Care of the woman with Dystocia related to Dysfunctional Uterine Contractions.

Dystocia - difficult labor.

Most common cause of dystocia is dysfunctional/uncoordinated uterine contractions, may result in prolonged labor.

Prolonged labor - lasting more than 24 hours

Normal uterine contractions pattern:  moderate or strong and regular
Early labor phase: 2-4 contractions in 10 minutes
Later phases: 4-5 contractions in 10 minutes

Tachysystolic Labor Patterns:  >5 contractions in 10 minutes, averaged over a 30-mins window.

Maternal Risks:

• increased discomfort due to uterine muscle anoxia (absence of oxygen)
• fatigue as patterns continue
• stress on coping abilities
• dehydration if labor is prolonged
• increased infection risks if labor is prologed

Fetal/Neonatal risks:

• nonreassuring fetal status because contractions and increased uterine tone interfere w/ the uteroplacental exchange of gases and nutrients.
• prolonged presurre on the fetal head, which may result in cephalohematoma, caput succedaneum, or excessive molding. 

Caput Succedaneum

Cephalohematoma

Clinical Therapy:

• bed rest and sedation to promote relaxation and reduced pain
• Often, pharmacologic intervention to promote sedation will stop tachysystolic contractions. 
• Pitocin and amniotomy (artificial rupture of membrane) may be considered if the pattern continues and developed into a prolonged latent phase. However, cephalopelvic disproportion (CPD) and fetal malpresentation need to be ruled out first. If CPD is present, labor is not stimulated because vaginal birth is not possible. Instead c/s will be performed. 
• CPD is said to be present if the maternal pelvic diameters are less than average, or if the fetus is particularly large or is in malpresentation or malposition.

Assessment and Diagnosis:

• Evaluate relationship between intensity of pain being experienced and the degree to which cervix is dilating and effacing.
• Note if anxiety is negatively affecting the labor progress
• Monitor for signs of nonreassuring fetal status.

Planning and Implementation:

• provide comfort and support to the laboring woman and her partner
• woman will be very uncomfortable due to increased force of contractions. Her anxiety and her partners anxiety will be very high. Work to reduce discomfort and promote more effective labor pattern
• Change of positions: left lateral side lying, high fowlers, on her knees with arms up, rocking in a rocking chair, sitting, walking.
• Soothing measures: quiet environment, back rub, therapeutic touch, music, visualization
• Comfort measures: mouth care, change of linens, effleurage, relaxation exercises
• Tub baths, warm shower can help promote comfort and uterine relaxation
• Provide information about the cause of tachysystolic labor pattern
• assure woman she's not overreacting
• patient education. She needs information about the dysfunctional labor pattern and the possible implications for her and her baby. This will relieve anxiety.
• Explain tx options
• offer opportunities to ask questions

Evaluation:

• Woman has increased comfort and decreased anxiety
• Woman and partner able to cope w/ the labor
• Woman experiences a more effective labor pattern

Hypotonic Labor Patterns:  fewer than 2-3 contractions in a 10-min period; develops in the active phase of labor; may occur when the uterus is overstretched from a twin gestation, or in the presence of a large fetus, hydramnios, or grand multiparity. Bladder or bowel distention and CPD may also be assoc. w/ this pattern.

Maternal Risks:

• exhaustion
• stress on coping abilities
• postpartum hemmorhage from insufficient uterine contractions ff birth
• intrauterine infection if labor is prolonged

Fetal/Neonatal Risks:

• nonreassuring fetal status due to prolonged labor pattern
• fetal sepsis from pathogen that ascend from the birth canal in the presence of ruptured membranes.

Clinical Therapy: The goal is to improve the quality of the uterine contractions and to ensure a safe outcome for mom and baby. 

• Stimulation of uterine contractions can be performed in several ways: Pitocin, amniotomy, and release of oxytocin due to nipples stimulation. 

• CPD, fetal malpresentation, and fetal immaturity need to be ruled out before Pitocin may be given to improve the quality of contractions. 

• IV fluids for hydration maintenance and prevention of maternal exhaustion. 

• Amniotomy may be used to stimulate labor process.  

• Electric breast pump can be applied or manual stimulation of nipples to help strengthen uterine contractions. Excellent starting point for women who wanted unmedicated birth. 

  • If labor pattern does not become effective or if other complications develop, c/s or other interventions may be necessary.  

 Assessment and Diagnosis:

• Assess ccontactions (frequency, intensity, duration), maternal VS and FHR.
• Assess s/s of infection and dehydration
• Observe coping mechanism
• Acute pain, ineffective coping, fatigue

 Planning and Implementation:

• promote maternal-fetal physical well being by frequent monitoring of contractions, maternal vs and fhr.
• Assess for presence of meconium if amniotic membranes were ruptured. Meconium indicates that the fetus is experiencing some form of stress w/c makes close observation of fetal status more critical.
• I/O record for maternal hydration or dehydration
• Encourage woman to void q2h, check bladder for distention.
• Monitor for s/s of infections (elevated temperature, chills, foul smelling amniotic fluid, fetal tachycardia)
• Keep vaginal examinations to a minimum to decrease risk for infections
• Emotional support
• Provide information about dysfunctional labor process and implications to mother and baby.
• Discuss disadvantages of and alternative tx

Evaluation:

• Woman maintains comfort during labor,
• Woman understand the type of labor pattern that is occurring and the tx plan.

