“acute coronary syndrome non st elevation myocardial infarction, hypertensive cardiovascular...

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c) Schematic Diagram (client – based) Non – modifiable Risk Factors: -68 y/o and above -Familial history of DM type 2 - Pacific Islander -Familial Modifiable Risk Factors: -Sedentary lifestyle -Previously known Impaired - Emotional Stress Fasting glucose -↑consumption of fatty, salty & sweet food Insulin resistance and desensitization ↓insulin production ↑glucagon Release Fats and Proteins breaks down to glucose Easy fatigability Complaint on his check up 5 years Impaired glucose absorption ↑blood glucose level Chronic glucose elevation HbA1c 11-25-09 10.9% Cellular starvatio n Polyphagia As verbalized by the patient, started 5 years ago until prior to ↑osmolality Fluid shifts ↑blood Cellular dehydration Thirst center ↑GFR Polydipsia As verbalized by the patient, started 5 years ago until prior Polyuria As verbalized by the patient, started 5 years ago until prior to admission Sluggish blood flow Glycoprotein cell wall deposits Narrowing of blood vessel 11-26-09 FBS= 192.91mg/dl HGT 11-25-09 309mg/dl, 159mg/dl 11-26-09 179,148,156 mg/dl 11-28-09 153, ↑Insulin Β cell Activation of satiety blood vessel ↓ perfusion ↑ Blood

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Page 1: “Acute Coronary Syndrome Non ST Elevation Myocardial Infarction, Hypertensive Cardiovascular Disease, Diabetes Mellitus Type 2, and Community Acquired Pneumonia” Client Centered

c) Schematic Diagram (client – based)

Non – modifiable Risk Factors:-68 y/o and above -Familial history of DM type 2- Pacific Islander -Familial history of hypertension

Modifiable Risk Factors:-Sedentary lifestyle -Previously known Impaired- Emotional Stress Fasting glucose-↑consumption of fatty, salty & sweet food

Insulin resistance and desensitization

↓insulin production ↑glucagonRelease

Fats and Proteins breaks down to glucose

Easy fatigability Complaint on his check up 5

years ago.

Impaired glucose absorption

↑blood glucose level

Chronic glucose elevationHbA1c 11-25-09 10.9%

Cellular starvation

PolyphagiaAs verbalized by the patient, started 5

years ago until prior to admission↑osmolality

Fluid shifts from IC to IV

↑blood volumeCellular dehydration

Thirst center activation ↑GFR

PolydipsiaAs verbalized by the patient,

started 5 years ago until prior to admission

PolyuriaAs verbalized by the patient,

started 5 years ago until prior to admission

Sluggish blood flow

Glycoprotein cell wall deposits

Narrowing of blood vessel

11-26-09 FBS= 192.91mg/dlHGT

11-25-09 309mg/dl, 159mg/dl11-26-09 179,148,156 mg/dl

11-28-09 153, 140mg/dl11-29-09 160, 155mg/dl

11-30-09 148mg/dl12-02-09 130mg/dl

↑Insulin demand

Β cell exhaustion

Activation of satiety center

blood vessel occlusion

↓ perfusion

↑ Blood viscosity

Page 2: “Acute Coronary Syndrome Non ST Elevation Myocardial Infarction, Hypertensive Cardiovascular Disease, Diabetes Mellitus Type 2, and Community Acquired Pneumonia” Client Centered

Small vessel disease

Accelerated atherosclerosis

Diabetic retinopathy

Blurring of visionEyeglass power of L-

250 R- 240

↑LDLJune 27, 2009

187 g/dl

Hypertension130 – 150/ 70 -90 mmHg as

verbalized by his daughter (usual BP prior to admission)

11-25-09 190/130 mmHg

Coronary Artery Disease

Plaque rupture

Platelet activation

Change in platelet shape

Platelet degranulation

↑ Expression of Platelet GP IIb/IIIa

Platelet adhesion to subendothelial

matrix

Release of Thromboxane A2, Serotonin and other platelet

aggregatory agent

Enhanced affinity to fibrinogen

Platelet aggregation

↓ Arterial lumen Plasma Coagulation System activation

Formation of thrombin

Enhances platelet aggregation

Converts fibrinogen to fibrin

Exposure of subendothelial matrix

Vasospasm dislodges thrombusCoronary occlusionImpaired cardiac perfusionIschemia of the tissue supplied by the arteryMyocardial cell deathAnaerobic glycolysisLactic acid productionAnginaMyocardial irritability↓cardiac contractility

Release of lysosomal enzymes

Impaired repolarization of the myocardiumECG changes ↑ CKMB

Irregular heart beatsSNS Stimulation

↓ ventricular function vasocontriction↑BP, HR, and O2 needs↓ CO

Blood pooling on left ventricle

Backflow of blood in the lungs

Pulmonary congestion

Adventitious Breath sounds

Productive cough↓ oxygenationDOBFatigue

Stabilization of fibrin clot

Page 3: “Acute Coronary Syndrome Non ST Elevation Myocardial Infarction, Hypertensive Cardiovascular Disease, Diabetes Mellitus Type 2, and Community Acquired Pneumonia” Client Centered

Nidus of rethrombosis

Hardening of the coronary arteries

Re-establishment of the endothelium with fibrotic tissue and thrombus

Vasospasm dislodges thrombus

Coronary occlusion

Impaired cardiac perfusion

Ischemia of the tissue supplied by the artery

Myocardial cell death

Anaerobic glycolysis

Lactic acid productionAngina11-25-09

Myocardial irritability

↓cardiac contractility2D – echo 11-27-09

thinned out akinetic entire interventricular septum from mid to apex, severe hypokinesia of all left

ventricular segments

Release of lysosomal enzymes

Impaired repolarization of the

myocardium

ECG changesST Depression

(11/25/09 9:00pm)

↑ CKMB11/25/09

47.4 mg/dL

Irregular heart beatsAfib RVR (11/25/09

9:30pm)

↓ ventricular function2D echo 11-27-09

left ventricular systolic function is severely

depressed

↓ CO2d echo 11-27-09

calculated ejection fraction of 34% by cube method and 25 +/- 25% by visual

estimated method

Blood pooling on left ventricle

Backflow of blood in the

lungs

Pulmonary congestionCXR result11/25/09

Adventitious Breath soundsCrackles 11/25-30/09

Productive cough11/25-30/09

↓ oxygenation

DOB11/25-28/09 2 LPM O2

supplementation

Fatigue11/25-28/09

↓ Serum Mg level11-25-09 0.65mg/dl