’t blend with T wave
- in MI: ST merges with T wave
stage 3 of MI:
formation of new Q waves
when does this occur?
what are the qualifications for this?
what does this indicate? reverisble?
what is this diagnostic for?
is there still ST elevation?
how long does it last?
- occurs 2-3 days later
- >.04 seconds wide and >1/3 height of R wave
- “death” has occured, not reversible
- diagnostic of MI
- by the point Q waves develop, ST returns to baseline
- persist for lifetime of pt
explain why there is Q wave formation when a MI has occured and the tissue is dead?
when mycardium dies, it is electrically silent and all the electrical stimulation is conducted AWAY from it, so that is why you get a DEEP NEGATIVE DEFLECTION Q wave
what leads might you see normal Q waves in because how the heart depolarizes?
left lateral leads
V5, V6, aVL and I
explain what reciprocal changes are and why you see them with MI?
leads at a distance from those showing ST segment elevation may show changes that are opposite those in the infarct leads: ST depression and T wave inversion
**think about it, as the tissue starts to die, the current is directed to other areas of the heart, so these new leads now see the current comming TOWARDS them so you will get tall R waves, ST deoression and T wave inversion**
keep in mind, not all of the reciprocal leads need to show changes, might only see it in 1 or not at all, totally depends!
what does the left main artery divide into and what are the two main areas this supplies?
- left anterior descending=anterior heart and interventricular septum
- left circumflex artery=lateral heart (left ventricle)
inferior MI
what artery would be blocked?
where do you see the changes?
where might you see reciprocal changes?
what other MI location might this commonly be paired with?
***what is something important you need to keep in mind when looking at change in V1-V3**
right coronary artery
changes in inferior leads II, aVF, III
reciprocal: lateral leads I and aVL
***If there are changes in V1-V3 as well where the R is super tall consider this person is having a posterior MI as welll since the right coronary arter also feeds the posterior wall!! DONT CONSIDER THESE RECIPROCAL CHANGES!!****
where do you see the lead changes for a inferior MI?
II, aVF, III
reciprocal if present in lateral leads! I and aVL
left lateral MI
what artery would be blocked?
where do you see the changes?
where might you see reciprocal changes?
left lateral circumflex artery
changes: I, aVL, V5, V6 (lateral leads)
reciprocal in: inferior leads!
what leads would you see changes if you were suspecting a lateral wall MI?
changes: aVL, I, V5, V6
reciprocal changes in inferior leads!
anterior MI
what artery would be blocked?
where do you see the changes?
where might you see reciprocal changes?
left anterior descending artery
changes: any precordials esp V1-V4
this can be easy to pick out with poor R wave progression
reciprocal: inferior leads
anterolateral MI
what artery would be blocked?
where do you see the changes?
where might you see reciprocal changes?
left main coronary artery
changes: I, aVL, all precordials
reciprocal changes: inferior leads
**think about it….the left main coronary supplies both the anterior and the lateral branches so therefore it makes sense you would have changes in both of these!
what does this show you?
anterior infarction
V1-V4 shows anterior heart
posterior MI
what artery is the most common cause of this?
where do you need to look for the changes and why?
what are two important things you MUST remember about this??
90% of patients are supplied by right coronary artery
changes: instead of ST elevation you see ST DEPRESSION and TALL R WAVE IN V1,
this is a mirror image of anterior infarcts because you don’t have leads that overly the posterior back
- must distinguish between this and right axis deviation because in RAD you will also have tall R wave so need to check V6 for large S wave
- often occurs with INFERIOR MI because they are from the same blood supply of the right cornary artery
in the pic…note tall R waves in V1, to rule our RAD, look at V6, there are tall R instead of deep S so this is posterior MI
what 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
transmural MI
through the entire thickness of the wall of the heart causing Q waves
subendocardial MI
only through a portion of the thickness of the heart
non Q wave infarction
what is the only thing that you would see on the EKG for this? what is abolustely pivotal that you do to determine if this was a MI?
the only EKG finding with non-q-wave infarctions are T wave inverisons and ST segment depressions (not elevation)
lower mortality rate
higher rate of reinfarct
*********in this case you check cardiac enzymes because if elvate this would suggest MI, where as if they were normal it would mean ischemia*****
how do you distinguish between angina on a EKG and non Q wave MI?
what are two things you need to do/use to distinguish between the two?
in non Q wave mi the indication is: ST dpression and T wave inversion which is the same as ANGINA
to tell the difference:
- order cardiac enzymes, elevated in MI
- ST depression and inversion will return to normal when angina ends (nitro), but non Q wave MI the depression and inversion will stay down for 48 hours
explain how prinzmetals angina shows on an EKG? how do you distinguish this from a STEMI?
angina that causes ST elevation from spasms
ST segments return quickly to baseline when patient is given antianginal medication
what is the magic number for pauses?
magic number is 3
3 seconds pause, if longer than this the heart doesn’t get blood to the organs, usually the brain is the first noticeable one so you get syncope, dizziness, and lightheadedness
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!
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
first degree AV block
what is this classified by?
what do you want to think of it as?
what causes this?
what type of heart do you find it in?
PR interval >.2 seconds!
want to look at the limb leads for this, think of it like a “delay”rather than a block
can be in normal or dieased hearts caused by prolonged delay at AV node or bundle of HIS causing a longer PR interval
sick sinus syndrome
what is this a combination of?
what is not work?
what percent will have AV node dysfunction?
what are the two presentations you might see?
how DX?
how to TX?
sinus arrest with alternations of paroxysms or atrial tachycardia and bradyarrythmias and clearly related to sinus node dysfunction (hence the name, duh)
“SA node dysfunction with symptoms”..most commonly cause by aging
40% will have AV node dysfunction
1. afib: controled or slow rate in the absence of meds
2. brady-tachy synddrome: artial tachyarrythmias and symptomatic bradycardia
DX: 24 hour holter monitor
tx: permanent dual chamber pacer with auto ICD
second degree AV block general
what happens in this type of block?
what do you have more of?
what are the two types?
not every atrial impulse is able to pass through the AV node into the ventricles
more QRS than P waves since not all of them make it through
Mobitze Type 1 second degree block: Wenchebach
Mobitz Type II second degree block
mobitz type 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
mobitz type II second degree AV block
where does this occur?
what is this defined as?
is this benign? what does pt usually need?
BELOW AV NODE IN BUNDLE OF HIS
dangerous and pt usually needs a pacemaker, can progress to third degree AV block
presence of a dropped beat WITHOUT lengthening of the PR interval, RANDOM dropped QRS,
CAN HAVE MORE THAN ONE IN A ROW
third degree AV block
what is this called?
what happens in this?
what should you look for in the rates?
“complete heart block” MEDICAL EMERGENCY!!!! ALWAYS NEED PACEMAKER
no atrial impulses make it through to stimulate the ventricles each are beating INDEPENDENTLY!! the block prevents the atria and ventricles from communicating
**QRS are wide and bizarre looking almost like PVCs since they are from ventricular origin**
AV dissociation where the ventricular rate is slower than the atrial rate
atria: 60-100
junctional: 40-60
ventricular: 30-45
THEY MARCH OUT INDEPENDENTLY!!
What are two really unique things that can cause a person to be in 3rd degree complete heart block?
- lyme disease…so check titers
- congenital heart block, they are born with it where their junction rythmn has been sufficient to supply blood so they are asymptomatic
what is the LEADING cause of COMPLETE HEART BLOCK?
degenerative disease of the conduction system
right bundle branch block
what are the two qualifying characteristics?
where do you see the reciprocal changes? what are the changes and why?
1. QRS >.12
2. V1 and V2 have R-S-R’ with rabbit ear appearance
reciprocal changes in lateral leads with DEEP S wave!
Handlers explaination: in RBBB, the left bundle branch still works so the conduction runs down the left side, usually on a EKG you only see the left ventricle contraction which gives you the R wave, however, in RBBB the left ventrcile is reponsible for causing the right ventricle to depolarize so the conduction goes from the left side over to the right cell by cell which is why depolarization has a longer duration and a R’ spike in V1 and V2, the R’ is the right ventricle depolarizing. this process is a left to right depolarization
left bundle branch block
what are the two qualifications for this?
what will you always have?
where do you see the reciprocal changes?
