Atelectasis

partly or completely collapse lungs
not a disease but a condition associated w/ many respiratory disorders.

Cause:
obstruction of the bronchus, may be small or the entire lobe.
compression of the lung by pneumothorax, pleural effusion, or tumor; loss of surfactant or inability to keep an alveoli open

Manifestation:
for small atelectasis - diminished breath sounds over the affected area
bigger one - absent breath sounds, tachycardia, tachypnea, hypoxemia, dyspnea, cyanosis, reduced chest expansion

do a chest x-ray or ct scan to determine cause

Tx:
prevention is important for high risk patients - chest physiotherapy
cough, deep breath, spirometry, chest therapy
bronchoscopy if there is an obstruction that needs to be remove
antibiotic therapy to treat infectious cause (focus is treating the underlying cause)

position on the unaffected side to promote gravity drainage of the affected side
frequent position change, ambulation, coughing, deep breathing
fluids will help liquify secretions

Dyslipidemia Pharmacology

Management of Dyslipidemia:

• Maintain optimal chlolesterol, LDL, triglyceride and HDL levels

• Total Cholesterol : <200
• LDL: <100
• Triglycerides: <150
• HDL: >40 for men; >50 for women

• Diet/Exercise: increase fiber and complex carbs. DASH diet, 30 minutes exercise most days of weeks. 

• Good for you: vit. B, C, E, red wine, grape juice, bioflavonoids, garluc, cucumin, gingko biloba

Drug class	Mechanism	Side effects & considerations
Statins (“-statin”)	Reduces LDL synthesis in liver	Muscle breakdown; liver dysfunction; fatigue; abdominal discomfort. Unsafe in pregnancy.
Bile acid sequestrants Cholestyramine (Questran)	Binds with bile acids in intestine; reduces cholesterol reabsorption from intestine	GI side effects; constipation; power mixes with liquid; take with adequate fluid
Cholesterol absorption inhibitors: ezetimibe (Zetia)	Blocks absorption of cholesterol from food in small intestine	Elevated liver enzymes, gallbladder/pancreatic dysfunction

HTN Pharmacology

Mechanisms of action of drugs for HTN:

• Decrease preload (fluid volume), SVR and force of cardiac contraction.
• Block cardiovascular response to catecholamines
• Block outflow of catecholamines 

Drug class	Mechanism	Side effects & considerations
Thiazide diuretics: HCTZ (hydrodiuril)	Promotes H2O & Na+ excretion; reduces SVR. First-line tx.	↓K+, ↑ glucose & triglycerides
Angiotensin-converting enzyme (ACE)inhibitors  (“-pril” drugs)	Blocks formation of angiotensin II; prevents vasoconstriction & Na+/H2O retention	Dry persistent cough; angioedema; K+ retention; unsafe in pregnancy; first-dose hypotension
Beta-blockers  (“-lol” drugs)	Blocks  β-1 receptors in heart & vascular smooth muscle	Contraindicated in COPD & asthma; hold for bradycardia. Fatigue; bradycardia; depression. Rebound HTN if DC’d

Angiotensin receptor blockers (ARBs) (“-sartan”)	Blocks angiotensin II receptors; prevents vasoconstriction & fluid retention	Expensive. For people who do not tolerate ACE-I. Unsafe in pregnancy.  ↑K+
Calcium channel blockers (“-ipine)	Blocks influx of calcium ions in cardiac & vascular cells	Reflex tachycardia; worsens heart failure; hypotension; heart block; constipation. Hold for bradycardia.
Alpha blockers  (“-zosin)	Blocks alpha adrenergic receptors on vascular smooth muscle	First-dose syncope; orthostatic hypotension & reflex tachycardia

Central sympatholytics: clonidine (Catapres)	Alpha-2 stimulant; inhibits outflow of catecholamines to heart & vessels; vasodilation,  ↓CO	Rebound HTN with abrupt DC of med. Sedation possible. Unsafe in pregnancy. Available TD patch.
Vasodilators: hydralazine (Apresoline)	Acts on peripheral arterioles, causing vasodilation	Injectable available. Monitor HR, pulse. Orthostatic hypotension. Do not DC abruptly.

Which drugs are appropriate?