•  

Anti-anginal Drugs

For treatment of angina pectoris (chest pain)
What causes angina? inadequate blood flow to the myocardium due to either plaque occlusions w/in or spasms of the coronary arteries. Decreased blood flow = decreased O2 to myocardium results in pain.
Anti-anginal drugs increase blood flow either by increasing oxygen supply or decreasing demand by the myocardium.
3 Types: Nitrates, Beta blockers, and Calcium Channel Blockers
Nitrates— major systemic effect is a reduction of venous tone, which decreases the workload of the heart and promotes vasodilation. Cause generalized vascular and coronary vasodilation, w/c increases blood flow through the coronary arteries to the myocardial cells. Reduces myocardial ischemia but can cause hypotension.

• Prototype drug: Nitroglcerin (Nitrostat, Nitrobid) - vasodilator; sublingual, the effects of SL last for 10minutes; client can use a maximum of 3 tablets, if pain is not relieve call 911.
• client may experience dizziness, faintness or headache as a result of peripheral vasodilation.
• causes relaxation and dilation, reduces cardiac preload and afterload and reduces myocardial 02 demand.
• ONSET: SL and IV, rapid 1-3mins; Trandermal 30-60minutes, patch should be removed nightly to avoid tolerance, 8-12 hour nitrate free interval. TD should be tapered.
• HA, hypotension, dizziness, weakness, faintness

Beta blockers—Why are they effective for angina? because by decreasing the heart rate and myocardial contractility, they reduced the need for oxygen consumption and consequently reduce anginal pain.

• decrease the workload of the heart and decrease oxygen demand.
• blocks beta-1 and beta-2
• decrease the effects of SNS by blocking the action of cathecolamines (epinephrine, norepinephrine), thereby reducing heart rate and BP
• used as antianginal, antidysrhythmic, and antihypertensive drugs
• should be tapered of to avoid reflex tachycardia and recurrence of anginal pain

Review side effects, contraindications:

• Contraindicated: pts who have low HR and BP; clients who have 2nd or 3rd degree AV block  

Calcium channel blockers—Why are they effective for angina?

• decrease workload of the heart, which decreases oxygen demand.
• Blocks influx of calcium into cardiac cells
• relax coronary artery spasm
• relax peripheral arterioles
• decrease cardiac contractility
• decrease afterload
• decrease peripheral resistance

Common side effects: Headache, peripheral edema, bradycardia, flushing, constipation, dizziness, hypotension

Nitrates and calcium channel blocker - effective in treating variant angina pectoris.
Beta blockers- for stable angina
Unstable angina, immediate medical care. Nitrates are usually given SQ and IV as needed. If cardiac pain continues, a beta blocker is given intravenously, if bblocker is not tolerated, calcium channel blocker can be used as substitute.

Cardiac Glycosides: Digoxin

Use: Increases contractility of cardiac muscle fibers
Indications: heart failure; heart rate control in atrial fibrillation
Desired results: Slows heart rate; decreases rate of cardiac electrical conduction; increases strength of cardiac muscle contraction. Improves heart failure symptoms by improving peripheral circulation, which increases fluid excretion.

Prototype drug: Digoxin (Lanoxin)—long half-life

• Narrow Therapeutic Window: therapeutic range = 0.5 (to treat HF) - 2.0 (best for atrial flutter or fibrillation) ng/ml
• Low serum potassium level (<3.5) can result in drug toxicity
• Bradycardia, N/V, visual “halos”, confusion
• Antidote: Digoxin immune Fab (Digibind)

Maintenance dose: 0.125 - 0.5 mg/dl. For older adults, dose is usually 0.125 mg/dl
Pulse rate should be above 60 beats/min.
Does not convert atrial fibrillation to normal heart rhythm. For mngmt. of atrial fibrillation, a calcium channel blocker, such as Calan may be prescribed. To prevent thromboemboli resulting from atrial fibrillation, Warfarin is prescribed concurrently w/ other drugs.
In clients w/ failing heart, cardiac glycosides increases myocardial contraction, w/c increases cardiac output and improves circulation and tissue perfusion. Because it decrease conduction through the AV node, the heart rate decreases.
Phenytoin and lidocaine are effective in treating digoxin induced ventricular dyshrythmias.
Lasix, HCTZ and systemic cortisone can cause hypokalemia. Patient should consume potassium rich foods or take potassium supplements.
Antacid can reduce Digoxin absorption so avoid taking it on the same time.

PHOSPHODIESTERASE INHIBITORS - Positive inotropic drug used for acute heart failure treatment
Promotes increase in cardiac muscle contraction, vasodilation

• IV drugs: inamrinone (Inocor), milrinone (Primacor) - increase stroke volume and cardiac output and promote vasodilation. Administered for no longer than 48-72 hours.

Used for short-term acute management of heart failure, requires cardiac monitoring during therapy for severe dysrhythmias can occur.

ATRIAL NATIURETIC PEPTIDE HORMONE
Nesiritide (Natrecor)— diuresis for heart failure treatment
Inhibits  ADH by increasing urine sodium loss. Promote vasodilation, diuresis and natriuresis. Useful for treating clients who have acute decompensated HF w/ dyspnea at rest or who have dyspnea w/ little exertion.

IV Fluids

Isotonic Solutions:

• 0.9% Saline (aka Normal Saline)
• Normal Saline is given to increase the amount of fluid in the blood vessels (intravascular space), without significantly changing the balance of electrolytes in the body.  This is useful for making sure a patient remains in a well-hydrated state of homeostasis.  Normal Saline also happens to be the only IV solution that can be infused at the same time as a blood product.
• Use to expand volume, dilute medications, and to keep vein open.
• Ringer’s Solution
• Lactated Ringers
• Ringer’s and Lactated Ringer’s Solutions contain a wider variety of electrolytes than Normal Saline, which makes them even more similar to what’s found in blood plasma.
• Use for fluid resuscitation
• 5% Dextrose in 0.225% Saline
• 5% Dextrose in Water (D5W) 
• The Isotonic Dextrose solutions have the same goal as the hypertonic dextrose solutions; to provide extra calories to the patient. Dextrose is just a sugar, which can be easily absorbed by the body and turned into energy.
• 5% Dextrose in Water is a special case. Although it is technically isotonic, it acts upon the body as if it is hypotonic as glucose is metabolized.

