Transcript Blood flow is abruptly and severely deprived of oxygen.

Myocardial Infarction
Angina Pectoris
What is an MI?
Myocardial Infarction
What causes an MI?
Blood flow is abruptly and severely
deprived of oxygen.
MI
Circumstances that
decrease the supply of blood
flow/oxygen to the heart….
MI
Circumstances that increase
the demand for oxygen
(MV02) by the
myocardium….
MI
Is angina and MI the
same thing?
Is it managed the same?
MI Angina Pectoris
Angina Pectoris is
temporary chest pain. No
permanent damage is
done to the myocardium.
MI
Why does pain occur when
there is a deficit of blood and
therefore oxygen to the
myocardium?
MI Stable Angina
Stable Angina: is usually
prompted by something
(exertion, stress) and is relieved
with rest, nitroglycerine, and
pharmacologic therapy taken
prophylactically.
MI
What meds did you talk
about in pharm could be
taken to address this
problem?
MI Unstable angina
Unstable angina: can occur
at rest, or while sleeping and is
unrelieved with intervention.
Requires prompt treatment!
MI Prinzmetal’s angina
Prinzmetal’s angina: is
associated with coronary
vasospasm.
May be relieved by exercise or
spontaneously.
MI – Prinzmetals angina
What type of
pharmacologic therapy do
you think is appropriate for
a patient with this type of
angina?
MI
Silent Ischemia =
Asymptomatic
What type of patient(s) that
we studied are likely to
experience silent ischemia?
Why?
MI
The degree of altered function
depends on the area of the
heart involved, and the size of
the infarct.
The occlusion of which vessel do you
think is associated with poor left
ventricular ejection?
MI
Why do you think that younger people
who suffer MIs with the same degree of
occlusion as their older counterparts
suffer more serious cardiac
debilitation?
MI- Definitions
Transmural MI- the entire thickness
of the myocardium in a region is
involved.
Subendocardial MI- the damage has
not penetrated through the entire
thickness of the myocardial wall.
MI -Location
The location of the infarct correlates with
the part of the coronary circulation
involved.
Inferior wall MI- right coronary artery
Anterior wall MI- left anterior
descending artery
Lateral/Posterior/Inferior MI- left
circumflex artery
MI- Signs and Symptoms
Chest pain
P--precipitating event
Q--quality of pain or discomfort
R--radiation of pain
S--severity of pain
– T--Time
MI-Signs and Symptoms
Abdominal pain
Nausea
SOB/dyspnea
Anxiety, weakness, fatique
Palpitations, diaphoresis, pallor
Women and MI symptoms
In a multi-center study of 515 women
who had an acute myocardial infarction
(MI), the most frequently reported
symptoms were unusual fatigue, sleep
disturbances, shortness of breath,
indigestion and anxiety.
MI- Management
Keep calm
Give 02
ECG
IV
Pain control
Labs..CK-MB, Troponin, Mypglobin, WBC
Cardiac Markers
Troponin T and I- Have a wider
diagnostic time frame than CK-MB
(myocardial muscle protein released
when there is injury to myo muscle.)
Creatine Kinase MB-peaks after 24 h
(enzyme specific to cardiac muscle)
Myoglobin- Not specific but pekas in 2
hours
Others- associated risk
CRP-Detects inflammation. Found that
it was elevated in MI pts
Homocysteine- An amino acid found to
be elevated in MI pts.
Both of these are used as detectors of MI
to find who is a high risk pts. Used for
primary prevention.
MI -Management
Antithrombotic therapy
o
ASA
o
Heparin
o
Thrombolytics
MI-Management
Anti-ischemic therapynitrates
beta-blockers
MI Management
Nitrates: Nitroglycerine
• Primarily affect venous blood
flow.
• Dilate large coronary arteries.
• Prevents Vasospasm.
• Increases coronary collateral
blood flow.
MI Management - nitro
•Therefore, what happens
to myocardial O2 supply?
Nitroglycerine
• By causing venodilation, the nitrates
bring about a decrease in venous
return, and therefore lower preload.
(LVEDV).
• There is decreased pressure in the
ventricle, resulting in decreased
workload on the heart
MI Management - nitro
•Therefore, what happens
to myocardial O2
demand?
MI- Management
Anti-ischemic therapy
Beta adrenergic blocking agents
compete with epinephrine and
norepinephrine at the receptor sites
located throughout the body.
MI- Management- beta
blockers
• When these beta blocker drugs block
the B1 receptors on the surface of
the heart:
• Heart rate is decreased
• Conduction through the AV node is
slowed
• Myocardial contractility is
decreased
MI- Management- beta
blockers
Therefore, what do you thing
happens to myocardial O2
consumption?
Catecholamine- s/p MI
What effect would catecholamine
release have on myocardial O2
consumption? Why is consumption
critical to reduce s/p MI?
MI- Complications
• 1.
Dysrhythmias: Why? What to do?
• 2.
Cardiogenic Shock: Why? What to do
• 3.
Heart Failure/Cardiogenic pulmonary edema:
Why? What will you see? What to do?
• 4.
Pulmonary embolism: Why after an MI?(afib)
What to do?
• 5.
Recurrent MI: Why? What to do?
EKG changes