1. >.12 QRS
2. Broad/notched QRS in V5/V6
ALWAYS WILL HAVE DOWNWARD Q or RS in V1
reciprocal in: V1/V2 with wide deep S wave
hemiblocks general
how do these occur?
what is this branch made up of?
what do they cause? what is normal?
what must you do to prove a hemiblock?
the left bundle branch is made up of two fasicles, so either of these can become individually blocked
1. left anterior fasicle
2. left posterior fasicle
they cause axis devation
they have NORMAL QRS, and must rule out other reasons for axis deviation (aka LVH, RVH)
left anterior hemiblock
where does this occur?
what are the qualifications? (3)
what are the steps to determine if this qualifies?
explain the direction of the vector and depolarization?
occurs on the left bundle branch!!
MOST COMMON HEMIBLOCK IN NORMAL AND DISEASED HEARTS!
1. NARROW QRS
2. left axis deviation > (-30)
3. NO OTHER CAUSES OF LAD
STEPS:
1. determina LAD via I and aVF
2. should also be negative in II (headed away and more neg)
rushes down the posterior fascile and swoops down and up traveling in a inferior superior, and right to left direction!! think about it
WHAT IS THE MOST COMMON HEMIBLOCK?
LEFT ANTERIOR FASICLE HEMIBLOCK
Left posterior fasicle
what type of hearts do yo usee this in?
what are the 3 qualifiations?
what is the direction and depoliarzation vector?
where do you see the R waves and S waves?
SICK HEARTS ONLY
1. narrow QRS
2. RAD
3. no other reason for RAD (like RVH)
4. tall R waves inferiouraly, deep S waves laterally
runs down the anterior fasicle traveling superior to inferiorly and left to right depolarization
myocardial ischemia
what is this and what is it caused by (3)? what determiens the severity? what are 3 contributatory factors? what how does it present as symptoms? what causes these symptoms in each?
temporary reduction of blood flow to an organ, potentially reversible, caused by mechanical, electrical, and valvular dysfunction
can be reversible or peremanent depending how long it has been happen for, can lead to infarction
this can cause angina when there is increased activity
Contributory factors: significant LVH, aortic stenosis, tachyarrythmias like afib/aflutter
symptomatic:
1. angina pectoris
1. O2 demand in the presence of fixed stenosis
- VASOSPAM and significant narrowing
1. prolonged decreaed O2=unstable angina or infarction
-acute thrombis likely present
sudden cardiac death in CHD
how soon does the pt die? what most likely causes it? when does this happen?
1. death within 1 hour after onset of symptoms usually within minutes
2. malignant arrhytmia commonly present
common presenting manifestation of CHD, frequent end point in patients with CHD propr to MI and imparied LV function
why are women often misdiagnosed when they have CHD? (3)
1. atypical symptoms: pain radiating to right arm, arm pain along
- many women produce false negative stress tests since single vessel disease more common
3. elderly or diabetic womeon complain of general malaise, loss of appetite, vague abdominal pain so if they have RF, GET EKG!!
stable angina pectoris
what does this pain feel like? is it reproducible? what are 3 things that make it better? what is the pattern? what are 6 things that can cause this? what are 4 things you might see to clue you into this?
chest discomfort described as
tightness, pressure, aching, choking that is often REPRODUCIBLE WITH ACTIVITY that resolve after cessation of activity, relaxation, or NTG
positive levine sign substernal to left sternum, with crescendo/decresendo pattern 1-5 mins, less likely to happen in AM (lower threshold)
can be brought on by: exertion, exercise, emotional stress,cold weather, cigarettes, sex
physical exam may be normal between episodes, may see xanthomas from hyperlidemia, AV nicking from HTN/DM, s4 gallop during angina, changes in BP
what are the 3 tests you can do to help identify stable pectoris for CAD? what do they show?
1. EKG:
normal between episodes
ST segment depression/T wave change during angina then normalize after angina passes
2. Stress EKG: most helpful non invasive tool
-increase workload with meds or exercise, compare resing and stress EKG for ischemia, may consider adding image to make it more specific, ability to detect dermines the amoutn of vessel involvment
3. coronary angiography- Gold standard for CAD
-tells which vessels are involved, degree of stenosis, and LV function
what is the drug you give for acute angina pectoris? or for prophylaxsis if the pt is going to be doing exercise?
sublingual NTG
reduces LV volume preload and decreasing O2 consumption
does this by causing venodilation, so that it decreases the amount of blood heading back to the heart, decreasing the volume and decreasing O2 demands
what are the 7 drugs you put someone on to help with chronic stable angina?
1. beta blockers ATENOLOL, METOROLOL: decreases HR, contractility, and BP improving exercise tolerance
*****REDUCE MORTALITY IN POST MI AND HF PATIENTS***
2. long acting nitrates isosorbide dinitrate
****DONT TAKE THIS WITH VIAGRA!!!!*****
****can develope nitrate tolerance so need to dose in intervals!!****
3. Non dihydropyridine calcium channel blockers dilate ARTERIES, decreasing afterload, decrease myocardial O2 consumption
4. dyhydropyridine calcium channel blockersamlodipine, nifedipine dilate ARTERIES, decrease afterload and myocardial O2 consumption
***best used in combination with a BB, reduce risk of HYPOTENSION**
5. diltiazem and verapamil used with nitrates, dilates arterioles decreasing afterload, decrease HR, and O2 consumption
***don’t use in HF patients!!***
6. ranolazine chronic angina that isn’t controled with the above
**increase QT interval, but won’t cause arrythmia**
7. antiplatelet drugs USED IN ALL PTS WITH CHD, PAD, AND CAROTID, DECREASES INCIDENCE OF CARDIAC DEATH AND MI, low dose asprin
when treating CHD patients, which drug do you not want to use in HF patients?
diltiazem and verapamil
when treating angina with a long term drug, which one do you NOT want to combine with viagra?
NITRO
isosorbide dinitrate
what drug do you not want to use in CHD in a patient that has asthma/COPD because it can cause bronchospasm?
nonselective beta blockers
Use selective beta blocker!!
what two drugs decrease the mortality post MI and in HF patients?
Beta blockers
Atenolol and metoprolol
what 4 groups of patients with CHD qualitfy for revascularization?
1. patients with unacceptable symptoms controlled with meds
2. 3 vessel CAD with LV dysfunction OR left main coronary stenosis that compromises Left anterior descending (LAD) LEFT main artery consider CABG!!
3. patients post MI with ongoing ischemia
4. acute MI
when should percutaneous coronary revascularization/catherterization be used for CHD?
what are the rates of restenosis with angioplasty, stent, and drug eluting stent? what do you do to compensate for this?
angioplasty restenosis rate: 30-40%
angioplasty with stent placement: 15-20%
drug eluting stents restenosis: 5-8%
- single or 2 vessel disease
- 3 vessels disease in pt that doens’t qualify for operative
drug eluting stents helped decrease rates of restenosis a lot, however probles with late thrombosis so requires intense anti-platelet RX of ASA and clopidogrel
coronary artery bypass for CHD
what happens during this procedure? which two vessels are most commonly used? which one is the best one to use and why? what two factors increase mortality rates?
coronary arteries are bypassed using arteries or veins, low mortality if LV preserved
saphenous veins and mammary arteries most commonly used
internal mammary artery graft has highest patency rate over time**BEST OPTION WHEN POSSIBLE because arteries last longer than veins**
mortality increase with age and EF
coronary vasospasm
what can bring this on? what does the spasms cause? what will the pt feel and what will you see on the EKG? what can happen if this doesn’t resolve?
can be in normal cornary arteries or superimposed o atherosclerotic ones, the spasms cause the artery to close
often induced by cold, emotional stress, meds, and cocaine
angina at rest with ST elevation
**can progress to MI if symptoms don’t resolve**
prinzmetals angina
what is this caused by? when do you get symptoms? who is it more common int? what does arteriography show? what are the two treatment options?
coronary ishchemia from vasospasms
symptoms at rest, usually in AM
women> men
ateriography shows normal looking arteries
Tx: nitrates and calcium channel blockers (dihyrdopyridines)
what percent of people with unstable angina remain unstable and need revascularization?
what percent improve medically? and what do you need to do before allowing them to leave?