Hypotonic Solutions: contain less solute than blood, which causes water to want to leave the hypotonic solution and enter an area that has a higher concentration of solute via osmosis.  When discussing IV fluids, that usually means that the water will want to leave the intravascular space and enter Red Blood Cells (RBCs).

• 0.45% Saline
• the most common reason to give 0.45% Saline is for true dehydration, which is when the body has lost water, without losing any electrolytes (this is different from fluid volume deficit, when the body loses BOTH water AND electrolytes).  In dehydration, the body already has a normal amount of electrolytes, so there is no need to provide more in the IV solution.  The patient simply needs some of their water replaced!
• *5% Dextrose in Water 
• this is technically isotonic, but once the dextrose is absorbed then it acts on the body as if it was hypotonic

Hypertonic Solutions: has a higher solute to solvent ratio than blood does. Blood basically becomes our definition of what “Isotonic” means. Useful for a patient who needs electrolytes but is already on fluid overload, such as in Heart Failure or severe edema.  That way you are providing the patient with needed electrolytes, but minimizing the extra water that their condition doesn’t get worse.

• 3% Saline
• typically used to treat severe cases of hyponatremia (low sodium).  This makes sense because if your blood stream has become hypotonic and it’s supposed to be isotonic, then adding a hypertonic solution will help increase the electrolyte imbalance back to normal levels. 
• Caution: You need to infuse the IV solution very slowly and cautiously, and watch the patient closely for any evidence of intravascular overload (too much fluid in the blood vessels).  This could be increased blood pressure, pulmonary edema (fluid in the lungs), or even hypernatremia (high sodium).
• 10% Dextrose in Water
• 5% Dextrose in 0.45% Saline
• 5% Dextrose in 0.9% Saline
• These three dextrose solutions are primarily used for the purpose of providing the patient with extra calories.

Heart failure

Preload is the amount of blood returning to the heart from the body via the Vena Cava.
After load is the amount of resistance the heart must pump against to eject blood from the heart into the body.

Cardiac output = SV X R stroke volume times rate is the amount of blood circulated through the body in a minute.

Stroke volume is the amount of blood pump from each ventricle during contraction
Starling’s Law of the Heart reflects the elasticity creating force of cardiac cells to contract. As heart goes into failure the cells are stretch and dilated and so loose the ability to contract with efficient force. Think of a rubber band, the more it is stretch and dilated the weaker it is and loses its recoil ability. This is the same physiology seen in heart failure.

How do the baroreceptors in the carotid arch influence hormone secretion in heart failure?
Baroreceptors sense the pressure with which the blood as ejected and fills the aorta. This is reflected in the blood pressure. If the pressure is low, word is sent out to secrete hormones of the body to contract the arteries, and retain fluid to fill the arteries thus raising the blood pressure.

Explain the role of these hormones in heart failure:
Adrenalin – causes vasoconstriction of blood vessels leading to hypertension
Aldosterone – binds with sodium to retain water and cause the symptom of edema
Antidiuretic Hormone closes the epithelial cells in the distal kidney tubule and thereby retains water that adds to the symptoms of hypertension and edema.
Renin is secreted by the juxtaglomulerus of the kidney in response to the request of the baroreceptors in the aortic arch. Renin then goes to the lungs to initiate the formation of Angiotensin I and II that will add to hypertension.
Angiotensin II goes to the cardiac cells to stimulate remodeling or the formation of immature cardiac cells that are not able to contract with the force necessary to eject the volume of blood necessary for adequate stroke volume, thus the cardiac output remains low and the heart continues into failure.

What is the physiology that causes the primary symptoms of dyspnea, edema, and fatigue in heart failure?
Dyspnea comes from lungs trying to compensate for decrease perfusion in alveoli.
Fatigue results from lack of oxygen and build up of carbon dioxide in cells as sluggish circulation cause tissues to not have normal cleaning and perfusion.
Edema is a safety mechanism to third space fluid and decrease the work load of the heart pumping blood.

Why does PND paroxysmal nocturnal dyspnea occur primarily at night?
Edema fluid held in the legs during the day while a person is sitting, returns to the general circulation when the person is horizontal in bed. This fluid causes overload and drowning sensation leading to symptoms of severe dyspnea, air hunger and pulmonary edema.

Contrast the etiology of left and right sided heart failure.
Left sided heart failure occurs after MI, hypertension, or other causes that weaken the pumping ability of the left ventricle. Occurs in response to resistance of blood pumping in afterload. Low blood flow over the carotid baroreceptors triggers the compensatory hormone mechanisms or Adrenalin, Aldosterone, ADH and Renin. Treatment is medication to reduce afterload or intraortic balloon pump is person goes into shock.

Right sided heart failure deals with preload. The edema fluid is trying to return to the already full distended right ventricle.

Think about it … blood can’t be pumped out to the body or lungs so ventricles are full of blood. Where is new blood trying to ender the heart going to go? It backs up so jugular veins distend and A/V waves can be seen when the heart contracts. The body employs safety measure of third spacing reducing the flow of blood back to the heart by pushing it into the tissues by increased hydrostatic pressure. This is similar to when a river is full of water; the water overflows the banks and seeps into the ground. Same thing in heart failure, the ground is the tissues of the body (pulmonary edema of lungs, ascites from the liver, and pitting edema in the legs.

