Exam 3 - Study Material Flashcards by Elias Cortez (2024)

• Acute nephritic syndrome is a group of symptoms that occur with some disorders that cause glomerulonephritis, or swelling and inflammation of the glomeruli in the kidney.
• Often caused by an immune response triggered by an infection or other disease
  
  • group A beta-hemolytic streptococcal infection of the throat
  • Precedes the onset of glomerulonephritis by 2-3 weeks.
  • Impetigo, acute viral infections, hepatitis B, mumps, varicella zoster, EBV, HIV, SLE

Symptoms:

• Hematuria (micro or macroscopic)
• Edema + HTN – most pts
• Azotemia
• Proteinuria
• ↑ BUN, ↑ Serum creatinine with ↓ UO

With severe disease:

• Headache
• Malaise
• Flank pain

Elderly Patients:

• Dyspnea
• Engorged neck veins
• Cardiomegaly
• Pulmonary edema

Atypical symptoms:

• Confusion
• seizures
• somnolence

• Hypertensive encephalopathy (medical emergency)
  
  • Goal: reduce BP w/o impairing renal function
• Heart failure
• Pulmonary edema

Prognosis: excellent & rarely causes CKD

• If residual streptococcal infection present, PCN is treatment of choice
• Dietary protein restricted when renal insufficiency present and nitrogen retention (↑ BUN)
• Sodium restriction for patients with hypertension, edema, and heart failure
• Carbohydrates given liberally to provide energy & reduce catabolism of protein
• Close monitoring of I&O
• Fluids given based on patient’s fluid loss & daily weight
• If tx effective, diuresis will begin ↓edema & BP
• Proteinuria & microscopic hematuria may persist for months

It Is:

• Glomerular disease with a progressive course leading to chronic kidney disease

Causes:

• Diabetic nephropathy
• Podocyte injury, progressive thickening & fibrosis of glomerular basem*nt membrane, & expansion of mesangial matrix
• Acute nephritic syndrome
• Hypertensive nephrosclerosis
• Hyperlipidemia
• Chronic tubulointersitial injury
• Hemodynamically mediated glomerular sclerosis

• Kidneys are reduced to as little as 1/5 their normal size and contain mostly fibrous tissue
• Kidney surface becomes rough and irregular
• Glomeruli and tubules become scarred
• Renal artery branches thicken
• Glomerular damage can progress to ESRD and require renal replacement therapies

• Symptoms vary-some patients with severe disease may have no symptoms for many years
• May be discovered with hypertension or elevated BUN, serum creatinine
• General symptoms reported:
  
  • –loss of weight & strength
  • –increasing irritability
  • –nocturia
  • –headaches
  • –dizziness
  • digestive problems

As disease progresses S/S of CKD and CRF develop

• Poorly nourished appearance w/ yellow-gray pigmentation of the skin
• Periorbital and peripheral edema
• Normal or severely elevated BP
• etinal findings: hemorrhage, exudate, narrowed tortuous arterioles, papilledema
• Anemia ⇉ pale mucous membranes
• Maybe cardiomegaly & S/S of CHF, lung base crackles

Later stage clinical manifestations:

• Peripheral neuropathy w/ ↓ deep tendon reflexes
• Confusion; limited attention span
• Pericarditis
  
  • –pericardial friction rub
  • –pulsus paradoxus (Drop in systolic BP greater than 10 when standing up)

Diagnostic Findings:

• UA: specific gravity <1.010, variable proteinuria & urinary casts (i.e., protein plugs secreted by damaged kidney tubules)
• When GFR gets low, it leads to:
  
  • –Hyperkalemia
  • –Metabolic acidosis
  • –Anemia
  • –Hypoalbuminemia
  • –Increased serum phosphorus
  • –Decreased serum calcium
  • –Mental status changes
  • –Impaired nerve conduction
• CXR: cardiac enlargement, pulmonary edema
• ECG: WNL; LVH; tall, tented (peaked) T waves
• CT and MRI: decrease in size of renal cortex

Treatment is guided by management of symptoms:

• HTN
• Na+ and H2O restriction
• –Anti-hypertensive medications

If the patient has fluid overload:

• Record daily weights
• Give diuretics

Nutrition:

• Protein - high biologic value (dairy products, eggs, meat)
• Calories – enough to spare protein for tissue growth/repair

UTIs: antibiotics to prevent further kidney damage

Dialysis – early in disease to ↓ complications, prevent fluid & electrolyte imbalances and keep pt in optimal physical condition

Anxiety – provide emotional support to pt/fam

W/O for elderly patients, easy fluid overload

It Is:

• Glomerular injury leading to the excretion of 3g or more of protein in the urine per day, hypoalbuminemia (albumin < 3g/dl), and peripheral edema

Causes:

• Primary - Lipoid nephrosis, membranous glomerulonephritis, and focal segmental glomerulosclerosis
• Secondary - Diabetes mellitus, amyloidosis, systemic lupus erthemoatosis.

Progression:

1. Glomerular injury → Altered gloomerular permeability and loss of negative charge →
2. ↑ filtration of plasma proteins →

3. Proteniuria →

A) Loss of transport proteins → ↓ Vitamin D & ↓ Thyroxine

B) Decreased immunoglobulins

4. Hypoalbuminemia →

A) Hepatic synthesis of lipoproteins →

B) Hyperlioproteinemia →

C) Lipiduria

5. ↓ Plasma oncotic pressure →
6. ↓ Plasma volume →
7. Na+ & H2O retention → Peripheral edema & ascites

• Irritability, headache, malaise
• Urinary excretion ≥ 3.5 g protein in 24 hr
• Proteinuria, lipiduria
• Hypoalbuminemia, hyperlipidemia
• Na+ retention → edema & ascites
  
  • Periorbital (eyes)
  • Dependent areas (sacrum, ankles, hands)
  • Ascites (abdomen)
  • Pitting edema
• Vitamin D deficiency (↓ serum transport proteins)
• Hypothyroidism (urinary loss of thyroid-binding protein & thyroxine)
• ↑ cholesterol & triglycerides

• Infection
• Thromboembolism
• Pulmonary emboli
• Acute Renal Failure
• Accelerated atherosclerosis

• Early stages of management are similar to that for acute glomerulonephritis; as condition worsens, management is similar to that of pt with ESRD
• Treat the underlying cause of proteinuria, slow progression of CKD, relieve symptoms
• If the patient has Edema: diuretics
• If Proteinuria: ACE inhibitors
• If Hyperlipidemia: lipid-lowering agents

• It is a genetic disorder characterized by the growth of numerous cysts in the kidneys, it is generally bilateral
• Caused by:
  
  • Cysts filled with fluid destroy nephrons
  • Cysts can profoundly enlarge kidneys, reducing kidney function, which leads to kidney failure

They are all caused due to the cyst growing in size:

• Hematuria
• Polyuria
• HTN
• Renal calculi
• UTIs
• Proteinuria
• Abdominal fullness
• Flank pain

• Family hx
• Enlarged cystic kidneys upon palpation of abd
• Kidney ultrasound

• No cure
• Supportive tx: BP & pain control, antibiotics
• RRT when kidneys fail

It Is:

• A sudden decline in kidney function with a ↓ in GFR and accumulation of nitogenous waste products in the blood as demonstrated by an elevation in plasma creatinine and BUN lvls.

