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OMS III > IM Cardio > Flashcards

IM Cardio Flashcards

1
Q

Features of the Chest pain that will not help determine a dx

A

associate with multiple dx and are therefore nonspecific

nausea

fever

sob

sweating

anxiety

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2
Q

what is the worst prognostic significance that goes along with chest pain

A

sob, if a fever is also present think pe or pneumonia

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3
Q

EKG

A

the best initial test for all forms of pain

in the officebased ambulatory setting you can expect the ekg to be normal most of the time but you cannot go on to other forms of testing until the ekg is performed

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4
Q

Enzymes (ck-mb-troponin)

A

these are not the answer in the office or ambulatory setting if you are being asked to evaluate chronic or stable chest pain, best answer in clinic would be to transfer pt to ed if they have acute chest pain

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5
Q

office (ambulatory clinic) chest pain for days to weeks

A

no enzymes

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6
Q

ed chest pain for minutes to hours

A

ekg then enzymes

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7
Q

Stress (exercise tolerance) testing

A

indispensible tool to evaluate chest pain when the etiology is not clear and the ekg is not diagnostic

ett is based on 2 factors:
you can read the ekg
the pts can exercise (get hr up to 85% of max)

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8
Q

maximum hr =

A

220 minus the age of the pt

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9
Q

stress testing is the answer when the etiology of the pain is..

A

uncertain and the ekg is not diagnostic

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10
Q

ischemia is detected by what on the ekg

A

st segment depression

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11
Q

what if you cannot read the ekg

A

if you cannot read the ekg bc of a baseline abnormality then the 2 best methods for detecting ischemia are:
nuclear isotope uptake thallium or sestamibi
echo detection of wall motion abnormalities

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12
Q

reasons for baseline ekg abnormalities are:

A

left bundle branch block

lvh

pacemaker

digoxin

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13
Q

thallium or sestamibi uptake

A

abnormalities are seen when the isotopes are not picked up

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14
Q

abnormalities on echo

A

decreased wall movement called

dyskinesis
akinesis
hypokinesis

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15
Q

ischemia vs infarction

A

ischemia or decreased perfusion will be detected by seeing a reversal of the decrease in thallium uptake or wall motion what will return to normal after a period of rest

infarction is irreversible or fixed that way

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16
Q

dipyridamole may provoke?

A

bronchospasm avoid in asthmatics

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17
Q

what if the pt cannot exercise

A

alternate methods of increasing myocardial oxygen consumption:

persantine (dipyridamole) or adenosine in combination with the use of nuclear isotopes such as thallium or sestamibi

dobutamine in combination with the use of echo: dobutamine will increase myocardial oxygen consumption and provoke ischemia detected as wall motion abnormalities on an echocardiogram

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18
Q

exercise tolerance testing

A

determpines persence of ischemia

set segment depression if ischemia is present

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19
Q

exercise thallium

A

inabelitiy to read the ekg or baseline st segment abnormalities

decreased uptake of nuclear isotope if ischemia is present

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20
Q

exercise echo

A

inabelitiy to read the ekg or baseline st segment abnormalities

wall motion abnormalities if ischemia is present

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21
Q

dipyridamole thallium

A

inability to exercise to target heart rate

decreased uptake of nuclear isotope if ischemia is present

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22
Q

dobutamine echo

A

inability to exercise to target heart rate

wall motion abnormalities if ischemia is present

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23
Q

whas is the right thing to do in a pt with reversable ischemia?

A

coronary angiography

isotope uptake will be normal at rest and decrease with exercise

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24
Q

reversible perfusion defects need?

A

catheterization, catheterization indicates which pts get bypass vs angioplasty vs medication alone

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25
Q

the 2 diff methods of detecting ischemia in terms of using nuclear isotopes or echo are essentially equal in terms of sensitivity and specificity

A

exercise thallium=exercise echo

dipyridamole thallium=dobutamine echo

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26
Q

coronary angiogrpahy

A

used to detect the anatomic location of coronary artery disease

a test to detect the presence of narrowing that is best managed with surgery, angioplasty or other methods

sometimes is it used if noninvasive tests like ekg or stree testing ore queivoal

most accurate method of detecting cad

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27
Q

angiography determines

A

bypass surgery vs angioplasty

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28
Q

stenosis less than 50% is

A

insignificant

surgically correctable disease begins with at least 70% stenosis

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29
Q

with 1 or 2 vessel disease on agniography

A

stent placement

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30
Q

with 3 vessel disease, left main or 2 vessel disease in diabetics

A

CABG

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31
Q

holter monitoring is used mainly for

A

rhythym evaluation

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32
Q

holter monitoring

A

continuous ambulatory ekg monitor that records the rhythym

useually 24 but can be used up to 72 hours

detects rhythym disorders like a fib, flutter, ectopy like premature beates, or v tach

it does not detect ischemia and is not accurate for evaluating the st segment

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33
Q

echocardiography is to evaluate

A

valve function
wall motion
and ef

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34
Q

dont put pts on a treadmill if

A

they are currently having chest pain

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35
Q

overview of treatment of chest pain

A

know what medications will lower mortality, dont need dose but know route of administration

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36
Q

nitro is used orally or by patch with

A

chronic angina

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37
Q

nitro is used as sl paste or iv with

A

acute angina

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38
Q

nonsepficie bta blockers such as propranolol are not used routinely in

A

cardiology

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39
Q

antiplatelet therapy

A

all pts with acute coronary syndromes (acs) should receive 2 antiplately meds immediatly upone arrival in the ed

the meds should be a combo of aspirin and either clopidogrel prasugrel or ticagrelor

all 3 inhibit the p2y12 receptor on the platelet

the use of 2 meds is for cute presentation and for coronary stenting not chronic or stable cad

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40
Q

antiplatelet therapy when angioplasty and stenting is planned

A

use ticagrelor or prasugrel, these best prevent restenosis of stenting

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41
Q

clopidogrel is used in

A

combo with aspirin on all acs

aspirin intolerance or allergy

recent angioplasty with stenting

is it rarely associated with ttp

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42
Q

best mortality benefit in chronic angina

A

aspirin and beta blockers

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43
Q

prasugrel

A

a thienopyridine medication in same class as clopidogrel

indicated as antiplatelet med that has its best evidence for use in those undergoing angioplasty and stenting

dangerous in pts 75 and older bc of hemorrhage and stroke

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44
Q

ticlopidine

A

used to inhibit platelets in the rare pt who is intolerant of both aspirin and clopidogrel

you cannot use if the reason for aspirin and clopidogrel intolerance is bleeding since it will inhibit platelets as well

causes neutropenia and ttp

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45
Q

ranolazine

A

additional therapy for angina fefractory or persistent through other treatment

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46
Q

ace inhibitors and arbs

A

low ejection fraction/systolic dysfunction (best mortality benefit)

regurgitant valvular disease

cough is the most common adverse effect of acei in up to 7% of pts

if causing hyperkalemia then switch to hydralazine and nitrates

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47
Q

hydralazine

A

direct acting arterial vasodilator

decreases afterload and has been shown to have a clear mortality benefit in pts with systolic dysfunction

should be used with nitrates to dilate the coronary arteries so that blood is not stolen away from coronary perfusion when afterolad is decreased with hydralazine

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48
Q

statins tip

A

cad with any ldl

the goal is at least an ldl

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49
Q

guidelines for using statins

A

when the ldl is above 100

cad with any ldl level

goal of ldl below 70 for those with cad and diabetes

everyone will agree that the goal for ldl with cad is below 100

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50
Q

cad equivalents for statin use

A

try to get ldl below 100

pad

carotid disease (not stroke)

aortic disease (artery not the valve)

stroke

dm

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51
Q

what is clear with lipid management

A

no cutoff point at which to start statins in those with cad stroke or pad, but they should all be on a statin

should not really be asked this on a test bc it is unclera the goal for ldl levels either below 70 or 100

is is clear that only statins are asociated with a definite mortality benefit in the managment of hyperlipidemia in any circumstance