Differentiate Cor Pulmonale from right sided heart failure.
Right sided heart failure occurs with MI, Cor Pulmonale occurs from COPD as heart has to pump against the resistance of lung tissue pathology.

Comparison of heart, kidney, and liver failure symptoms

Symptom	heart	kidney	liver
Ascitesedema	ADH, renin, Aldosterone secretion, venous congestion into right ventricleIncreased hydrostatic pressure	ADH, renin, Aldosterone secretion, venous congestionLack of output	Decreased albuminPortal hypertension, increased capillary pressure, obstruction of venous flow
hypertension	ADH, renin, Aldosterone secretion, arterial congestion, edema, arterial constriction	ADH, renin, Aldosterone secretion, fluid retention	Liver does not metabolize aldosterone
breath		acetone	Fetor hepaticus
Change sensorium	Decreased circulation and oxygen	Increased nitrogen and acidosis	Ammonia and nitrogen
hepatomegaly	Venous engorgement		Scar tissue, inflammation
puritis		Uric acid crystals, uremic frost	Bile salts and jaundice
anemia	Low hemoglobin and oxygen carrying power	Lack of erythropoietin	Inability to metabolize hemoglobin and clotting factors
Diagnostic labs	H &H, BNP, Aldosterone	BUN, creatinine, electrolytes Creatinine clearance	AST, ALT, PT, BUN, A/G ratio
acidosis	Decrease CO, inadequate tissue perfusion, decrease oxygen exchange in cells, lactic acidosis	Hydrogen retention
anorexia	Venous stasis in the abdominal organs, ascites	Toxins, ammonia	Ascites, toxins
diet	DASH, low sodium, cholesterol, low triglycerides, and fluid restriction	Low sodium, potassium, protein, fluid restriction, high carbohydrate	High carbohydrate, low protein, low sodium
hepatomegaly	venous engorgement		Inflammation, scar tissue
Treatments	diuretics	dialysis	Diuretics, SPA

Hypovolemia & Hypervolemia tx

Hypovolemia:

• Oral rehydration, 1500mL/day
• Carbohydrate/electrolyte solution such as sports drink, gingerale, pedialyte
• IV theraphy
• Isotonic solutions are used to expand plasma volume preferably LR
• 0.45% w/ or w/out added electrolytes for maintenance

Hypervolemia:

• Diuretics = loop, thiazide-type, potassium sparing i.e lasix, HCTZ, aldactone
• Restrict fluid intake
• Restrict sodium intake
• Too much water retention can lead to cerebral edema or pulmonary edema.

Hypernatremia tx

• Oral or IV water replacement
• Hypotonic IV fluids such as 0.45% NaCl solution or
• 5% Dextrose in water (isotonic solution but becomes hypotonic when glucose is metabolized)
• Diuretics may be given to increase sodium excretion (for excess sodium)
• Restrict sodium in diet
• Give isotonic solutions

Hyponatremia tx

• When both sodium and water have been lost, replace both water and sodium w/ isotonic ringer or isotonic saline.
• Hypertonic (3% or 5% NaCl) may be necessary if pt. have very low plasma volume
• For dilutional hyponatremia, administer loop diuretic and restrict fluids.
• For mild hyponatremia, increasing fluid intake of sodium may restore the balance

Risk for ineffective cerebral tissue perfusion. Brain cell swells increasing cranial pressure.

Hyperkalemia tx

• Calcium Gluconate or Calcium Chloride
• Kayexelate and Sorbitol
• Sodium Bicarbonate espescially for metabolic acidosis related
• Insulin, Glucose, Hypertonic IV
• Potassium wasting diuretics i.e lasix/furosemide
• Dialysis if renal failure is the cause
• Avoid salt substitute, high in K

Hypokalemia tx

Cause: GI loss: suctioning, vomiting, emesis, diarrhea, high dose loop diuretics, penicillin G, steroids, poor nutrition

Treatment:

• KCl, Potassium sparing diuretics (aldactone), parenteral nutrition 
• Oral or parenteral K supplements
• NPO, Potassium Chloride (KCl) is added to IV fluids; 10 mEq/hr

Diet: banana, oranges, potatoes, tomatoes, avocado, spinach, meat, seafood, milk and yogurt

Watch out for digoxin toxicity!
NEVER, EVER give K as an IV push. Very lethal. Use for lethal injection.

Priority: effects of hypokalemia on cardiac impulse transmission, and cardiac + skeletal muscle function, decrease CO, activity intolerance, imbalanced fluid volume 

Hypercalcemia tx

• Acute, loop diuretics i.e lasix to promote elimination of excess calcium
• Acute, Calcitonin will promote the uptake of calcium in bones and rapidly lower serum Ca level; 
• slows the release of calcium from bones into bloodstream, thereby keeping blood levels of calcium to a minimum
• Biphosphonate ( pamidronate, etidronate), inhibit bone resorption
• IV plincamycin (mithramycin), inhibit bone resorption
• Sodium phosphate or Potassium phosphate; increase in phosphate = decrease in calcium
• Glucocorticoids (cortisone), compete with vitamin D and low calcium diet to decrease GI absorption of calcium, inhibit bone resorption and increase urinary excretion of calcium
• Isotonic IV, to replace sodium and restore vascular volume. 
• Sodium excretion is accompanied by calcium.
• Watch out for hypervolemia because of isotonic IV.

