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Nurse’s Guide to COPD: Patho, Assessments, Diagnosis, Interventions, & Medications



Chronic obstructive pulmonary disease (COPD) is the 8th leading cause of hospitalization in the United States and the 3rd leading cause of death. Nurses are involved with COPD care across the spectrum, from outpatient and home care education to intensive care and hospice management. COPD is a disease characterized by airflow limitation that is not fully reversible. COPD includes diseases that obstruct airflow, including emphysema and chronic bronchitis. Separate diseases like asthma, cystic fibrosis, and bronchiectasis were previously classified as types of chronic obstructive lung disease. Current guidelines place asthma in a separate category designated as an abnormal airway condition involving reversible inflammation.

Chronic bronchitis is defined as the presence of a chronic productive cough for a 3-month period during 2 consecutive years. Emphysema is defined as an abnormal, irreversible enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of alveolar walls. Airflow limitation in emphysema is due to loss of elastic recoil of the interstitial tissue that aids in exhalation. Chronic bronchitis is characterized by a narrowing of airways and an increase in airway resistance. Although these are 2 discrete diseases and some patients may display signs of both, most fall somewhere in the middle of the spectrum between the 2 conditions. CAUSES

Risk factors for COPD include environmental exposures and host factors. Exposure to tobacco smoke accounts for an estimated 80 – 90% of all cases. Other risk factors include prolonged and intense exposure to occupational dusts and chemicals, indoor air pollution, and outdoor air pollution, which adds to the total burden of inhaled particles. The following are possible causative factors in COPD:

  • horoscope by date of birth matchmaking Cigarette Smoking: Induces macrophages to release neutrophil chemotactic factors and elastases, which destroy tissue integrity and elasticity. The lack of tissue elasticity compromises the patient’s ability to exhale sufficient volume at a necessary speed leading to air trapping.
  • Secondhand Smoke: Increases the risk of respiratory infections, increases asthma symptoms, and leads to appreciable reductions in pulmonary function.
  • Alpha 1 Antitrypsin Deficiency: Genetically susceptible patients become sensitive to environmental factors (smoking, pollution, allergens, etc.) and in time develop COPD symptoms. Carriers must be identified early to reduce exposure and delay symptoms. Alpha-protease inhibitor replacement therapy slows the progression.


  • seminar für binäre optionen Environmental Exposure: Long-term exposure from living near highly-trafficked areas creates exposure to air pollution and may produce COPD symptoms, especially in patients with asthma.
  • follow Airway Hyperresponsiveness: Patients who have nonspecific airway hyperreactivity and also smoke are at a significantly higher risk of symptoms of COPD.
  • see url Intravenous Drug Abuse: Approximately 2 – 3% of people who abuse IV drugs will develop emphysema secondary to pulmonary vascular damage produced by impurities injected directly into the circulatory system and carried to the lungs.
  • Connective Tissue Disorders: Marfan syndrome and other connective tissue disorders can harm elastin, collagen, and other connective tissues responsible for the dynamics of passive breathing.


In COPD, limited airflow is both progressive and associated with an abnormal inflammatory response to irritating particles and gases in the lungs. The inflammatory response occurs throughout the airways, parenchyma, and pulmonary vasculature. Narrowing of the airways occurs as the body attempts to repair the changes related to chronic inflammation. Eventually, scarring takes place due to this repeated process.

Airflow obstruction may also be due to parenchymal destruction from emphysema, most notably in the alveoli. Emphysema results in permanent enlargement of airspaces distal to the terminal bronchioles. This creates a decline in alveolar surface area as the walls between individual alveoli are destroyed. Elastic recoil is lost in this process as well as support structure. Airflow becomes limited when the lungs fail to deflate efficiently and surrounding tissue collapses, impeding movement of air.

Chronic bronchitis is characterized by deformed airways and narrow lumens. Airway structural changes include ciliary abnormalities, atrophy, smooth muscle hyperplasia, inflammation, and bronchial wall thickening. As damage accumulates to the mucociliary elevator, mobilization of secretions becomes difficult. Distortion of the airways from fibrosis warps their shape, creating a unique setting for the collection of mucous as well as mucous plugging.

Hyperinflation is the central mechanism that produces shortness of breath in this patient population. The ability for a patient with COPD to inhale is not altered. However, expelling air is hampered by damaged airways. During exercise or exertion the patient’s respiratory rate may rise creating less time to exhale before the next inhalation. The patient’s lungs begin to air-trap as a result of the unmet demand for additional time to exhale through poorly functioning airways. The oxygen is quickly extracted from this trapped air. The patient may become hypoxemic, especially if emphysema is present because the surface area needed to extract oxygen is significantly reduced in the alveoli.

je cherche 1 prenom garcon arabe bГ©bГ© EPIDEMIOLOGY & PROGNOSIS

In 2011, an estimated 12.5 million adults in the U.S. had COPD. However, under-diagnosis leads experts to believe that the number may be closer to 24 million based on documented impaired lung function. That same year, 10.1 million Americans had a diagnosis of chronic bronchitis. The highest rate of chronic bronchitis was in older adults age 65 years or greater. Emphysema affects a total of 4.7 million people. The prevalence of COPD varies considerably by state, from < 4% in Washington to > 9% in Alabama. Based on spirometry results, studies have determined that approximately 1 in 5 patients older than 30 years with at least a 10-year history of smoking are likely to have COPD.