20% will remain unstable and need revascularization
80% will get better clinicallly and need to get stress test once stable, if they produce a positive test then it might be an indication for revascularization
unstable angina
what is this? what are you at high risk for? how do you differentiate between this and a NSTEMI? what are the two presentations of this? what are two things you do to diagnose this? what are the two things you need to do for tx and the three drugs they need to be on?
angina at rest with minimal activity >10 minutes
GET VERY CLOSE TO HAVING A MI BUT DONT, RIGHT AT THE BRINK OF CELL NECROSIS BUT TISSUE HASN’T DIED YET, high risk for developing MI in following days/weeks so much treat aggressively and quickly
VERY SIMULAR TO NSTEMI, except in unstable angina negative cardiac markers
new onset: angina
accerating or cresendo angina in pt with previously stable angina (gets worse doing less activity)
DX:
NEGATIVE CARDIAC ENZYMES
EKG: ST depression, T wave inversion
Tx:
- HOSPITALIZE THEM!! BEDREST!!
- full anticoagulation and antiplatelet therapy
-HEPARIN +ASA+
prasurgrel/ticagrelor/clopidigrel OR glycoprotein IIb/IIIa
3. nitrates, Beta blockers, and Ca-blockers to decrease MVO2
what percent of people with unstable angina will have abnormal EKG?
50%
so worry about the 50% that have a normal one, still might need to work them up
since the pathology of unstable angina and NSTEMI are the same….what is the only thing that you use to tell them apart?
cardiac enzymes
ck-creatine kinase
MB
troponins
these indicate cell death and that the scale has tipped over the point of unstable angina and cell death is occuring, this is a myocardial infarction
non-stemi acute myocardial infarction
what is this caused by? what is this nickname for these? relate to morality? why must we treat aggressively? how do you differentiate between that and unstable angina?
infarcts caused by prolonged ischemia
CAD to plaque rupture to platelets to clotting to thrombus
small infarcts that are unstable and could go on to cause a bigger infarct so that is why we treat aggressively
“incomplete infarcts” with lower initial mortality but high risk of re-infarction with HIGH MORTALITY
DX: like unstable angine with POSITIVE CARDIAC ENZYMES
for someone who has had a STEMI (infarct), what do you need to get before they leave the hospital?
stress test!! low level
then maximal stress 6 weeks post MI
want to make sure they can saftely return home
what is really important to know about the use of NSAIDS in MI patients (NSTEMI OR STEMI)
increase risk of reccurent MI by 50% post 1st MI.
includes ALL nsaids, short and long term use!!
what is the in hospital mortality rate of MI?
10-15% determined by the size of the MI
what is 5 things a patient is at risk for post MI?
- recurrent ischemic pattern
- nonSTEMI infarct
- HF
- low level stress test causing ishcemia
- high grade ventricular arrythmia
acute myocardial infarction
STEMI
what is the cause of this? what does it lead to? what does patient complain of? what does this most likely occur? how does the patient appeare (3)? what often accompanies this? what are 6 signts of this? what are the 5 things you use to diagnose this?
prolonged ischemia resulting from inadequate tissue profusion leading to cell death and necrosis
total occulsion CAD to plaque to rupture to platelets to clotting, to occlusive thrombus
“elephant sitting on my chest and the worst pain I have felt in my life”
often early in the AM since coronary tone, SEVERE PAIN, anxious, diaphoretic, and distress, LV dysfunction
variable pulse and BP, S4 gallop, apical mitral regurgitation, cold, cyanotic, low CO, ST elevation
DX:
- Creatinine kinase (CK) ALWAYS ELEVATED!
check CK-MB, specific to damanged heart muscle
2. troponins cTnl represents muscle breakdown, sensitive to small infarcts
3. leukocytosis
4. EKG ELEVATED ST
5. echo left ventricular function, identify mitral regurge
what are the treatments for a acute STEMI? (3)
1
1
2
1. percutaneous coronary intervention to reprofuse tissue (CATH)
- goal: open artery within 3 hours of onset of symptoms
goal: open atery within 90 mins presenting to hospital
***If within hour and a half of hospital that does this, consider transfer!!! Must also have CABG CAPABILITY****
2. thrombolytic (finbrinolytic) therapy: done if no access to cath lab, t-PA (altepase)
-done when ST elevation >1 mm in tow or more adjacent leads
50% reduction in mortality if given withint 1-3 hrs of symptoms
3. post thrombolytic management
a. ASA ongoing
b. heparin 24 hours
what are 3 drugs taht might be used to try to help in a actue MI early on pre hospital or in the ED?
- morphine sulfaste
- aspirin in ED
- nitro IV
what are the contraindications (4) and realtive contraindications (1) for thromboltic therapy for a STEMI?
absolute contraindications:
- uncontrolled HTN
- stroke within 1 year
3. cerebral hemmorahage
4. recent head trauma
relative contraindications:
- abdominal or thoracic surgery within 3 weeks
what are three indications of rapid REPROFUSION seen in MI post thromboltic therapy administration?
- rapid resolution of pain
- ventricular arrythmia (PVCs, VT, AVIR)
- rapid evolution of EFG (often q waves)
what percent of infarct related vessels with reocclude during hospitalization post STEMI?
10-20%
what is the preferred method to treat a STEMI in elderly?
percutaneous coronary intervention….CATH
if you are within 1.5 hours of a hospital that does acute angioplasty….what should you think about with a STEMI?
transferring them!! instead of giving them thrombolytics!
what 5 medications is a person who had a STEMI put on after intervention or thrombolytic therapy?
1. BETA BLOCKERS: decreases wall tension preventing MI complications, decreases morality!
2. nitrates
2.5 heparin
3. asprin/clopidigrel
4. ACE inhibitors: i_mprove short and long term survival, decrease LV remodeling post MI,_** great for **large infarcts
5. alosterone blockers
6. statins LDL goal
what are 5 complications of an acute MI?
- atrial and ventricular arrythmias
- left ventricular dysfunction
3. mitral regurgitation, murmer from papillary muscle dysfunction
4. hyptension and shock
- ventricular aneurysm formation
explain the pathway for some with a suspected MI?
what are the drugs that you use to treat unstable angina or NSTEMI?
- full anticoagulation and antiplatelet therapy
-HEPARIN +ASA+
prasurgrel/ticagrelor/clopidigrel OR glycoprotein IIb/IIIa
- nitrates
3. Beta blockers
4. Ca-blockers
what is the TIMI test?
allows you to score the risk of a patient who you think is having a ACS
scores of >3 are high risk
explain when the CK MB isoenzymes rise, peak, and fall?
rise: 4-6 hours
peak: 16-24 hours
fall: 2-3 days
explain when the troponin cTnI rise, fall, and stay elevated? what is diagnostic? what is good about this test?
rise: 4-6
peak: 8-12
remains elevated: 5-7 days
dianostic if >.1, abornal if >.05
This test is the most specific and sensitve, can test for small MI
what are the differences between the symptoms seen with left and right sided dilated cardiomyopathy?
Left sided: DOE, orthopnea, PND, weakness, fatigue, peripheral edema, etc.
Right sided: unexplained weight gain, peripheral edema, abdominal fullness (hepatomegaly, ascites).
dilated cardiomyopathy
who is this most common in? what does this reduce? what part of the heart does this effect? what is the biggest hint to this? what are two things you might hear? what might you see on examinatin of the neck? what are four causes of this? what do you do to diagnose? tx 4 classes?
MOST commony type of cardiomyopathy, esp in black men
often caused by post infectious-myocarditis, toxix alcohol, endocrine, “ischemia cardiomyopathy”
reduced strength of ventricular contraction,
causing dilation of left ventricle, left or biventricular failure causing dyspnea, s3 gallop, pulmonary crackles, increase JVP cardiomegaly, PMI displaced laterally, TR murmer
causes: genetic abnormalities (25-30%), alcohol consumption, postpartum, idiopathic
DX:
- do echo/doppler
- EKG, nonspecific changes excludes other diagnosis
CXR: cardiomegaly
Tx:
- ACE to decrease afterload
- Beta blockers
- dieuretics/nitrates
- anticoag unless contraindicated
what is the prognosis for dilated cardiomyopathy?
what is it dependent on?
what is the mortality for class 4 pateitns?
what about if cardiact transplant?
what are the 3 meds to decrease mortality?