Causes:

• Extracellular volume depletion from:
  
  • Hemorrhage
  • Diuretics
  • V/D
• Impaired cardiac efficiency from
  
  • MI, heart failure, cardiogenic shock
  • Dysrhythmias
  • ↓ RBF
• Toxic/inflammatory injury to kidney cells that may be minimal or severe

• **Lethargy **
• Dry skin
• Drowsiness
• Headache
• Muscle twitching
• Seizures

• Renal sonogram: anatomic changes
• ↑ BUN, ↑ creatinine
• risk for hyperkalemia (& dysrhythmias)
• metabolic acidosis (Due to decreased renal excretion and HCO3)
• anemia (from decreased EPO)

It Is:

• Reduced effecitve arterial blood volume casuses renal hypoperfusion that occurs rapidly over a period of hours with ↑ BUN and plassma creatinine lvls.

Causes:

• Renal artery thrombosis
• Hypotension rlated to hypovolemia (dehydration, diarrhea, fluid shifts) or hemorrhage
• Renal vasoconstriction
• Kidney edema

Progression:

1. ↓ renal blood flow → hypoperfusion →
2. ↓ GFR →
3. ↑ Proximal tubule Na+ and H2O reabsorpton →
4. ↑ Aldosterone and ADH secretion →
5. ↑ Distal tubule Na+ and H2O reabsorption →
6. Oliguria

Manifestations:

• Oliguria (UO < 30 mL/hr, < 400 mL/24 hr)
• Hyperkalemia (K+ > 6.5 mEq/L)
• ↑ serum creatinine, ↑ BUN

Treatment:

• IV glucose & insulin (carries K+ intracellularly)
• IV NaHCO3- (shifts K+ intracellular for H+)
• dialysis/CRRT (clean out BUN & Creatinine)

1. Ischemia induced acute tubular necrosis
2. Nephrotoxic induced acute tubular necrosis

• It kidney failure caused by direct damage to the kidneys by inflammation, toxins, durgs, infection, or reduced blood supply
• Can be due to parenchymal damage to glomeruli or tubules
  
  • Prolonged renal ischemia from

◦Myoglobinuria (trauma)

◦Hemoglobinuria (transfusion reaction)
* Nephroxic agents

◦ aminoglycosides (gentamicin, tobramycin)

◦ radiopaque contrast

◦ heavy metals, chemicals

◦ NSAIDS, ACE inhibitors
* Infections (acute pyelonephritis, glomerulonephritis)

Antibiotics:

• Aminoglycosides (gentamicin & tobramycin)
• Amphotericin B
• Vancomycin
• MONITOR KIDNEY FUNCTION BEFORE GIVING DRUG

Other Drugs:

• NSAIDS
• Radiocontrast
  
  • prehydration with saline
  • admin of N-acetylcysteine + sodium bicarbonate

• It is a sudden obstruction of urine flow due to an enlarged prostate, kidney stones, bladder tumor, or injury
• Problems below the kidneys that result in increased pressure due to problems with urinary tract outflow:
• Urinary tract obstruction:
  
  • calculi (stones)
  • tumors
  • benign prostatic hyperplasia
  • Strictures
  • blood clots

1. Initiation
2. Oliguria-↑ in serum concentration of urea, creatinine, uric acid, potassium, magnesium
3. Diuresis-gradual ↑ in UO; watch for dehydration
4. Recovery

Monitor fluid & electrolyte status:

• Hyperkalemia!
• VFs-use smallest amt possible
• UO, daily weight, edema
• heart and lung sounds
• Breathing effort

Help reduce metabolic rate:

• Bed rest (so need help turning, coughing, deep breathing)
• Prevent/treat fever

Prevent infection:

• Invasive lines
• Catheters

Skin care:

• Dry and edematous skin – moisturize
• Tissue toxins – use measures to minimize itching
• RUB don’t scratch

It is:

• The progressive loss of renal function associated with systemic diseases

Causes:

• Diabetes mellitus (#1)
• Hypertension (#2)
• Systemic lupus erthematosus
• Intrinsic kidney disease
• Acute kidney injury

Progression:

1. Progressive kidney damage →
2. Loss of nephron mass → suriving nephrons to sustain kidney function →
3. Nephron hypertrophy and hyperfunction in their rates of filtration, reabsorption, and secretions →
4. Maintainance of solute and H2O regulatin in presence of ↓ GFR →
5. Until Kidney function < 25% →
6. Loss of nephrons → ↑ Angiotensin II
7. Destruction of the remaining glomeruli →
   
   1. ↓ erythropoietin → ↓ RBCs → Anemia
   2. Retention of urine → edema → Hypertension
   3. Retenion of blood, urea, creatinine, K+ & P (-3) → hyperkalemia & hypocalcemia → bone growth arrest
8. Capillary hypertension →
9. ↑ Glomerular permeability and filtration → proteinuria
10. ↑ Tubular protein reabsorption →
11. Tubulointerstitial inflammation & fibrosis →
12. Renal scarring

• ↓GFR & creatinine clearance
• ↑serum creatinine & BUN
  • serum creatinine-more sensitive indicator of renal function than BUN
• Sodium & water retention
• Metabolic acidosis
• Anemia
• ↓calcium & ↑ phosphorus

Medications:

• Calcium & phosphorus binders
• Antihypertensive & cardiovascular agents
• Antiseizure agents
• Erythropoietin (Epogen)
• Give all of these meds with food

Diet:

• protein restriction; allowed protein must be of high biologic value (e.g., dairy, eggs, meats)
• fluid restriction-500-600 ml/day more than previous day’s UO
• carbs, fats, vitamin supplements
• monitor potassium intake

**Dialysis **

It Is:

• An infection of one or both upper urinary tracts, that is the ureter, renal pelvis, and kidney interstitium
• Common in young adult women

Most common causes:

1. Urinary obstruction
2. Reflux of urine from the bladder (vesicouretral reflux)

• Problem occurs from: E. Coli, Proteus, Pseudomonas (from urethral instrumentation or urinary tract surgery)

Progression:

1. Microorganisms spread by ascending uropathic ureters →
2. Infection →
3. Local Inflammation (affects the pelvis, calyces, and medulla) →
4. Medullary infiltration of WBCs →
5. Renal edema → Purulent urine
6. Healing → scar tissue → fibrosis → atrophy of affected tubules

DOES NOT USUALLY EFFECT THE GLOMERULUS

Manifestations:

