Cardiology [MYOCARDIAL ISCHEMIA]

Cardiology
[MYOCARDIAL ISCHEMIA]
Introduction
Myocardial ischemia is produced where there is an occlusion to
blood flow. It’s caused by chronically progressive
atherosclerosis limiting perfusion to the myocardium. This
produces ischemia when cardiac demand increases; there’s an
imbalance in the demand to supply ratio. When an acute
thrombus forms from endothelial injury the lumen can quickly
become occluded (an MI). Over time, the patient will undergo
infarction with permanent loss of myocardial tissue.
Risk Factors
HTN
Smoking
Dyslipidemia
DM
Cocaine
Risk Factors
Since this is a result of progressive atherosclerosis those things
which perpetuate atherosclerosis will lead to ischemic heart
disease. Risk factors provide something to fix and help steer the
diagnosis. What makes this interesting is HOW you fix these risk
factors. They’re HTN, smoking, dyslipidemia, diabetes, and
drug use (i.e. cocaine).
Patient Presentation
Myocardial ischemia on its own is painful. It causes a crushing,
retrosternal chest pain that will radiate down the arm and up
the jaw. It may also present with dyspnea. Ischemia on its own
will not cause mechanical failure. Other signs and symptoms will
be a result of myocardial infarction and necrosis. If the Left
Heart fails it’s pulmonary edema. If the Right Heart fails it’s
hypotension and peripheral edema. Any infarct can produce
arrhythmias: atrial, ventricular - whatever. Separating severity
of ischemia is typically based on whether or not the pain is
relieved with rest and/or nitrates. Beyond that, laboratories are
needed to differentiate between the “bad ones” (STEMI,
NSTEMI).
Diagnosis
The first test is the ECG. It’s noninvasive, cheap, and able to
detect the highest acuity disease (STEMI). It also establishes an
admission baseline for comparison. A 12-Lead ECG is best. ST
segment elevation = transmural infarct = STEMI.
To rule out active myocardial infarct you need cardiac
biomarkers (Troponins, CKMB, etc). These are released from
dying or dead myocytes. They separate unstable angina from
NSTEMI.
Pain
Relief
Biomarkers
ST ∆s
Pathology
Stable
Angina
Exercise
Rest +
Nitrates
Ø
Ø
70%
Unstable
Angina
@ rest
Ø
NSTEMI
STEMI
@ rest
Ø
@ rest
Ø
Ø
Ø
90%
↑
Ø
90%
↑
↑
100%
Typical
Levine Sign
Crushing Chest Pain
Pale, Cool, Diaphoretic
Sense of Impending Doom
Diagnosis
In Acute disease (guy in the ER with active chest pain)
get EKG, Troponins, and Cath.
In Chronic disease (guy in office with an h/o chest pain)
get an EKG and Echo/Stress Test.
Chest Pain
ST ∆s
EKG
Multiple options exist for confirming the diagnosis of myocardial
ischemia based on severity and acuity. There is the stress test (for
someone who has neither NSTEMI nor STEMI) and the best test
which is coronary catheterization. The higher the acuity, the
more likely the cath. Let’s talk about the low-acuity setting first.
Able to
Exercise
STEMI
Emergently
ST∆s
Routine tests such as CXR / CBC / TSH / CMP are obtained but
do not influence the diagnosis or management.
Atypical
Fatigue
Malaise
SOB
CATH
NSTEMI
Biomarkers
Troponin,
CKMB
Unstable Angina
Stress Test
Unable To
Exercise
Treadmill Dobutamine
or Adenosine
Normal
EKG
Abnormal
EKG
EKG test
Echo or
Thallium
Treat with
medications then…
Manage
Medically
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Cardiology
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[MYOCARDIAL ISCHEMIA]
Diagnostic Modalities
The stress test
a) Treadmill stress test - Requires the patient to be able to
exercise (80% of max heart rate) and requires a normal ECG.