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52
Q

most common adverse effects of statins

A

liver dysfunction will occure in 1% and they will get elevated transaminases

myositis elevation of cpk or rhabdomyolysis occurs in .1% of pts

dont routinely check for cpk unless symptoms are present

test ast and alt routinely even w/o symptoms

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53
Q

other lipid lowering therapies

A

niacin, gemfibrozil, cholestyramine and ezetimibe all have beneficial effects on lipid profiles but none are initial therapy bc they have a mortality benefit on cad

nicain and givric acid derivatives like gemfibrozil have some mortality benefit but not as much as the statins

statins ahve an antioxidant effect on the endothelial lining of the coronary arteries that gives a benefit that transcends simply lowering the ldl number

only use when cant get ldl down with statin or they are intolerant to statins with liver failure myositis or allergic

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54
Q

niacin

A

associate with glucose intolerance, elevation of uric acid level, and itchiness from atransient release of histamine

excellent drug to add to statins if full lipid contorl is not achieved with statins

although statins exercise and cessation of tobacco will all raise the hdl level nicain will raise hdl more

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55
Q

gemfibrozil

A

fibric acid derivatives lower triglyceride levels somewhat more than statins, but lower tris alone has not proven to be as sueful as the straightforward mortality benefit of statins

use caution when adding fibrates to statins bc of an increased risk of myositis

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56
Q

cholestyramine

A

bile acid sequestrant has significant interactions with other meds in the gut and may block their absorption

can cause constipation and flatus

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57
Q

ezetimibe

A

lowers ldl without any evidence of actual benefit to teh pt

ldl elvels are an imperfect marker of benefit with cholesterol lowering therapies

no better than a placebo with mi stroke or death

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58
Q

what is clear with lipid lowering therapy

A

statins lower mortality the most

adverse effects of other agents are well established

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59
Q

statin ae

A

elevation of transaminases (lfts)

myositis

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60
Q

niacin ae

A

elevation in glucose and uric acid level

pruritus

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61
Q

fibric acid derivatives ae

A

increased risk of myositis when combined with statins

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62
Q

cholestyramine ae

A

flatus and abdominal cramping

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63
Q

ezetimibe ae

A

well tolerated and nearly useless

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64
Q

check ast and alt when using

A

statins

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65
Q

dihydropyridine ccbs may increase mortality in pt with

A

cad bc of their effect in raising heart tartes

reflex tachycardia

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66
Q

none of the ccb have been shown to lower mortality in

A

cad

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67
Q

although ccbs are negative inotropes

A

they acutally increase myocardial o2 consumption because of reflex tachycardia

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68
Q

bottom line is do not routinely use ccbs in

A

cad

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69
Q

ccbs verapamil and dilitazem are used in pts who cannot tolerate b blockers bc of

A

severe asthma

70% of people with reactive airway disease can toerate beta1 specific blockers

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70
Q

use ccbs (verapamil and diltiazem) in CAD only with:

A

severe asthma precluding the use of beta blockers

prinzmetal variant angina

cocaine induced chest pain (bblockers are ci)

inability to control pain with maximum medical therapy

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71
Q

adverse effects of ccbs

A

edema

constipation (verapamil most often)

heat blocke (rare)

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72
Q

revascularization

A

angiography is indipsensible in evaluating a pt for the possibility of revasuclarizations which is either coronary bypass surgery or angioplasty

symptoms alone cannot tell the number of vessels involved what vessels or the degree of stenosis

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73
Q

cabg

A

lowers mortality only in a few specific circumstances with very severe disease such as:

3 vessels with at least 70% stenosis in each vessel

left main coronary artery occlusion

two vessel disease in a pt with dm

persistent symptoms despite maximal medical therapy

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74
Q

cabg long term mortality

A

benefit is greater with the most severe disease such as those with left v dysfunction. the immediate operative moratlity may be greater in pts with an ef below 35% but in the long term those surviving hte procedure will do better in those with 3 vessel and left v dysfunction

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75
Q

cabg internal mammary artery grafts

A

last on avg 10 years before they occlude

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76
Q

cabg saphenous vein grafts

A

remain patent reliably for only 5 years

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77
Q

PCI

A

is commonly referred to as angioplasty

intervention is more precise bc there are other interventions besides angioplasty

it is the best therapy in acs esp in those with st segment elevation

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78
Q

the mortality benefit of pci is hard to demonstrate in

A

chronic stable angina

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79
Q

maximal medical therapy with aspirin b blockers acei/arbs and statins has been proven to have equal or evern superior benefit compared to pci in

A

stable cad

pci is more definitive in terms of decreaseing dependence on meds and decreaseing frequency of painful angina episodes

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80
Q

ACS

definition

A

it is impossible to determine the precise etiology of acs from history and physical exam alone

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81
Q

ACS

risk factors

A

same as cad

htn dm tobacco

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82
Q

why are acs associate with an s4

A

bc of ischemia leading to noncompliance in the lv

s4 gallop is the sound of atrial systole as blood is ejected form the atrium into a stiff v

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83
Q

pulsus paradoxus

A

a decrease in p of greater than 10 mm hg on inspiration

associated with cardiac tamponade

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84
Q

kussmaul sign

A

an increase in jvp on inhalation most often assocaited with constrictive pericaditis or restrictive cardiomyopathy

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85
Q

triphasic scratchy sound

A

pericardial friction rub

mi (dressler syndrome), occurs several days after an MI and is much rarer than simple ventricular ischemia

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86
Q

continous machinery murmur

A

pda

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87
Q

there are no specific physical findings that allow you to answer a most likely diagnosis question in terms of st elevation or depression w/out

A

an ekg

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88
Q

a displaced pmi

A

is characteristic of lvh as well as dilated cardiomyopathy

it cannot occur with an acs

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89
Q

leads v2-v4

A

anterior wall of lv

worst place to have mi

mortality is 30-4-% within 1 year

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90
Q

leads 2 3 and avf

A

inferior all of of lv

mortality is 5% within 1 year

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91
Q

pr interval grater than 200 milliseconds

A

first degree heart block

little pathologic potential, esp when isolated

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92
Q

pvcs and apcs

A

are associated with the later development of more severe arrhythymias but no additional therapy is needed if magnesium and paotssium levels are normal

we dont like to see pvcs but theri presence does not require any changes in management

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93
Q

st depression in v1 and v2

A

suggestive of a posterior wall mi

bc the lead are read in opposite direction of the rest of the leads

low mortality and no additional therapy is needed

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94
Q

rbbb

A

benign compared to a new leftbb

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95
Q

most important step for an acute mi

A

give aspirin, lowers mortality

morphine oxygen and nitro should all be given but they do not lower mortality and so they are not as important as aspirin

give apsirinr simultaneously while activating the cath lab

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96
Q

when do you give clopidogrel with acute mi

A

when pt cant tolerate aspirin or has undergone agnipolasty with stenting

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97
Q

always initate therapy and testing before what with mi

A

move the pt

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98
Q

b blockers and mi

A

they lower mortality but are not critically dependant on time

same thing with acei and statins

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99
Q

EKG and mi

time to becoming abnormal

duration of abnormality

A

immediately at onset of pain

st elevation progresses to q waves over several days to a week

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100
Q

myoglobin and mi

time to becoming abnormal

duration of abnormality

A

1-4 hours

1-2 days

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101
Q

ck-mb

time to becoming abnormal

duration of abnormality

A

4-6 hours

1-2 days

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102
Q

troponin and mi

time to becoming abnormal

duration of abnormality

A

4-6 hours

10-14 days

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103
Q

the use of troponing level is not without its difficulties

A

troponin cannot distinguish a reinfarction occuring several days after the first event

renal insufficiency can result in false positive tests since troponin is excreted through the kidney

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104
Q

MI reinfarction

A

when a pt has a new episode of pain within a few days of the first cardiac event the management is:

perfomr an ekg to detect new st segment abnormalities

check ck-mb levels, after a few days from initial infarction they go back down and so an elevation will tell you it is a new infarction

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105
Q

mi icu monitoring

A

placed here after initial management is put in place

continuous rhythm monitoring improves survival and outcome

the most common cuase of death in the first several days after an mi is ventricular arrhythmia (tach and fib)

rapid performance of electrical cardioversion or defib is available

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106
Q

ck mb should be gone in

A

24-48 hours

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107
Q

st elevation mi treatment

A

initially with aspirin

clopidogrel is often used if there is an allergy to aspirin but prasugrel and ticagrelor are alternatives to clopidogrel that are superior if stenting happens

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108
Q

angiolplasty is superior to thrombolytics in terms of:

