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PATHOPHYSIOLOGY

Non-modifiable

Age – 77 years old

Gender – Male

Previous attack of MI (April 2011)

Race: Asian 1 of 100

Heredity: Hypertension

Modifiable

Anemia

Diabetes mellitus

Alcoholism

Smoking (1 pack X10)

Low activity

Activation of latelet

Formation of thrombus

Narrows or blockage of 

cardiac artery

Emboli formation

Ischemia of tissue inThe region supplied by

coronary artery

ECG: 5/24/11Cannot r/oinferolateral wall

ischemia

Angina

Predisposing factors to contribute to

blood vessel wall injury and change in

condition of Coronary Artery by plaque

formation

Embolus travels to the heart

Embolus travels to the heart

Decreased oxygen supply tocardiac muscle resulting

anaerobic mechanism

Myocardial Injury leading tocell death

MYOCARDIALCARDIACMARKERS:↑ Troponin I:

Embolus travels to the brain

Blood flow obstructed bythrombus formation

Decrease Cerebral Perfusion

Cerebral Tissue Necrosis

CVD INFARCT

SIGNS AND SYMPTOMS

Impaired motor functions: unilaterallimb weaknessLeft sided hemiparesisDecreased Level of ConsciousnessHeadacheVision Disturbance: Ptosis

Esomolol 10mg IV now

Citicoline 1 IV 8

O2 @ 10LPM via facemask

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Plasma protein

& water leak out

& move into the

interstitiumPULMONARY

EDEMA

Decreased Left

Ventricular Function

Decreased Cardiac

Output

Decrease Renal Perfusion

Activation of (RAAS)Renin AngiotensionAldosterone System

Release of Renin; with thepresence of 

Angiotensinogen,

Angiotensin I will beproduced

Angiotensin II

HypertensionBP: 150/100

Stimulation of AdrenalCortex

Release of Aldosterone

Sodium and Water Reabsorption

Increase Circulating BloodVolume

Further Increases CardiacWorkload and May worsen

fluid overload andCongestion

Bilateral Crackles

PeripheralVasoconstriction

↑ Sodium: 154

Increase CardiacWork load

Increase HeartRate: 120

Cardiac remodelingto keep up with theincreasing cardiac

demand

ECG Result:Left Ventricular HypertrophyLeft Atrial Enlargement

Furosemide 40mg IVNOW

Remainingfunctioning musclescannot keep up with

demands

Impaired GasExchage

Respiratory rate:32

Difficulty of Breathing

Intubation:CMV ModeFiO2: 100%PF:60BUR: 24

Combivent +SalbutamolNebulization

every 6hours

Cardiogenic shockMI Killips IV

Hypotension[Palpatory 50]

Dopamine drip;Dopamine 4amps +250 D5W to run for 4mcg/kg/min

Levophed drip:

Levophed 4mg/ml +250cc D5w to run at2mg/kg/min

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Cardiogenic shock

Decreased circulating bloodsupply to vital organs

MULTIPLE ORGAN FAILURE

Risk Factors for PNEUMONIA

• The elderly and very young.

• People with chronic or severe medicalconditions, such as lung problems, heartdisease, nervous system (neurologic)disorders, and cancer.

• People who have been in the intensivecare unit (ICU). Patients who lie flat on

their backs are at particular risk for aspiration.

SEPTIC SHOCK

Decreased oxygen supply toKidneys

Decreased oxygen supply toLiver 

Lobules necrotized due toinadequate O2 supply

Nephrons necrotize due toinadequate O2 supply

ACUTE KIDNEY INJURY

↑ Creatinine: 626↑ BUN: 11mmol/LHematuria: +++Proteinuria: +

Inability to produceerythropoietin

Decreased RBC: 1.94Hct: 0.19Hgb: 60

Blood Transfusion 4units PRBC

Inability of the Liver tosynthesize protein

Decreased estimated plateletProlonged PT: 17.9

Decreased Albumin: 22.9

Decreased oncotic pressure

Bipedal Edema Grade 2

Inability toreabsorbNaHCO3

NaHCO350meqs slow IVpush NOW then

100 meqs inD5W 250cc x 24

hours

Metabolic Acidosis

DEATH[June 1, 2011]

LEGENDS:

Disease Process

Symptoms

Laboratory and DxResults

Medications andManagement

Highlighted Disease

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Inhalation of microorganism that have

been released into the air when an

individual cough, sneeze or talk.

Aspiration of Streptococcus Pneumoniae

Released of Multiple inflammatory

Cellular infiltration and immune response↑ WBC:

Microorganism release toxins that can

cause further lung damage

Infiltration, bronchospasm

Damage of bronchial mucous

membranes and alveolo capillary

membranes

Filling of infectious debris and exudates

in the terminal bronchioles (edema)

Dyspnea and to ventilation and perfusion

mismatching and hypoxemia

+ Wheezes,DOB, PO2-↓52, PCO2-↑50Respi.Acidosis

Venous blood entering the pulmonary

circulation processes through the under 

ventilated area and travel to the left side

of the heart poorly oxygenated

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Pulmonary congestion and cardiac arrrest

Bacteremia

gram-negative organism gram-

positive organism

Released of endotoxins, proteases

Act as triggering molecules and

result in activation of 

Neotrophil, endothelial, andmonocyte-macrophage cell

activity

Kinin systemCoagulation cascadeComplement system

Released of proinflammatory cytokines

Endothelial cell damage

Decreased systemic vascular resistance

Depressed myocardial function

Leukopenia

Tissue necrosis

Vascular leakage

thrombocytopenia

O2 Sa

70%

PO2-

Cellular infiltrationand immune

↑ WBC-

Microorganism release

toxins that can causeInfiltration,

Damage of bronchial mucous

membranes and alveolo capillary

Filling of infectious

debris and exudates inthe terminal

+

Wheezes,DOB,

Dyspnea and to

ventilation andperfusion

Alteration in Cellular permeability

Fluid shifting resulting to third

spacing

Decreased circulating blood volume

SEPTIC SHOCK

↑ WBC: 38.12Positive Bacteria in theUrine