Hypocalcemia tx

• Oral or IV calcium
• Severe hypocalcemia, need IV to avoid airway obstruction
• Calcium Chloride or Calcium gluconate
• IV CaCl is more irritating to the veins.
• Rapid drug administration can lead to bradycardia and possible cardiac arrest due to over correction resulting to hypercalcemia
• PO Calcium: for asymptomatic hypocalcemia
• Calcium Carbonate
• Calcium Gluconate
• Calcium Lactate
• Calcium supplements + viamin D or vitamin D alone to increase absorption of Calcium
• Antacid, to lower phosphorus level; decrease in phosphorus = increase in calcium

Respiratory Alkalosis treatment

• Anxiety disorder, breathe into a paper bag
• Sedative or antianxiety medication may be needed
• If excessive mechanical ventilation is the cause, adjust the ventilator setting
• If hypoxia is the cause, administer oxygen
• S/S: mimic heart attack, chest tightness etc

Respiratory Acidosis treatment

• Bronchodilator, to open the airway
• Antibiotics, to treat respiratory infection
• Naloxone (Narcan)m antidote for excess narcotics or anesthesia
• Respiratory support, may require intubation and mechanical ventilation to improve gas exchange and alveolar ventilation
• Hydrate up to 3000 mL/day
• Breathing tx, percussion, vibration, postural drainage as ordered
• Lower PaCO2 slowly to avoid complication i.e cardiac dysrhytmia and cerebral perfusion
• Administer O2 cautiously
• COPD - O2 narcosis
• Teach pursed lip breathing
• Monitor for respiratory depression.
• Restoring effective alveolar ventilation and gas exchange is the priority.

Metabolic Alkalosis treatment

Possible cause: gastric suctioning, vomiting, anorexia, ingestion of bicarbonate (Alka-seltzer, Soda Bicarbonate)

Decrease Cl = Increase CHO3
Give Cl to reverse the result

• Potassium Chloride (KCl)
• Sodium Chloride (NaCl)
• Potassium restores serum and intracellular K levels
• Chloride promotes renal  excretion of Bicarbonate
• NaCl, restore fluid volume deficits that can contribute to metabolic alkalosis

• Severe alkalosis, an acidifying solution such as Ammonium Chloride may be administered.
• Treat underlying cause
• Priority: impaired gas exchange / hypoxemia
• May lead to hypokalemia and hypovolemia

Metabolic Acidosis Treatment

• Sodium Bicarbonate - alkalinizing solutions to reduce the effect of the acidosis on cardiac function.
• IV for acute
• PO for chronic

• Treat underlying cause:
• DKA - insulin and fluids
• ETOH acidosis - glucose and saline
• Lactic Acidosis - treat underlying cause and improve tissue perfusion
• Renal failure 
• Diarrhea - fluid and electrolyte replacement

• Monitor for decrease CO because of metabolic acidosis and hyperkalemia
• Monitor lab values, ABG, electrolytes, creatinine and BUN for renal
• Monitor for dysrhytmias
• further decrease CO intensify acidosis
• As PH falls, mental functioning declines leading to confusion, stupor and decreasing LOC

May lead to hypokalemia and metabolic alkalosis if bicarbonate is not watch closely. Can also cause hypernatremia, hyperosmolarity and hypervolemia.

Lower Respiratory Tract Drugs

COPD 

• Emphysema, chronic bronchitis

• Caused by chronic inflammation in respiratory tract due to exposure to irritants (tobacco smoke, environmental pollutants)

• Treatment: Limit exposure to irritants; increase PO fluid intake; breathing exercises; medications—same as asthma treatment

ASTHMA

• Reactive airway disorder—bronchospasm, difficulty breathing

• Mast cell overreactivity—histamine, cytokines, eosinophils released which causes airway edema, smooth muscle constriction, oversecretion of mucus

• Treatment: Avoidance of triggers; management of allergies; avoidance of drugs (ASA, NSAIDS, Beta blockers) that can worsen symptoms

ALPHA & BETA ADRENERGIC AGONISTS

• Albuterol (Proventil, Ventolin)
• Used for bronchodilation
• Stimulates Beta receptors
• Side effects: Beta 1 stimulation (tachycardia, nervousness)
• Terbutaline—similar drug (also used for preterm labor)
• Levobuterol (Xopenex)—similar to albuterol; fewer cardiac side effects; expensive
• Isoproterenol (Isuprel)—Beta 1 & Beta 2 stimulation
• Can be given by IV for severe asthma attacks

• Epinephrine (Adrenalin)
• Stimulates Alpha 1, Beta 1, Beta 2 receptors
• Produces bronchodilation
• Tachycardia, elevates blood pressure; risk of arrhythmias

ANTICHOLINERGICS

• Ipratropium (Atrovent)—Prototype drug
• Prevents bronchoconstriction (end result = bronchodilation)
• Side effects: decreased SLUDGE (dry mouth common)
• Use before inhaled steroid if using dual therapy
• Combination with albuterol=Combivent inhaler

METHYLXANTHINES

• Theophylline (Theo-Dur) & aminophylline—chemically related
• Similar to caffeine—side effects similar
• Narrow therapeutic window
• Not recommended in people with cardiac, renal, hepatic disease or seizures
• Long-acting; mostly used in maintenance of stable asthma

LEUKOTRIENE RECEPTOR ANTAGONISTS

• Montelukast (Singulair)—Prototype drug
• For maintenance/prophylactic therapy of asthma
• Administered by PO route; long-acting
• Decreases inflammatory response; decreases bronchoconstriction
• Few serious side effects; not indicated for acute asthmatic attacks

GLUCOCORTICOIDS (AKA STEROIDS)

• Indicated for acute exacerbations of COPD or asthma
• Action: Decreases inflammatory response
• Many side effects: Elevated blood glucose, increased risk of infection; high doses must be tapered over 1-2 weeks (risk of adrenal suppression); weight gain; fluid retention; osteoporosis & cataracts with long-term therapy
• Systemic effects less with inhaled corticosteroids
• Most common side effect with inhaled: thrush
• Prevent thrush by rinsing mouth after each use