A

survival and mortality benefit

fewer hemorrhagic complications

likelihood of developing complications of mi (less arrhythmia less chf fewer ruptures of septum free wall and papillary muscle ruptures)

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109
Q

door to balloon or pci time is

A

less than 90 minutes

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110
Q

complications of pci

A

rupture of coronary artery on inflation of balloon

restenosis (thrombosis) of the vessel after the angioplasty

hematoma at the site of entry into the artery

only 20% of us hosptials can do angioplasty bc they have no cath lab

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111
Q

how to reduce the risk of restenosis after pci

A

the palcement of drug eluting stents aht inhibit the local t cell response (paclitaxel, sirolimus)

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112
Q

rate of restenosis within 6 monts of pci

A

no stenting 30-40%

bare metal stent 15-30%

drug eluting stent

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113
Q

what do you do if pt has ci to thrombolytics

A

transfer somewhere with a cath lab

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114
Q

absolute ci to thrombolytics

A

major bleeding into the bowel (melena) or brain (any type of cns bleeding)

recent surgery (within the last 2 weeks)

htn above 180/110

nonhemorrhagic stroke within the last 6 months

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115
Q

heme positive brown stool is not a ci to use

A

thrombolytics

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116
Q

the mortality benefit of thrombolytics extends out to

A

12 hours from the onset of chest pain

50% improvement rate if given within 2 hours

should receive thrombolytics withing 30 minutes of coming through the door

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117
Q

MI treatment indications and benefits

aspirin

A

everyone

the best initial therapy

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118
Q

MI treatment indications and benefits

clopidogrel or prausgrel or ticagrelor

A

those underoing angioplasty or stenting

second antiplatelet drug with aspirin

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119
Q

MI treatment indications and benefits

beta blockers

A

everyone

effect is not dependent on time

started any time during admission

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120
Q

MI treatment indications and benefits

acei/arb

A

everyone

benefit best with ejection fraction below 40%

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121
Q

MI treatment indications and benefits

statins

A

everyone

goal ldl

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122
Q

MI treatment indications and benefits

oxygen,nitrates

A

everyone

no clear mortality benefit

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123
Q

MI treatment indications and benefits

heparin

A

after thrombolytic/pci to prevent restenosis

inital therapy with st depression and other nonst elevation events (unstable angina)

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124
Q

MI treatment indications and benefits

ccb

A

cant use beta blockers

cocaine induced pain

prinzmetal or vasospastic variant angina

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125
Q

door to needle time

A

under 30 minutes

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126
Q

when the pt has acs and there is no st segment elevation (so if the pt has depression) there is no benefit from what?

A

thrombolytic therapy or pci

give heparin instead

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127
Q

glycoprotein IIb/IIIa inhibitors

A

abciximab tirofiban eptifibatide

used in coronoray syndromes in those who are to undergo angioplasty and stenting

are not benefical in acute st elevation infarctions unless underoing stenting or angioplasty

inhibit the aggregation of platelets

lead to a reduction in mortality in those with st depression particularly in pts whose troponin or ckmb levels rise and who then develop a mi requiring pci with stenting

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128
Q

Cardiac events when to use aspirin

A

stable angina

unstable angina/non-st elevation MI

st elevation mi

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129
Q

Cardiac events when to use beta blockers

A

stable angina

unstable angina/non-st elevation MI

st elevation mi

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130
Q

Cardiac events when to use nitrates

A

stable angina

unstable angina/non-st elevation MI

st elevation mi

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131
Q

Cardiac events when to use heparin (enoxaparin)

A

unstable angina/non-st elevation MI

st elevation mi

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132
Q

Cardiac events when to use GPIIb/IIIa

A

unstable angina/non-st elevation

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133
Q

Cardiac events when to use thrombolytics

A

st elvation mi, but not as good as pci

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134
Q

Cardiac events when to use ccbs

A

never

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135
Q

Cardiac events when to use warfarin

A

never acutely

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136
Q

Cardiac events when to use antiplatelet drug

A

unstable angina/non-st elevation MI

st elevation mi

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137
Q

tpa (thrombolytics) are only beneficial with

A

St elevation MI

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138
Q

heparin is best for

A

non st elevation mi

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139
Q

GPIIa/IIIb inhibitors are best for

A

non st elevation mi and those undergoing pci and stenting

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140
Q

what has no clear mortality bneefit in ACS

A

ccb and warfarin

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141
Q

low molecular weight heparin is superior to

A

unfactionated heparin in terms of mortality benefit

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142
Q

absolute contraindications to stenting

A

major bleeding (bowel/brain)

recent surgery (less than 2 weeks)

severe htn (greater than 180/110)

nonhemorrhagic stroke (less than 6 months)

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143
Q

In non-st elevation ACS, when all medications have been given and the pt is not better

A

urgent angiography, and possible angioplasty (PCI) should be done

no better means: 
   persistent pain
   s3 gallop or CHF developing
   worse EKG changes or sustained ventricular tachycardia
   rising troponin levels
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144
Q

starving hearts have v tachy

A

open it fast with PCI

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145
Q

complications of acute mi are an excellent source of

A

what is the most likely diagnosis

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146
Q

sinus bradycardia

A

very common in assocaition with mi bc of vascular insufficiency of the SA node

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147
Q

3rd degree (complete) AV Block

A

cannon A waves, produced by atrial systole against a closed tricuspid valve, the tricuspid valve is closed bc the of the 3rd degree AV block causes the atria and ventricles to contract seperately and out of coordination with each other

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148
Q

Cannon A Wave

A

3rd degree block

the bounding jugulovenous wave bouncing up into the neck

look for an association with right ventricular infarction and 3rd degree AV block

all symptomatic bradycardias are treated first with atropine and then by placing a pacemaker if the atropine is not effective

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149
Q

Tachycardia causes

A

R ventricular infarction

tamponade/free wall rupture

ventricular tachycardia/ventricular fibrillation

valve or septal rupture

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150
Q

Right ventricular infarction

A

association with new inferior wall mi and clear lungs

you cannot get blood into the lungs if the blood cannot get into the heart

diagnose by flipping ekg from usual left side of chest to the right side, st elevation in RV4 is the most specific finding

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151
Q

the Right coronary artery supplies

A

Right Ventricle

AB node

inferior wall of heart

-this is hwy up to 40% of inferior wal mi will have a right ventricular infarction

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152
Q

How to treat RV infarction

A

high volume fluid replacement

dont use nitroglycerin they worsen cardiac filling

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153
Q

Tamponade/free wall rupture

A

it usually takes several days after an infarction for the wall to scar and weaken enough for it to rupture

look for sudden loss of pulse

lungs are clear

cause of pulseless electrical activity

diagnose with emergency echo

emergency pericardiocentesis is done on the on the way to the OR

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154
Q

ventricular tachy/ventricular fibrillation

A

both can cause sudden death and there is no way to distinguish them without an ekg if they cause sudden loss of pulse. both are treated with cardioversion/defibrillation

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155
Q

Valve or septal rupture

A

both present with new onset of a murmur and pumonary congestion. mitral regurgitation murmur is best heard at the apex with radiation to the axilla. ventricular septal rupture is best heard at the lower left sternal border

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156
Q

most accurate test for valve rupture and septal rupture

A

echocardiogram

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157
Q

look for a step up on oxygen saturation as you go from the right atrium to the right ventricle to hand you the diagnosis of

A

septal rupture

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158
Q

intraaortic balloon pump

A

is the answer when there is acute pump failure from an anatomic problem that can be fixed in the operating room

IABP contracts and relaxes in sync with natureal heartbeat, it gives a push forward to the blood

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159
Q

IABP is never a

A

permanent device, it serves as a bridge to surgery for valve replacement or transplant for 24-48 hours

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160
Q

Extension of the infarction/reinfarction

A

when a pt presents with either an inferior or anterior infarction, it is common for a second event to infarct a second geographic area of the heart

look for recurrence of pain new rales on exam a new bump up in ckmb and even sudden onset of pulmonary edema

repeat ekg and reterat with angioplasty and sometimes thrombolytic in addittion to usual meds (asprin, metoprolol nitrates, ACE, statins)

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161
Q

aneurysm/mural thrombus

A

detected with echocardiography. most aneursyms do not need specific therapy, treated with heparin and followed by warfarin