A clinical scoring system was developed called the BODE index. This system was developed to approximate a patient’s risk of death or hospitalization. The point system is as follows:

  • see BMI
    • > 21 = 0
    • < 21 = 1




  • Modified Medical Research Council (MMRC) dyspnea scale
    • MMRC 0: Dyspneic on strenuous exercise
      • 0 points
    • MMRC 1: Dyspneic on walking a slight hill
      • 0 points
    • MMRC 2: Dyspneic on walking level ground, must stop occasionally due to breathlessness
      • 1 point
    • MMRC 3: Dyspneic after walking 100 yards or a few minutes
      • 2 points
    • MMRC 4: Cannot leave house; dyspneic doing activities of daily living
      • 3 points


  • Six-minute walking distance
    • > 350 meters = 0
    • 250-349 meters = 1
    • 150-249 meters = 2
    • < 149 meters = 3


The predicted 4-year survival based on the BODE index:

  • 0-2 points = 80%
  • 3-4 points = 67%
  • 5-6 points = 57%
  • 7-10 points = 18%



A mixture of symptoms of reactive airway disease, emphysema, and chronic bronchitis are usually present in patients diagnosed with COPD. The following symptoms are typically found in this patient population:

  • Wheezing
  • Productive cough
  • Dyspnea
  • Respiratory infection


The following physical signs are present in more advanced stages of COPD:

  • JVD
  • Cyanosis
  • Dyspnea and tachypnea on exertion
  • Accessory muscle use
  • Peripheral edema


Chest exam:


  • Wheezes, crackles, & decreased breath sounds
  • Prolonged expiratory period
  • Hyperinflation
  • Percussive hyper-resonance


Chronic bronchitis:

  • Productive cough
  • Obesity & Cyanosis (“blue bloater”)
  • Accessory muscle use
  • Right-sided heart failure with edema
  • Wheezes & Rhonchi



  • Non-productive cough
  • Cachexia
  • Barrel chest with significant air-trapping
  • Pursed-lip breathing (“pink puffer”)
  • Hyper-resonance in chest




  • History: An accurate history, which will assist with the differential diagnosis, should include:


  • Family history of heart and lung disease
  • Childhood diseases
  • Environmental exposures to gas and dust
  • Occupational exposure
  • Tobacco use:
    • 1 pack-year = 20 cigarettes/day for 1 year
    • 10 pack-year = 1 pack/day for 10 years
  • Oxygen saturation: Goal pulse oximeter > 92%
  • ABG:
    • pH < 7.2 consider invasive or non-invasive positive pressure ventilation strategies
    • PaCO2 > 55 mmHg assess baseline and pH for correlation
    • PaO2 < 60 mmHg consider supplemental oxygen, be mindful of O2-induced hypoventilation
  • Infection:
    • temperature
    • sputum volume, color, tenacity, and smell
    • mucous membranes for hydration
    • palpate tactile fremitus
  • Skin:
    • cyanosis
    • clubbing
    • edema
  • Breathing:
    • dyspnea
    • pursed lip breathing
    • symmetrical chest expansion
    • intercostal retractions
    • tracheal deviation
    • respiratory rate > 20 bpm
    • ability to speak
    • tripod position: use of arms to press down and raise rib cage to produce greater diaphragmatic downward excursion
  • Breath Sounds:
    • rhonchi
    • wheezing
    • crackles
    • diminished/absent
  • Chest X-ray:
    • pulmonary congestion: heart failure
    • pneumothorax
    • secretions consolidation: infection
    • blunted costophrenic angle: hyperinflation
  • LOC: somnolence can be a byproduct of hypercapnia, exhaustion, or both. Patient may be in danger of impending respiratory failure
  • Level of Activity: exercise tolerance
  • Sleep Patterns: orthopnea may indicate right-sided heart failure and pulmonary congestion when recumbent
  • Nutrition:
    • obesity with chronic bronchitis
    • cachexia with emphysema
    • bowel sounds diminished from shunting of blood to more vital organs during periods of hypoxia
    • oral hygiene may lead to lowered appetite
  • Knowledge:
    • breathing exercises
    • coughing & deep breathing
    • oral care
    • risk for infection
    • triggers
      • cold air
      • pollen
      • smoke
    • smoking cessation
    • alternating rest & activity
    • pursed lip breathing
    • follow-up care
    • oxygen safety
    • inhaler technique