• Acute fever, chills, and flank/groin pain (similar to UTI)
• Polyuria
• N/V
• leukocytosis, WBC casts
• Frequecy, dysuria (pain when peeing), CVA tenderness, may precede systemic signs and symptoms

Diagnostics:

• CT or US - to locate obstructions in the urinary tract
• IV pyelogram - to identify functional or structural renal abnormalities
• Urine C&S to identify causative organisms
  
  • Two weeks after antibiotic tx completed, urine is re-cultured, then monthly for several months

Treatment:

• Antibiotics (for 2 weeks) and hydration

1. Kidney stones - Obstruction and statis of urine contributing to bacteriuria nad hydronephrosis, irritation off epithelial linning with entrapement of bacteria
2. Vesicouretral reflux - Chronic reflux of urine up the ureter and into the kidney during micturition contributing to bacterial infection
3. Pregnancy - Dialation and relaxation of ureter with hydroureter and hydronephrosis, partly caused by obstrution from enlarged uterus and partly from ureteral relaxation caused by higher progesterone levels
4. Neurogenic bladder - Neurologic impariment interfering with normal baldder and urethral sphincter contraction with residual urine and ascending infection
5. Instrumentation - Intoduction of organisms into urethra nad bladder by catheters and endoscopes introduced into the urinary tracy for diagnositc purposes
6. Femal sexual trauma - Movement of organisms from the urethra into the bladder with infection and retrograde spread to kidney.

It Is:

• Persistent or recurrent infection of one or both kidneys leading to scarring, which can leadto kidney failure.

Causes:

• Idiopathic
• May be associated with vesicoureteral reflux or renal stones.
• Drug toxicity (NSAID’s)
• Ischemia
• Immunecomplex diseases

Progression:

1. Urinary tract obstruction (kidney stones) or Vesicoureteral reflux →
2. Presistent infections →
3. Progressive inflammation in interstitial spaces between tubules→
4. Alterations of the renal pelvis and calyces →
5. Destruction of the tubules, atrophy or dilation and diffuse scarring →
6. impaired urine concentrating ability →
7. Chronic kidney failure →
8. Inability to conserve sodium → hyperkalemia → metabolic acidosis

• no symptoms of infection unless acute exacerbation
• fatigue
• headache
• poor appetite
• polyuria
• excessive thirst
• weight loss

Persistent, recurring infection can produce scarring of kidneys leading to renal failure

Diagnostics:

• IV urogram
• BUN and Creatinine levels
• Creatinine clearance

Complications:

• End-stage renal disease (ESRD)
• Hypertension
• Formation of kidney stones

Treatment:

• Long-term prophylactic antimicrobial therapy
• Forced fluids, antipyretics, antibiotics, bedrest

It is:

• The formation of kidney stones
• Formation not clearly understood; dehydration?

S/S:

• No symptoms vs. excruciating pain
• Hematuria, pyuria, N/V/D
• Confirmed by KUB or US

Medications / treatment:

• Opioid analgesics & NSAIDs; hydration
• Procedures for stone removal + stent

Nursing interventions:

• Encourage ambulation; strain urine
• Have the Pt report ↓UO, bloody/cloudy urine, fever, pain

• Risk for Fluid Volume Deficit
• Acute pain
• Ineffective Renal Tissue Perfusion
• Impaired Urinary Elimination
• Hyperthermia

• Hemodialysis
• Continuous renal replacement therapy (CRRT)
• Peritoneal dialysis

• It is the removal of waste products such as creatinine and urea and free water from the blood, and can be short or long term
• Chronic hemodialysis
  • 3X/week for 3-4 hours as outpatient
  • home hemodialysis

• Hemodialysis (HD) goal: toxic nitrogenous substance removal from blood + H2O removal
• HD based on principles of diffusion, osmosis, and ultrafiltration

• heart failure, CHD, angina, stroke, PVD
• anemia
• gastric ulcers, nausea/vomiting, malnutrition
• bone pain & fractures
• HTN, hypotension
• itching
• sleep disturbances
• SOB
• Muscle cramping

Dialyzer-artificial kidney (replaces glomeruli & tubules)

• Diffusion & osmosis occur as waste products move from an area of higher concentration (blood stream) to an area of lesser concentration (dialysate fluid) through a semipermeable membrane (peritoneum)
• Dialysate should be warmed via dry heat- heating cabinet, incubator, or heating pad
• Exchange-infusion, dwell, & drainage of dialysate

Peritonitis:

• most common & most serious complication of PD
• first sign-cloudy dialysate drainage; abdominal pain & rebound tenderness occur much later
• hypotension

Leakage:

• of the dialysate through catheter site
• avoid by use of small dialysate volumes

Bleeding:

• bloody effluent (drainage) may be seen w/ menstruating women
• expected after newly inserted catheters

Protect vascular access:

• Check patency-bruit or thrill
• No BPs on vascular access extremity
• Take precautions w/ IV therapy: slow, minimal

Detect cardiac & respiratory complications:

• fluid overload, HF, pulm edema→crackles
• pericarditis→chest pain, low-grade fever, frict rub

Control electrolyte levels:

• monitor daily labs
• blood transfusions during HD

Manage discomfort & pain:

• itching-antihistamine (diphenhydramine/Benadryl)
• pain-analgesics

Monitor BP:

• HTN common b/c of fluid overload + renin oversecretion
• withhold daily antihypertensives until after dialysis

Prevent infection:

• ESRD pts have low WBCs, low RBCs, & impaired plt func
• wash hands

Care for catheter site:

• Do not submerge PD catheter in water
• Catheter site care w/ soap & water-during showering

Watch out for nephrotoxic meds

Avoid meds with potassium & magnesium

• Acts on ascending loop of Henle to block reabsorption of Na+ and Cl-
• This also inhibits potassium recycling = ↓ in potassium
• Loss of volume
• Relaxation of venous smooth muscle

• ↓ Pulmonary edema r/t congestive heart failure (CHF)
• Edematous states – of hepatic, cardiac, or renal origin that has been unresponsive to other diuretics
• ↓ Hypertension not controlled by other diuretics – but can add a thiazide diuretic (no benefit to combining furosemide with another high-ceiling/loop agent)

• Hyponatremia
• hypochloremia
• Hypocalcemia
• hypomagnesemia
• dehydration
• Hypokalemia
  
  • If serum K+ falls below 3.5 mEq/L tx with K supplements or use K-sparing diuretic
• Hypotension
• Ototoxicity
• Hyperglycemia
• Hyperruricemia (a lot of peeing)

• Digoxin [hypokalemia from loops produces ↑ risk of dig-induced toxicity (ventricular dysrhythmias)
• Ototoxic drugs
• Lithium – in general, diuretics result in decreased renal lithium clearance = ↓ lithium excretion, so it can accumulate to toxic levels in the blood
• Antihypertensive agents – lower BP already, now add loss of fluid volume and relaxation of venous smooth muscle
• NSAIDs (Nonsteroidal anti-inflammatory drugs) – *blunts efx of furosemide

