Pathophysiology of Myocardial Infarction, COPD, BPH Predisposing factors: age - 89 y.o. gender - male History of CHF - jan.

2010

injury on endot elium from pla!ue deposits increased permea"ility ad esion of molecules monocyte# platelet ad erence# lipid accumulation aggregation of monocytes and macrop age progressi$e t ic%ening of lumen narro&ing of artery occlusion in "lood flo& decreased coronary "lood flo&

inade!uate supply of o'ygen to eart mu isc emia# increased cellular ypo'ia anearo"ic meta"olism and increase in lactic acid production release of damage to cardiac cells necrosis (yocardial infarction failure of cardiac compensatory mec anism decreased myocardial contractility decreased cardiac output decreased arterial pressure stimulation of "aroreceptors

stimulation of sympat etic receptors increase perip eral $asoconstriction increased afterload and cardiac output

increased myocardial increased eart rate

decreased diastolic fi

decreased myocardia diastolic failure impairment of left $enticle to fill up &it "lood increased pressure in left atrium and pulmonary $asculature increase in left atrial and left $entricular end diastolic pressures congestion of pulmonary circulation accumulation of fluid in t e lungs ,--./ -0P1-2 )2-3-10+ (inimal a4iness in t e rig t "ase.

o"struction of airflo& from fluid accumulation and mucus production loss of elasticity of lung fi"ers impaired e'piratory flo&rate increased air trapping air&ay collapse destruction of al$eolar tissue decreased surface for gas e'c ange C1P5 acti$ity intolerance dyspnea

constipation

Precipitating Factors sedentary lifetyle ypertension diet C.5 - jan. 2010

on of molecules lipid accumulation macrop age

ng of lumen

Hematocrit Platelet Count Neutrophils "#mphoc#tes $onoc#tes

(2-5-10) (2-7-10) (2-9-10) 35.5 35.5 39.1 124 109 145 9.2 !4.9 5!.9 20. 10.9 30.5 .5 9.7 !.2

"lood flo&

f o'ygen to eart muscles

%& se'ment (epression an( &-)a*e in*ersion + in(icates pattern o, ischemia

c est pain

roduction release of meta"olites )e.g. * ions# lactic acid# car"on dio'ide# adenosine+

- )a*e present + tissue necrosis

presence of 78 and 73 eart sounds

y mec anism

at etic receptors ypertrop y of cardiac muscle

ncreased myocardial contractility

ncreased eart rate

decreased diastolic filling

decreased myocardial tissue perfusion

X-RAY REPORT (2-4-10) Heart is enlar'e( )ith C& ratio o, .7!. .mpression/ Car(iome'al# "0 an( "1 ,orm. 1theromatous thoracic aorta. Consi(er Pneumonia2 ri'ht 3ase

t e rig t "ase.

c est pain

decreased circulation

plaqued and narrowed blood vessels present

(2-1-10) 4 &he mi((le cere3ral arteries are ca

C2 scan

5istri"ution of of cere"ral "lood flo& )C9F+ decrease Distribution cerebral blood flow (CBF) decrease 5ecrease "lood flo& to to middle artery Decrease blood flow middle cere"ral carrotid artery

Decrease blood flow to middle carrotid artery

Hypo'iaHypoxia of t e of left emisp ere the left hemisphere :sc emia

Ischemia

5istur"ance of t of ecellular cellular meta"olism Disturbance metabolism ;se of anaero"ic meta"olism se of anaerobic metabolism .ccumulation of lactic !ccumulation of acid lactic acid 5ecrease cellular pH Decrease cellular pH 5ecrease Decrease .2P production !"# production :nduction of e'citoto'icity Induction of excitotoxicity

onia2 ri'ht 3ase

Increase concentration of $lutamate aspartate in the extracellular spa

1pening of Ca c annel %penin$ of Ca channels

#ersistent depolari&ation (influx of Ca' (a' Cl ions' efflux of

CaCa acti$ated relase of ofdestructive distructi$ activated release e lipases' endonucleas )proteases# lipases# <<<<<<<<< -elease of cyto%ines *elease of cyto+ines =oss of cellular integrity ,oss of cellular inte$rity Cell deat >ecrosis
Cell death (ecrosis Infarction

(proteases' lipases'ordon

-ig t sided &ea%ness slurring of speec facial asymmetry decreased mentation dysp agia

,essions formed

e cere3ral arteries are calci,ie(.

.2P production Decrease !"# production

of e'citoto'icity nduction of excitotoxicity

concentration of $lutamate and ate in the extracellular space

<<<<<<<<<< %penin$ of Ca channels

ersistent depolari&ation f Ca' (a' Cl ions' efflux of ))

ed relase of ofdestructive distructi$e en4ymes ed release en&ymes (proteases' lipases' endonucleaseas) # lipases# <<<<<<<<<
(proteases' lipases'ordonucleases)

cyto%ines *elease of cyto+ines

CT SCAN REPORT

(2-1-10)

lular integrity ,oss of cellular inte$rity

Cell death (ecrosis Infarction ,essions formed

4 &here are punctuate h#po(ensities in the peri *entricular )hite matter.

2 ere is a 2.2 cm ypodense focus in t e left mid peri $entricular & ite

Consi(er small *essel ischemic chan'es 3oth peri *entricular )hite matter.. Consi(er an in,arct2 le,t mi( peri *entricular )hite matter li5el# ol(.

Course of diseasse signs and symptoms la"oratory results diagnosis direct realtion possi"le outcome

)hite matter.

peri $entricular & ite matter.

lar )hite matter..

Course of diseasse signs and symptoms a"oratory results

direct realtion possi"le outcome