Dependent on length of Sx and functional class. If onset recent, some recovery of ventricular function can occur.
Class IV patients: 50% one year mortality
Cardiac Transplantation: >70% 5yr. survival
Only meds that may improve survival are ACEI (or ARB’s), ß-Blockers and Spironolactone.
hypertrophic cardiomyopathy
what does the patient present with? what might be the first presentation? what are four things you might find on exam? what are the two DX and what is most important? what are the four treatment options?
massive hypertrophy, **usually of septum (assymetric septal hypertrophy)**, left ventricle
unrelated to pressure overload, present at birth, diastolic dysfunction, suddent death in athletes! (small left ventricle so can’t get enough blood and the leaflet blocks the outflow tract)
OFTEN ASYMPTOMATIC IN CHILDREN patients present with dyspnea and angina, syncope and arrythmia like Afib that can lead to sudden decompensation and sudden death may be the first presentation in young athletes during strenous activity!!!!!
on exam: sustained PMI, loud s4 and S3, loud harsh aortic outflow murmer cresendo-decreshendo is charactericstic (INCREASED MURMER WITH VALSALVA AND STAND, DECREASED SQUATTING!!!) KEY!! variable systolic murmer, jugular venous pulsations bisferiens pulse with double/triple pulse because the ventricle is contracting against the obstuction of the aorta by MV leaflet
DX:
EKG: might show LVH
echo: key!! show LVH, asymmetrical septal hypetrophy and small left ventricle, and diastolic dysfunction
tx:
- Beta blockers, calcium channel blockers (verapamil)
- myomectomy (to remove extra septal muscle)
- ablation, ICD, dual chamber pacers and mitral valve replacements as needed
hypertrophic cardiomyopathy
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
hypertrophic cardiomyopathy
explain what is going on on in the heart?
“handler: the area right below the aorta outflow tract narrorws because the intraventricular septum grows and it closes off, so the mitral valve leaflets move abnormally towrads the intraventricular septum and blocks this area so the blood can’t get out of the left ventricle, this is dynamic meand the amount of blocking depends on the activity you are doing”
obstruction: MV moves abnormally towards the intraventricular septum obstructing the Left ventricular outflow tract
myocardial fiber hypertrophy and disarray
mitral valve often thickens causing abnormal movement blocks the blood getting out of the heart
restrictive cardiomyopathies
what is this caused by? what three things might you see this in? how does the pt present and what else do they often have? what is the Dx and what might you need to get? what is the tx?
fibrosis/infiltration of the ventricular wall because of collagen defects like causing the ridgid walls to prevent diastolic filling
characteristic: abnormal diastolic function
pts present with dereased exercise tolerance, in sever get right sided HF, pulomary hypertension usually present, jugula venous distension, S3/S4, inspiratory increase in venous pressure (KUSSMALS SIGN)
DX:
echo!!! may need endomyocardial biopsy
see LV wall thickening
decreased diastolic relaxation
tx: diuretics and cardiac transplant in extreme, CCB might help with symptoms
what percent of people with restrictive cardiomyopathy die within the first 10 years?
90%
can’t treat it, just help with symptoms
CCB might help in some patients
what are the 6 causes of restrictive cardiomyopathy?
Amyloidosis
Hemochromatosis
Fabry Disease
Gaucher Disease
Endomyocardial Fibrosis-Loeffler Endocarditis-hypereosinofilia syndrome
explain the role of LDL and HDL?
LDL: carries lipid to the arteries after being oxidized
HDL: removes lipids from the arteries
**together these contribute the the managing of atherosclerosis**
role of tryglycerides is unknown
what is the major source of endogenously derived cholesterol?
what about exogenously?
liver and intestines
exogenously: diet
what is the rate limiting step in the liver in cholesterol biosynthesis?
what happens when you increase your dietary cholesterol?
converting HMG CoA to mevalonic acid by HMG CoA reductase
**this is where statins work**
when you increase intake of dietary cholesterol_: down regulation of LDL receptors and elevation of LDL cholesterol_
what can reducing the amount of total and LDL cholesterol do? (2)
- significantly reduce mortality and mobidity of coronary heart disease
- slow progression of atherosclerosis
how much greater is the risk of recurrent MI in someone with CHD?
5-7x greater!
how many times greater is the risk of develiping CHD in someone who has PAD, carotid disease, or aortic disease?
4-6 times greater
what are the goals for LDL lowering?
TRICK QUESTION…there are no goal levels anymore, it is based on intensity of statin therapy!!!
what was the main point from the PROVE-IT-TIMI 22 test?
lower we can lower the LDL the better we are at preventing ASCVD and progression
get it down and keep it down
pericarditis
what does the pain feel like and where is it?? what are 4 things that make the pain worse? what is one thing that makes the pain better? what are four things that can cause this?
irritation of the parietal pleura adjacent to pericardium
often following autoimmune disorders SLE, post MI, **viral infections most common COXSACKIE B VIRUS**, neoplasm chest irriation, dresslers syndrome
retrosternal/left precordial pain, may radiate to tip of left shoulder
“KNIFE LIKE STABBING” that is severe!
provoking: breathing, changing positions, laying down, swallowing
palliating: leaning foward
pericarditis
what will you heart? 2
what are 5 things that make this worse?
what are 2 things that make it better?
what will you see on the EKG that is pivitol to identify?
what are the two PIVITOL THINGS YOU SEE/LOOK FOR ON ECHO???
CP, pericardial friction rub scratching, grating from epicardium and pericardium grating on each other usually heart two components (Systolic/diastolic)”evanesence” here today gone tom” venricular systole and early diastole
provoking: pain is worse laying supine, with inspiration, coughing, swallowing, laughing, pain just as bad as MI
Palliating: leaning forward, sitting up
_***YOU GET ST ELEVATION IN ALL LEADS EXCEPT AVR and V1!!!!!!***_ (must distinguish from early polarization with healthy individuals which causes ST elevation)
ECHO EVERY PATIENT MUST HAVE THIS DONE!!!!: may see small pericardial effusion and make sure they don’t have tamponade cause if this progresses could be dangerous also tells you if there is abnormal LV size and function which would indicate MYOCARDITIS as well, in pericarditis you DONT see this!!!
pericarditits tx
what are the 3 treatments?
how long does it take to recover?
- bedrest until pain and fever resolve, most treated as out patient
- NSAIDS for pain VERY EFFECTIVE!!! (opposit as myocarditis)
3. DONT USE ANTICOAGULATION
- takes 2-4 weeks to recover
pulmonary edema
explain how this happens? what does it indicate? what are 8 characteristics of the pt if they present with this?
most severe and dangerous side effect of acute heart failure
- hypertension and back up causes pressure to increase in capillary bed
- fluid moves into the alveoli causing stiffness and preventing the lungs from expanding
- hemoglobin not oxygenated resulting in SOB and cyanosis
grasping for air, rapid pulse, skin moist and cool, lips and nails cyanotic, confusion, stupor, frothy pink cough, crackles
pulmonary hypertension
what is it and what are the two types? what should you remember about this system?
the pulmonary circulation is usually a low pressure system
pulmonary hypertension: increase in pressure of the pulmomary system, usually the pulmonary arteries
this system is selfperpetuating, once you have pulmonary hypertension, you get structual abnormalities that include smooth muscle hypertropy and proliferation of vessel intima making the problem worse
- secondary pulmonary hypertension (most common)
- primary pulmonary hypertension
secondary pulmonary hypertension
What makes it “secondary” HTN?
what are the two most common causes?
what are the two challenges faced with these two causes?
what are 4 things that cause it?
how do you dx/tx it?
