Class 11: Multisystem dysfunction Flashcards
Tonicity + isotonic solution
-Fluid that has same osmolality as normal plasma: NS, D5W (hypotonic in body), RL
-Used to replace fluid loss
Tonicity + hypertonic solution
Fluid that has a higher osmolality than normal plasma: Admixed solutions e.g. TPN; 3% saline; mannitol; & D50S
Tonicity + hypotonic solutions
-Fluid that has a lower osmolality than normal plasma: 0.45% saline
-Used to replace fluid without giving electrolytes
Tonicity + isotonic
Placing a cell into an isotonic solution will have no net effect on the cell as the tonicity (osmolality) of the cell equals to the fluid
Tonicity + hypertonic
Placing a cell into a hypertonic solution will draw water out on the cell and the cell will shrink
Tonicity + hypotonic
Placing a cell into a hypotonic solution will shift fluid into the cell and the cell will swell & possibly burst
Anything other than a isotonic solution can…
-Cause fluid shifts in the vein used for infusion & consequently, the vessel may become more easily damaged and inflamed
Hypertonic cells..
Shrink and are damaged. (That’s why hypertonic solutions are generally infused through a central venous catheter)
Hypotonic cells…
Swell and infusion may infiltrate
Slide 5
Fluid shifts & edema + osmotic pressure GOES w/ card 1
-Power of the solution to draw water across a semi permeable membrane
-Isotonic crystalloid solution (NS & RL)
Fluid shifts & edema + oncotic pressure
-Plasma proteins exert this pressure and as a result pull water from the interstitial space into the vascular system
-Colloid solution (large proteins: albumin, globulin, fibrinogen)
Fluid shifts & edema + hydrostatic pressure…
-In the arterial (30-40 mmHg) and venous (10-15 mmHg) ends of capillary
-Force blood exerts against vascular walls
Fluid shifts & edema + capillary permeability
Is increased for pts with burns, or allergic inflammatory reactions
Oral fluid and electrolyte replacement in acid-base imbalances + isotonic solutions (D5W)
0.9% NS, RL, & D5W in 0.225% saline
Oral fluid and electrolyte replacement in acid-base imbalances + hypotonic solutions (0.45% saline)
D5W (physiologically)
Oral fluid and electrolyte replacement in acid-base imbalances + hypertonic solutions (D10W)
3.0% saline , D5W in 0.45% saline, & D5W in 0.9% NS
Edema + peripheral vs local
-Peripheral– Systemic swelling & pitting edema
-Local e.g. Ascites
Systemic signs of edema
BP & CVP alterations occur
Fluid shifts + serum osmolality
Measure of solute concentration of the blood [sodium, glucose and urea] (↑ = fluid volume deficit, ↓ = fluid volume excess)
Fluid shift + urine osmolality
Measure of solute concentration of urine [nitrogenous wastes – creatinine, urea, and uric acid] (↑ = fluid volume deficit, ↓ = fluid volume excess)
Risk of fluid shifts in infants
Infants have proportionately more body water, a lot of which is in the extracellular space. This is more easily lost from the body so infants can become dehydrated easily
Others at risk for fluid shifts
-Elderly, who can’t compensate for fluid shifts
-Anyone with GI problems
Sodium & volume imbalances nursing diagnosis + ECF volume excess
-Ineffective airway clearance r/t Na+ & H2O retention
-Risk for impaired skin integrity r/t edema
-Disturbed body image & altered body appearance r/t edema
-(P) complication of pulmonary edema or ascites
Sodium & volume imbalances nursing diagnosis + ECF volume deficit
-Deficient fluid volume r/t ↑ECF losses or ↓ fluid intake
-Decreased CO r/t ↑ECF losses or ↓ fluid intake
-(P) complication of hypovolemic shock
Sodium & volume imbalances nursing diagnosis + hypernatremia
Risk for injury r/t to altered sensorium/seizures & abnormal CNS function
Sodium & volume imbalances nursing diagnosis + hyponatremia
Risk for injury r/t to altered sensorium/↓LOC & abnormal CNS function
ABG values
pH, CO2, HCO3-, & PaO2
Normal PaO2
80-110mmHg
Mild hypoxemia
60-79mmHg
Moderate hypoxemia
40-59mmHg
Severe hypoxemia
<39mmHg
Slide 15
Electrolyte imbalances
Abnormalities, causes and consequences associated with three critical electrolytes: Sodium, potassium, & calcium
Slide 17
Na+ is a major
Cation of ECF
Na+ has a
Water retaining effect; take caution with CHF & MI pts
Na+ is responsible for
Conduction of neuromuscular impulses via the sodium/potassium pump
Na+ is involved in
Enzymatic activity
Na+ regulates
Acid-base balance by combining with chloride or bicarbonate ions
Hyponatremia causes
Vomitting/diarrhea
Etiology of hyponatremia
Burns, inflammation, vomiting/diarrhea, gastric suction, perspiration, continuous D5W IV & SIADH
Drugs that cause hyponatremia
Lasix, mannitol & thiazides
Hypernatremia is caused by