• Increase renal excretion of sodium, chloride, potassium, and water
• Elevate levels of uric acid and glucose
• Promote renal calcium retention
• Loss of volume
• Relaxation of venous smooth muscle

early segment of the distal convoluted tubule

• To treat essential hypertension – 1st line choice for most people
• To treat edema – preferred drug for mild to moderate HF and hepatic & renal edema
• To treat diabetes insipidus – don’t know how it works
• May protect from post menopausal osteoporosis

• Hyponatremia
• Hypokalemia
  
  • If serum K+ falls below 3.5 mEq/L tx with K supplements (or eating K rich foods) or use K-sparing diuretic
• Hypomagnesemia
• hypochloremia
• dehydration
• Promotes renal calcium retention
• NO OTOTOXICITY
• Hyperuricemia
• Hyperglycemia
  
  • usually only in DM pts…who may need larger doses of insulin or oral hypoglycemic drug
• Impact on lipids - ↑ LDL, cholesterol, total cholesterol & trigs

• Digoxin - If combined will further lower K+ lvls
• NSAIDs may blunt diuretic effect
• Lithium supplements - If combined can increase lithium levels due to retained lithium in kidneys
• Can be combined with ototoxic agents without increased risk of hearing loss

• Aldosterone antagonist (blocker)
  
  • Spironolactone
• Nonaldosterone antagonists (blockers)
  
  • Triamterene
  • Amiloride

• Blocks aldosterone in the distal nephron
• Retention of potassium
  
  • (hyperkalemia >5 mEq/L – mostly if used alone)
  • Increased excretion of sodium & passive loss of water
• Slows myocardial remodeling & fibrosis
• Reduces Baroreceptor activation
• ​gynecomastia in men

**NOTE: this is a Aldosterone antagonist **

• Pts w/ with Hypertension – ↓ BP
• Pts w/ with Edematous states – ↓ BP
• Pts w/ Heart failure – decreases mortality in severe failure
• Pts w/ primary hyperaldosteronism – blocks aldosterone from being formed
• **Potent antagonist of the androgen (testosterone) receptor as well as an inhibitor of androgen production **

• Hyperkalemia – possible fatal dysrhythmias; cell uptake of insulin could ↓ K+ levels by K+ uptake into cells
• Endocrine effects – gynecomastia, menstrual irregularities, impotence, hirsutism, & deepening of the voice

• Thiazide and loop diuretics – counteract K-wasting
• Agents that raise potassium levels (because this drug ↑ K+ lvls), such as:
  
  • K supplements
  • Salt substitutes (KCl)
  • Or other K-sparing diuretic
  • ACE-inhibitors
  • ARBs
  • Direct renin inhibitors

• Block actions/access* of angiotensin II
• Cause dilation of arterioles and veins
• Prevent angiotensin II from inducing pathologic changes in cardiac structure
• Decrease release of aldosterone:
  
  • ↑ renal excretion of Na & water
  • Hyperkalemia – K retention (more from ARBs than ACE-I)
• Increase renal excretion of sodium and water
• Do not increase levels of bradykinin (no blocking of enzyme)
  
  • no cough

• Hypertension, heart failure, myocardial infarction, stoke & death
  
  • improves LV ejection fraction, reduce HF symptoms, increase exercise tolerance
  • ↓ bradykinin lvls – no cough
• Diabetic nephropathy - mitigates progression
• If unable to tolerate ACE inhibitors: protection against MI, stroke, and death from cardiovascular (CV) causes in high-risk patients
• Migraine headache – prophylactically (candesartan)
• Slowed development of diabetic retinopathy (losartan)

• Polyuria (increased production of urine) & polydipsia (increased thirst)
• Low urine specific gravity ( less than 1.010)
• Low urine osmolality (less than 200mOsm/kg)
• Hypernatremia
• High serum osmolality (greater than 300mOsm/kg)
• Continued diuresis diuresis despite serum sodium levels greater than 145

Normal range is between 0.6-1.2 mg/dL

• Creatine clerance is a natural substance produced by muscle breakdown and is released into the blood at a relatively constant rate
• It is freely filtered at the glomerulus and is not reabsorbed by the renal tubules
• Creatine clerance overestimates the GFR but it is within tolerable limits, therefore creatine clerance provides a good estimate of GFR.
• As renal function declines, creatinine clearance decreases
  *

• BUN is the concentration of urea nitrogen in the blood, and it reflects the GFR and urine-concentrating capacity
• Because urea is filtered at the glomerulus, BUN lvls ↑, when GFR ↓
• Dehydration &/ acute/chronic renal failure → ↑ BUN lvls
• Normal range is 10-20 mg/dl
• BUN is affered by altered protein intake and protein catabolism and is a poor measure of GFR

• Arteriovenous fistula (AVF) is preferred for perm access
• in a fistula you want to hear a bruit, feel the thrill
• Complications: Watch out for hypovolemia, hypotension,

• Slowly progressive disease of airflow obstruction, associated with an abnormal inflammatory response of the lungs that is not completely reversible
• Includes emphysema and chronic bronchitis
• Preventable and treatable, but difficult to reverse damage

Usually due to:

1. Inflammation of airway
2. Parenchyma damage
3. Decrease of elastic recoil

• Chronic bronchitis- mucus production & persistent cough
• Emphysema- Over distention of air spaces & alveolar walls destroyed
• May have one or combination

Asthma is considered a distinct, separate disorder, not a type of COPD.

Primary symptoms:

• Cough
• Sputum production
• Dyspnea

Additional symptoms:

• Wheezing and crackles
• Weight loss
• Pale to cyanotic
• Barrel chest (emphysema)
• Use of accessory muscles
• Prolonged expiration
• Orthopnea
• Cardiac dysrhythmias
• Congestion and hyperinflation on CXR
• Polycythemia
• Hypoxemia

• Occurs when the Hct in the blood is above reference range values
• With COPD there is an increase in RBC from chronic low O2 levels
• Polycythemia indicates a disease or disorder

• —Respiratory failure
• —Pulmonary hypertension with consequent heart failure
• —Cor Pulmonale, one of the complications of emphysema, is right-sided heart failure brought on by pulmonary hypertension.
  
