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Echo 2 > C14: Ischemic HD > Flashcards

C14: Ischemic HD Flashcards

1
Q

2 causes of ischemic HD/CAD

which is more common

A

atherosclerosis - more common

non-atherosclerotic causes

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2
Q

most common symptom of CAD

A

angina

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3
Q

what is acute coronary syndrome

2 types

A

when the patient is having a heart attack

  1. STEMI - ST elevation MI
  2. NSTEMI - non-ST elevation MI
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4
Q

non-atherosclerotic causes of CAD

A 
emboli to the coronaries
traume
dissection of the AO
arteritis/vasculitis
radiation
coronary spasm which cause angina
cocaine/amphetamines
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5
Q

describe ischemia of the heart

A

decreased blood supply to the myocardium or increased demand for blood

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6
Q

most common causes of ischemia of the heart

A

coronary artery disease - plaque in the vessel that impedes blood flow

increased metabolic demand - hypertrophic cardiomyopathy or AS (more work or high afterload)

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7
Q

describe infarction

A

death or necrosis of tissue due to prolonged ischemia of total occlusion of blood flow…. everything downstream of the occlusion dies unless theres collateral circulation from another vessel

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8
Q

is ischemia and infarct reversible

A

only ischemia

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9
Q

when does cell death start and complete w/ infarction

A

starts to happen w/in 1 hour and is completed by 4 hours (death in transmural w/in 4 hours)

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10
Q

symptoms of ischemia

MI?

A

SOB, fatigue
angina

same, but add sweating, nausea and vomitting, anxiety

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11
Q

why does angina occur

how does it feel

A

reduction in 02 delivery to part of the myocardium due to CA stenosis or spasm

heaviness, during or aching pain in the chest +/- left arm

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12
Q

what can cause coronary artery spasms

A

stress, exercise, alcohol, smoking, cold, cocaine

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13
Q

which gender tends to have atypical symptoms of angina

what are those symptoms

A

women

pain in the jaw, neck, arm, back

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14
Q

2 main types of angina w/ CAD caused by atherosclerosis

describe them

A

stable

  • occurs when a stenosis is > 70%
  • predictable and regular chest pain
  • relieved w/ rest or nitro and manageable w/ medication or angioplasty

unstable

  • more intense, painful and not predictable
  • maybe due to plaque rupture
  • may require immediate bypass or PCI
  • medication helps to minimally stabilize

“stable” refers to the stability of the patient

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15
Q

other less common types of angina

A

variant angina - due to coronary A spam

microvascular angina - “cardiac syndrome x” maybe due to microvascular dysfunction

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16
Q

common place for CA plaque

A

just distal to a bifurcation

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17
Q

describe the plaque that typically causes un-stable angina

A

a thrombus has formed through a torn plaque but doesnt completely occlude the vessel

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18
Q

common re-perfusion options w/ an MI

how is plaque diagnosed first?

A

PCI - percutaneous coronary intervention (angioplasty)

angiogram

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19
Q

if an angiogram is + for plaque, how is an angioplasty performed

A
  • catheter inserted into the stenosed artery
  • balloon inflated to displace the plaque
  • steroid producing stent placed in the artery to hold the plaque back, plaque helps the stent stick (steroid allows the endothelium to grow back through the stent)
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20
Q

what is done before a CABG

what does the surgery include?

A

angiogram and echo done first

open heart surgery, heart and lung bypass machine…

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21
Q

when is a CABG performed

A
  • when the blockage is unreachable percutaneously w/ a catheter
  • there are too many blockages to stent (>3 or 4)
  • vessel becomes unable or ruptures during PCI
  • patient presents late w/ MI (b/c cell death will already be occurring)
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22
Q

which vessels are usually used in a CABG

A

GSV or internal mammary artery used… attach one end proximal and one end distal to the blockage

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23
Q

disadvantages of a CABG

A
  • higher mortality and morbidity rates… more severe risks
  • longer recovery time
  • cant be done on frail patients
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24
Q

survival rate of patient drops by what % for every minute w/ no pulse… what do you do once pulse is back

A

10%… thrombolytics, PCI or emergency bypass

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25
Q

sequence of events in cardiac arrest

A

MI > arrhythmias (VT, VF) . asystole

…needs CPR and defibrillator

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26
Q

treatment for patients post MI or ischemia

A

modify risk factors

medication

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27
Q

what risk factors should be modified post MI or ischemia

A 
stop smoking
lower fat in diet, alcohol, sat
exercise
manage stress
lose weight
lower BP
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28
Q

what medication is used for chest pain relief

what effect do they have

A

nitrates/nitroglycerines

vasodilation which lowers systemic vascular resistance since the plaque covers less surface area, but can also affect veins and lead to congestion