  • Arterial Blood Gas
    • May have mild to moderate hypoxemia
    • Hypercapnia develops with progression of disease
    • Renal compensation occurs with chronically elevated PaCO2 as evidenced by increased HCO3 & normalized pH
    • pH < 7.2 signals acute distress
  • Hematocrit
    • Polycythemia may develop due to chronic moderate hypoxemia
    • Hct > 52% for males, and 47% for females
  • Serum Chemistry
    • May retain Na
    • Diuretics & Beta-adrenergics may decrease K
    • Beta-adrenergics decrease Ca & Mg
    • Monitor increased HCO3 as a sign of compensated respiratory acidosis
  • B-Type Natriuretic Peptide
    • Elevation can differentiate CHF exacerbation from COPD
  • Alpha-1 Antitrypsin
    • AAT < 11 mmol/L can explain COPD symptoms in patients < 40 yrs
  • Cytologic Exam
    • Rule out malignancy
  • Sputum Sample
    • Chronic bronchitis = mucoid
    • Purulent = presence of neutrophils
    • Increased production = exacerbation
    • Streptococcus pneumoniae & Haemophilus influenza are common
  • Chest X-ray
    • Emphysema = hyperinflation, flattening of diaphragm, diminished heart shadow (pictured below)
    • Chronic bronchitis = bronchovascular markings & cardiomegaly


  • Bronchogram
    • Shows cylindrical dilation of bronchi on inspiration
    • Shows bronchial collapse on forced expiration (emphysema)
    • Show enlarged mucous ducts (chronic bronchitis)
  • Six-Minute Walking Distance
    • Part of BODE index described above
    • Desaturations predict mortality rates
  • Exercise ECG/Stress Test
    • Evaluate effectiveness of bronchodilator therapy
    • Plan & evaluate exercise regimen
    • Assess degree of pulmonary dysfunction
  • Pulmonary Function Test (PFT)
    • Total lung capacity = increased
    • Functional residual capacity = increased
    • Residual volume = increased
    • Vital capacity = decreased
    • FEV1 = no increased response to bronchodilator therapy
    • Carbon monoxide diffusing capacity (DLCO) = decreased with emphysema
    • FEV1/FVC = < 80%

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The ultimate aim of care is to increase or maintain the patient’s functional status. Management focuses on optimizing lung function, avoiding infection, adhering to treatment schedules, and avoiding exacerbations. Education is essential for patient investment and ownership of treatment.

  • Ineffective Airway Clearance
    • Assist patient to comfortable position
    • Remove environmental gas, dust, smoke, micro-fibers
    • PO fluids 3000 mL/day between meals
    • Mucolytics: N-acetylcysteine


  • Impaired Gas Exchange
    • Elevate HOB
    • Provide rest
    • Encourage pursed-lip breathing
    • Encourage cough and suction PRN
    • Provide O2 if SpO2 < 92%
    • Home O2 for sustained PaO2 < 55 mmHg, educate on fire safety
    • Non-invasive positive pressure ventilation (NIPPV) = CPAP or BiPAP


  • Imbalanced Nutrition
    • Frequent oral care
    • Drink before or after meals
    • No carbonated beverages (bloating)
    • Supplemental O2 during meals


  • Risk for Infection
    • Encourage coughing & deep breathing
    • Document temp. & sputum character
    • Use spacer & rinse/spit after corticosteroid inhaler
    • Administer antibiotics as ordered


  • Smoking Cessation
    • Personalize the message
    • Choose quit date
    • Educate on expected effects: increased mucous production, lethargy, anxiety
    • Inquire about social support
    • Follow-up support from health care team or support group
    • Pharmacological support: chantix, wellbutrin, nicotine patch, etc.


  • Airway Inflammation
    • Inhaled corticosteroids
    • Azithromycin


  • Vaccination
    • Pneumococcal vaccine for all patients > 65 years
    • Influenza annually for all COPD patients



– Albuterol

  • Trade Name: Proventil, Ventolin, Proair
  • Indication: Acute bronchospasm
  • Action: Relaxes bronchial smooth muscle by activating beta-2 receptors with slight effect on beta-1 and heart rate, dilate bronchial airways
  • Class: Beta-2 agonist
  • Considerations:
    • 1 – 2 inhalations q4 – 6h
    • Duration 3 – 6h
    • May cause tremor or tachycardia
    • Take last dose several hours before bedtime
    • Review proper inhaler technique with patient

– Salmeterol

  • Trade Name: Serevent Diskus
  • Indication: Prevention of COPD or asthma related bronchospasms
  • Action: Long-acting beta-2 agonist stimulates receptors and relaxes bronchial smooth muscle with little effect on heart rate
  • Class: Beta-2 agonist
  • Considerations:
    • 2 inhalations aerosol (42 mcg) or 1 powder diskus (50 mcg) b.i.d. 12h apart
    • Duration 12h, do not use for acute asthma
    • Withhold and notify physician if bronchospasms occur after use
    • May cause tachycardia
    • Monitor LFT’s
    • Take 30 – 60 min prior to exercise

– Ipratropium

  • Trade Name: Atrovent
  • Indication: COPD
  • Action: Parasympatholytic agent that inhibits vagally mediated reflexes by antagonizing acetylcholine leading to bronchodilation
  • Class: Anticholinergic, Respiratory
  • Considerations:
    • 2 inhalations of MDI q.i.d. at no less than 4h intervals
    • Not intended for PRN use due to delayed onset
    • Anticholinergic effect may lead to blurred vision, nausea, dry mouth, and constipation
    • May change urinary pattern in older adults
    • Review proper inhaler technique with patient