CROMOLYN & NEDOCROMIL

• Cromolyn (Intal)—Prophylactic treatment of asthma
• Chronic therapy; available by PO route
• Inhibits release of histamine
• Side effects:  rebound bronchospasm if abruptly discontinued
• Commonly used in children with asthma

Upper Respiratory System Drugs

Upper Respiratory Disorders:
 Involves nasopharynx, pharynx, larynx, sinuses: Colds, rhinitis, sinusitis, pharyngitis

• ANTIHISTAMINES
• Block H1 and/or H2 receptors 
• Side effects: Decreased SLUDGE (anticholinergic), drowsiness
• Prototype drug: Diphenhydramine (Benadryl)—1st generation—PO, injectable (can be used for emergencies)
• 2nd generation antihistamines: Cetirizine (Zyrtec), fexofenadine (Allegra), loratidine (Claritin)—available only by PO

• DECONGESTANTS
• Alpha adrenergic effects
• Administered by nasal spray, PO
• Drugs: Ephedrine, pseudoephedrine (Sudaphed), phenylephrine (Neo-Synephrine), oxymetazoline (Afrin)—spray
• Side effects: Rebound congestion with overuse of spray; systemic: elevated BP, elevated blood glucose; dysrhythmias; avoid stimulants

• INTRANASAL GLUCOCORTICOIDS
• Systemic side effects rare; may cause nasal dryness
• Drugs: Fluticasone (Flonase), Triamcinolone (Nasacort)

• ANTITUSSIVES
• Suppress cough reflex
• Prototype drug: Dextromethorphan (Robitussin, Delsym)
• Available OTC
• Intoxication at high doses

• EXPECTORANTS
• Liquify sputum for easier production with coughing
• Need to increase PO fluid itake
• Drug: Guaifenesin (Robitussin, Mucinex)

Anti-Emetics

Chemoreceptor trigger zone (CTZ) & vomiting center in brain

OTC:

• Benadryl, Antivert, Dramamine
• also effective on motion sickness
• decrease SLUDGE (salivation, lacrimation, urination, defecation, GI distress, emesis), drowsiness
• Best taken 30 minutes before travel

Prescription:
Dopamine antagonists: Phenothiazines

• Phenergan -- oral, IV, rectal; 
• EPS side effects; drowsiness, 
• must be diluted prior to IV administration (> or = 10mL); 
• sleep and fall precaution; 
• Phenergan should be administered with caution to a client who has a history of hypertension.
• Reglan -- stimulate peristalsis

Serotonin Receptor Antagonists

• Zofran -- can be used prophylactically(prevention) or for acute n/v; 
• PO or IV; 
• pre-surgery, during surgery, post-surgery

Cannabinoids:

• Marinol -- for N/V associated with chemo & for appetite stimulation in AIDS patients
• Side effects: impaired cognition, drowsiness, euphoria, dry mouth

ALL: absence of n/v determines effectiveness

Macrolides

Tx of  respiratory tract infections, H. pylori, skin, PID, skin, bacterial STD's, MRSA
Take on empty stomach

• Prototype drug: Azithromycin (Zithromax) - "Z-pack"
• monitor for hepatotoxicity and ototoxicity
• assess liver enzymes on a regular basis

• Other Drugs: Erythromycin, Clarithromycin, Clindamycin, Vancomycin
• monitor for renal and hepatic function
• monitor for signs of colitis (diarrhea, abdominal cramping)
• monitor for ototoxicity

• Vancomycin: monitor for red man syndrome, nephrotoxicity (creatinine and Urine output); peak and through levels; infuse slowly - may cause IV site pain.

• Erythromycin: drug of choice when penicillin is not an option due to hypersensitivity

Antimicrobial Therapy

Sensitivity and resistance:

• Any medication allergy should be reported to the healthcare provider.
• Fluids should be encouraged with antibiotic therapy.
• To obtain the most accurate culture, culture should be obtained before antibiotic therapy begins.
• The entire course of the medication should be taken to ensure eradication of the infection and decreased resistance, even if the client’s symptoms has normalized. Resistance occurs when microbes become de-sensitized to an antimicrobial. 
• Multiantibiotic therapy delays development of resistance.
• When microbe is resistant to an antibiotic, antibiotic therapy must be changed. Bacteria mutate if they are in contact with antibiotics for extended periods.
• May decrease effectiveness of oral contraceptives
• Monitor for superinfections (fungal, C.difficile, vaginitis)
• Monitor for organ toxicity ( kidney and liver) (BUN and Creatinine level)
• Monitor for allergy/hypersensitivity
• High peak levels may indicate that the medication is above the toxic level.
• Medication levels must be maintained above the Minimum Effective Concentration throughout therapy to ensure that bacterial resistance does not occur.

Cephalosporins

Derived from fungus
Interferes w/ cell wall synthesis
Similar to PCN but resistant to beta-lactamase enzyme
Potential cross-allergy in those w/ PCN allergies. The nurse should administer the medication and carefully observe for allergic reaction.

• Prototype: Cefaclor, Cefazolin
• Interaction w/ alcohol, probenicid (treats gout) (decreases excretion of ceph; raises level of drug)
• Interaction w/ erythromycin will produce a decrease in the action of the Cefaclor.
• Side effects: GI (anorexia, nausea, vomiting), headache, dizziness, itching, rash, increased blood clotting time, nephrotoxicity
• Monitor renal and hepatic function, vital signs, urine output; monitor for superinfections

Penicillin

Derived from mold
Prevents cell from forming cell wall

• Prototype: amoxicillin, penicillin G, ampicillin
• no acidic fruits and juices
• Penicillin combined w/ beta-lactamase inhibitors: Augmentin, Zosyn, Timentin
• amplifies antimicrobial effect

Common drug allergy/hypersensitivity, drug-resistance issue, generally safe in pregnancy

General Antimicrobial guidelines:

• Any medication allergy should be reported to the healthcare provider.
• Fluids should be encouraged with antibiotic therapy.
• To obtain the most accurate culture, culture should be obtained before antibiotic therapy begins.
• The entire course of the medication should be taken to ensure eradication of the infection and decreased resistance, even if the client’s symptoms has normalized.