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29
Q

how are nitroglycerines administered

A

pills, spray

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30
Q

medical treatment post MI or ischemia

A

anticoagulants - breaks the fibrin strands to avoid clotting

antiplatelets - makes platelets more slippers

beta blockers - improve survival by lower demand for 02

calcium channel blockers - lower muscle contraction

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31
Q

how can we diagnose IHD (ischemic HD)

A
  • ECG: ST depression or elevation
  • stress test
  • echo
  • MIBI (nuclear stress testing)
  • cardiac CT or MRI to look for profusion defects
  • coronary angiogram
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32
Q

gold standard for diagnosis of IHD

A

coronary angiogram

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33
Q

why does an acute MI required bloodwork

A

to look for enzymes released w/ myocardium injury and when the cells start to die:

creatine kinase myocardial band
troponin

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34
Q

when could creatine kinase myocardial band and troponin be increased w/ an MI

A

acute stress

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35
Q

acute MI management

A

MONA - morphine, oxygen, nitrates, ASA/aspirin
heparin or thrombolysis
re-perfusion

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36
Q

which differential diagnoses for MI need to be R/O

A

AO dissection
tension pneumothorax
pericardial disease
pleural effusion

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37
Q

which type of thrombolytic is the most effective MI clot busting medication

what does it do

A

TPA - tissue plasminogen activator

cuts (“lyse”) the long chains of plasminogen to prevent it from forming fibrin strands in blood clots (also used for DVT and PE)

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38
Q

types of TPAs

A

streptokinase

urokinase

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39
Q

describe an STEMI MI

A
  • MI w/ ST elevation over the affected area on ECG… usually a transmural infarct from endocardium to epicardium
  • often an anterior MI, look at anterior leads
40
Q

describe an NSTEMI MI

A
  • MI w/o ST elevation on ECG… can cause the ST segment to become depressed instead of elevated, usually a subendocardial infarct only
  • the infarct causes a zone of ischemia w/ a small zone of cell death only
41
Q

what causes the ST segment to become depressed w/ an STEMI

A

the area of cell death around the zone on ischemia which is irritated

42
Q

the ST segment is isoelectric w/ which other segment

A

PR segment or TP segment (?)

43
Q

in general, what does ST depression mean

A

ischemia

44
Q

in general, what does ST elevation mean

A

infarction

45
Q

how will the Q wave change w/ both a STEMI and NSTMI

A

STEMI - abnormal Q wave, will be larger

NSTEMI - normal Q wave

46
Q

unstable angina an be confused w/ what cardiac events

A

STEMI and NSTEMI

47
Q

general ECG changes seen w/ MI or ischemia

A

arrhythmias - originating in the ventricle due to irritated tissue
conduction defects like AV block and LBBB
peaked T waves (acute MI)
symmetric flat or reversed T waves (chronic ischemia)

48
Q

what could a LBBB potential indicate

A

MI

49
Q

describe 1st, 2nd and 3rd degree block

A

1: PR segment is prolonger
2: PR gets progressive longer until the QRS is dropped
3: P and QRS dissociation

50
Q

how does the LAD run on the surface of the heart

what does it mainly supply

A

along the anterior IVS… supplied most of the anterior wall and septum

51
Q

how does the circumflex run on the surface of the heart

gives rise to which artery 10% of the time (left dominant)

A

runs laterally along the AV sulcus towards the posterior of the heart

PDA

52
Q

how does the LAD run on the surface of the heart

gives rise to which artery 90% of the time (right dominant)

which areas of the conduction system does it supply

A

runs laterally towards the back of the heart

PDA

supplied the SA and AV nodes

53
Q

how do we asses the kinetics of the walls

can perfusion be adequate at rest

A

wall motion index or strain

yes

54
Q

good tool to use if you cant tell if the walls are thickening or moving well

A

m-mode

55
Q

does the absence of a resting wall motion abnormality excuse the possibility of ischemia

A

no

56
Q

define hypokinesis

A

reduced wall thickening and motion - <40% but > 5%

normal is > 40% thickening

57
Q

how do we score each of the 16 segments on motion

A

from 1-4

1: normal
2: hypokinetic
3: akinetic
4: dyskinetic or aneurysmal

58
Q

how do you do a wall motion score index

A

take the sum of all wall motion scores and divide it by the # of segments visualized

…if segment not seen in at least 2 views then dont include it in the denominator

59
Q

what does a higher wall motion score mean

A

higher = lower systolic function of the LV

60
Q

what is a sigmoid septum

A

focal basal septal hypertrophy due to myocardial disarray… more common in diabetics and old patients