  • Monitor heart failure – BP/HR, BNP, Lung sounds, edema, CXR, EF
• —Pneumothorax
• —Infection
• —Other comorbidities related to smoking and aging which include ischemic heart disease and lung cancer

• —Defined as an acute worsening of symptoms characterized by increased dyspnea, mucous production, hyperinflation and air trapping which may be triggered by infection or environmental pollutants
• —Mortality increases as the frequency of exacerbations occur.
• They can be caused by medicine noncompliance

• —Advancing age - strong predictive risk factor of COPDE
• —Pulmonary secretion clearance is reduced with age which puts the patient at increased risk for infection
• —Declines in immunity may also be partially responsible

• —Spirometry
• —Chest X-ray: increased bronchovascular markings
• —Sputum sample for culture and sensitivity
• —ABGs: respiratory acidosis
• —CBC: increased RBCs
• —Pulmonary Function Tests: decreased forced expiration, decreased vital capacity
• —EKG

• Breath sounds/ capillary refill & skin color / hydration status, sputum
• Pulse oximetry/ABG
• Spirometry (FEV not accurate in COPDE)
• Labs - ABG’s CBC, Chemistry panels
• Cardiac status as needed
• Other physical symptoms (see complications)
• Holistic assessment: physical, psychosocial, cognitive, spiritual

Ineffective airway clearance related to:

• — bronchoconstriction
• — increased sputum production
• — ineffective cough
• — fatigue/ lack of energy
• — bronchopulmonary infection

Ineffective breathing pattern related to:

• — shortness of breath
• — mucus
• — bronchoconstriction
• airway irritants

—Impaired gas exchange r/t

• Ventilation perfusion inequality

—Activity intolerance r/t

• Imbalance between oxygen supply with demand

—Imbalanced Nutrition: less than body requirements r/t

• Anorexia

—Disturbed sleep pattern r/t

• Discomfort
• Sleeping position

—Self-care deficit (hygiene) r/t

• Fatigue secondary to inc. respiratory effort & ventilation & oxygenation insufficiency

• Fowler’s; forward-leaning positions
• O2 as ordered (supplemental O2 to mechanical ventilation)
  
  • If give too much O2, then O2 suppresses the hypoxic drive to breathe. The hypoxia is the stimulus to breathe
• Pulse oximetry / ABGs / cardiac monitor as needed
• Respiratory therapy (breathing treatments)
• Start IV/ give meds as ordered (bronchodilators, antibiotics, steroids, anxiolytics, antidepressants)
• Nicotine patch
• Decrease patient’s anxiety- psychosocial support

• Quit smoking
• Supplemental oxygen, ventilator support, walker, wheelchair, nebulizer
• Home Health/SNF
• —Meds/Inhalers/Nebs - bronchodilators, antibiotics, steroids, anxiolytics, antidepressants
• —Pulmonary Rehab - maintaining functional ability
• Fall prevention
• Prevent respiratory infections
• Proper nutrition to prevent muscle wasting
• Crucial to prevent exacerbations
• May need:
  
  • Lung Transplantation
  • Lung volume reduction surgery

• Defined as the presence of cough and sputum (with no other known cause) for at least 2 months in each of two consecutive years.
• It is caused by Inflammation of the airways due to irritants (smoking, bacteria, virus…) and results in increase mucous production (d/t increase in number of goblet cells)
  
  • Mucous plugging results in reduction of ciliary function, thickened bronchial walls (narrowing), alveolar damage and fibrosis.
  • Patient becomes more susceptible to infection, exacerbations are more likely during the winter when viral and bacterial infections more prevalent.

• Cyanotic apperance
• Recurrent cough & sputum production
• Hypoxia
• Hypercapnia
• Acidosis
• Edematous
• Increased RR
• Exertional dyspnea
• Cor Pulmonale
• Use of accessory muscles to breathe

Impairment of O2 and CO2 exchange results from destruction of walls of over distended alveoli which leads to:

• O2 unable to diffuse through capillaries
• Permanent over inflation of alveoli
• Increased airway resistance
• Loss of elastic recoil
• Dead space: lung area where no gas exchange can occur and impaired oxygen diffusion à hypoxemia
• Impaired elimination of CO2àhypercapnia, respiratory acidosis
• Increased anterioposterior diameter increases: barrel chest; air gets in, but cannot get out.

• ↑ CO2 retention (this leads to the pink apperance)
• Minimal cyanosis
• Purse lip breathing
• Dyspnea
• Hyperresonance on cheast percussion
• Orthopenic
• Barrel chest
• Exertional dyspnea
• Prolonged expiratory time
• Speaks in short jerky sentences
• Anxious
• Use of accessory muscles to breathe
• Thin apperance

It is a reversible chronic inflammatory disease of the airways that causes airway hyperresponsiveness, mucosal edema, and and mucus production.

Causes:

• Triggers; genetic component: +25 genes associated with asthma
• Respiratory infections and colds
• Cigarette smoke; 2nd hand smoke
• Allergens such as pollen, mold, animal dander, feathers, dust, food & co*ckroaches
• Exercise
• Exposure to cold air or sudden temperature change
• Odors and fumes
• Excitement or stress

• Diffuse airway inflammation and narrowing
• Bronchoconstriction of smooth muscles
• Increased vascular permeability
• Increased mucous gland secretion
• Increased airway resistance from spasm
• Increased lung compliance
• Impaired mucociliary function
• Altered gas exchange: respiratory acidosis

1. Allergens/triggers →
2. production of IgE →
3. IgE attach to mast cells and basophils →
4. Activates release of histamine, bradykinin, prostanoids, cytokines, leukotrienes →
5. Swelling, airway constriction

Airway “remodeling” may occur in response to chronic inflammation, causing further airway narrowing.

• —Dyspnea, breathlessness, chest tightness, cough
• —Wheezing (inspiratory and/or expiratory)
• —Increased P, R, BP; Pallor
• —Anxiety, restlessness
• —Use of accessory muscles, nasal flaring, retractions
• If uncorrected leads to status asthmaticus: s/s continue despite treatment à air trapping & V/Q mismatch à respiratory distress, cyanosis

1. Frequent cough, especially at night
2. Losing your breath easily or shortness of breath
3. Feeling very tired or weak when exercising
4. Wheezing or coughing after excercise
5. Feeling tired, easily upset, grouchy, or moody
6. Decreases or changes in lung function as measured on a peak flow meter
7. Signs of a cold or allergies
8. Trouble sleeping

1. ‘STEP’ therapy for asthma (see link in previous slide)
2. Know the triggers for asthma & chronic bronchitis
3. Do not delay professional treatment for any breathing problems; controlled breathing techniques
4. Staying hydrated (follow any fluid restrictions if have heart disease); take meds as prescribed
5. Know home equipment- peak flow meter, O2, spacer, & inhalers

• It is a Medical emergency, which has a sudden or gradual onset, and is not responsive to usual therapy.
• Triggered by viral infection, stress, D/C meds, etc.