Hypertensive crisis

Hypertensive Crisis:

• sudden, dangerous, elevation in BP
• can lead to organ and tissue damage quickly
• BP is > 180/120
• Symptoms: headache, confusion, vision changes, chest pain, dyspnea, sensory deficit, seizure activity 
• Goal: reduce BP by no more than 25% w/in an hour, then toward 160/100 w/in 2-6hours. 
• It is important to avoid rapid or excessive BP decreases that may lead to renal, cerebral or cardiac ischemia.
• IV medication for rapid and predictable action
• Nipride - vasodilator, easy to titrate
• Vasodilator - nitroglycerin, apresoline
• Enalaprilat - ace inhibitor

Heart Failure

Heart failure develops when the heart cannot effectively fill or contract w/ adequate strength to function as a pump to meet the needs of the body. As a result, cardiac output falls, leading to decreased tissue perfusion. The body initially adjusts to reduced cardiac output by activating compensatory mechanisms to restore tissue perfusion. These normal mechanisms may result in vascular congestion -- hence, the commonly used term congestive heart failure. As these mechanisms are exhausted, heart failure ensues, w/ increased morbidity and mortality.

Depending upon the cause, HF presents initially as right sided heart failure or left sided heart failure; as it progresses, the other side becomes affected

Left heart failure:

• the left ventricle has reduced capacity to pump blood into systemic circulation causing decreased cardiac output and stasis or backup of blood into the pulmonary circulation
• due to coronary artery disease, hypertension, cardiomyopathy, rheumatic heart disease
• Presenting symptoms: dyspnea on exertion (1st sign), orthopnea, PND, new s3, crackles; pulmonary edema.

Right heart failure:

•  the right ventricle has reduced capacity to pump blood into pulmonary circulation causing stasis or back up of blood into the venous circulation
• due to COPD, pulmonary embolism, rv infarct
• usually called cor pulmonale
• Presenting symptoms: edema of lower extremities, jugular venous distention, abdominal discomfort and nausea occur from fluid congestion in the abdominal organs

Both sides:

•  Presenting symptoms are unexplained fatigue, decrease exercise tolerance, unexplained altered mental status

Further clarification:

• Fall in cardiac output activates mechanisms that cause increased salt and water retention which causes weight gain and further increases pressures in the capillaries, resulting in edema
• Nocturia develops as edema fluid from dependent tissues is reabsorbed when the patient is supine
• Paroxysal nocturnal dyspnea, a frightening condition in w/c the pt. awakens at night acutely short of breath. It occurs when edema fluid that has accumulated during the day is reabsorbed into the circulation at night, causing fluid overload and pulmonary congestion
• Congestive hepatomegaly and splenomegaly caused by engorgement of the portal venous system results in increased abdominal pressure, ascites and GI problems. 
• Prolonged RHF may lead to impaired liver function

Main goals for care:

• slow progression
• reduce cardiac workload
• improve cardiac function
• control fluid retention

Pneumothorax

Accumulation of air in the pleural space.
Can occur spontaneously, w/out apparent reason, as a complication of preexisting lung disease, as a result of blunt or penetrating trauma to the chest or from thoracentesis.

Manifestation:
dyspnea, tachycardia, tachypnea, absent breath sounds or diminished, hyperesonant percussion on affected side, chest pain, anxiety, shock (late symptoms)

TENSION PNEUMOTHORAX (expanding): hypotension, shock, tracheal deviation (late but definitive sign), distended neck veins

Treatment:
chest tubes to allow the lung to re-expand; low-level suction helps reestablish negative pressure
large bore needle or plastic IV cath may be inserted thru the chest wall as emergency tx of tension pneumothorax.

Pleural Effusion

Collection of excess fluid in the pleural space. Either from systemic or local cause.
Pleural space normally contains 10-20 mL of serous fluid.

Systemic disorder that may lead to pleural effusion:

• heart failure
• renal or liver disease
• connective tissue disorder
• RA
• SLE

Local conditions that may lead to pleural effusion:

• pneumonia
• atelectasis
• TB
• lung cancer
• trauma

Manifestations:
diminished or absent breath sounds, dyspnea (difficult or labored breathing), pain (early sign), dull percussion

Treatments:
thoracentesis
treat cause

Pneumonia

@risk:
people over 65 with chronic cardiac or respiratory conditions, dm, alcoholism or other chronic diseases
immunocompromised people
chronic renal failure
people receiving chemotherapy

Prevention is a key component in managing pneumonia.
Pneumonia and flu vaccine. Revacination of pneumonia vaccine recommended for age >65 and who were immunized 5 years previously. Flu vaccine is yearly.