61
Q

what can cause myocardial disarray

A

reduced perfusion to that segment

62
Q

how does the movement of a a sigmoid septum often appear

A

hypokinetic

63
Q

what can a sigmoid septum cause

A

subAO stenosis and LVOT acceleration, especially if the patient is hypovolemic

64
Q

prognosis for sigmoid septum

A

correlated w/ increased risk for adverse cardiac events

65
Q

another name for sigmoid septum

A

septal knuckle

66
Q

post MI complications

A 
secondary MR due to pap muscle dysfunction from ischemia
thrombus formation
aneurysms
Dresslers syndrome
acquired VSD from myocardial necrosis
CHF
systolic and diastolic dysfunction
ventricular arrhythmia
67
Q

is an isolated RV MI rare

what is it usually associated w/

A

yes

inferior MI - perfused by the RCA

68
Q

is an RV MI associated w/ more pap muscle dysfunction than an LV MI

A

yes

69
Q

IHD/CAD complications

A

pap muscle dysfunction

70
Q

what does pap muscle dysfunction cause

A

improper contraction of the pap muscles and underlying wall segment leading to functional, eccentric MR

71
Q

rupture of a pap muscle is more common in which type of MI

A

inferior

72
Q

another name for ischemic MR

A

functional MR

73
Q

were is a thrombus usually located post MI

types

A

apex - will look like an echo dense mass

protruding or mural/laminar

74
Q

in how many views must you see a thrombus to diagnoses

A

at least 2

75
Q

what type of frequency should you use to assess a clot at the apex

A

high frequency

76
Q

describe a VSD or wall rupture post MI

what might you see, or hear w/ auscultation

A
  • rupture of IVS, usually the inferior septum
  • will hear a loud harsh systolic murmur @ L sternal border
  • thrill
  • high velocity flow across septum
  • flow into pericardial w/ wall rupture
77
Q

why do clots often form at the apex w/ a new MI

A

large ares of the heart no longer contracting…. and the lowest velocity flow is there.. risk drops w/ use of antithrombotics

78
Q

clots are more common when the MI affects which area of the heart?

A

anterior - most common

inferior

79
Q

at what time to clots form post MI

A

50% w/in the first 2 days

95% w/in 2 weeks

80
Q

when would an emboli most likely embolize

A

1-3 months post MI (10% of thrombus embolize)

81
Q

what increases the risks for embolization

A

protruding clot
larger size
mobile
adjacent to a hypermobile segment

82
Q

how does a laminar thrombus appear at the apex

do laminar thromboses tend to be acute or chronic

A

flat, but apex gets thicker

chronic, press flattens it out over time

83
Q

when should you be very suspicious of a laminar thrombus

A

if the anterior and septal walls are akinetic

84
Q

how should you investigate a thrombus at the apex

A

zoom
use a higher frequency
use colour doppler and lower the scale… if not a clot colour will enter the suspected area, if it is, colour will stop where the clot begins

85
Q

describe a protruding thrombus

is it likely acute or chronic

A

may be less echogenic than laminar thrombus and more mobile… protrudes into LV cavity

acute

86
Q

can a clot be transitioning b/w protruding and laminar?

A

yes, it could have characteristics of both

87
Q

4 applications of contrast

A
  1. detect shunts
  2. enhance doppler signals
  3. LV opacification
  4. myocardial perfusion to assess CA and defects

…helps to visualize the LV when visibility is porr

88
Q

Rt heart applications for contrast

what type of contrast is used

A

look for shunts

agitated saline w/ bubbles > 5 microns that don’t pass through the lungs

89
Q

what does it mean if the agitated saline bubbles are seen in the Lt heart

A

theres a possible shunt

90
Q

Lt heart applications for contrast

what type of contrast is used

A

LV opacification and wall motion analysis

smaller size, 1-5 microns that pass through the heart

91
Q

are true and false aneurysms a post Mi complication

A

yes

92
Q

describe a pseudoaneurysm

A

abrupt wall rupture… has a narrow neck that connects to the pericardium sometimes

may be filled w/ thrombus

93
Q

describe a true aneurysm

where is it usually located

A

all 3 layers are involved… has a wide neck and tapering appearance

may leak into pericardium

apex

94
Q

how does a VSD or wall rupture happen post Mi

A

MI damages the wall and it becomes thin and necrotic… the wall weakens and ruptures creating a shunt, or leaking into pericardium

95
Q

what is Dresslers syndrome

w/ what type of MI is it more common

A

post MI acute pericarditis due to an autoimmune rxn to the necrotic tissue…. often occurs w/ an anterior MI

96
Q

3 main features of Dresslers syndrome

A
  1. fever
  2. pleuritic pain (lungs)
  3. pericardial effusion
  4. tamponade (rare)
97
Q

appearance of pericardium w/ Dresslers syndrome

A

bright over an area of abnormal wall motion

Echo 2 (15 decks)

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