– Fluticasone

  • Trade Name: Flovent
  • Indication: COPD, Asthma
  • Action: Exhibits anti-inflammatory effects on neutrophils, eosinophils, macrophages, mast cells, and histamine
  • Class: Corticosteroid
  • Considerations:
    • Inhaled powder 100 – 250 mcg q12h
    • Rinse mouth after use to prevent oral candidiasis
    • May increase intraocular pressure with cataracts and glaucoma
    • Adrenal insufficiency may occur after abrupt withdrawal
    • May suppress growth in children
    • Immune-suppression possible with long term use

– Prednisone

  • Trade Name: Rayos
  • Indication: Acute exacerbation of COPD
  • Action: Elicits mild mineralocorticoid activity and moderate anti-inflammatory effects by suppressing migration of PMN’s and fibroblasts, reversing capillary permeability, and stabilizing lysosomes
  • Class: Corticosteroid
  • Considerations:
    • PO 40 mg q12h X 3 – 5 days
    • Can lead to immune-suppression with prolonged use, monitor for poor wound healing
    • Give at mealtime to avoid gastric irritation
    • Do not abruptly stop, reduce dose gradually
    • Monitor BG, weight, sleep patterns, and blood pressure closely
    • Monitor for adrenal suppression
    • Monitor bone density

– Albuterol/ipratropium

  • Trade Name: Combivent
  • Indication: COPD patients who require second bronchodilator
  • Action: Bronchodilation through beta-2 adrenergic and anticholinergic mediated antagonization of vagal reflexes
  • Class: Respiratory inhalant combo
  • Considerations:
    • Aerosol 100 mcg/20 mcg 1 puff q6h, not to exceed 6 per day
    • Anticholinergic effect may lead to blurred vision, nausea, dry mouth, and constipation
    • May change urinary pattern in older adults
    • May cause tremor or tachycardia
    • Take last dose several hours before bedtime
    • Review proper inhaler technique with patient

– Budesonide/formoterol

  • Trade Name: Symbicort
  • Indication: COPD uncontrolled with mono-therapy
  • Action: Decreased inflammation of airways through inhibition of inflammatory cells and long-acting beta-2 adrenergic agonism with rapid onset leading to bronchodilation
  • Class: Respiratory inhalant combo
  • Considerations:
    • 160 mcg/9 mcg (2 puffs of 80 mcg/4.5 mcg) q12h
    • Implement step-down therapy as soon as possible to prevent long-term issues with corticosteroids like immune-suppression, adrenal suppression, and decreased bone density
    • Not for relief of acute asthma symptoms
    • Monitor blood pressure and heart rate
    • Rinse mouth after using to avoid oral candidiasis

Show Me Your Stethoscope

An article from William R. Blythe, MD on the importance of nurses…

“The truth about Nurses, from an ungrateful, selfish, arrogant Surgeon

Yesterday I posted a silly photo in support of this movement, but tonight I want to say something serious while there is ample attention.

When a patient comes to our hospital for surgery, these are the people who take care of them:

The Pre-Op Nurses meet the patient, make sure they are ready for surgery, complete mountains of paperwork, reconcile their medications, sign permits, check labs, answer questions, allay fears, and make certain the patient is properly prepared for surgery. And they put up with me.

The Circulator Nurse is in charge of the OR. She makes certain the room, equipment, personnel, implants, disposables, medications and every other detail are ready. She oversees that everything is checked twice, that everything is documented properly and that the proper surgery is performed on the right part and the right patient every time. Her job is to ensure that we do everything right, every time, with no exceptions. She makes certain that every sponge, needle, gauze, blade and specimen are properly accounted for. And she puts up with me.

My CRNA puts the patient to sleep and attends to them through every moment. She listens to their every breath and heartbeat. She makes sure they are asleep, safe and comfortable. She holds children her lap and talks to them like a mother while they go to sleep. She makes certain every patient goes to sleep and wakes back up as safely as possible every time, no exception. And she puts up with me.

The people who operate directly with me are Nurses or Techs, not doctors. They make sure we have the proper instruments and equipment. My Scrub hands me what I need before I ask for it. She can anticipate what I am going to need next better than I can many times. She makes my job easy and she makes me look like I know what I am doing when sometimes I am less certain. The person across the table from me is often an RNFA or SFA. They operate directly with me – tie the knots, cut the suture, retract, hold, pull, control the bleeders, close the wounds and a million other things. I simply could not do what I do without them. And they put up with me.

The PACU Nurses take the patients from the CRNA and recover them from anesthesia and surgery. They assess and dress wounds. They treat pain and anxiety and fear. They hold screaming babies in their arms until they are awake. They hold hands of grown men who are disoriented and fearful. They re-assure and calm the parents, children and spouses of the patients. They give wound, medication and discharge instructions, and they transfer patients to their room. They land the plane, and it’s as important a job as any in the world. And they put up with me.