S/S:
fever, SOB, purulent sputum, rhonchi, crackles, pain, labored breathing
Vitals: increased HR, respiratory rate and temperature, decrease spO2, 
Elderly and immunocompromised: decrease LOC may be the only symptoms

Medications:
Antibiotics to eradicate the infection, culture 1st to identify the right antibiotics to be prescribed
Bronchodilators yp reduce bronchospasm and improve ventilation
agent to break up mucus or reduce its viscosity i.e mucomyst

Treatments:
increase fluid intake to 2500-3000 mL per day - to liquify secretion, making it easy to expectorate and cough up. IV fluids and nutrition
Incentive spirometry to promote deep breathing, coughing and clearance of respiratory secretions.
Endotracheal suctioning if cough is ineffective
Bronchoscopy can also be use to perform pulmonary toilet and remove secretions
Oxygen therapy
Chest physiotherapy
Promote rest to reduce metabolic and oxygen needs

Priority Nursing Diagnosis:
Ineffective airway clearance
Ineffective breathing pattern
Activity intolerance

Considerations:
High Fowler position promotes lung expansion
frequent position change and ambulation facilitate movement of secretions
Coughing, deep breathing and suctioning help clear airways
A liberal fluid intake helps liquify secretions, facilitating clearance

Test 2 outline for respiratory meds

Bronchodilators:

• Anticholinergic: ipatropium(atrovent), itotropium(spiriva)
• first line unless contraindicated, dry mouth is the side effect
• Beta-2 agonist: albuterol, levalbuterol
• work faster than anticholinergic, best for emergencies, stimulate CNS is the side effects
• Methylxantines: Theodur, it also increases mucociliary action
• side effects: toxicity possible, n/v, seizures, insomnia

 Corticosteroids: decrease inflammation, increase sensitivity to cathecolamines

• Systemic: Prednisone, Hydrocortisone, Methylprednisolone
• Many side effects such as hyperglcemia,infection, tachycardia, easy bruising, weight gain
• Inhaled: fluticasone, beclamethasone
• for COPD maintenance, less side effects than systemic; rinse mouth after each use to prevent oral thrush

AntiHistamines:

• 1st generation: Benadryl; sedating, drowsiness, dry mouth
• 2nd generation: Claritin, Allegra; less sedating than 1st gen

Mucolytics: decrease thickness of mucous i.e Mucinex

Influenza

Cause: viral
Droplet transmission; can lead to pneumonia 
Symptoms: malaise, fever, cough, sore throat
Treatment: symptom relief, rest
Prevention: vaccination, isolation, hygiene
Tamiflu & Relenza shorten duration and decrease symptoms
Vaccinate annually (different strains)

Acute Bronchitis

Inflammation of the bronchi.
Typically follows a viral upper respiratory infection
can be caused by bacteria or viruses
Common in older adult

Risk Factors:
immunocompromise and cigarette smoking

Manifestations:
nonproductive coughs that later become productive
chest pain
moderate fever
malaise

Treatment:
A chest x-ray may be ordered to rule out pneumonia, because the presenting manifestations can be similar.
rest, increased fluid intake, stop smoking
aspirin or acetaminophen to relieve fever and malaise
antibiotics for bacterial infection
OTC expectorant cough medication i.e mucinex or delsym

Book info:
The diagnosis of acute bronchitis typically is based on the history and clinical presentation. A chest x-ray may be ordered to rule out pneumonia, because the presenting manifestations can be similar. Other diagnostic testing and hospitalization are rarely indicated. Treatment is symptomatic and includes rest, increased fluid intake, and the use of aspirin or acetaminophen to relieve fever and malaise. Many physicians prescribe a broad-spectrum antibiotic such as erythromycin or penicillin, because approximately 50% of acute bronchitis is bacterial in origin. An expectorant cough medication is recommended for use during the day and a cough suppressant for night to facilitate rest.

Thoracentesis

Done to obtain a specimen of pleural fluid for diagnosis
used as a procedure to remove pleural fluid (pleural effusion) or instill medication
fluid removed is limited to 1200-1500 mL at one time to reduce the risk of cardiovascular collapse from rapid removal of too much fluid.

Pre-op:
requires informed consent
upright position,leaning forward w/ arms and head supported on anchored overbed table. This position spreads the ribs, enlarging the intercostal space for needle insertion.
coach patient to hold breathe or breathe out.

Post-procedure:
Chest x-ray is taken to check for pneumothorax, which is a possible complication for thoracentesis

Bronchoscopy

Direct visualization of the larynx, trachea and bronchi thru a bronchoscope to identify lesions, remove foreign bodies and secretions, obtain tissue for biopsy and improve tracheobronchial drainage.

Pre-op:
assess for hypersensitivity to anesthetics, antibiotics iodine or contract dyes
NPO for 8-12 hours
remove dentures, contact lenses, jewelry
assess vitals

Post-op:
assess for complication i.e laryngeal edema, bronchospasm, pneumothorax, cardiac dysrhythmias, bleeding
monitor for s/s of respiratory difficulty and hemoptysis (bloody sputum)
keep on NPO until gag reflex is back
no smoking for at least 6-8 hours cuz it may cause coughing and bleeding

Normal: blood-tinged sputum, hoarseness and sore throat
Report: pain, bleeding, respiratory difficulty

Obstructive sleep apnea

Intermittent absence of airflow through the mouth and nose during sleep. A serious and potentially life threatening disorder.

Manifestations:
loud, cyclic snoring
excessive daytime sleepiness, HA, irritability, restless sleep,
personality changes, depression, HTN, intellectual impairment, increases risk for heart failure

Risk Factors:
male, increasing age, obesity
large neck circumference
use of alcohol and CNS depressants

Treatments:
weight reduction, alcohol abstinence, improving nasal patency
avoid supine position for sleep
use of oral appliances designed to keep the mandible and tongue forward
tonsillectomy and adenoidectomy

CPAP/BiPAP - tx of choice

• positive pressure generated by an air compressor and administered thru a tight-fitting nasal mask splints the pharyngeal airway, preventing collapse and obstruction
• humidifier needed to prevent irritation and dryness
• BiPAP delivers higher pressure during inspiration and lower pressure during expiration, providing less resistance to exhaling
• continous usage at night
• adequate fluid intake to maintain moist mucous membrane

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.