162
Q

bradycardia, cannon a waves

A

third-degree AV block

163
Q

no cannon A waves

A

sinus bradycardia

164
Q

sudden loss of pulse, jugulovenous distention

A

tamponade/wall rupture

165
Q

IWMI in history, clear lungs, tachycardia, hypotension with nitroglycerin

A

RV infarction

166
Q

new murmur, rales/congestion

A

valve rupture

167
Q

new murmur, increase in oxygen saturation on eneterin the right ventricle

A

septal rupture

168
Q

loss of pulse, need ekg to answer question

A

ventricular fibrillation

169
Q

Detection of persistent ischemia

A

everyone gets a stress test prior to discharge

the stress test determines if angiography is needed

angiography determines the need for revascularization such as angioplasty or bypass surgery

170
Q

do not do a stress test if the pt remains

A

symptomatic, go straight to angiography

171
Q

do not do agniography if reversible sign of myocardial ischemia are

A

absent

there is no point in revascularizine to mycardium that is dead (infarcted)

172
Q

Post MI stress test

A

identify those with residual ischeia prior to leaving the hospital. do not just cath (angiography) everyone

173
Q

postinfarction routine medications

A 
everyone should go home on:
   aspirin
   beta blockers (metoprolol)
   statins
   ACEI
   clopidogrel or prasugrel or ticagrelor: for those intolerant of aspirin or post-stenting
   ARBs: those with a cough on ACEI
174
Q

ACEI are best for anterior wall infarctions bc

A

of the high likelihood of developing systolic dysfunction

175
Q

dipyridamole is never the right choice for

A

CAD

176
Q

Prphylactic antiarrhythmic medications

A

do not use amiodarone, flecainide, or any rhythm-controlling medication to prevent the development of ventricular tachycardia or fibrillation

do not be fooled by the question describing frequent PVCs and ectopy.

prophylactic antiarrhythmics increase mortality

177
Q

sexual issues postinfarction

tested very frequently, know these things

A

do not combine nitrates with sildenafil, can get hypotension bc they are both vasodilators

erectile dysfunction postinfarction is most commonly from anxity, however of all the medications that cause erectile dysfunction beta blockers is the most common

the pt does not have to wait after an MI to reengage in sexual activity. if the pt is symptom free, sexual activity may begin immediatly . this is bc sexual activity usually does not last long enough to constitute an excessive increase in myocardial oxygen consumption

if the post mi stress test is described as normal the pt can renegage in any form of exercise program as tolerated including sex

178
Q

Congestive Heart Failure

definition

A

sob (dyspnea) is the essential fature of cgf

it is a dysfunction of the heart as a pump of blood, resulting in an insufficent oxygen delivery to tissues accompanie by the accumulation of fluid in the lungs

systolic dysfunction is a low ef

dyastolic dysfunction is the inability of the heart to relax and receive blood, ef is normal and can even be increased

179
Q

Postinfarction Routine Medications

everyone goes home on

A

aspirin

beta blockers (metroprolol)

statins

ACE inhibitors

clopidogrel or ticagrelor or prasugrel: only if intolerant to aspirin

ARBs: if you get a cough with ACEI

180
Q

Ace inhibitors are best for?

bc of the high likelihood of developing systolic dysfunction

A

anterior wall infarctions

181
Q

Prophylactic antiarrhythmic medications

A

do not use amiodarone, flecainide, or any rhythm-controlling medication to prevent the development of ventricular tachycardia or fibrillation.

182
Q

prophylactic antiarrhythmics increase

A

mortality

183
Q

do not be fooled by the question describing frequent pvcs and

A

ectopy

184
Q

dipyridamole is never the right choice for

A

cad

185
Q

Causes of systolic dysfunction

htn

A

htn resulting in a cardiomyopathy or abnormality of the myocardial muscle is the most common cause of chf

initially when caused by htn there is preservation of the ef, over time the heart dilates resulting in systolic dysfunction and low ejection fraction

186
Q

valvular heard disease of all types results in

A

chf

187
Q

causes of systolic dysfunction

mi

A

very common cause of dilated cardiomyopathy and decreased ef

188
Q

ch in us adults is the most common cause of

A

being admitted to the hospital

admitted repeatedly due to complications

189
Q

Infarction>?>?>?

A

dialtion, regurgitation, chf

190
Q

common causes of chf

A

infarction, cardiomyopathy, and valve disease account for most cases (over 95%)

alcohol
postviral myocarditis (idiopathic)
radiation
adriamycin (doxyrubicin)
chagas disease and other infection
hemochromatosis (and causes restrictive cardiomyopathy
thyroid disease
peripartum cardiomyopathy
thiamine deficiency
191
Q

CHF presentation

major

A

dyspnea (sob), is the indispensible clue (on exertion)

pulmonary edema (clinical diagnosis)

Look for what is the most likely dx question, dont lead labs and test just physical and history

192
Q

chf presentation

others

A

orthopnea

peripheral edema

rales on lung exam

jvd

paroxysnal nocturnal dyspnea

s3 gallop

193
Q

Most likely dx for dyspnea,

sudden onset clear lungs

A

pulmonary embolus

194
Q

Most likely dx for dyspnea,

sudden onset, wheezing, increased expiratory phase

A

asthma

195
Q

Most likely dx for dyspnea,

slower, fever, sputum, unilateral rales/rhonchi

A

pneumonia

196
Q

Most likely dx for dyspnea,

decreased breath sounds unilaterally, tracheal deviation

A

pneumothorax

197
Q

Most likely dx for dyspnea,

circumoral numbness, caffeine use, hx of anxiety

A

panic attack

198
Q

Most likely dx for dyspnea,

pallor, gradual over days to weeks

A

anemia

199
Q

Most likely dx for dyspnea,

pulsus paradoxus, decreased heart sounds, jvd

A

tamponade

200
Q

Most likely dx for dyspnea,

palpitations, syncope

A

arrhythmia of almost any kind

201
Q

Most likely dx for dyspnea,

dullness to percussion at bases

A

pleural effusion

202
Q

Most likely dx for dyspnea,

long smoking hx, barrel ches

A

copd

203
Q

Most likely dx for dyspnea,

recent anesthetic use, brown blood not improved with oxygen, clear lungs on auscultation, cyanosis

A

methemoglobinemia

204
Q

Most likely dx for dyspnea,

burning building or car, wood burning stove in winter, suicide attempt

A

co

205
Q

the s4 heart sound comes during

A

pq interval

206
Q

the s3 heart sound comes during

A

tp interval

207
Q

chf diagnostic tests differences

A

know the setting like er vs office

presence of acute symptoms of dyspnea at the time of presentation

208
Q

every pt with chf must undergo

A

echocardiography to evaluate ef

209
Q

echocardiography

A

most important of all tests for chf

most reliable way to distinguish between systolic and diastolic dysfunction (xray ekg and bnp and anp cannot)

210
Q

best initial test for ef

A

transthoracic echo

211
Q

most accurate test for ef

A

multiple gated acquisition scan (muga) or nuclear ventriculography

212
Q

transesophageal echo

A

is more accurate than transthoracic echo and muga or nuclear ventrulography in evaluation heart valve function and diameter

however it is not necessary for evaluatig chf

213
Q

when should you answer nuclear ventriculography

A

nucelar testing for the best precision is rarely needed , but if a person is received chemo (doxorubicin) or you are trying to give the max amount of chemo to cure a lymphoma but ensure you are not causing cardiomyopathy

214
Q

nuclear ventriculography gives precise evaluation of

A

wall motion abnormalities

215
Q

when do you answer BNP

A

in a pt with acute sob in whome the etiology of the dyspnea is not clear and you cannot wait for an echo to be done, a normal bnp excludes chf and the reason behind the dyspnea

216
Q

Test to determine cause/etiology of chf

ekg

A

mi

heart block

217
Q

Test to determine cause/etiology of chf

chest cray

A

dialted cariomopathy

218
Q

Test to determine cause/etiology of chf

hotler monitor

A

paroxysmal arrhythmias

219
Q

Test to determine cause/etiology of chf

cardiac catherterization

A

precise valve diameters

septal defects

220
Q

Test to determine cause/etiology of chf

CBC

A

anemia

221
Q

Test to determine cause/etiology of chf

thyroid function

A

both high and low thyroid levels can cause CHF

222
Q

Test to determine cause/etiology of chf

endomyocardial biopsy

A

rarely done

excludes infiltrative disease such as sarcoidosis or amylid when other sites for biopsy are inconclusive

biopys is mosst accurate test for some infections

223
Q

Test to determine cause/etiology of chf

swan-ganz right heart catheterization

A

distinguishes chf from ards, not routine

224
Q

Treatment for systolic dysfunction (low ef)

