PATHOPHYSIOLOGY

Predisposing Age- 73 years old Hereditary- HPN, DM Gender- female Hx of Cholecystectomy (NMMC; 1995) Menopause (starts at age 42 years old; Menarche starts at age 13 yrs.old.) DM II (1999; usual glucose level: 140-160mg/dL; highest level: 300mg/dL) Precipitating >HPN (37 yrs old; usual BP 140/90; highest BP is 200/110mmHg) >Inc. serum Cholesterol level: 231mg/dL >Lack of exercise/activity >Obesity (BMI of 27 kg/m2, IBW: 48.96kg)

Increase shearing force of the arterial wall by the condition of the blood Nonspecific injury to arterial wall (endothelial injury) in the coronary artery

Diagnostic: CBC: Eosinophils-16.4%(0.006.00) Diagnostic: Blood Chemistry: Cholesterol-231 mg/dl (0-200 mg/dl) Triglycerides-191 mg/dL (0-150 mg/dl) Medication: >Atorvastatin Calcium (Lipitor)80mg 1 tab OD @ HS (Antilipidemics) >Enoxaparine Sodium (Lovenox)-o.6ml SC q12 (Antilipemics) >Aspirin (Aspilet EC)-80mg 1tab od (Nonopioid analgesics and antipyretics; antiplatelet) >Clopidogrel (Platexan) 75mg/tab, 4tabs now, then OD (Adenosine diphosphate (ADP) receptor antagonist

Desquamation of endothelial lining and stimulation of Mast cells to produce inflammation Increase permeability/adhesion molecules, Lipids (LDL, VLDL) and activation of platelets assimilation into the area Oxidized LDL attracts monocytes and macrophages to the site and plaques begin to form from cells and smooth muscle cells develop to form foam cells into thrombus

Diagnostic: >X-Ray Report (Chest AP- Sitting) Impressions: Medication: Atherosclerosis thoracic aorta. > >Amlodipine Besylate (Norvasc)Color Flow Doppler 50mg 1 tab Rupture of atherosclerotic plaque Conclusion: OD (Calcium-channel (cap) and Increase adhesion of a) blockers; Antianginals)motion abnormality Segmental wall >Nitroglycerin (Glyceryl these molecules and increase indicative of coronary artery disease Signs/ symptoms: Signs/ b) Trinitrate)-10mg Patch scleroses. Aortic and mitral thrombus/blood clot formation Right& left subcostal Coronary Ischemia and Ischemia symptoms: c) (Nitrates/Vasodilators; Aortic regurgitation, 1+ margin chest pain-5-6/10 Antianginals)regurgitation, trivial >Cold, by d) Mitral of tissue in the region supplied Diagnostic: pain scale; pain occur >Isosorbide Mononitrate (Imdur) Clammy skin Medication: Interventions: Diagnostic: >ECG tracing: the artery Occlusion and stenosis/narrowing of the even during exertion or 30mg 1 tab OD >prolonged/d> Metoprolol Tartrate >Obtained a 12 rest; heaviness and Clinical Chemistry: ST-depression & Signs/ symptoms: at lead ECG as coronary artery and leads to coronary (Nitrates/Vasodilators; ecreased Signs/ prescribed tightness of chest with (Toprol-XL) 50mg 1tab Decreased Calcium refill of 5 T wave >decreased capillary Antianginals) vasoconstriction Diagnostic:Signs/ symptoms: Interventions: symptoms: >Administered O2 inhalation via nasal 8.3 mg/dl inversion capillary refillBID (beta-adrenergic secs dyspnea; pain radiates 1tab of 5 secondsChemistry: Interventions: Signs/ Signs/ symptoms: >Jugular Increase demand for oxygen and glucose in the >Aspirin(Aspilet EC) 80mg cannula at 2L/min Clinical blockers, Dysrhythmias(bradycardia; >O2 therapy via nasal vein (8.4 10.2 mg/dl) >Clinical >RR: 26 cpm; tachypneic up to the neck and chin; od (Nonopioid analgesics) >increased Anti-dysrhythmics) >O2 therapy via Interventions: andAltered repolarization of nitrogensymptoms: cannula at 2L/min >tachycardia; PR:49-59bpm; tachycardia; distention >Advised to perform deep breathing Decreased Peripheral Anaerobic metabolism tissues leads to diminishedUrea Chemistry: myocardial >dyspnea >Diazepam (Valium)-5mg 1 tabIncrease guarding behavior, facial BP 22mg/dl (7-cell nasal cannula at (JVD)(Sept.4PR:130-150bpm NPO at 8cm Stimulation of sympathetic Increased Stimulation of cardiac sensory nerve exercises andgrimace; pursed-lip of used Acid production >Spironoloctone(Aldac Hypokalemia and Cardiac Increase >bradycardia; vasoconstriction and the myocardium that altered PR 130-150bpm); causedLactic of tachycarsia by increased oxygenation, Cellular hypoxia of can >use of accessory muscles to BID (Anxiolytics) 170/110mmHtone) 25mg 1tab OD 5,2009) except >palpitations noted decreased blood flowdecreased 17mg/dL) palpitations; dizziness Decreased Increase system to stimulate 2L/min myocardial release of breathingkinins,for O2 & glucose preload nervous PR: 49-59bpm endings to transmit 130-150bpm; ions, with techniquecentral mild to the potassium nervous Output to demand Unstable Angina breathe oxygen membrane lead 3.0 mmoL/L integrity > Metoprolol Tartrate (Toprol-XL) g Decreased norepinephrine and left ventricular >Elevated HOB P.O meds Increased after Increased Heart >maintained anxiety; body weakness relaxing environment (Potassium Sparing (3.5- 5.1 contractility needs adrenal medulla system to cause pain Pectoris prostaglandins >nasal flaring to the kidneys cardiac output 50mg 1tab BID (beta-adrenergic in the tissues/hypoxia Atherosclerosi s