increase in pulmonary pressures due to secondary cause
most common: cardiac or pulmonary causes
Challenges:
- if from back flow from cardiac issues: the HTN causes the arteries SM hypertrophy and proliferation of intima…perpetuating the problem
- if from respiratory and hypoxia: the vessels constrict more, perpetuating the problem
***YOU CAN’T WIN EITHER WAY!!***
1. mitral valve/left ventricular dysfunction: increased LA pressure, backs into pulmonary venous to pumonary arterial, leads to thickening of pulmonary arteries, perpretuating the problem and causing sustained HTN
2. pulmonary thromboemboli
3. hypoxemia from COPD/interstital lung disease: for some strange reason the pulmonary arteries constrict under hypoxic environment unlike regular arteries, this perpetuates the problem
4. high altitudes/sleep apnea
DX: radiographic, echo, US
Tx: treat underlying cause
primary pulmonary arterial HTN (PAH)
what is this? what changes in the artery cause this? what three things does it lead to? what is the inheritance pattern? what two things is it associated with for causes? what two compounds do these patients have significantly decreased levels? what are their 2 symptoms? what are the four tx options?
elevation in pulmonary arterial pressure in the absense of an identified cardiopulmonary reason
abnormal proliferation and contraction of vascular SM, coagulation abnormalities, and marked intima fibrosis leading to obliteration and obstruction of pulmonary arteries and aterioles leading to progressive right sided HF__, low CO, and death
autosomal dominant
can be associated with appetite suppressing drugs fenfluramine and HIV!!!!!
reduced levels of NO and prostacyclin which are potent vasodilators
sob with marked periphreal edema
Tx: CCB, prostacyclin analogs, endothelin antagonist, PDE5 inhibitors
cardiogenic shock
what is this? what are 3 causes and what is the most common? what does it activate? what are the 3 charactersitics?
when the heart fails to pump blood sufficiently to meet the needs of the body
hypotension, hypoprofusion, hypoxemia despite adequate volume
Most common cause: AMI
also: myocardial contusion, acute mitral valve regurg to papillary muscle rupture
**since there isn’t enough profusion, causes activation of the sympathetic and renin-angiotensin system which makes the problem worse because it increases afterload and preload overwheling the heart**
cardiogenic shock
what are the 6 characteristics of this you would see/find on the patient?
- lips, nails, and skin become cyanotic
- mean arterial and systolic pressure drop due to poor stroke volume
- 5 narrow pulse pressure
- normal diastolic pressure
- rise of pulmonary capillary wedge of 15 mmHg
- neurologic changes because of low CO and brain profusion
cardiogenic shock
what are the two treatment options? pharm (3)? non pharm (1)?
pharm goal: increase contractility without increasing HR
1. dopamine #1 choice
- dobutamine or NE
non pharm: mechanical intraaortic balloon pump via cath
- pumps in synchrony with the heart
- inserted into decending aorta
- inflates during diastole and pushes the blood along, relaxes during systole
- enhances coronary and systemic profusion and decreases afterload and myocardial oxygen demands since not working as hard
explain the relationship between lipids and athlerosclerosis?
(both LDL and HDL)
- vascular injury like smoking DM facilitates the uptake of lipoproteins
- increase in LDL (oxidized) directly leads to vascular damage and premature atherosclerosis
- LDL oxidation is nessacary for endothelia damage
- HDL: cardioprotective and prevents the oxidation of LDL, reverse transporter of cholesterol
what are four things you might find if a patient that has hyperlipidemia?
- athlerosclerosis disease like PVD, CHD
- eruptive xanthomas: can be seen on the buttocks with extremely high levels of triglycerides
- tendinous xanthomas: very high LDL, nodules on tendons most commonly on achilles, back of hand, and patella
- xanthelasma: yellow plaque on the skin around the eyes
dyslipidemia in adults is heavilly influenced by what three things?
how is it usually detected?
what are four conditions that make people more apt to get dyslipidemia?
diet, lifestyle and genetics
often detected in asymptomatic adults during routine blood screening
- DIABETES MELLITUS
- nephrotic syndrome
- Chronic renal failure
- hypothyroidism
those who have athlerosclerosis commonly have….
dyslipidemia
what is the difference between
primary prevention
seconday prevention
for dyslipidemia?
primary prevetion: lowering cholesterol/LDL will prevent NEW ONSET CHD, they don’t have it yet and you want to prevent them from getting it!
secondary prevention: lowering cholesterol/LDL will prevent recurring coronary events, they already have it so you want to prevent progression
goal: decrease total mortality in presences of existing disease
explain the four treatment groups and what type of statin therapy they would recieve?
familia dyslipidemia
what is defective in these individuals?
what are the levels for heter/homozygotes?
what are three things you might find on PE?
lack LDL receptors or they are defective so the LDL isn’t taken up by the liver to be degraded
heterozygotes: have total cholesterol at birth >350 with high LDL
homoxygotes: have total chonesterol >700 with high LDL
PE: tendon xanthomas, xanthelasma, cutaneous xanthomas
explain the 10 year risk score calculator used to calculate someones risk of cardiac event for LDL?
who are the equations for?
how many RF input?
what BP does it use?
what do you do for others?
- has separate equations for men and women, whites and blacks
- inputs 9 RFs to calculate risk
- can’t calculate for <40 year olds so must use clinical judgement
- uses SYSTOLIC BP!!
- for other ethnicities use sex appropriate white patient equation
who will be on a statin?
basically anyone over 63
explain the risks for Altherosclerotic even with dyslipidemia in:
hispanics, asians, indians
Hispanic american and asian america lower risk than whites
american indian higher than whites
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 <.9
**you need to use clinical judgement!!**
how much can you expect high intensity statins to lower LDL?
what are the two drugs?
lowers LDL by 50%
atorvastatin, rousuvastatin
how much can you expect a moderate intensity statin to lower LDL?
what are the drugs?
lowers LDL by 30-50%
simvastatin, pravastatin, lovastatin or lower dose of atorvastatin, rousuvastatin
what should you always use first in the treatment of elevated LDL?
***always use statins first unless for some reason the pt can’t tolerate them!**
hypertriglyceridemia
are you at risk for developing CAD?
what is this associated with?
why do you treat? when?
what are 3 things it is associated with for dxs?
what are the 2 tx options?
risk for developing CAD is controversial, however, may play a role when LDL is also elevated
associated with Very low density lipoprotein (triglycerides)
inverse relationship between VLDL and HDL….so therefore treat hypertriglyceridemia >200
associated with obesity, T2DM, metabolic syndrome
TX:
- very sensitive to diet, weight reduction and exercise
- fibrinic acid or niacin
HDL
what does this do? is it good or bad?
who is it reduced in 3?
what is it increased in 4?
what does it have a inverse relationship with?
CARDIOPROTECTIVE: facilitates removal of cholesterol in tissues, so has direct protective effects
reduced amount in: smokers, inactivity, and obesity
increases in: increases with: weight reduction, exercise, smoking cessation, estrogen therapy
strong inverse relationship between HDL and CV events, more HDL the less CV events
what is interesting about HDL?
drugs that raise HDL-C do not reduce CV events–its the particle not its cholesterol that makes the HDL anti-atherogenic
what are the 5 lifestyle adjustments you can make to decrease dyslipidemia?
- smoking cessation
- decrease intake of saturated fats
- decrease total calories
- increase physical activity
- decrease sodium intake
what is the ideal diet for a person with dyslipidemia?
diet is a major contributor to lipoprotein disorders
<30% fat
<7% saturated fat
<200 mg cholesterol
replace fats with carbohydrates
what is the goal weight reduction in dyslipidemia?
minimum 10% weight reduction
HMG CoA inhibitos
what do these do?
what is important about the dosing?
what can it cause
what are two SE?
rate limiting step in cholesterol synthesis; up regulates LDL receptors
- low dose gives you the most bang for your buck, increasing dose you see less effective
- can cause chemical diabetes but the benefits outweigh the risks
- myalgia
4. myositis and rhabdomyolysis
what 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!!!
bile acid sequestrants
what do they do?
what do they decrease?
what can the cause as SE?
stimulate the conversion of cholesterol to bile acids in the liver and upregulate bile acids in the liver
decreases LDL
constipation, GI issues
nicotinic acids
what does it decrease? what does it raise?
what is one strange symptom you many need to pretreat?
how should it be dosed?
what shouldn’t you use this with?
decrease VLDL
lowers triglycerides
raises HDL 20-30%
GI DISRESS, flushing/itching (pretreat with ASA
start with low dose and work upwards
don’t use with statins, increase risk for myopathy!!
ezetimibe
what does this work in combination with?
what does this achieve?
who do you not use this in?
what does it do?
when added to a statin there was additional LDL lowering up to 25% and likely has synergistic effect
this plus low/moderate dose statin is more effective in lowering LDL than doubling the dose of a statin!!!
no in hepatic disease
inhibits intestinal absorption
PCSK9 inhibitor
alirocumab
what does the PCSK9 enzyme do?
what type of drug is this?
how much does it lower LDL?
what two groups of people is it indicated for?