A

acei or arb

bblockers

spironolactone

diuretics

digoxin

225
Q

acei and arbs with chf

A

give to all pts with systolic dysfunction at any stage of the disease, benefits occur with any drug in the class

226
Q

bblockers with chf

A

there is only evidence that the following drugs will offer benefit

metoprolol b1 antagonist
bisoprolol b1 antagonist
carvedilol nonspecific bblocker and alpha1 antagonist

227
Q

benefits of bblockers in chf is

A

antiischemic effect

decrease in heart rate leading to decreased oxygen consumption

antiarrhythmic effect

228
Q

what is the most common cause of death from chf

A

arrhythmia/sudden death

ischemia>ventricular arrhythmias>sudden death

bblockers can stop this

229
Q

do not give blockers with acute

A

chf

230
Q

spironolactone in chf

A

beneficial bc it inhibits the effects of aldosterone

only effective in advanced and serious stages of CHF (3 and 4)

ae: hyperkalemia and gynecomastia

not used at a high enough dose to exhibit diuretic activity

231
Q

what is the management of a pt with severe chf who develops gynecomastia

A

switch spironolactone to eplerenone

232
Q

diuretics control symptoms of chf they do not

A

improve mortality

233
Q

diuretics in chf

A

inital therapy of chf with low ejection fraction often includes a loop diuretic in combo with an ace or arb

use any loop

spr

234
Q

Digoxin in chf

A

does not lower mortality in chf (know this)

used to control sympotms of dyspnea, and will decrease hospital admissions

235
Q

do positive inotropes lower chf mortality?

A

digoxin, milrinonr, amrinone, and dobutamine

no they do not

236
Q

what do you do if pt has elevated k in serum and they are on lisinopril for chf

A

switch it for hydralzine and nitro

these have been shown to increase survival with systolic dysfunction

237
Q

candesartan is associated with

A

hyperkalemia

238
Q

know what drugs lower mortality in

A

chf

239
Q

Devices for CHF Treatment

A

implantable defibrillator

biventricular pacemaker

240
Q

implantable defibrillator

A

for those with ischemic cardiomyopathy and an ef below 35%. these devics have s much as a 25% relative reduction in the risk of death. remember that arrhythmia and sudden death is the most common cause of death in CHF

241
Q

Biventricular pacemaker

A

indicated in those with dilated cardiomyopathy and an ef under 35% and a wide QRS above 120 milliseconds who have persistent symptoms

it resynchronizes the heart when there is a conduction defect. many pts who would otherwise be heading to a cardiac tranplantation have had their symptoms markedly improved with the biventricular pacemaker

242
Q

do not confuse the biventricular pacemeaker with a

A

dual chamber pacemaker with a wire in both an atrium and a ventricle

243
Q

ccb’s provide no clear benefit in

A

systolic dysfunction, some ccb’s can actually raise mortality

244
Q

CHF Transplantation

A

when maximal medical theraphy (ACEI, BB, Spironolactone, diuretics, and digoxin) and possible the biventricular pacemaker fail to control symptoms of CHF, then the only alternative is to seek cardiac transplantation

245
Q

Routine anticoagulationwith warfarin is always? in the absence of a clot in the heart

A

wrong

246
Q

Drugs that have mortality benefit in systolic dysfunction

A 
ACEI/ARB
beta blockers
spironolactone or eplerenone
hydralazine/nitrates
implantable defibrillator
247
Q

Treatment for diastolic dysfunction (CHF with preserved ejection fraction)

A

beta blhave clear benefit

digoxin has no clear benefit

diurectics are used to control symptoms of fluid overload

ACEi and ARBs havve unclear benefit in diastolic dysfunction

248
Q

do not confuse diastolic dysfunction with

A

HOCM

249
Q

HOCM

A

congenital disease with an asymmetrically enlarged (hypertrophic) septum leading to an obsruction of the left ventricular outflow tract.

diuretics are contraindicated bc they increase the obstruction

250
Q

clearly beneficial in diastolic dysfunction

A

beta blockers and diuretics

251
Q

clearly not beneficial in diastolic dysfunction

A

digoxin and spironolactone

uncertain: ACEI, ARs and hydralazine

252
Q

Acute Pulmonary Edema

definition

A

pulmonary edema is the worst or most severe from of CHF. pulmonary edema is the rapid onset of fluid accumulating in the lungs

253
Q

Acute pulmonary edema

presentation

A

acute onset of SOB associated with:

rales 
JVD
S3 gallop
Edema
Orthopnea

there can be ascites and enlargement of the liver and spleen if there has been sufficient time for the chronic passive congestion of the right side of the heart to prevent filling of the heart

254
Q

Acute Pulmonary Edema

Diagnostic Tests

A 
Brain natriuretic peptide
cxr
oximetry/arterial blood gases
EKG
Echocardiography
255
Q

BNP for pulmonary edema

A

this is used if the diagnosis of the etiology of the sob is not clear. a normal BNP level excludes pulmonary edema

256
Q

CXR for pulmonary edema

A

you will see vascular congestion with filling of the blood vessels towards the head (cephalization of flow). ordinarily, most flow in the lungs is at the bases bc of simple gravity. in more chronic cases, there will be enlargement of the heart and pleural effusions

257
Q

oximetry/arterial blood gases for pulmonary edema

A

hypoxia is expected. until the acute disease is extremely severe, there is also respiratory alkalosisbc of hyperventilation. bc of the increased respiratory rate, carbon dioxide leaves more easily than oxygen enters the bloodstream.

258
Q

EKG for pulmonary edema

A

most important test to do acutely, bc the ekg can lead to a change in immediate therapy

if atrial fibrillation, atrial flutter, or ventricular tachycardia is the cuase of pulmonary edema, the first thin to do is to perfomr rapid, synchronized cardioversion in order to restore atrial systole and to return the atrial contribution to cardiac output. normally atrial systole contributes only 10% to 20% of cardiac output. if the heart is diseased from dilated cardiomyopathy, decreased ejection fraction, or valvular heart disease, then the atrial conribution to cardiac output.

259
Q

if acute pulmonary edema is from an arrhythmia the fast way to fix it is with

A

cardioversion

260
Q

Echocardiography for pulmonary edema

A

this should be done in all pts to determine if there is systolic or diastolic dysfunction. this makes no difference acutely if there is pulmonary edema bc the initial therapy does not differ.

261
Q

best initial therapy for acute pulmonary edema

A

to remove a large volume of fluid from the vascular space so diuretics

oximetry should be done but should not alter acute management bc we now must give oxygen bc the pt complains of sob and she is hyperventilating

echo should be done but it doenst need to be done urgently

ramipril or any other acei or arb should be used if there is systolic dysfunction with a low ejection fraction, but it does not make a diff in an acutely stable pt (the sam eis true of metoprolol)

262
Q

nesiritide is a therapeutic iv for of atrial natriuretic peptide

A

nesiritide functions in much the same was as nitrates. bc is is only a weak diuretic there is no proven mortality benefit in pulmonary edema

263
Q

pulmonary edema treatment

A

preload reduction

positive inotropic agents

afterload reduction

264
Q

pulmonary edema

preload reduction

A

initial therapy is:

oxygen
loop diuretics such as furosemide or bumetinide
morphine
nitrates

removing 1 or 2 liters of fluid from the vascular space and the lungs is the best thing that can be done acutely to decrease symptoms

265
Q

pulmonary edema

positive inotropic agents

A

dobutamine can be used in the acute setting of pts placed in the ICU when their sob did not respond to therapy acutely with preload reduction

amrinone and milrinone are phosphodiesterase inhibitors that perfrom the same role. they increase contractility and decrease afterload

digoxin is a positive inotrope that increases contractility but it will not have this effect for several weeks after starting its use. there is no benefit of using digoxin in the acute setting

266
Q

pulmonary edema

afterload reduction

A

acei and arbs are used on discharge for long-term use in all pts with systolic dysfunction and low ejection fraction. in an acute setting nitroprusside and intravenous hydralazine can be used.