Leads to:

• Severe bronchospasms/air trapping
• Hypoxemia
• Expiratory flow/volume decrease
• Fatigue
• Respiratory failure

• Absence of a wheeze is called a “silent chest” and is an emergency
• Hyperinflated chest
• Hypoxemia
• Hypocapnia initially, followed by hypercapnia
• Marked respiratory distress
• Marked wheezing
• Use of accessory muscles
• Extreme anxiety
• Fear of suffocation
• Diaphoresis
• Tachycardia

Correct hypoxemia to achieve PaO2 > 60 - may require intubation

This will require the use of:

• β-adrenergic agonist nebulizer
• Arterial line placement
• IV corticosteroids
• IV mag sulfate

• Subjective data, if appropriate; brief history
• Breath sounds/ capillary refill & skin color / hydration status
• Pulse oximetry/ ABGs
• Cardiac status, as needed
• Other physical symptoms (see manifestations)
• Holistic assessment: physical, psychosocial, cognitive, spiritual

• —Ineffective airway clearance
• —Anxiety
• —Impaired gas exchange
• —Ineffective breathing pattern
• —Ineffective therapeutic regimen
• —Imbalance nutrition: less than body requirements
• —Disturbed sleep pattern
• —Risk for infection/actual infection
• —Decrease cardiac output
• —Activity intolerance

• Fowler’s; forward-leaning positions
• O2 as ordered; usually cannula at first
• Pulse oximetry / ABGs / cardiac monitor as needed
• Respiratory therapy (breathing treatments)
• Start IV/ give meds as ordered
• Decrease patient’s anxiety / work with family

• Acute inflammation of lung parenchyma caused by various microorganisms, including bacteria, mycobacteria, fungi, and viruses.
• The edema associated with inflammation stiffens the lung, decreases lung compliance, and vital capacity, and causes hypoxemia.

• Community-acquired (CAP)
  
  • Steptococcus, Mycoplasma, Haemophilus influenzae
  • Occurs within < 48 hours of admission
• Healthcare-associated (HCAP)
  
  • Often multi-drug resistant organisms
  • Occurs within > 48 hours of admission
• Hospital-acquired (HAP)
  
  • Enterobacter, E.Coli, H.influenzae, Klebsiella, Pseudomonas
  • Occurs within > 48 hours of admission
• Ventilator-associated (VAP)
  
  • Subtype of HAP; most common infection seen in the ICU
• Immuno-compromised
  
  • Pneumocystis pneumonia (PCP), fungal, and mycobacterium tuberculosis
• Aspiration

• Older adult
• Immobility
• Chronicity/ decreased immune system
• Exposure to foreign materials
• Nosocomial factors (tracheal intubation, feeding techniques)
• Not following health professionals’ advice (hand washing, vaccines, immediate attention for meds)

• —Dry or wet cough
• —Tired, body aches
• —Fever, chills
• —Short of breath
• —Wheezes, rhonchi
• —Chest pain
• —Tachycardia
• —Dyspnea, Syncope, cyanosis
• —Older patients: Mild fever, confusion and/or tachypnea might be the only sign

• Establish adequate ventilation/ perfusion
• Empiric antibiotics; Treat the organism based on sputum C & S
• Bronchodilators
• Antipyretics
• Analgesics
• Nutrition, hydration, pulmonary hygiene
• Patient teaching & concept of prevention (hand washing)

**—Vital signs: **

• respiratory rate, pulse oximetry, temperature, cyanosis, lung sounds - wheezing, rales or diminished breath sounds

—Sputum color, amount, consistency

—Assess for exposure of tuberculosis

• Encourage coughing and deep breathing and use of incentive spirometer
• Change pts. position frequently and ambulate to mobilize secretions
• Semi-Fowler’s position to facilitate lung expansion
• Nasotracheal suction if pt. unable to clear secretions
• Encourage fluids, unless contraindicated
• Provide balance of rest and activity
• Provide CPT
• Health Promotion
  
  • Prevention
  • Immunizations: Pneumococcal

Ineffective Airway Clearance

a. Assess resp status, SpO2, VS, breath sounds, skin color
b. Assess cough & sputum
c. Monitor ABGs, as ordered; report abnormal values
d. Position in Fowler’s/high-Fowler’s
e. Assist with C & DB
f. Provide fluids
g. Assist with chest physiotherapy
h. Administer medications/assess effectiveness

Ineffective Breathing Pattern

a. Provide for rest
b. Assess for pain/provide analgesia
c. Administer O2 as ordered.

Activity Intolerance

a. Assess effect of activity
b. Assist with ADLs
c. Schedule activities/rest
d. Provide emotional support/encourage family presence & help

• —Oxygen assessment documentation
• —Blood culture before 1st antibiotic
• —Initial antibiotic within 6 hours of triage time
• —Appropriate antibiotics given
• —Influenza/Pneumococcal vaccination given/or documented
• —Documentation of smoking cessation
• —Nicoderm patch if patient refuses to quit smoking

• Acute viral infection of respiratory tract; highly contagious
• Different viral strains, usually known as types A, B, and C
• Symptoms: acute onset of myalgia, fever, cough, sore throat, head aches, and can progress to pneumonia symptoms (esp in older adult)
• Patients are contagious 1 day before symptoms start and 7 days after they start

• Diagnosis early to receive anti-viral medication: need to be given within 48 hours of intial symptoms for effectiveness
• Treatment targeted at symptom relief: antipyretics and antitussives
• Rest, hydration, nutrition
• Prevent pneumonia
• Teaching: hand washing, avoid crowds, annual influenza vaccination

• Highly communicable disease caused by Mycobacterium tuberculosis
• M. tuberculosis is an aerobic bacterium, primarily affecting the pulmonary system, especially the upper lobes where oxygen content is highest.
  
  • Granulomas develop in the lung tissue
• It can also affect other areas of the body, such as brain, intestines, peritoneum, kidney, joints, and liver.
• Major public health concern- globally, every second someone infected

• Spread by droplet nuclei
• Microorganisms usually lodge in upper lobe
• Multiply & cause inflammation
• Can migrate through lymph system
• Tubercle= granulomatous lesion
• Bacilli in tubercles can be dormant or become active
• Compromised immune system or live bacilli can spread through to other organs

1. Infectiousness of person
2. —Environment of exposure
3. Duration of exposure
4. —Virulence of organism:

• —Multidrug-resistant (MDR-TB)
• —Extensively (CDC) drug-resistant (XDR-TB); “extreme”- lay term

• Foreign-born: e.g., Asia, Africa, Russia
• Close contacts: same living environment
• Health care workers: high-risk patients
• Substance abusers: e.g., injection/ inhalation
• Other high-risk populations: e.g., homeless persons, migrant farm workers, prisoners
• Immunocompromised individuals ie. HIV/AIDS, diabetes mellitus, cancer
• International travelers

• —Cough for several weeks
• —Fever for more than a week
• —Night sweats
• —Weight loss
• —Weakness
• —Chest pain/pleurisy
• —Coughing up blood
• —Fatigue
• Anorexia

• Mantoux test: simple skin test
• QuantiFERON-TB Gold (OFT): blood test
• Direct microscopic exam of sputum: acid-fast bacilli (AFB)
• Radiographic evidence: CXR
• Culture of specimens
• History & clinical findings

• —Nursing care plan: education/ prevention
• Directly Observed Therapy Strategy (DOTS)
• Drug therapy
• Monitoring of drug therapy
• Notify MD of side effects
• BCG vaccine – efficacy questioned