PCSK9: an enzyme that binds to LDL receptors on the liver and promote receptor degredation preventing LDL-C clearance from the blood
this drug: monoclonal antibody given SQ
lowers LDL by 40% or more in pts already taking maximal tolerated doses of statins “get extra burst to lower it even more!!
indications: heterozygous familial hypercholesterolemia OR patients with ASCVD already taking max doses of statin
whats the general rule of thumb for somoene needing treatment of dyslipidemia?
STATIN FIRST, increased to maximum as necessary
if unable to use statins (myopathy) consider non-statins
what is the treatment reccomendations for
hypertriglyceridemia with mild cholesterolemia?
- gemfribrozil (fibrinic acid), fenofibrate (fibrinic acid), niacin
2. must control diabetes, reduce smoking, ETOH, and lose weight
- Still elevated: add statin if LDL remains above goal
postural hypotension
who does this usually occur in?
what happens in this?
what happens to the blood…what does this cause?
what are 5 symptoms?
what are the 2 tx methods?
usually occurs in pts with injuries at T4-T6 and above and is related to the interruption of descending control of sympatetic outflow to blood vessels in the extremities and abdomen
- pooling of blood impairs the return of venous blood to the heart, causing a decrease in cardiac output along with a drop in arterial pressure
dizziness, palor, excessive sweating, blurred vision, possible fainting
tx: prevented by slow changes in position and measures to improve venous return
orthostatic hypotension
what is this characterized by?
what happens in this?
what are the requirements?
what are two symptoms you might seE?
what are the 4 treatment options?
abnormal drop in BP that occurs when a person stands after a long period of being seated or supine
blood temporarily shifted to the lower part of the body, with an accompaning decrease in central blood volume and arterial pressure
def: systolic drop of 20 mmHg and diastolic drop of 10mmHg after 3 mins of standing
in orthostatic HTN: absense of normal circulatory reflexes or BV so blood pools in the lower extremity causeing cardiac output drop, BP drop, and BF to brain to decrease
dizziness, syncope
TX:
- gradual ambulation to allow patient time to adjust
- avoid situations that cause excessive dilation (alcohol, exercising)
- avoidance of excessive dieuretics
- TEDS/abdominal support brace
what are the 3 most common causes of orthostatic hypotension?
how do you dx it?
1. drug induced hypotension: HTN and psychotropic drugs most common
2. getting old: esp after 7o, have arterial pressure instability and postural hypotension
3. bedrest and immobility: esp after 3-4 days
4. Automonic nervous system disorders: parkinsons, Shy-drager syndrome
DX:
- taking orthostatic BP
- tilt table method
pericardial effusion
what is this? what are 5 things that can cause it?
what can it limit if large enough?
how do you dx?
what are the tx options? (5 total)
accumulation of fluid in the pericardial cavity from inflamatory or infectious process that includes pericarditis >50ml
also from:
- neoplasms
- cardiac surgery
- trauma
small pericardial effusions: can be asymptomatic
sudden acclumination of 200mL may raise intracardiac pressure enough to signiciantly limit venous return to the heart
DX: echo
Tx: depends on extent
- diuretics, NSAIDS, colchicine or corticosteroids to help minimze fluid accumulation
- pericardiocentesis, initial tx of choice for large pericardial effusion
pericardial effusion without cardiac compression
what can this occur with?
what symptsom might you have?
what is important to see on EKG?
what is the best techique used to identify TAMPONADE?
can occur with pericarditis
symptoms if present: hiccups, nasues, coup, chest pressure
CXR: cardiomegaly >250 ml
EKG: decreased WRS voltage
echo: best technique to identify TAMPONADE
Tx: depends on if pt is hemodynamically stable or not
pericardial effusion with compression of the heart causes
temponade
cardiac tamponade
what is this?
what are 5 things that can cause this?
what are two things this reduces?
5 symptoms, which is most important?
how does the patient appeare?
what makes the problem worse?
compression on the heart due to the acccumulation of fluid or blood in the pericardial sac LIFE THREATENING
- trauma
- rupture of the heart post MI
- complication from a cath
- aortic dissection
- PERICARDIAL EFFUSION
increased intracardial pressure limits ventricular filling and reduces stroke volume and cardiac output **heart doesn’t fill properlly with blood**
elevated venous pressure, increase JVP, fall in systolic BP, narrowed pulse pressure, circulatory shock, **pulsus paradox** (drop >10 mmHg in the systolic BP during Insppiration this occurs because the left ventricle is more compressed because of fluid inthe sac so left ventricle has signifcantly less filling and stroke volume)
**appeare acutely ill**
since less blood getting ot the body, the sympathetic system is stimulated which prepetuates the problem
pericardial effusion with compression of the heart
TAMONADE
what happens in this?
what are TWO things that are limited here?
fatal?
what happens to the pressures in RV and LV and CO?
What is the IMPORTANT THING YOU SEE?!?!!?
increasing pericardial fluid raises intrapericardial pressure resulting in compression of the heart
limits ventricular fillling and reduces stroke volume
FATAL IF NOT RECOGNIZED EARLY
causes CARDIAC TAMPONADE, compression of the heart:
1. equilibration of LV and RV diastolic pressure
2. marked decrease in CO
- BECKS TRIAD: decline in arterial pressure, elevation of venous pressure, quiet heart
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
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
tako-tsubo cardiomyopathy
what is this caused by?
by what hormone?
what does it minic?
what do they see when they go in for cath/angiography?
who is this common in?
what will you see on the echo?
what does it ressembly?
“broken heart disease”
stress cardiomyopathy, outpouring of catecholamines in response to stress…causes LV insult
90% in women
**presentation mimics STEMI!** modest elevation of troponins absence of obstructive CAD when they go in to do a cath or angiography…all the arteries clear
DX:
echo- significant LV dysfunction with anterior, apical, and inferior wall ballooning resembling a fishing pout “the apex doesn’t move making a balloon appearance”
myocarditis
what is this?
what is the most common cause of this (3)?
what are the 8 causes of this?
a primary inflammatory process of the myocardium, most often caused by infectious agent
viral origin most common: coxsackievirus B, A, HIV, CMV etc
bacterial
fungal: aspergillos, candidiasis
parasitic: trypanosoma cruzi “changas”
Rickettsial
tx:
supportive
antimicrobial if identified agent biopsy guided
AVOID NSAIDS, can make it worse!
myocarditis
what might you see before this?
what might be the initial presentation?
what are 3 symptoms?
what are two ways you can dx this?
PRODOMAL VIRAL SYNDROME followed by symptoms of mycarditis (CP, dyspnea)
HF MAY BE THE INITIAL PRESENTATION!!!
Tachycardia, muffled heart sounds, elevated temp
DX:
difficult to confirm diagnosis
viral titer
endomyocardial biopsy may isolate virus (rare) or show characteristic pathology of myositis-inflammatory infiltrate
what is the critial difference in the treatment between pericarditis and myocarditis?
pericarditis: NSAIDS…respond within a couple hours NORMAL LV FUNCTION and SIZE
myocarditis: NO NSAIDS EVER….MAKE IT WORSE DECREASE IN LV FUNCTION AND INCREASE SIZE
***must do a echo to look for the presense of myocarditis….
what 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******
constrictive pericarditis
explain the pathophys of this?
5 causes
initial episode of pericarditis transitions to a chronic stage with fibrosis and calcification and THICKENING of the pericardium RESTRICTION OF FILLING
failure of blood to get into the heart because of the contricted pericarditis
obliteration of the pericardial space with fusion of pericardium to the epicardium
picture the outside of you heart wrapped in ductape that you havd such stiffening of the walls that it is unable to relax properally so you get elevation of diastolic pressures in all cardiac chambers, decrease stroke volume, get less blood to the body
activates the RAAS exacerbating the probelm and appeares like right sided heart failure
causes:
radiation, TB, uremia, neoplastic, postpericardotomy (post heart surgery)
constrictive pericarditis
what do you see on PE?
