1. What acute pathophysiological condition(s) have led to
John’s current presentation? Ensure to explain the associated underlying
pathophysiological mechanisms and provide evidence for your answer.
most likely suffering from ischemic chest pain caused by myocardial ischemia
that developed into a myocardial infarction distal to his right coronary artery
superior to his marginal branch due to his potential past medical history of
atherosclerosis, angina, and hypertension.
of medications including ECASA (anti-platelet drug), Atorvastatin Calcium
(lipid-lowering agent), Irbesartan/Hydrochlorothiazide (antihypertensive), and Bisoprolol
Fumarate (anti-hypertensive) provide evidence that John has a history of
atherosclerosis, angina, and hypertension as these medications suppress the
effects of both conditions (Schull, 2013, p.19, p.113, p.153, p. 1419).
is the hardening and thickening of the artery walls due to the accumulation of
fat-laden foam cells, LDL molecules, and smooth muscle cells forming plaque in
the tunica media (McCance, 2014, p.1145). John has hypertension and high LDL
levels in his blood, and these factors can cause damage to the endothelial
cells of the coronary arteries. When an injury to the endothelial cells of the
coronary arteries occurs, the cells become inflamed and can not create normal
quantities of antithrombotic and vasodilating cytokines. Many inflammatory
cytokines are released and macrophages bind to injured endothelium and release
enzymes that oxidize LDL and injures the tunica intima further, causing an
increase in permeability. LDL enters the tunica media and becomes oxidized,
which draws macrophages into the tunica media as well. Macrophages begin to
engulf the oxidized LDL, and become fat-laden foam cells (McCance, 2014, p.1145).
After fat-laden foam cells and LDL accumulate in significant amounts around the
vessel, smooth muscle cells proliferate into the tunica media and produce
collagen. This concoction of LDL, fat-laden foam cells, smooth muscle cells,
and collagen form plaque. Over time plaque buildup in the tunica media causes
the tunica intima to become hard and form a fibrous cap (McCance, 2014, p.1147).
Angina is chest
pain that is caused by reduced blood flow to the heart through the coronary
arteries. John has a high risk of angina because of his weight and high blood
LDL levels (Huether, 2017, p. 1834). John’s angina can be recognized as
unstable angina, as Jessica stated that “his back and shoulders had been
bothering him all day”, “John began complaining of chest pain”, and “he was ‘dizzy’
and … ‘felt as though he was going to pass out'”. John also presented as diaphoretic
and had vomited before EMS arrival. Common signs and symptoms of unstable
angina are pain or discomfort in the back and chest, sweating, nausea,
vomiting, dizziness, fatigue, and any symptoms lasting longer than 15 minutes (Medscape
/ Caroline, 2016, p. 1047). In unstable angina, the fibrous cap in the coronary
artery has ruptured and causes platelet aggregation. Platelets begin to clot over
rupture, and convert fibrinogen into fibrin creating a fibrin mesh blocking the
blood vessel (Grossman, 2014, p. 803). This blockage causes a myocardial
infarction in John’s heart.
2. Explain the pathophysiology behind each of
John’s signs and symptoms.
John currently has a pulse deficit between the
palpated carotid pulse and the cardiac monitor pulse. John’s pulse on the
cardiac monitor is ~108 bpm with occasional premature ventricular contractions
whereas his palpated pulse is 52 weak and irregular (Caroline, 2016, p. 1043).
Premature ventricular contractions are common in patients with myocardial
infarctions, and are caused in John’s condition because of heart failure and a
reduction of preload (Grossman, 2014, p.807 / Mayo Clinic / NCBI).
John’s diaphoresis is caused by the sympathetic
nervous system activating the “fight or flight” response (Web MD).
John was experiencing chest pain with back and
shoulder discomfort due to referred visceral pain deriving from the ischemic
chest pain. Pain originating in his heart from his myocardial infarction is
hard to localize and is often felt in a site far removed, in this case his back
and shoulders. This is because visceral and somatic afferent neurons converge
on the same neurons of the spinal cord (Grossman, 2014, p. 437).
John’s low blood pressure is due to his low
perfusing heart rate and damage to his right ventricles. Damage to his right
ventricle causes contractility to diminish, which in turn diminishes the amount
of preload the right ventricle can take and ultimately lowers cardiac output (Grossman,
2014, p. 726). This hypotension is also the cause of John’s dizziness and
feeling of potential syncope (Healthline). This hypotension is also the reason
for his mottling as his systolic blood pressure is not enough to pump blood to
his extremities (Grossman, 2014, p. 754).
the pathophysiological mechanisms responsible for this presentation. How does
it explain the diagnostic information you have obtained?
Johns heart has experienced necrosis to the
myocytes in the right ventricle due to his myocardial infarction. I am seeing
pulseless electrical activity on the cardiac monitor caused by the SA and AV
nodes firing without any contractions (Grossman, 2014, p. 797). There are no
contractions in the heart due to necrosis. John’s end-tidal CO2 has diminished significantly
because of the lack of perfusion in the lungs due to the cardiac arrest (Caroline,
2016, p. 993).
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