• Airborne infection: coughing, sneezing
• Droplet nuclei- 3 feet; family members
• Classic symptoms
• Encourage health care & compliance-incentives
• Medication side effects – jaundice, bleeding, N/V, aches/pains (monitor LFTs)
• Social support; social stigma- Holistic approach
• Mandatory reporting

• Treatment of identified lesions depends on whether the patient has active disease or hs only be exposed to the disease
• Treatment is difficult because the bacterium has a waxy substance on the capsule that makes penetration and destruction difficult
• Multidrug regimen most effective to destroy organism quickly and minimize drug-resistant
• Individuals with active TB are treated for 6-9 months; HIV patients treated for longer period
• After 2-3 weeks of treatment, the risk of transmission is greatly reduced
• Individuals exposed to active TB are treated with preventative Isoniazid for 9 to 12 months

• Importance of teaching:
• Side effects
• ETOH intake
• Drug interactions
• Routine monitoring: e.g., kidneys, liver, eye exams
• Use in pregnancy
• Encourage relationship with practitioner

• Isoniazid
• Rifampin
• Ethambutol
• Pyrazinamide
• Rifabutin
• Rifapentine

Many TB meds can cause toxic effects such as hepatotoxicity, nephrotoxicity, neurotoxicity, optic neuritis, or ototoxicity. Teach the client about the signs of toxicity and to notify HCP if signs arise.

• —Second-line Agents
• —Used in combo with 1st line meds; more toxic
  
  • Amikacin
  • Cipro, Levofloxacin
  • Cycloserine
  • Capreomycin sulfate
  • Streptomycin

Many TB meds can cause toxic effects such as hepatotoxicity, nephrotoxicity, neurotoxicity, optic neuritis, or ototoxicity. Teach the client about the signs of toxicity and to notify HCP if signs arise.

• Be educated
• Independent actions- ISOLATION & infection control nurse
• Use *Negative air-flow rooms/HEPA filters *
• Be aware: coughing, risk factors, read chart
• Wash your hands- always for any infection control!
• Call the practitioner if patient has symptoms

• Patients taught to cover their mouth & nose when coughing, using a tissue.
• Private room with air exchange - air exchange at least 6 times per hour and two of the exchanges being fresh air from outside. Air exhausted to the outside.
• When patient leaves their room, must wear a particulate respirator (PR) mask.
• Air pressure in patient’s room, must be negative.
• High-energy particulate air (HEPA) filters in rooms.
• Ultraviolet lights.
• 3 consecutive negative smears for TB, patient does not have to wear a mask.
• HCWs using PR mask - refitted annually.
• HCWs tested annually with PPD.
• If exposed to TB, then have PPD 8 to 12 weeks after exposure.
• If work in area where exposure is possible (ie, tracheal suctioning or bronchoscopy) - then have PPD every 6 months. Determined by CDC.
• If convert from negative PPD status to positive, must have exam to rule out active TB. Consider INH therapy or annual CXR.

• Air accumulation in pleural space
  
  • Rupture of visceral or parietal pleura
  • Air destroys negative pressure; lung collapses
• Can be Spontaneous
  
  • Rupture of bleb

Types of pnuemothorax include:

1. traumatic
2. tension
3. simple

• Depend on size & cause
• Sudden pleural pain
• Tachypnea, tachycardia
• Increased oxygen demand
• Dyspnea (degree depends on size)
• Absent or decreased breath sounds affected side
• Air movement thru open wound (open pneumothorax)
• Subcutaneous emphysema
• Confirmed by CXR

• Oxygen therapy
• Vented dressing (stabilize impaled object) with open pneumothorax
• Chest tube insertion
• Surgical intervention

Physical assessment:

• Degree of respiratory distress
• Evidence of chest trauma
• Vital signs
• SpO2
• Skin color
• LOC
• Breath sounds & respiratory excursion
• Position of trachea
• Neck vein distention

Impaired gas exchange, Ineffective breathing pattern, Ineffective airway clearance:

• Maintain open airway
• Assess VS, Breath sounds, SpO2 (q4hrs)
• Position in Fowler’s or semi-Fowler’s
• Administer oxygen/assess effectiveness
• Administer analgesia/assess effectiveness
• Maintain/monitor chest tube function (q2hrs)
• Provide for adequate rest
• Increase patient mobility (once stabilized)

Decreased cardiac output (tension pneumothorax, hemothorax):

• Monitor VS
• Administer fluids (crystalloids, colloids)
• Monitor I&O
• Monitor H&H, RBCs, platelets

Risk for infection:

• Chest tube care/site care
• Wound care (open pneumothorax)
• Monitor/interpret labs
• Monitor VS
• Administer antibiotics

• Fractured rib (blunt trauma)
  
  • Closed pneumothorax
• Open (penetrating trauma)
• Sucking chest wound
• Iatrogenic (central line, thoracentesis, mechanical ventilation)—

Site of the pleural rupture acts as one-way valve:

• Air enters on inspiration
• Air does not escape during expiration
• More & more air enters pleural space
• Pressure builds & compresses lung tissue & mediastinum (heart & great vessels)

Clinical Manifestations:

• Severe dyspnea/hypoxemia
• Hypotension
• Absent breath sounds affected side
• Tracheal deviation
• Neck vein distention

Collaborative Care-Emergency Situation:

• Oxygen
• Needle thoracotomy/Chest tube insertion
• Monitor EKG, VS
• Possible intubation

Accumulation of blood in intrapleural space caused by:

• Blunt/penetrating trauma
• Rib fractures
• Lung parenchymal (pulmonary contusion)

Clinical Manifestations:

• Decreased/absent breath sounds
• Decreased chest expansion
• Decreased percussion noted

—Refers to the extravasation of fluid from the pulmonary vasculature into the interstitium & alveoli of the lung

—Causes:

• Increased capillary hydrostatic pressure
• Increased capillary permeability
• Decreased oncotic pressure
• Lymphatic obstruction

—Stage I – fluid transfer is increased into the lung interstitium because lymphatic flow increases

—

—Stage 2 – The capacity of the lymphatics to drain excess fluid is overwhelmed and fluid begins to accumulate in the interstitial space that surrounds the bronchioles & lung vasculature

—

—Stage 3 – as fluid continues to build up, increased pressure causes it to track into the interstitial space around the alveoli & disruption to the alveolar membrane occurs. Gas exchange becomes impaired

• —Infectious pulmonary edema (viral or bacterial)
• —Inhaled toxins
• —Circulating toxins
• —Vasoactive substances (histamine, kinins)
• —Disseminated intravascular coagulation
• —Immunologic reactions
• —Radiation pneumonia
• —Uremia
• —Near-drowning
• —Aspiration pneumonia
• —Smoke inhalation
• —ARDS

—Can develop slowly or acutely

—Early signs:

• Shortness of breath on exertion
• Sudden respiratory distress after sleep
• Difficulty breathing unless sitting upright
• Cough

