Pathophysiology of Myocardial Infarction, COPD, BPH

Predisposing factors:
age - 89 y.o.
gender - male
History of CHF - jan.2010

injury on endothelium from plaque deposits

increased permeability adhesion of molecules

monocyte, platelet adherence, lipid accumulation

aggregation of monocytes and macrophage

progressive thickening of lumen

narrowing of artery

occlusion in blood flow

decreased coronary blood flow

inadequate supply of oxygen to heart mu

ischemia, increased cellular hypoxia

anearobic metabolism and increase in lactic acid production release of

damage to cardiac cells

necrosis

Myocardial infarction

failure of cardiac compensatory mechanism

decreased myocardial contractility

decreased cardiac output

decreased arterial pressure

stimulation of baroreceptors
 stimulation of sympathetic receptors

increase peripheral vasoconstriction increased myocardial

increased afterload and cardiac output increased heart rate

decreased diastolic fi

decreased myocardia

diastolic failure

impairment of left venticle to fill up with blood

increased pressure in left atrium and pulmonary vasculature

increase in left atrial and left ventricular end diastolic pressures

congestion of pulmonary circulation

X-RAY REPORT (2-4-10)
accumulation of fluid in the lungs Minimal haziness in the right base.

obstruction of airflow from fluid accumulation and mucus production

loss of elasticity of lung fibers

impaired expiratory flowrate

increased air trapping

airway collapse

destruction of alveolar tissue

decreased surface for gas exchange

COPD dyspnea

activity intolerance

constipation
 Precipitating Factors
sedentary lifetyle
hypertension
diet
CAD - jan. 2010

on of molecules

lipid accumulation (2-5-10) (2-7-10) (2-9-10)

Hematocrit 35.5 35.5 39.1
macrophage Platelet Count 124 109 145
Neutrophils 69.2 84.9 58.9
ng of lumen Lymphocytes 20.6 10.9 30.5
Monocytes 6.5 9.7 8.2

`
blood flow

f oxygen to heart muscles

ST segment depression and T-wave inversion – indicates pattern of ischemia

roduction release of metabolites (e.g. K ions, lactic acid, carbon dioxide, adenosine) chest pain

Q wave present – tissue necrosis

presence of S3 and S4 heart sounds

y mechanism
athetic receptors
ncreased myocardial contractility
ncreased heart rate
decreased diastolic filling
decreased myocardial tissue perfusion
the right base.
hypertrophy of cardiac muscle
X-RAY REPORT (2-4-10)
Heart is enlarged with CT ratio of .78.
Impression:
Cardiomegaly LV and LA form.
Atheromatous thoracic aorta. Consider Pneumonia, right base
chest pain

decreased circulation
CT scan (2-1-10)
plaqued and narrowed blood vessels present > The middle cerebral arteries are ca

Distribution of of
Distribution cerebral bloodflow
cerebral blood flow (CBF)
(CBF) decrease
decrease

Decrease blood
Decrease flowflow
blood to to
middle
middle cerebral artery
carrotid artery
 Decrease blood flow to middle carrotid artery

HypoxiaHypoxia
of the of
left
thehemisphere
left hemisphere

Ischemia Ischemia

Disturbance of the
Disturbance cellular
of cellular metabolism
metabolism

Use of anaerobic metabolism

Use of anaerobic metabolism Decrease Decrease
ATP production
ATP production

onia, right base Accumulation of lactic

Accumulation of acid
lactic acid Induction of excitotoxicity
Induction of excitotoxicity

Decrease cellular
DecreasepHcellular pH Increase concentration of glutamate
aspartate in the extracellular spa

Opening ofOpening
Ca channel
of Ca channels

Persistent depolarization
(influx of Ca, Na, Cl ions, efflux of

CaCa
activated relase of
activated release ofdestructive
distructive
lipases, endonucleas
(proteases, lipases, ?????????
(proteases, lipases,ordon

Release of cytokines
Release of cytokines

Loss of cellular
Loss ofintegrity
cellular integrity

Cell death Cell death

Necrosis Necrosis

Infarction

Right sided weakness Lessions formed

slurring of speech

facial asymmetry

decreased mentation

dysphagia
e cerebral arteries are calcified.
ATP production
Decrease ATP production

of excitotoxicity
nduction of excitotoxicity

concentration of glutamate and

ate in the extracellular space

??????????
Opening of Ca channels

ersistent depolarization
f Ca, Na, Cl ions, efflux of K)

ed relase of
ed release ofdestructive
distructive enzymes
enzymes (proteases,
lipases, endonucleaseas)
, lipases, ?????????
(proteases, lipases,ordonucleases)

cytokines
Release of cytokines CT SCAN REPORT (2-1-10)

lular
Loss ofintegrity
cellular integrity > There are punctuate hypodensities in the peri ventricular white matter.
There is a 2.2 cm hypodense focus in the left mid peri ventricular white
Cell death
Consider small vessel ischemic changes both peri ventricular white matter..
Necrosis Consider an infarct, left mid peri ventricular white matter likely old.

Infarction

Lessions formed
Course of diseasse
signs and symptoms
laboratory results
diagnosis

direct realtion
possible outcome
 white matter.
peri ventricular white matter.

lar white matter..

Course of diseasse
signs and symptoms
aboratory results

direct realtion
possible outcome