The Nurses in the ICU and Floor take care of the patients, not me. The ICU nurses are infinitely more capable of monitoring and assessing sick patients than am I. I try to stay out of their way and let them do their job, and they let me know when they need me. The Floor Nurses take care of every detail of every patient: What and when they eat; medications; wound care; ambulation; checking vitals, labs, weights, sugars, pulse oximetry, I’s & O’s; draw and check labs; start and re-start IV’s; and countless other things that only nurses understand. They spend time with the patient and family all day. They educate and answer questions. They pray with the patient and family. They cry when their patients die. And they put up with me.

The truth is that if a patient is in the hospital for 48 hours, they may see me for the smallest fraction of that time. I say a brief hello before surgery, I operate, I speak to the family, and I make rounds each morning. I may spend 15 minutes each day at any one patient’s bedside. The rest of it – every second, every bit, every detail, everything – is performed by the Nurses. Honestly, the one who probably needs the stethoscope least is me.

And in the end, through it all, they put up with me!”Show Me Your Stethoscope

Sepsis Nursing Treatment & Medications



Septicemia is a systemic inflammatory response to an infection that causes circulatory dysfunction.  When infections become blood borne and spread throughout the body, capillaries become more permeable, hypotension occurs, coagulation increases, and immune mediators are released. Infections leading to sepsis are usually bacterial but can also be fungal or viral. The term sepsis is often used interchangeable with septicemia and refers to a bloodstream infection. Sepsis can occur with or without organ dysfunction, depending on severity. Sepsis can be further classified as follows:

  • Systemic Inflammatory Response (SIRS): Infection in conjunction with the systemic inflammatory response syndrome.
    • Temperature > 38 C
    • Heart rate > 90 bpm
    • Respiratory rate > 20 bpm
    • WBC > 12,000/mm3
  • Severe Sepsis: Sepsis complicated by organ dysfunction.
  • Septic Shock: Sepsis causing acute circulatory collapse resulting in refractory hypotension unrelieved by intravenous volume resuscitation.

Sepsis is typically associated with a causative condition primarily from the skin, abdomen, lungs, or urinary tract, such as bowel perforation, pneumonia, pyelonephritis, renal abscess, or urosepsis related to a urinary tract obstruction.


Sepsis, or septic shock, is associated with direct introduction of pathogenic microorganisms. The most common iatrogenic sources are central or peripheral venous catheters, catheter-associated urinary tract infections (CAUTI), surgical site infections (SSI), and ventilator-associated pneumonia (VAP). Despite only accounting for 2% of hospitalizations in 2008, sepsis caused 17% of all in-hospital deaths. In a hospital setting, 50% of all sepsis cases start as an infection in the lungs. No definitive source is found in 1/3 to ½ of all documented cases.

The rate of hospitalization for septicemia has more than doubled since 2000. The sharp rise in cases has been attributed to microbial resistance due to increased use of antibiotics, greater use of invasive procedures, an aging population with more chronic illnesses, immunosuppressive drugs, chemotherapy, transplantation, increasing microbial resistance to antibiotics, and greater awareness of sepsis resulting in more frequent and accurate medical diagnosis and coding.


The pathophysiology of sepsis is complex and related to the pathogen and its virulence and the patient’s immune status. Sepsis is characterized by a systemic inflammatory response resulting in systemic vasodilatation, hypotension, increased cardiac output and eventual end-organ damage caused by limited oxygen extraction by the tissues. The primary effects come from endogenous cytokine release (i.e. tumor necrosis factor, interleukins) and the inflammatory cascade in response to circulating bacterial products. Impaired pulmonary, hepatic, or renal function may result from excessive cytokine release. Disordered coagulation results in activation of the clotting cascade and a reduction in the natural inhibitors of clotting, such as activated protein C. Once initiated, the process is self-perpetuating without regard to the initial infection. Microcirculatory blood flow is impeded by an increase in thrombosis formation and reduced fibrinolysis (clot breakdown), microcirculatory ischemia, and eventual multiple organ dysfunction (MODS).

The stages of sepsis can be divided as follows:

  • Infectious insult
  • Initial systemic response
  • Overwhelming systemic response
  • Anti-inflammatory reaction
  • Immunomodulatory failure


Septicemia can quickly become life threatening if not recognized early and treated aggressively. Patients hospitalized for septicemia have twice the average length of stay versus patients hospitalized for other conditions and are eight times more likely to die during their hospitalization. Approximately 30-70% of patients with septic shock die. Patients who survive severe sepsis are more likely to have permanent organ damage including cognitive impairment and physical disability.

Several prognostic assessments exist to stratify sepsis outcomes. Lactate levels have been shown to be directly proportional mortality rate. The APACHE II scale can help classify the severity of the disease by calculating a score based on physiological measurements including: arterial pH, potassium, creatinine, hematocrit, and Glasgow coma scale. Without progression to septic shock, approximately 20-35% of patients still do not survive.