Send him/her on an exercise and stop the test when there are
EKG changes (ST depression or T wave inversion) or Chest
Pain. If positive, go immediately to cath.
b) Dobutamine Stress Test – Uses a pharmacological challenge
and an Echo. Under the challenge (85% max HR), the echo will
pick up hypokinesis or akinesis (decreased wall motion).
Areas that are infarcted will persist with akinesis even at rest.
Areas that become ischemic under stress (become akinetic) will
move again after dobutamine is removed (revealing
salvageable tissue).
c) Nuclear Stress Test – Thallium looks like sodium to the heart.
It will be picked up by myocytes and light up healthy tissue.
Infarcted tissue will not under both rest and exercise. Ischemic
tissue will not under stress, but will at rest (revealing
salvageable tissue).
Catheterization
This is the best test for the diagnosis of coronary artery disease.
It assesses the severity of stenosis AND helps rule out
Prinzmetal’s angina (clean coronary arteries producing
ischemia as a product of vasospasm - treat with CCB).
Therapy
Adjust risk factors
a. LDL – the goal is to ↓ LDL < 100 or <70 for active disease and
get ↑HDL > 40. Do this with statins. Other drugs exist, but
start with statins. Use Fibrates if there is a contraindication to
statins.
b. DM – tight glucose control to near normal values (80-120 or
HgbA1C < 7%) with oral medications or insulin.
c. HTN – regular control of blood pressure to <140 / <90 with
Beta-Blockers (reduce arrhythmias) and ACE-inhibitors.
Titrate heart rate to between 50-65bpm and 75% of the heart
rate that produced symptoms on stress test.
Reduce Risk of Thrombosis
Manage this with either Aspirin (Cox-Inhibitor) or Clopidogrel
(ADP-inhibitor) long term. Those spiffy Glycoprotein IIb/IIIa
inhibitors like Abciximab are useful in the patient going for cath
with stenting for additional antiplatelet effect, but they are not for
long term.
Surgical Management
Surgical management choices are angioplasty or CABG. The
decision is made based on the severity of occlusive disease. If it’s
really bad (i.e. requires multiple stents) do a CABG. If the
atherosclerosis is global and no ground can be found for the stent,
do CABG. Stents are now drug-eluding (require Clopidogrel) or
bare-metal (do not require Clopidogrel)
Thrombolytics
Either the administration of tPA (within 12 hours of onset) or
heparin is done only when catheterization is not available AND
they are in an acute disease (NSTEMI or STEMI).
Can’t Exercise: Peripheral Vascular Disease,
Claudication, vasculitis, diabetic ulcers, SOB at rest, etc.
Can’t Read ECG: Any BBB or old infarct
“Dead Things Don’t Move”
Stress
Normal
Wall
Motion
Akinesis
Akinesis
No Dz
Ischemia
Infarct
Normal
Wall
Motion
Normal
Wall
Motion
Akinesis
At Rest
Acute Presentation: MONA-BASH
Morphine
Beta-Blocker
Oxygen
ACE-inhibitor
Nitrates
Statin
Aspirin
Heparin
Treatment
Statins
β-Blockers
ACE-i
ASA
Clopidogrel
Angioplasty
CABG
tPA
Heparin
When to use it
Goals
Any ACS
LDL < 70
HDL > 40
Any ACS
SBP < 140
DBP < 90
Any ACS
SBP < 140
DBP < 90
Any ACS
No goal
ASA allergy or
No goal
drug-eluding
stents
ST↑ or + Stress; 1 or 2 vessel disease
ST↑ or + Stress; Left-Mainstem or 3 vessel disease
ST↑ or + Stress; no PCI available, no transport
ST↑ or + Stress; contraindication to tPA,
CATH
Angioplasty
(PCI)
Left Mainstem
1,2 Vessel
CATH
CABG
3 Vessel Disease
Surgery = Left Mainstem OR 3-vessel disease; surgery = CABG
Angioplasty = 1,2 Vessel Disease
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