5 things on PE
what do you see on CXR?
what do you see on ECHO?
- pedal edema
- abdominal ascites
- hepatomegaly
- elevated JVP KUSSMAULS SIGN (distension of neck veins during inspiration)
- KNOCK HEARD ALONG left sternal border: diastolic sound that is the sudden cessation of ventricular filling
CXR: calcification 50%
EKG: low QRS voltage
echo: pericardium densely thickened, immobile, dilation of hepatic veins
constrictive pericarditis
supportive other than pericardiectomy
Wolf Parkinson White syndrome
what is this caused by?
what does this create?
what are the 3 qualifications?
what 3 things can’t you read?
accessory patway through bundle of kent
VIA REENTRY
associated with arrythmias like PSVT and Afib that can induce vfib
qualifications:
- delta wave “slurring/upstroke on QRS”
2. shortened PR <.12
3. widened QRS
**cant read the presense of:
Q waves for MI
LVH
ischemia**
wolf parkinson white tx
what are two important distinctions you need to make?
what are four drugs used for the first?
what about for the second?
and if these don’t work?
what is the best option for most patients!
VERY IMPORTANT!!
IF REENTRANT PSVT ONLY with WPW:** **accelerates conduction leading to Vfib use drugs that block AV node conductions
- adenosine
- BB
- diltiazem
- verapamil
IF AFIB/AFLUTTER with WPW: looks a lot like vtach but WPW is IIRREGULAR!!! so its not vtach!!!the ABOVE DRUGS COULD CAUSE THEM TO GO INTO VFIB!!!! THIS WILL BE AN EXAM QUESTIONS!!! accelerates the conduction
- procainamide
2. amiodarone
***If these don’t work….CARDIOVERT THEM!!***
tx of choices for most patient ablation to the accesssory pathway! 90% effective and currative
what is an important thing to know about WPW with PSVT vs WPW with Afib/aflutter
If PSVT/WPW treat with a drug that slows AV conduction: adenosine, BB, diltiazem, verapamil
if Afib/Aflutter/WPW: DO NOT USE THE ABOVE DRUGS IN THIS PATIENT!!!! the ventricular rate is already normal, so slowiing it even more you will cause them to go into vfib
how do you tell if someone has WPW with either PSVT/afib/aflutter?
look at the ventricular rate
if greater than 200 ventricular rate likely is WPW syndrome
in WPW how do you differentiate between WPW/PSVT and WPW/afib?
**this is important because it differentiates tx causes..fatal if misused?***
look at the R-R
- ventricular rate >200
- Look at the R-R to see if regular or irregular
afib: irregular R-R
PSVT: regular R-R
***since the EKGS look funny since so fast you have to use this method to determine if WPW is suposected and guide the treatment between the two***
explain why giving the AV slowing drugs are back in pt with WPW and afib/aflutter are COMPLETELY CONTRAINDICATED AND CAN KILL THE PT!?
the AV node in WPW with afib actually keeps the ventricular rate lower than if the accessory pathway alone.
if you slow the av node you are allowing more impulses down the accessory pathway and it speeds up ventricular rate too much that it can cause the person to go into dangerous vtach/vfib
lown-ganong-levine syndome
what is this caused by?
what are the qualifications?
James fibers bypass track
Qualifications:
1. PR interval <.12, NO DETLA WAVE
2. QRS not widened
Digoxin Toxicity
what does this increase?
what can it cause (5)? which is most common?
what is the characteristic wave?
narrow therapeutic to toxic ration
potent stimulator of arrythmia
increases automaticity
can cause any arrythmias but Multiform PVCs most common that can turn into VTACH
- atrial tach with AV block
- accelerated junctional rythmn
- 1* HB, 2* HB
ST CHANGES WITH SCOOPING/LADLE appearance
hypokalemia
what are the 3 qualifications?
Qualifications:
- ST depression
- flattening of the T wave
- U wave presence after the T wave
hyperkalemia
what can this lead to?
what are the three steps of this characterized by?
can lead to Vfib and death
STEPS:
- diffus T wave peaking throughout EKG…this is different than the peaking you see in a MI because MI is only in the leads you would get a infarct….don’t get infarct in all the leads indicated with diffuse T wave peaking
- PR elongates, drops the P wave, continues peaking
- QRS WIDENS TO SINE WAVE which can turn into vfib
first pic is the peaked t waves
second pic is the sine waves
how do you calculate the length of the QT interval?
2 ways
- QT interval should not exceed 50% of the R-R, doesn’t apply once HR>110
- QT=square root of RR
normal <.41
what can cause QT prolongation?
3 electrolyte conditions
7 drugs
1 hypertrophy
- hypocalcemia.hypercalcemia
- hypokalemia
- digoxin
- macrolides
- antifungals
- class IA, IC, III antriarrythmics
- TRICYCLIC ANTIDEPRESSANTS
8. LVH
what are two congenital disease that can cause increase in QT PROLONGATION?
- jervell and lang-neilsen syndrome: autosomal dominant and associated with deafness
2. romano-ward syndrome: autosomal dominant
what is the danger associated with prolonged QT interval?
can cause dangerous arrythmias
explain what is important to remember about the EKG of someone with pericarditis?
what test must yu older and what is the ONLY thing you want to treat with?
ST ELEVATION IN ALL OF THE LEADS
…eventually this goes down and the T waves invert **think about it, pts don’t infarct the entire heart all at once so this indicates it is likely from another cause like pericarditis**
DO CARDIAC ULTRASOUND and treat with NSAIDS!!! ONLY TREAT WITH ANTIINFLAMMATORIES…..3-4 hours the pain should go away!!***
early repolarization
who do you find this in?
who does it present in?
what does it make them at increased risk for?
what do you do about it?
normal variant that causes ST elevation in YOUNG men more than women
see a little ST elevation in young healthy person in multiple leads!
they are at increased risk for sudden death becuase more likely to enter arrythmia with this variant
***DONT DO ANYTHING WITH THEM…(she wrote this down***
no one really knows what to do with these pts
how can stroke or intracerebral bleed present on EKG?
mimics ischemia with T wave inversion, need pt hx
sinus arrythmia
rate?
rythmn?
p waves?
QRS?
causes?
rate? slight irregularity of sinus rythmn
rythmn? slightly irregular
p waves? yes
QRS? narrow
1. phasic speeding up with inspiration and slowing down with expiration or reponse to variety of stressors
2. variation in vagal tone as result of herring breuer reflex
TX: doesn’t warrant Rx therapy, tx underlying cause
sinus bradycardia
rate?
rythmn?
p waves?
QRS?
when might you see this and what might accompany it?
who is this common in?
what 3 drugs can cause this?
rate?
rythmn? regular
p waves? yes
QRS? narrow
causes? common rythmn seen in early stage of acute MI
- may be seen during sleep when vagal tone takes over rate can drop into 40s
2. can be accompanied by pauses ~2 seconds in sleep
3. normal in well trained athletes
- can be caused by meds beta blockers, diltaizem, verapamil
premature atrial contractions
rate?
rythmn?
p waves?
QRS?
where is this blocked?
if no p wave?
what can this cause?
what are 4 precipitory causes?
what do you do to tx?
ATRIAL RE-ENTRY or increase AUTOMATICITY, premature atrial depolarization
rate? single beat
rythmn? premature complex
p waves? yes, but looks different than a regular p wave
QRS? narrow
other?
1. if early coduction can be blocked at AV node
2. if there is no preceeding p wave then it is called junctional premature beat (only difference)
**can initiate supraventricular tachycardias in suseptible individuals PSVT, Afib, Aflutter**
precipitory factors: ETOH, TABACCO, CAFFEINE, ADRENERGIC STIMULATANS
tx: remove precipitating
atrial flutter
rate?
rythmn?
p waves?
QRS?
other? 4 things!
what are the two treatment options?