Taking an accurate patient history is important in determining the potential source of sepsis. This will help guide essential antimicrobial therapy. Due to the vague nature and systemic progression of sepsis, it is difficult to determine the source without reviewing all systems and performing a thorough physical assessment. Most signs and symptoms relate to hypotension, coagulopathy, infection, and hypoperfusion of organs. The following are general signs and symptoms and special considerations:

  • Fever > 38 C or < 36 C
  • HR > 90 bpm
  • RR > 20 bpm
  • WBC > 12,000/mm3
  • Shaking or chills
  • Altered mental status
  • Oliguria: < 0.5 mL/kg/hour
  • Warm skin with dilatation of the superficial vessels
  • Cold skin with inadequacy of organ perfusion


  • IV line infection:
    • Almost always central line site vs. peripheral or arterial lines
    • Suspect if other potential sources are eliminated and patient has long-term IV line in place
  • Gastrointestinal or genitourinary infections:
    • Ileus: absent bowel sounds
    • History of pyelonephritis, renal abscess acute prostatitis, or prostatic abscess
    • Abdominal pain suggests pancreatitis or peritonitis
    • Right upper quadrant tenderness suggests gallbladder etiology
    • Right lower quadrant tenderness suggests appendicitis or Crohn’s complications
    • Left lower quadrant tenderness suggests diverticulitis
    • Abnormalities on rectal exam like severe tenderness suggest a prostatic abscess
    • Costovertebral angle tenderness suggests pyelonephritis
    • Elderly may have peritonitis without rebound tenderness of the abdomen
  • Urosepsis: Most common cause of sepsis in pregnancy secondary to obstructed urinary tract
  • Burns
  • Asplenia: No spleen
  • Gastrointestinal Disorders:
    • Intestinal obstruction
    • Gallbladder disease
    • Colon disease
    • Abscess
    • Liver disease
    • GI surgery
  • Ethanol abuse
  • Genitourinary Disorders:
    • Renal calculi
    • Pyelonephritis
    • Urinary tract obstruction
    • Acute prostatitis
    • Prostatic abscess
    • Renal insufficiency
    • GU catheters
  • Diabetes mellitus
  • Lung Disorders:
    • Empyema
    • Lower respiratory tract infection
    • Community-acquired pneumonia
    • Lung abscess
  • Immunocompromised
  • Bacterial endocarditis


  • Lactate: Marker for cellular hypoxia, normal 0.5-2.2 mmol/L, above 4.0 mmol/L = 27% mortality rate
  • Complete blood count: Anemia, elevated or low white blood cell count, or thrombocytopenia
  • Arterial blood gas: metabolic acidosis and arterial hypoxemia (PaO2/FiO2 < 300 mmHg)
  • Blood Glucose: Septic patients can have > 140 mg/dL without diabetes
  • Creatinine: > 0.5 mg/dL
  • Troponin T: > 0.1 ug/L in 85% of sepsis without coronary syndrome
  • Cultures: Blood, IV catheter tip, or urine cultures on admission before starting antibiotics to determine specific microbial target
  • Gram stain blood: Differentiate between gram positive and gram negative organisms
  • Urinalysis: Perform gram stain and culture
  • C-Reactive Protein: identify presence of inflammation and monitor response to treatment
  • Procalcitonin: Evaluate risk of developing system bacterial infection
  • Presepsin: Early risk stratification
  • Clotting screen: D-dimer and fibrinogen will reveal disseminated intravascular coagulation
  • Chest X-ray: Rule out pneumonia
  • Abdominal CT or MRI: Assess for peritonitis, abdominal abscesses, and renal pathology
  • Abdominal Ultrasound: Exam liver, gall bladder, pancreas, and biliary tract for obstruction
  • Thoracentesis: Patients with significant pleural effusions
  • Paracentesis: Patients with ascites
  • Swan-Ganz catheterization: Guides fluid management and reveals left ventricular dysfunction
  • Invasive investigation: Lumbar puncture, bronchoscopy, laparoscopy, lymph node biopsy