• Labored & rapid breathing (leads to respiratory alkalosis)
• Frothy or bloody sputum
• Tachycardia
• Cardiac arrhythmias
• Cold, clammy, sweaty, bluish skin
• Decreased blood pressure
• Thready pulse
• Anxiety
• Pulse oximetry is commonly less than 85% & arterial Po2 of 30-50 mmHG

—Medical treatment:

• Find and treat underlying cause
• O2 via nasal cannula or mask
• Intubation & mechanical ventilation maybe necessary
• Furosemide (Lasix) – increases urine output and works quickly to remove excess fluid from the body
• Morphine – decreases anxiety & work load of breathing
• Dobutamine – dilates the peripheral vessels to decrease the work load of left ventricle
• Aspirin - helps decrease blood viscosity for easy delivery

• Identify type of artificial airway or supplemental oxygen
• Check respirations for rate, depth, rhythm, symmetry, accessory muscle use
• Sputum – if present, note color, consistency, & odor of sputum
  
  • Pink Frothy is usually noted with pulmonary edema
• Auscultate breath sounds for equality and/or adventitious breath sounds (would hear crackles)

• Monitor for symptoms of heart failure/decreased cardiac output
• Monitor vital signs
• Observe for confusion, restlessness, agitation
• Monitor for chest pain, discomfort (note severity, radiation, and duration)
• Cardiac monitor for dysrhythmias
• Monitor I & O
• Note results of EKG, chest x-ray, & other diagnostic exams
• —Monitor lab work such as ABGs, CBC, electrolytes
• —Place patient in semi-Fowlers of upright position
• —Activity/rest balance
• —Diet sodium restricted, low cholesterol, limit caffeine
• —Serve smaller more frequent meals
• —Monitor bowel and bladder function
• —Minimize environmental stimuli
• —Daily weights
• —Refer appropriately (heart failure programs, cardiac rehab., support groups)

• s/s of heart failure
• Importance of smoking cessation/ avoidance of alcohol
• Stress reduction
• Diet restrictions
• Assist patient to understand need for lifestyle changes
• Side effects of medications
• Early reporting of SOB or other respiratory difficulty
• Provide specific self-care & disease process information to patient prior to discharge

It is a collection of fluid in pleural space:

• vSource: blood vessels or lymphatics; lesions
• Fluids compress lung tissue (atelectasis occurs)
• Lung does not collapse

Types:

• Transudative: watery; low in protein
• Exudative: high amount of WBCs & proteins

Clinical Manifestations:

• Dyspnea
• Pleuritic pain
• Dullness to percussion, decrease breath sounds (hyperressonance)
• CXR

Collaborative Care:

• Treat underlying cause
• Thoracentesis

• —Dyspnea with activity and/or rest
• —Tachycardia, dysrhythmias, S3 heart sound, hypo or hypertension
• —Fear, anxiety
• —Pain aggravated by inspiration, possibility of spread to neck, shoulders, abdomen
• —Tachypnea, use of accessory muscles in chest, intercostal retraction, decreased breath sounds, decreased fremitus (effected side
• —Skin – pale, cyanosis, sweating

—Transudative effusions usually form as a result of excess capillary fluid leakage into the pleural space, and can be caused by:

• Congestive heart failure
• Nephrotic syndrome
• Cirrhosis of liver
• Pulmonary embolism
• Hypothyroidism

—Exudative effusions are often more serious than transudative effusions. They are formed as a result of inflammation of the pleura caused by:

• —Pneumonia
• —Lung Cancer; other cancers
• —Connective tissue diseases
• —Pulmonary embolism
• —Asbestosis
• —Tuberculosis
• Radiotherapy

Ineffective breathing pattern:

• —Identify etiology or trigger factor
• —Assess respiratory function (changes in vital signs, O2 sat, cyanosis)
• —Auscultation for breath sounds
• —Note position of the chest & trachea
• —Comfortable position – usually HOB up
• —Give oxygen and monitor
• —Monitor chest tube if inserted

Chest Pain:

• —Assess for presence of pain, the scale and intensity of pain
• —Teach patient about pain management & relaxation with distraction
• —Secure chest tube to restrict movement and avoid irritation
• —Provide analgesics as indicated
• —Evaluate effectiveness of pain reduction measures

• Informed consent
• Position pt upright, leaning forward
• Obtain equipment
• Monitor pulse, color, SpO2
• Apply dressing over site
• Monitor closely after procedure; I & O

• Promote ventilation & re-expansion of the lung
• Pneumonectomy – should not be turned on unoperative side
• Maintain a clear airway
• Maintain a closed drainage system (if used)
• Promote arm exercises on affected side (PROM)
• Promote nutrition
• Monitor incision for bleeding & subcutaneous emphysema
• Remain in ICU until extubated & hemodynamically stable
• Then O2 at 6L/min via NC

1. Stasis - decreased blood flow
2. Endothelial injury - damage to the inside of the blood vessel
3. Hypercoagulability - blood clots likely

• —Careful assessment including risk factors, physical exam
• —Ambulation, active & passive leg exercises
• —Do not sit or lie in bed for prolonged period—
• —Do not cross legs; wear constrictive clothing; dangle or place feet in dependent positions for long periods of time
• —Sequential compression devices
• —Prophylactic heparin or lovenox

• Venous stasis
• Hypercoagulable states
• Immobilization
• Surgery & trauma
• Pregnancy
• OCPs & estrogen replacement
• Malignancy
• Acute medical illnesses
• IV drug abuse
• Heparin-associated thrombocytopenia
• Varicose veins
• Venous pacemakers
• Inflammatory bowel disease
• Lupus

• Travel of 4 hours or more in the past month
• Surgery within the last 3 months
• Malignancy, especially lung cancer
• Current, or past hx of thrombophlebitis
• Trauma to lower extremities & pelvis during past 3 months
• Smoking
• Central venous instrumentation in past 3 months
• Stroke, paresis, or paralysis
• Prior pulmonary embolus
• Heart failure
• COPD

• Tachypnea (RR > 16/min)
• Rales
• Accentuated 2nd heart sound
• Tachycardia (HR>100)
• Fever (temp > 37.8C)
• Diaphoresis
• S3 or S4 gallop
• Clinical S/S suggesting
  
  • Thrombophlebitis
• Lower extremity edema – DVT

• Monitor vital signs, ABGs
• Position patient in high Fowler’s position
• Administer oxygen as ordered
• Bedrest
• Medications - anticoagulants

—Anticoagulants:

• Heparin – weight based protocols
  
  • Monitoring PTT, INR; therapeutic range 2.0-2.5
  • S/E – bleeding; antidote = Protamine Sulfate
• Warfarin (Coumadin)
  
  • Monitoring PT, INR
  • Important to keep the same brand of coumadin
• Enoxaparin (Lovenox)
  
  • High doses SC
  • Require less frequent monitoring