Medication: >Losartan Potassium (Cozaar)-100mg 1tab OD (Angiotensin II antagonists) >Captopril(Capoten)-25mg tab BID (Angiotensin II antagonists)

Renin (released from kidneys) to split off angiotensinogen to form angiotensin I Angiotensin-converting enzyme (ACE) removes and converts Angiotensin I into Angiotensin II which promotes vasoconstriction Antidiuretic hormone Sodium retention by released from Angiotensin II stimulates kidneys and promotes an hypothalamus to increase adrenal cortex releaseby increased plasma reabsorption of water aldosterone osmotic to increased blood kidneys pressure

Medication: >Spironoloctone (Aldactone) 25mg 1 tab OD (Distal Tubule Diuretics/ Potassium Sparing Diuretics)

Constipation prior to admission (resolved Sept 1,2009)

Medication: Semma cone (Senokot)-30ml OD PO Lactulose (Chephulac)-30ml od PO Diarrhea resolved (Sept. 3, 2009)

Increased blood pressure

Overloading of blood in the ventricles of the heart

Interventions: Hold laxatives 2xday as indicated

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Signs/ symptoms: >BP170/110mmHg(hypertensive) >temp-36.8C >Dizziness(10 days prior to admission until assessment day >faintness(10days prior to admission)

Excessive stretch and decreased contraction occur

Increase workload of the heart

Diagnostic: >Echocardiography Conclusion: Concentric left ventricular hypertrophy with left ventricular diastolic dysfunction

Thickening of the cardiac muscle that leads to Left Ventricular Hypertrophy

Hypertensive Cardiovascular Disease (HCVD)

COMPLICATIONS: Myocardial Infarction Dysrhythmias Cardiogenic shock Pulmonary embolism Recurrent Myocardial Infarction Ventricular aneurysms Rupture of the heart Pericarditis Death