  • ICU admission for monitoring and treatment
  • Lactate: Obtain initial serum level and regular follow-ups
  • Foley insertion: Monitor urine output closely to guide therapy and fluid replacement, goal > 0.5 mL/kg/hour
  • Intravenous antimicrobials: Cultures followed by broad-spectrum antibiotics given intravenously. Antivirals and antifungals may also be required. Once organism is isolated through lab cultures, the regimen may be targeted for the pathogen. Empirical combination therapy should not last longer than 3-6 days. Reducing to single therapy should be done as soon as the pathogen profile is known:
    • IV line infections: Line removal then meropenem or cefepime
    • MRSA: Linezolid, vancomycin, or daptomycin
    • Biliary tract infections: Imipenem, meropenem, piperacillin-tazobactam, or ampicillin-sulbactam
    • Abdominal and pelvic infections: Imipenem, meropenem, piperacillin-tazobactam, ampicillin-sulbactam, or tigecycline; clindamycin or metronidazole plus aztreonam, levofloxacin, or an aminoglycoside
    • Urosepsis: Aztreonam, levofloxacin, a cephalosporin, or an aminoglycoside
    • Enterococci: Ampicillin or vancomycin;
    • Vancomycin-resistant enterococcal urosepsis: Linezolid or daptomycin;
    • Community-acquired urosepsis: Levofloxacin, aztreonam, or an aminoglycoside plus ampicillin
    • Nosocomial urosepsis: Piperacillin, imipenem, or meropenem
    • Pneumococcal sepsis: Cephalosporins, carbapenem, or vancomycin
    • Sepsis of unknown origin: Meropenem, imipenem, piperacillin-tazobactam, or tigecycline; metronidazole plus either levofloxacin, aztreonam, cefepime, or ceftriaxone
  • Fluid Resuscitation:
    • Crystalloid 30 mL/kg: If hypotensive
    • Crystalloid 4-6 Liters total: Often required for septic shock
    • Colloids IV: Osmotic force may counteract third-spacing from increased capillary permeability, used only when unresponsive to isotonic crystalloids
    • Monitor fluid overload: dyspnea, crackles, JVD, pulmonary edema
  • Transfusions:
    • RBC transfusion: If patient’s hemoglobin falls below 7 g/dL
    • Platelet transfusion: Severe sepsis causes thrombocytopenia, transfuse < 20,000
    • FFP, Fibrinogen, or Cryoprecipitate: Consider with DIC, active bleeding, elevated PT, and decreased fibrinogen
  • External cooling: Fever control which may reduce vasopressor requirements
  • Enteral nutrition: Electrolyte and protein deficiencies are common, do not give parenterally, caution ileus
  • Vasopressors:
    • Indicated for hypotension that does not respond to initial fluid resuscitation
    • MAP > 65 mmHg: Administer fluids & vasopressors
    • CVP > 8 mmHg: Monitor central venous pressure to guide fluid resuscitation and vasopressors
    • ScvO2 = 70%: Monitor central venous oxygen saturation for cellular supply and demand
  • Supplemental oxygen: Monitor respiratory effort closely as respiratory failure is a risk
  • Dialysis: Patient may experience kidney failure
  • Monitor blood glucose: Goal < 150 mg/dL
  • DVT prophylaxis: heparin when not contraindicated, SCD’s
  • Asepsis: Maintain strict aseptic technique
  • Mechanical ventilation:
    • Acute Respiratory Distress Syndrome (ARDS) carries very poor prognosis
    • Tidal volume 5-8 mL/kg
    • Elongated inspiratory time
    • Sufficient PEEP
    • Peak pressure < 30 cmH2O



– Norepinephrine

  • Trade Name: Levophed
  • Indication: Acute hypotension, sepsis, septic shock
  • Action: Increases blood pressure, cardiac output, and heart rate, beta-1 and alpha-adrenergic effects with moderate beta-2,
  • Class: Alpha/Beta adrenergic agonist
  • Considerations:
    • First line treatment of septic hypoperfusion unresponsive to fluids
    • 2-1.5 ug/kg/min up to 3 ug/kg/min due to alpha down-regulation in sepsis
    • Monitor blood pressure closely
    • Splanchnic (abdominal) perfusion can become compromised from prolonged administration
    • Caution IV site extravasation

– Dopamine

  • Trade Name: Intropin
  • Indication: Hypotension, low cardiac output, hypoperfusion of vital organs, raises mean arterial pressure in septic shock patients after fluid resuscitation has failed
  • Action: Endogenous catecholamine, stimulating dopaminergic and adrenergic receptors
  • Class: Inotropic agent
  • Considerations:
    • Low dose (1-5 mcg/kg/min) produces renal and mesenteric vasodilation
    • Moderate dose (5-15 mcg/kg/min) produces cardiac stimulation and renal vasodilation
    • High dose (20-50 mcg/kg/min) stimulates alpha receptors producing systemic vasoconstriction and increased mean arterial pressure
    • Use with caution in angina due to increased oxygen demand of heart
    • Always fluid resuscitate first
    • Prevent tissue damage at IV site by monitoring for extravasation

– Hydrocortisone

  • Trade Name: SoluCortef
  • Indication: Vasopressor-refractory shock or adrenal insufficiency secondary to cortisol stimulation test, improved survival of ARDS
  • Action: Controls or prevents inflammation by reducing rate of protein synthesis and suppressing migration of polymorphonuclear leukocytes and fibroblasts, reverses capillary permeability
  • Class: Corticosteroid, Glucocorticoid
  • Considerations:
    • High-dose corticosteroids should not be used with sever sepsis
    • Lower-dose (physiologic) steroids are beneficial for patient with adrenal insufficiency
    • Measuring cortisol levels before and 30 minutes after IV administration of ACTH can reveal adrenal insufficiency
    • Majority of patients with vasopressor-refractory sepsis benefit
    • Hydrocortisone 100 mg IV or Dexamethasone 10 mg IV