267
Q

Valvular Heart Disease

Definition

A

all valvular heart disease can be congenital in nature.

rheumatic fever can lead to any form of valve disease but ms is the ost common

aging can automaticallybe associated with as

regurgitant disease is most commonly caused by htn and ischemic heart disease

infarction automatically leads to regurgitation, which leads to dilation

268
Q

all forms of valvular heart disease are associated with

A

SOB and many signs and symptoms of CHF

only the murmurs are specific in terms of presentation

269
Q

lesions of the right side of the heart

A

tricuspid and pulmonic valve

increase in intensity or loudness with inhalation

inhalation will increase venous return to the right side of the heart

270
Q

lesions of the left side of the heart

A

mitral and aortic

increase with exhalation

exhalation will squeeze blood out of the lungs into the left side of the heart

271
Q

best initaial test for valvular heart disease

A

echocardiogram

272
Q

most sensitive and specific test for valvular heart disease

A

transesophageal is better than transthoracic

273
Q

most accurate test for valvular heart disease

A

catheterization

allows the most precise measurement of valvular diameter, as well as the exact pressure gradient across the valve

274
Q

what test is not specific in regard to valvular heart disease

A

ekg, it shows hypertrophy of chambers but you cannot confirm a diagnosis of valvular disease with it

275
Q

xray evaluation of cardiac chamber size is neither the

A

most accurate or the best initial test

276
Q

treatment for vlavular heart disease

A

all of them are assocaited with fluid in the lungs to use diuretics

ms dilate with a balloon

as needs surgical removal

regurgitant lesion respond best to vasodilator therapy with ACEi ABs nifedipine or hydralazine

surgical replacement of regurgitant lesions must be done before the heart diltes too much, if it dose surgery wont help

if the myocardium stretches too much it wont go back to normal

when the end systolic diameter expands you must replace the valve

277
Q

Mitral Stenosis

Definition/Etiology

A

most often caused by rhuematic fever, making it uncommon in the US

critical narrowing is valve surface area that is less than 1cmsquared

treat if it is symptomatic, dont treat if asymptomatic

278
Q

look for pregnancy and immigran in the hx as a clue to answering what is the most likely diagnosis to?

A

Mitral stenosis

279
Q

pregnancy related cardiomyopathy

A

pregancy is associated with a 50% increase in plasma volume which must travers a narrow valve

also during delivery contraction of the uterus can squeeze as much as 500 ml extra blood into cirucaltion

280
Q

most pts with mitral stenosis are

A

immigrants to us from places where rhuematic fever is still common

281
Q

mitral stenosis often present sin

A

young adult pts

282
Q

Mitral stenosis presentation

A

SOB and CHF as well as

dysphagia from left atrium pressing on esophagus
hoarseness from la pressing on laryngeal nerve
atrial fibrilation and stroke from enormous la
hemoptysis

283
Q

Mitral stenosis physical findings

A

murmurs in diastole, just after an opening snap. squatting and leg raising increase the intesnity from increased venous return to the heart

284
Q

mistral stenosis diagnostic tests

A

echo
ekg
cxr: la hypertrophy

285
Q

mitral stenosis echo

A

tte is the best initial test

tee is more accurate test

catheterization is the most accurate diagnostic test

these rules are true for all valvular diseases

286
Q

mistral stenosis ekg

A

atrial rhythm disturbance, particularly atrial fibrillation, is very common. left atrial hypertrophy shows up as a biphasic p wave in leads v1 and v2

287
Q

mitral stenosis cxr

A

straightening of the left heart border
elevation of the left main stem bronchus
second bubble behind the heart

288
Q

mitral stenosis treatment

A

diuretics and sodium restirction (when fluid overload is present in the lungs)

balloon valvuloplasty (done with a chatheter)

valve replacement (only when a cahteter procedure cannot be done)

warfarin for atrial fibrillation (to an inr of 2-3)

rate control of afib (with digoxin, beta blockers, or diltiazem/verapamil

289
Q

Aortic Stenosis definition/etiology

A

aortic stenosis can be caused by a congenital bicuspid valve or with increasing clacification as people age

290
Q

Aortic stenosis presentation

A

Angina: most common presentation

Syncope

CHF: poorest prognosis with 2 year average survival

291
Q

aortic stenosis murmur

A

as systolic, crescendo decrescendo murmur peaking in a diamond shape in mid systole

hear best at the 2nd right intercostal space and radiates to the carotid artery

valsalva and standing improve or decrease the intesity of the murmur from decreased venous return to the heart

handrip softens the murmur bc of decreased ejection of blood

292
Q

aortic stenosis diagnostic tests

A

tte then tee hten catheterization

293
Q

aortic stenosis ekg

A

lvh

s wave in v1 plus an r wave in v5 greater than 35 millimeters

294
Q

Aortic stenosis treatment

A

valve replacemnt is the only trule effective therapy for as

diuretics can be used to decrease chf but pts do not tolerate volume dpeletion very well

balloon valvuloplasty is not routinely done for as. this is bc the main mechanism for developing as is calcifications which does not improve very well with balloon valvuloplasty, balloon catheter procedures are done only if surgery is not an option secondary to the instability or fragility of the pt

295
Q

mitral regurgitation definition/etiology

A

mr is an abnormal backward flow of blood thorugh a mitral valve that does not fit together. htn, endocarditis, myocardial infarction iwth papillary muscle rupture, or any other reason that the heart dilates will lead to MR

296
Q

mitral regurgitation presentation

A

mr presents with the same signs and symptoms as CHF. the only unque findings is the murmur, which is pansystolic (holosystolic), obscuring both S1 and S2.

the murmur radiates to the axilla

handgrip will worsen the murmur by pushing more blood backwards thorugh the valve, handgrip increases afterload and will worsen the urmurs of both aortic regurg and mitral regurg

squatting and leg raising will also worsen mr by increaseing venous return to the heart

all left sided murmurs except mitral valve prolapse and hypertrophic obstructive cardiomyopathywill increase with expiration

297
Q

mr is diagnosed with

A

echo

298
Q

mitral regurgitation treatment

A

Vasodilators: ACE ad ARBs are best, they decrease the rate of progression of a regurgitant valve

Digoxin and diuretics may be used sometimes as htey would b ein any form of CHF

Valve replacement is indicated when the heart starts to dilated. do not wait for left vetricular end systolic diameter to become too large bc the damage will be irreversible, if it is above 40 mm or the ef drops below 60%, surgical valve repair or replacement is indicated

299
Q

Aortic Regurgitation

Definition/etiology

A

AR is caused by anything that makes the heart or aorta dilated in size:

mi
htn
endocarditis
margan syndrome or cystic medial necrosis
inflammatory disorders usch as ankylosing spondylitis or Reiter Syndrome
syphilis

300
Q

AR

Presentation

A 
CHF
wide pulse pressure
water-hammer (wide-boudning) pulse
quincke pulse (pulsations in nail bed)
hill sign (BP in legs as much as 40 mmhg above arm BP)
head bobbing (de musset sign)
301
Q

AR

Murmur

A

it gives a diastolic, decresecendo murmur heard best at the lower left sternal border.Valsalva and stanidn make it better. handgrip which increaes afterload by compressing the arteries of the arms make it worse

302
Q

AR

diagnostic tests

A

Echo

ekg and cxr may show LVH

303
Q

AR

Treatment

A

ACEi/ARBS or nifedipine as vasodilators will increase forward flow of blood and delay progression

digoxin and diuretics have littley benefit

surgical vvalve replacement is used when there is acute valve rupture such as with mi. rpelace or repair the valve before the left ventricle dialtes excessively. ef less than 55% or left ventricular end systolic diameter greater than 55 mm. repairing hte valve means tightening the ends of the valve with sutures this decrease regurg w/o the need for anticoagulation

304
Q

Mitral valve prolapse

definition/etiology

A

mvp is so common as to be considered a normal anatomic variant occurring in as much as 2-5% of the populations, particulary in women. other causes are marfan and ehlers danlos syndrome

305
Q

mvp

presentation

A

most often asymptomatic, usually not associated with chf

most common:

atypical chest pain
palpitations
panic attack

306
Q

mvp

murmur

A

midsystolic click that when severe is assocaited with amurmur just after the click from mitral regurgitation

valsalva and standing which decrese venous return tot he heart will worsen mvp

anything htat increase left ventricular chamber size like squatting or handgrip improves mvp