PreHypertension: lifestyle modifications
Stage 1: diuretic first, maybe add beta blocker or Ace inhibitor
Stage 2: more aggresive tx. more meds
Heart Failure: no calcium channel blockers; Beta blockers used cautiously
African American: Respond better to diuretics and calcium channel blockers
African American & elderly: More sensitive to effects of sodium in diet

HTN tx

Lifestyle modifications are recommended for all patients whose blood pressure falls within the prehypertension range and everyone with intermittent or sustained hypertension. These modifications include weight loss, dietary changes, restricted alcohol use and cigarette smoking, increased physical activity, and stress reduction. Dietary approaches to managing hypertension focus on reducing sodium intake, maintaining adequate potassium and calcium intakes, and reducing total and saturated fat intake. The DASH diet has proven beneficial effects in lowering blood pressure. Regular exercise reduces blood pressure and contributes to weight loss, stress reduction, and feelings of overall well-being. Previously sedentary patients are encouraged to engage in aerobic exercise for 30 to 45 minutes per day most days of the week. Isometric exercise, such as weight training, may not be appropriate, as it can raise the systolic blood pressure.

Hypertension management focuses on reducing the blood pressure to less than 140 mmHg systolic and 90 mmHg diastolic. The ultimate goal of hypertension management is to reduce cardiovascular and renal morbidity and mortality. The risk of cardiovascular complications decreases when the average blood pressure is less than 140/90; when the patient also has diabetes or renal disease, the treatment goal is a blood pressure less than 130/80.

Hypertension Manifestations

Primary HTN:

• Asymptomatic, marked only by elevated BP. Elevated BP are intitially transient but eventually become transient.
• Vague symptoms, headache usually in the back of the head and neck, may be present on awakening, subsiding during the day.
• nocturia, confuson, n/v and visual disturbance.

Sustained HTN:
- affects the cardiovascular, neurologic and renal systems
- workload of left ventricle increases, leading to ventricular hypertrophy, w/c then increases the risk for HF, CHD and dysrhythmias.
- accelerated atherosclerosis increases risk for cerebral infarction (stroke).

Modifiable Risk Factors:
- High sodium intake
- low K, Ca, and Mg intake
- obesity
- excess alcohol consumption
- insulin resistance
Nonmodifiable Risk Factors:
- genetic
- family hx
- age
- race

Hypertension Pathophysiology

Consistent BP readings >140 mmHg systolic or 90 mmHg diastolic OR taking antihypertensive medications to control BP

Chronic condition: medications are a "treatment" not a "cure".
Major risk factor for the development of cardiovascular and cerebrovascular disease.

Cardiac Output - ejection of blood from the heart during systole. Determined by the blood volume and the ability of the ventricles to fill and effectively pump that blood.

Increased CO or increased PVR cause the BP to rise.

• SNS stimulation. Baroreceptors signal SNS when the MAP changes. Drop in MAP stimulates SNS, increasing HR, CO and constricting arterioles. As a result, BP rises. A rise in MAP has the opposite effect. 
• Circulating epinephrine and norepinephrine have the same effect as SNS stimulation.
• Atrial Natriuretic Peptide (ANP) is released from atrial cells in response to stretching by excess blood volume. It promotes vasodilation and sodium and water excretion, lowering BP.
• RAAS responds to renal perfusion. Angiotensin II is a potent vasoconstrictor. It stimulates adrenal medulla to release Aldosterone, both SVR and CO increase raising BP.
• Adrenomedullin, potent vasodilator.
• Vasopressin or ADH, promotes water retention and vasoconstriction, raising BP.
• Local factors such as inflammatory mediators and various metabolites can promote vasodilation, affecting BP.
• Excess insulin has several effects that potentiall contribute to HTN: 
• sodium retention by the kidneys
• increased SNS activity
• hypertrophy of vascular smooth muscle
• changes in ion transport across cell membranes

Classification	Systolic BP	Diastolic BP
Optimal	<120 mmHg	<80 mmHg
Pre-hypertensive	120-139 mmHg	80-89 mmHg
Stage I HTN	140-159 mmHg	90-99 mmHg
Stage II HTN	≥ 160 mmHg	≥  100 mmHg

Diagnosis:

Systolic blood pressure of 140 mmHg or higher, or diastolic pressure of 90 mmHg or higher, based on the average of three or more readings taken on separate occasions.