– Epinephrine

  • Trade Name: Adrenalin
  • Indication: Second-line agent for persistent hypotension despite fluid, norepinephrine, and dopamine administration, can be used in cardiac arrest
  • Action: Mainly alpha-adrenergic stimulation causing systemic vasoconstriction, strong beta-1 and beta-2 resulting in increased cardiac output, heart rate, and bronchial smooth muscle relaxation
  • Class: Alpha & Beta adrenergic agonist
  • Considerations:
    • Tachyarrhythmias and myocardial ischemia can result from strong beta-1 stimulation
    • Rapid increase in blood pressure can cause cerebral hemorrhage
    • May increase lactate and blood glucose levels
    • Gut ischemia from diversion of blood flow, must monitor bowels
    • 1-10 mcg/min IV infusion, titrate to effect

– Vasopressin

  • Trade Name: ADH, Vasostrict
  • Indication: Second-line agent for vasodilatory shock, should be used to supplement concurrent use of norepinephrine
  • Action: Endogenous peptide normally released from posterior pituitary that vasoconstricts without inotropic or chronotropic effects, stimulates peristalsis
  • Class: Antidiuretic hormone analog, Vasopressor
  • Considerations:
    • 03 U/min IV infusion added to norepinephrine as a therapy to treat unresponsiveness and reduce requirements for catecholamines
    • Restores effectiveness of catecholamine first-line agents
    • Increases renal perfusion and stimulates peristalsis

– Insulin

  • Trade Name: Humulin R, Novolin R
  • Indication: Glycemic control and avoidance further inflammatory response
  • Action: Reduces cytokine release, prevents polyneuropathy and myopathy, attenuates inflammation, and can decrease lactate formation
  • Class: Antidiabetic, Insulins
  • Considerations:
    • Previous recommendations were blood glucose levels 80-110 mg/dL but episodes of hypoglycemia negated any potential benefits
    • Recent sepsis-specific recommendations call for maintaining glucose level below 180 mg/dL
    • Administer in drip form according to ICU IV insulin infusion protocol
    • Insulin needs to be on connected to carrier line with fluid to infuse continuously
    • Blood glucose checks usually hourly

– Heparin

  • Trade Name: No trade name
  • Indication: Prevention of DVT or thrombosis-dominant disseminated intravascular coagulation (DIC)
  • Action: Inactivates factor Xa and inhibits conversion of Prothrombin to thrombin, inactivates factors IX, X, XI, and XII, and inhibits activation of factor VIII
  • Class: Anticoagulant
  • Considerations:
    • Only administer in the absence of active bleeding or thrombocytopenia
    • Caution creatinine clearance less than 30 mL/min
    • When contraindicated, use compression stockings or sequential compression devices
    • Also use in presence of inadequate perfusion to extremities or vascular skin infarctions
    • Weight-based dosing starting at 10 U/kg/hr with goal aPTT of 1.5-2.5 longer than patient’s pretreatment level

– Albumin

  • Trade Name: Albuminar, Alba
  • Indication: Hypovolemia and hypotension after substantial amounts of crystalloids have been administered
  • Action: Intravascular volume expansion through mobilization of fluids from interstitial spaces
  • Class: Volume expander
  • Considerations:
    • Increases circulating plasma volume by 3.5 times the volume infused within 15 minutes
    • Hemodilution lowers hematocrit and lowers blood viscosity
    • Monitor for signs of volume overload: dyspnea, JVD, crackles, pulmonary edema
    • Crystalloids should be given in 2-4 times greater quantity first
    • Results should be evident in CVP, PAOP, and urine output

– Phenylephrine

  • Trade Name: Vazculep
  • Indication: Second-line vasopressor for persistent hypotension despite maximal doses of norepinephrine and dopamine
  • Action: Strictly alpha-receptor agonist resulting in increased peripheral vascular resistance and blood pressure at the expense of cardiac output, heart rate and renal perfusion
  • Class: Alpha 1 agonist
  • Considerations:
    • 80-200 mcg/min IV infusion
    • Caution with cerebrovascular insufficiency and cardiovascular disease
    • Consider as first-line agent with tachycardia as it will reduce heart rate quickly and reliably while other catecholamine agents can exacerbate tachycardia
    • Extravasation can cause tissue ischemia
    • Reflex bradycardia should be considered in patients with low heart rates
    • Decrease in cardiac output can be detrimental in patients with hypermetabolic state like sepsis

5 Step EKG for Nurses

It’s not hieroglyphic.  Let me be specific.  Our notion of heart motion can be un-sci-en-tif-ic.

That’s a Blood Hound Gang inspired rhyme to illustrate how the EKG can appear incoherent to a novice nurse who fails to employ a systematic approach to interpreting electrophysiology.  I have included a brief summary of key points concerning the EKG, along with a 5-step approach to help students and new graduate nurses grasp some seemingly difficult concepts…

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ABG Interpretation for Nurses

When interpreting an arterial blood gas result I like to take a systematic, yet contextual, approach.  Other methods that I have seen on the internet focus on isolating parameters such as PaCO2 and HCO3 and using steadfast rules based on their behavior to classify the blood gas results.  One such method that I have seen […]