307
Q

mvp

diagnostic tests

A

cho is best

catheterization is done rarely bc you rarely replace the valve

308
Q

cardiomyopathy

definition

A

abnomral function of the heart muscle, the origins of all defects are in an abnomrally contracting or relaxing myocardium

309
Q

cardiomyopathy etiology

A

dilated, systolic dysfunction and low ejection fraction are often used interchangeably

hypertrophic cardiomyopathy is often interchaged with diastolic dysfunction, cardiac failure with preserved ef

310
Q

cardiomyopathy

presentation

A

sob worsened by exertion

edema
rales
jvd

311
Q

best initial test for cardiomyopathy

A

echo it is also the most accurate

ekg and cxr are unspeficif but still are perfroed

312
Q

cardiomyopathy treatment

A

diuretics for all of them

the onl real function difference in the management of pts is their treatment for each kind

313
Q

murmurs that do not increase with expiration

A

hocm

mvp

314
Q

dilated cardiomyopathy

etiology

A 
alcohol
postviral myocrditis
radiation
toxins like doxorubicin
chagas disease
315
Q

dilated cardiomyopahty

presentation

A

dyspnea gallop edema and thoser symptoms like chf

316
Q

dilated cardiomyopathy

diagnostic tests

A

cho then ekg and cxr are not specific

317
Q

dilated cardiomyopathy

treatment

A

ACEi arbs bblockers (metoprolil or carvedilol) spironolactone all lower mortality

diuretics and digoxin are used to control symptoms

if the qrs is wider than 120 use a bivientricular pacmeaker that improves symptoms and survival

automated implantable cardioverter/defibrillator has morality benefit in some pts

318
Q

hypetrophic cardiomyopathy

definition/etiology

A

most common cause of cardiomyopahty

in hcm a rxn to stressors on the heart such as htn, the heart hypertrophies to carry the load but then has a hard time relaxing in diastole, then the pt becomes sob

in hocm it is a gneetic dosrder with an abnomral shape sto the septum of the heart that forms an anatomic obstruction bewtween the setum and the valve leaflet to block blood leaving hte heart

319
Q

difference between hcm and other forms of cardiomyopathy

A

s4 gallop

fewer signs of right heart failure such as ascites and enlargment of the liver and spleen

320
Q

hocm

A

dyspnea
chest pain
syncope and lightheadedness
sudden death in athletes
worse with anything that increases heaert rate (dehydration diuretics and exercise)
worse with anything that decreases left ventricular chamber size (acei arbs digoxin hydralazine, valsalva, and standing suddenly)

321
Q

hocm diganostic tests

A

echo is the best initial test

the septum is 1.5 times the thickness of the posterior wall

322
Q

hypertrophic cardiomyopathy treatment

A

beta blockers are the best initial therapy for hocm and hcm

negative inotropis like verapamil and disopyramide are helpful

diuretics may help in hcm but they are ci in hocm

323
Q

hocm specific thearpy

A

implantable defibrillators - shoudl be used in any hocm pt with syncope

ablation of the septum shoudl first be tried with a catheter placing absolute alcohol in the muslce causing samll infarctions. if sx persist surgical myomectoy removing part of the septum is the ultimate therapy

324
Q

systolic anterior motion (sam) of the mitral valve is classic for?

A

hocm

it contributes to obstruction

325
Q

catheterization is the most accurate test for

A

determining the precise gradients of pressure across the chamber

326
Q

hypertrophic cardiomyopathy ekg

A

nonspecific st and t wave changes are common

lvh is common

ekg can be normal in a quarter

327
Q

septal q waves are common in

A

hocm but no in mi

328
Q

digoxin and sprinolactone are definitely always wrong in

A

hypertrophic cardiomyopathy

329
Q

surgical myomectomy is the therapy for hypertrophic cardiomyopathy only if

A

all medical and catheter procedures fail

330
Q

hypertrophic cardiomyopathy therapy

A

b blocerks
diuretics
ace and arb ar unclear

331
Q

dilated cardiomyopathy therapy

A 
bblockers
diuretics
ace and arb
spironolactone
digoxin
332
Q

in hocm acei and diuretics definitely

A

do not help this is the majore difference between hocm and hcm

333
Q

restrictive cardiomyopathy

definition

A

combines the worst apsects of both dilated and hypertrophic cardiomyopathy, the heart neither contracts nor relaxes normally bc it is infiltrated with substances creating immobility

334
Q

restrictive cardiomyopathy

etiology

A

sarcoidosis

amyloid

hemochromatosis

endomyocardial fibrosis

scleroderma

335
Q

restrictive cardiomyopathy

presentation

A

dyspnea is most common complaint with signs of r heart failure like edema ascites jvd and liver and spleenomegaly

pulmonary htn is common bc of an increase in wedge pressure

336
Q

kussmaul sign

A

increase in jvp on inhalation is common in restrictive cardiomypathy

337
Q

restrictive cardiomyopathy

diagnostic tests

A

echo is best initial

ekg show low voltage

ef may be normal or elevated

amyloid presents with speckling of the septum on echo or mri

most accurate itest in an endomyocardial biopsy (rarley done they usually take a bipsy from somerhwer else in the body)

338
Q

restrictive cardiomopathy

treatment

A

treat the underlying cause

diuretics may relieve some of the pulmonary htn and signs of right heart failure

thre is no other clear therapy

339
Q

more blood increase all murmurs except

A

mvp and hocm

340
Q

squatting/leg raising effect on murmurs

A

increases: mitral and aortic stenosis, mitral and aortic regurgitation
decreases: mvp and hoxm

341
Q

standing/valsalva effect on murmur

A

increases: mvp and hoxm
decreases: mitral and aortic stenosis, mitral and aortic regurg

342
Q

standing and valsalva do what to venous return to the heart

A

decreases

343
Q

standing from a squatting psoition will

A

open the venous capacitance vessels of the legs

344
Q

valsalve is exhalation against a closed glottis

A

this increases intrathoracic pressure, when this happens it makes it harder for blood to return to the right side of the heart

345
Q

standing or valvsalva=

A

diuretic use

these ar esimilar to using a diuretic. stenotic and regurgitant murmurs are all treated iwth diuretics and or salt restirciton so the anuevers of standing and valsalva will improve them

mvp and hocm have worsening of thei cardiac physiology with diuretics. diuretics decrease left ventricular chamber size, and owrse the regurgitation of mvp and the obstruction of hoxm. hence standing and valsalva will worsen them

346
Q

less blood decreases all murmurs except

A

mvp and hocm

347
Q

handip and amyl nitrate on murmurs

A

the contraction of the muslces of the arms will compress the arteries of the upper extrmeity such as the brachial radial and ulnar arteries . this increases afterload by obstructing the ability of blood to empty the heart

amyl nitrate is a direct arteriolar vasodilator. amyl nitrate stimulates the effect of ACE inhibitors or ARBS on the heart. any valvular disease that is treated with an acei/arb will improve with amyl nitrate. Improve means a softer murmur.

348
Q

handgrip=

A

fuller left ventricle

349
Q

amyl nitrate=

A

acei=emptier left ventricle

350
Q

handgrip decreases

A

left ventricular emptying

351
Q

amyl nitrate increases

A

left ventricular emptying

352
Q

handgrip and amyl nitrate have no meaningful effect on

A

mitral stenosis, in hte same way ACEi has no meaningful effect on MS

353
Q

handgrip and amyl nitrate effect on AS

A

Hand grip: decreases

Amyl nitrate: increases

354
Q

handgrip and amyl nitrate effect on ms

A

Hand grip:no effect

Amyl nitrate: no effect

355
Q

handgrip and amyl nitrate effect on ar

A

Hand grip:increases

Amyl nitrate: decreases

356
Q

handgrip and amyl nitrate effect on mr

A

Hand grip: increases

Amyl nitrate: decreases

357
Q

handgrip and amyl nitrate effect on mvp

A

Hand grip: decreases

Amyl nitrate: increases

358
Q

handgrip and amyl nitrate effect on hoxm

A

Hand grip: decreases

Amyl nitrate: increases

359
Q

manuever are like treatment

A

since regurgitant lesions are treated with ACEi, ARBs, and nifedipine as vasodilators, it is understandable that amyl nitrate decreases the intesnity of these lesions, since it increases the forward flow of lbood and decreases the regurgitant, backward flow of blood

handrgip decreases ventricular empying by increasein afterlaod. this will ipmrove the lesions of MVP and HOCM. a biggr fuller heart improves the obstruction of HOCM. with amyl nitrate, the emptier heart is samller such as would occur with diuretics, dehydration, and tachycardia. thiat is why amyl nitrate will worsen MVP and HOCM

360
Q

handrip impvoes hoxm bc the heart is

A

larger (more full), which decreases the obstruction

361
Q

Pericardial disease

A

the causes of pericardititis, pericardial tampnae and constictive pericarditis have considerable overlap. if the etiology of pericarditis is assocaited with the extravasation of a great deal of fluid, then tamponade can occur. if the cause of pericarditis is chronic then pts can develop the fibrosis and calcification of the pericardium that leads to constrictive pericaditis.