Peripheral Vascular System

Arterial Circulation
The factors that affect arterial circulation are blood flow, peripheral vascular resistance and blood pressure.

Blood Flow - volume transported in a vessel, in an organ, or throughout the entire circulation over a given period of time, mL/min.

Peripheral Vascular Resistance (PVR) - opposing forces or impedance to blood flow as the arterial channels become more and more distant from the heart.

3 Factors of PVR:

•  the greater the viscosity or thickness of the blood the greater the resistance to moving and flowing
• the longer the vessel, the greater the resistance to blood flow.
• the smaller the diameter of a vessel, the greater the friction against the walls of the vessel thus the greater the impedance to blood flow.

Blood Pressure - force exerted against the walls of the arteries by the blood as it is pumped from the heart. Most accurately referred to as mean arterial pressure (MAP).

MAP = CO x PVR

Blood flow, PVR and BP, which influence arterial circulation, are in turn influenced by various factors:

SNS: vasoconstriction thereby increasing BP

PNS: vasodilation of the arterioles, lowering BP

Baroreceptors in the aortic arch, carotid sinus, and other large vessels can cause reflex SNS stimulation, resulting in vasoconstriction, increased HR and increased BP.

Kidneys: when BP decreases, the kidneys initiate RAAS which stimulates vasoconstriction, resulting in the release of Aldosterone, increasing sodium and water retention. In addition, pituitary release ADH to promote renal reabsorption of water. Net result is an increase in blood volume and consequent increase in CO and BP

Temperature: Cold causes vasoconstriction, whereas warmth produces vasodilation.

Chemicals, hormones and drugs influence BP by affecting CO and/or PVR i.e Epinephrine causes vasoconstriction and increased HR; Prostaglandins dilate blood vessels; Endothelin is a potent vasocontrictor; Nicotine causes vasoconstriction; alcohol and histamine causes vasodilation.

Salt, saturated fats and cholesterol elevate BP by affecting blood volume and vessel diameter.

Other factors that may also affect BP:

• Race
• Gender
• Age
• Weight
• Time of day
• Position
• Exercise
• Emotional state

LeMone/Burke/Bauldoff

p 876-879

CKD and HTN

Hypertension - sustained elevation of the systemic blood pressure, can result from or cause kidney disease.

Prolonged HTN damages the walls of arterioles and accelerates the process of atherosclerosis. This damage primarily affects the heart, brain, kidneys, eyes and major blood vessels.

In the kidney, GFR declines and tubular function is affected, resulting in proteinuria and microscopic hematuria.

Uncontrolled or poorly controlled HTN is the second leading cause of CKD.

Management of HTN to maintain the BP w/in an optimal range is vital to prevent kidney damage. When HTN is secondary to kidney disease, adequate BP control can slow the decline in renal function.

LeMone/Burke/Bauldoff 

p.830-831

Lab Values

Laboratory Normal Reference Ranges: Metabolic Panel

Laboratory Test	Reference Range
Sodium (Na+)	135-145 mEq/L
Potassium (K+)	3.5-5.5 mEq/L
Chloride (Cl-)	95-110 mmol/L
Glucose (fasting)	70-120 (***double-check)
Blood Urea Nitrogen (BUN)	5-25 mg/dL
Creatinine	0.5-1.5 mg/dL
Calcium (Ca²+)	9-11 mg/dL
Magnesium (Mg²+)	1.5-2 mEq/L
Total bilirubin	0.1-1 mg/dL
Miscellaneous Chemistry Labs
Albumin	3.5-5 g/dL
Prealbumin	15-36 mg/dL
Hemoglobin A1C (HgbA1C)	≤ 7%
Serum Osmolarity	275-295 mOsm/L

Complete Blood Count (CBC)

Laboratory Test	Reference Range
White Blood Cells (WBC)	5,000-10,000/mm³
Band Neutrophils	≤ 8%
Hemoglobin (Hgb)	12-18 g/dL
Hematocrit (Hct)	36-54%
Platelets (Plt)	150,000-400,000/microliter

Arterial Blood Gas (ABG)

Laboratory Test	Reference Range
pH	7.35-7.45
pO₂	75-100 mmHg
pCO₂	35-45 mmHg
HCO₃	22-26 mEq/L