RENTRY CIRCUIT around annulus of tricuspid valve
250-350 flutter waves
regular
no p waves, flutter waves
QRS narrow
- most common presentation is 2:1 AV block with QRS ~150 bpm
- SAW TOOTH APPEARANCE in II, III, aVF
- after meds given to slow AV conduction given, most common form of block is 4:1 with ventricular rate ~75 (only this if have been treated with meds, usually 2:1)
- carotid masage can help slow VR down, allowing flutter waves to be seen
underlying heart disease ALWAYS present
TX:
-DC cardioversion
-ablation
-may need meds to prevent occurance
atrial fib
rate?
rythmn?
p waves?
QRS?
MULTIPLE REENTRANT CIRCUITS IN THE ATRIA
rate? 400-600 atrial contractions (blocked at AV by refractory period)
rythmn? irregullarly iregular supraventricular
p waves? NO!!! undulating baseline
QRS? narrow QRS
other:
- in new/untreated onset without med control: ventricular rate is very fast 120-180 bpm
- can be paryoxsmal or persistent
atrial fib
is this in healthy people?
what are 3 things that can cause this in healthy people?
what percent of people have this attributed to cardiac or pulmonary disease?
what do you do if hemodynamicaly unstable? how to test?
what are three things that can be caused by excessive ventricular rate?
can be in healthy individuals without heart disease caused by emotional stress, post surgery, ETOH “holiday heart”
can be “lone” without any precipitating factors
95% in presence of cardiac or pulmonary disease
first goal: access hemodynamic stablilty by pulse …if not stable DC cardioversion
excessive ventricular rate can cause hypotension, pulmonary congestion, CP
how long do you need to have afib to be at risk for thromboemboli?
48-72 hours
lone atrial fibrillation
what is this characteristics of this?
what happens in this?
what is the natural progression of this?
tx?
electrical disturbance in the absence of cardiac or systemic disease
paroxysmal episodes of symptomatic afib that revert to NSR spontaneously with brief course of meds
natural history: increased frequency of episodes over time and becomes harder to maintain NSR with meds
Tx:
dependent of frequency of episodes
evaluation and Tx
new onset afib
what are 3 things you should look for?
3 tests?
rapid control in ED?
drug for recent onset?
if these don’t work?
look for underlying cardiac, pulmonary, and systemic disease
Dx:
Ekg
echo (to check for heart abnormalities)
throid function test (hyperthroidism can cause afib)
TX:
1. first goal: acute/rapid rate control in ED is initial goal: IV diltiazem or Beta blockers
2. ibutilitde Type III for recent onset **THIS IS A PHARM CARDIOVERTER***
3. if these don’t work than proceed to CARDIOVERSION
if pt has been in afib >72 hours what do you need to do before cardioversion? 2 drugs
anticoag for 3 weeks before cardioversion with
coumadin, dabigatran
*****if the patient can’t tell you exactly when it started you MUST DO THIS AND DELAY CARDIOVERSION!!!! don’t put them on a BB just put them on a anticoagulation……the only way to get around this is to do a TEE to check for a clot if the person needs to be converted sooner******
what are the two management strategies for Afib?
are they both ok to use?
- rythmn control
- rate control
****both rythmn control and rate control are acceptable long term strategies to prevent morality, stroke, and quality of life, choice of tx strategy is based on SYMPTOMS!! risk of bleeding, and side effects of the anti-arrhymics***
rythmn control method for
chronic/recurrent Afib
what is the goal of this method?
what are benefits/negatives?
if you can’t cardiovert via meds, what are your next two options?
what two meds do you use to prevent afib recurrance?
what percent will have afib reocurrance?
goal: cardiovert to NSR and use drug to maintain SR (often young people so that way they have no limitations)
benefits: increase cardiac output/function
negatives: side effects of meds and reccurances
if you can’t cardiovert with med
- DC cardioversion after being on antiarrythmic: 90% successful
- if recurrence: DEFINITIVE RX: ABLATION VIA CATH (eliminates Pacs that initiate afib)
drugs to maintain SR once cardioverted
- Type IC fleocainide
- type III amiodarone
50% WILL HAVE RECURRANCE RATE
rate control approach for chronic/reccurent afib
what is the goal of this?
benefit? negatives?
what are the 3 drugs you can accomplish this with and what DO THEY NEED TO BE ON???
goal: leave in afib and anticoagulate with warfarin
benefit: no cardioversion
bad: increase risk of bleeding from anticoagulant
chronic rate control with drugs
1. diltiazem
2. beta blockers
3. digoxin in eldery/sendentary
PLUS
LIFE LONG ANTICOAGULATION WITH WARFARIN TO PREVENT EMBOLISM, use ASA in elderly
premature ventricular contractions (PVCs)
what is this the most common of?
reentry or automaticity?
QRS? p waves? rythmn? after? shape? what type of hearts? pattern?
most common ventricular rythmn
reentry more than automaticity
premature QRS complex that is wide and biazarre
no p waves
WIDE QRS >.12
irregularlly iregular, or regularly irregular (trigeminiy)
often followed by a pause
uniform or multiform
healthy and diseased hearts
bigeminy and trigeminy
premature ventricular contractions
who are these in?
what are they associated with? (2)
what might a person have if they are symptomatic? (2)
tx?
common in healthy and diseased hearts
in the presense of underlying heart disease they are associated with suddent death and LV dysfunction
PE: palpatations, fullness in the neck, or asymptomatic
TX:
if no cardiac disease: don’t do anything
in cardiac disease: new studies show that even though there is increased risk of sudden death….new studies show treating the PVCs increased mortality
case and point, never treat these
ventricular tachycardia
what is this defined as?
what is sustained mean?
is the heart diseased?
hemodynamicaly stable?
what does it deteriorate into?
what are 3 thing syou see this in what can it indicate?
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, syncope and collapse
deteriorates into vfib
occurs with: CHD/mi (first 24-48 hours), cardiomyopathies, drug admin and often reflects severe LV dysfunction
if a person who has had a MI has Vtach within 1st 6 weeks their prognosis is…..
POOR!!
what are four reverisble risk factors for vtach?
ischemia, acute MI, electrolyte imbalance, drug toxicity
what are the treatment options for vtach?
2 tx for stable individuals?
3 tx for unstbale individuals?
if hemodynamically stable:
- amiodarone
- synchronized cardioversion
if hemodynamically unstable:
1. DC cardioversion
ablation/antiarrythmic AMIORDARONE DOC
implantable ICD for significant LV dysfunction
what should you conside if a patient is in afib and the ventricular rate is >200 bpm?
consider afib with WPW syndrome
*****don’t see Delta wave here so determined based on the rate!!!****
first priortiy during afib?
assess hemodynamic stability
most patients are stable which would cause you to do a DC cardioversion (electrical shock)
ventricular fibrillation
what is this?
what is this the most common cause of?
when does it most likely occur?
it can follow the administration of what?
does it contain any waves?
terminal arrhythmia associated with death
most common cause of cardiac death, often in early AM
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)
causes: sometimes occurs following administration of antriarrythmic drugs esp with patients with prolonged QT interval
UNDILATIONS ONLY, choatic oftren preceeded with vtach
rarely seen in pts with structually normal hearts
brugada syndrome
what is this an abnormality of?
3 qualifications?
inherited cardiac disease with abnormal Na channels predisposed to dangerous arrythmia
- coved ST elevation in V1-V3
- RBBB
- T wave inversion
what is the tx for resusitated vfib?
- correct metabolic abnormalties
- treat underlying cause
3. absence of MI, active ischemia, metabolic abnormalities, drug or other reversible causes warrants ICD placement +/- antiarrhythmics
many recent trials have shown ICD to be the ONLY EFFECTIVE long term intervention that improves long term mortality
paroxysmal supraventricular tachycardia (PSVT)
rate?
rythmn?
p waves?
QRS?
who is it in? tx? 3 causes? what are the 3 treatment options?
AV NODAL REENTRY!
abrupt onset and termination
carotid massage may help terminate
150-220
regular
not usually present
narrow QRS
- most in young healthy people without cardiac disease, can tell you the second it started and stopped.
- try valsalva or carotid massage to convert patient out of it
3. cardiovert with adenosine 90-95% of the time if carotid massage doesn’t work
4. selective ablation to part of AV node using radio frequency to prevent PSVT if the meds don’t keep the patient in PSVT
- can be caused by coffee, alcohol, and excitement