362
Q

pericarditis

A

any infection, inflammatory disorder, connective tissue disorder, trauma to the chest, or cancer of an organ anatomically near the heart can cause pericariditis. the most common infection is viral however staphylococcus, streptococcus, fungi, and othe ragents can cause pericarditis in the sam waythat virtually any infection can cause pneymonia. sle is the most common connective tissue dorder, but wegeners granulomatosis, goodpasture syndrome, ra, polyarteritis nodosa and other diosrders can cause pericarditis

363
Q

what is the most likely diagnosis

pericarditis

A

sharp chest pain that changes in intensity with respiration as well as the position of the body

pain is worse by lying glat and improved by sitting up. this is probably from a change in the level of tension or stretch of the pericardium

ekg shows st segment elevation in all eads, but the most specific finding is pr segment depression

364
Q

colchicine decreases recurrences of

A

pericarditis

365
Q

pereicarditis treatment

A

treat the underlying cause. for the majority, no clear cause is identified, and these “idiopathic” cases are generally presumed to be viral in etiology with coxsackie b virus. these cases are treated with nsaids such as ibu naproxen indomehtacin or any other drug in the class. colchicine decreases recurrences. if a choice calls for nsaid and colchicine is is the correct answer

366
Q

pericardial tamponade

definition/etiology

A

any of the cuaes of preicarditis can extravasate enough fluid to cause tamponade. compression of the chambers of the heart starts on the right side bc the walls are thinner. as little as 50ml of fluid accumulating acutely can cause tamponade. if accumulating over weeks to monthes the pericardium will stretch to accomodate as much as 2 liters of fluid. tamponade can also be from trauma with a bleed into the pericardium this requires emergent thoracotomy

367
Q

physical findings with tamponade

A

pulsus paradoxus - decrease of more than 10 mmhg in blood pressure on inhalation

368
Q

cardiac tamponade most likely dx

A

hypotension
tachycardia
distended neck veins
clear lungs

369
Q

most appropriate test for cardiac tamponade

A

echo

370
Q

cardiac tamponade diagnostic tests

A

ekg: electrical alternans (different heights of QRS complexes between beats)

CXR: enlarged cardiac shadow expanding in both directions (globular heart)

Echo: right atrial and ventricular dastolic collapse

Right heart catheterization: equalization of pressures in diastole

371
Q

Cardiac tamponade treatment

A

percardiocentesis: needle drainage will rapidly reexpand the heart

iv fluids

a hole or window placed into the pericardium for recurrent cases

372
Q

diuretics will decrease intracardiac filling pressure and may markedly worsen

A

the collapse of the right heart

373
Q

constrictive pericarditis

A

any cause of pericarditis can result in sufficient calcification and fibrosis to prevent filling of the right side of the heart if it is chornic, such as tuberculosis

374
Q

constrictive percarditis

what is the most likely dx

A

signs of right heart failure such as:

edema
ascites
enlargement of the liver and spleen
jvd

is is a combination of physical finding and calcification on cxr

375
Q

what findings are most likely to be assocaited with this pts

constrictive pericarditis

A

kussmaul sign: increase in JVD on inhalation (normally the neck veins should go down on inhalation)

knock: this is an extra heart sound in dastole from ventricular filling. as the heart fills to its maximum, it hits the stiff, rigid pericardium with a knock

376
Q

diagnostic tests for constrictive pericarditis

A

best initial test is cxr, it shows the calcification and fibrosis

CT and MRI are moth more accurate, but would not be done if a chest xray were not done first

an echocardiogram is often indispensible in order to exclude right entricular hypertrophy of cardiomyopathy as a cause of the presentation. the myocardium moves nomrally in those with constrictive pericarditis

377
Q

constricitve pericarditis treatement

A

Diuretics: used first to decompress the filling of the heart and relieve edema and organomegaly

surgical removal of the pericardium

378
Q

Peripheral Artery Disease

definition and etiology

A

stenosis of peripheral arteries with the same causative factors as cad and carotid disease such as:

diabetes mellitus
hyperlipidemia
htn
tobacco smoking

379
Q

what is the most likely diagnosis

pad

A

leg pain in the calves with exertion, relieved by rest
loss of hair follicles, sweat glands, and sebaceous glands
skin becomes smooth and shiny

380
Q

spinal stenosis pain is worse when walking

A

down hills bc of leaning back

381
Q

diagnostic tests

pad

A

best inital test is the ankle brachial index, normally equal or slightly greater in the ankles bc of gravity. if the difference is greater than 10% (ABI less than 0.9) then disease is present

most accurate test is an angiogram but this is not necessary unless specific revascularization will be done

382
Q

Treatment

pad

A

best inital therapy is: aspirin, stopping smoking, cilostazol

sinlge most effective medication is cilostazol

surgery is done to bypass stenosis if these medical therapies are not effective

383
Q

routine screening for pad

A

there is none bc there is no mortality benefit to be obtained

384
Q

in all major vascular disease, control each of the following:

A

BP
LDL below 100
Diabetes

385
Q

calcium blockers do not help

A

PAD

386
Q

Aortic Disease tip

the most frequently tested points regarding aortic disease are:

A

diagnosis and treatment of acute dissection

screening recommendations

387
Q

Best initial test for Chest pain with pain also between the scapulae

A

although ont as sensitive as other tests the cxr may show wiedening of the mediastinum which is an excellent clue as to the presence of aortic dissection

388
Q

key points for presence of aortic dissction

A

pain between the scapulae

difference in bp between the arms

389
Q

most accurate test for aortic dissection

A

angiography, most sensitive and specific

also the ost invasive and most lilely to have allergic reaction and renal faiulre to contrast

390
Q

there is no difference in the accuracy of what tests for aortic dissection

A

MRA, CT or TEE

391
Q

in aortic dissetion the most important step is to control what?

A

BP, do this with

bblockers (decreases the shearing forces that are worsening the dissection, must be started before nitroprusside to protect agaisnt relfex tachycardia or nitro)

nitroprusside

surgical correction

392
Q

screening for aortic anuerysm

A

men over 65 who have smoked with US

393
Q

new onset of backpain in a pt over 65

A

do an us to rule at aaa

394
Q

worst form of heart disease in pregnancy

A

peripartum cardiomyopathy, if you get this with persistent lv dysfunction, you will make it worse if you get pregnant again

395
Q

Peripartum Cardiomyopathy

A

it is unknown why there are antibodies made against the myocardium in some prenant women. the LV dysfunction is often reversible and short tem. if the LV dysfunction does not improve then the person must undergo cardiac transplantation

396
Q

medical therapy for peripartum cardiomyopathy

A

same as for dilated cardiomyopathy

ACEi/ARB
bblockers
spironolactone
diuretics
digoxin
397
Q

repeat pregnancy in peripartum cardiomyopathy will provoke

A

enormous antibody production against the myocardium

398
Q

when does peripartum cardiomyopathy develop

A

after delivery in most cases, why you cane use acei or arbs

399
Q

eisenmerger syndrome

A

development of a right to left shunt from pulmonary htn, develops in a person with a ventricular septal defect who has significant left to right shunting htat eventually leads to the development of pulmonary htn, when pulmonary htn becomes very severe then the shunt reverses and right to left shunting develops

400
Q

if peripartum cardiomyopahty isnot one of the choices in asking “what is teh worst cardiac disease in pregnant women?” then l

A

eisenmenger

401
Q

pregnancy increases plasma volume by 50%

A

ms will worsen but not as much as peripartum cardiomyopathy or eisenmenger

OMS III (21 decks)

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