CHF, cushing’s disease, hepatic failure, dehydration & vomiting/diarrhea
Drugs causing hypernatremia
Cough medicines, cortisone, antibiotics, laxatives, methyldopa & hydralazine
Consequences of hyponatremia
-Edema, confusion and giddiness leading to coma
-If water retention occurs rapidly it can lead to HF or pulmonary edema
-Hyponatremia with fluid loss will cause hypotension & tachycardia
Consequences of hypernatremia
CNS: Lethargy & confusion progressing to coma. Increased neuromuscular irritability which can progress to convulsions
Nursing interventions of aNa+
-Monitor serum sodium levels, for S&S of hyponatremia, VS & ins/outs
-Recognize symptoms of SIADH after surgery
-Educate your patient on the DASH diet
K+
-Found most abundantly in ICF
-Narrow range and cardiac arrest could occur if serum level is too high or too low
-80-90% is excreted by the kidneys; therefore kidney function very important
Etiology of hypokalemia
Vomitting/diarrhea, malnutrition, stress, gastric suctioning & burns
Drugs that cause hypokalemia
Lasix, cortisone, estrogen, gentamicin, bicarbonate, insulin, laxatives, kayexalate & ASA
Etiology of hyperkalemia
Reduced U/O, acute renal failure, Addison’s disease & metabolic acidosis
Addisons disease
Adrenal insufficiency, decreased steroid production of cortisol
Drugs that cause hyperkalemia
Spironolactone, Penicillin G potassium, heparin, epinephrine & histamine
Consequences of hypokalemia
Alkalosis, hypoventilation, muscle weakness, arrhythmias & possibility of cardiac arrest
Consequences of hyperkalemia
Skeletal muscle weakness, flaccid paralysis, bradycardia, arrhythmias and cardiac arrest
Nursing interventions with aK+
-Monitor trends of serum levels, VS, ins/outs
-Assess medications for addition or depletion of potassium
-Ask your patient about their diet
Etiology of hypercalcemia
Hyperparathyroidism, excessive vitamin D ingestion, prolonged immobilization (or weightlessness), renal disease preventing excretion, malignancies, and Cushing’s disease accompanied by osteoporosis
Consequences of hypercalcemia
Bone wasting, pathological fractures, kidney stones, deep muscle pain, N/V, arrhythmias/arrest, respiratory depression and coma
Etiology of hypocalcemia
Vitamin D deficiency, increased excretion in stress and increased protein intake, diarrhea & burns
Consequences of hypocalcemia
Tingling of fingers, tremors, tetany, convulsions, and depressed excitability of myocardial muscle
Slide 29-31 lab values
Hemoglobin
Protein found in red blood cells, gives blood its red colour, O2 carrier & is composed of iron
Low hemoglobin is caused by
Anemia, hemorrhage, leukemias, excess fluids, thalassemia & kidney disease
Drugs causing low hemoglobin
Penicillin, ASA, antineoplastic drugs, hydralazine & MAO inhibitors
High hemoglobin is caused by
Dehydration, hemoconcentration, polycythemia, high altitude, COPD, CHF & severe burns
Drugs that cause high hemoglobin
Gentamicin & methyldopa
Nursing interventions of aHemoglobin
Monitor VS especially if patient hemorrhaging, trends of hemoglobin, for signs of anemia, S&S of dehydration
Tx of aHemoglobin
Iron supplement or dietary modification to increase iron
Slide 35
Hematocrit
-Percentage of the blood volume occupied by red blood cells
-Indicator of hydration status
Low hematocrit is caused by
Acute blood loss, anemia, leukemia, protein malnutrition, vitamin deficiencies & RA
Drugs causing low hematocrit
Antineoplastic agents, penicillin & radioactive agents
Etiology of high hematocrit
Hemoconcentration, dehydration/hypovolemia, severe diarrhea, polycythemia vera, diabetic acidosis, surgery & burns
Nursing interventions of aHematocrit
Monitor VS for signs of shock, may require blood transfusion, may require fluid administration d/t dehydration & hypovolemia
Platelets
-AKA thrombocytes
-Help in the clotting process by gathering at a bleeding site and clumping together to form a plug
Low platelets (thrombocytopenia) causes
Bruising, aBleeding, purpura & petechiae
Etiology of low platelets (thrombocytopenia)
Bleeding, Von Willebrand’s disease, leukemia & liver cirrhosis
Drugs causing low platelet levels
Aspirin, ibuprofen, indocin, valium & theophylline
High platelets (thrombocythemia) causes
Hypercoagulability, DM & increases the risk for CVA and MI
Nursing interventions of aPlatelets
-May require transfusion, check for bleeding tendencies and assess for petechiae/purpura
-Educate your patient on impact of medications such as aspirin and coumadin and side effects such as decreased platelets and clotting time
WBC
-Part of the body’s defense system
-Help determine the presence of an infection or blood cancer such as leukemia
WBC + neutrophils
-Most abundant WBC’s
-First line of defence againts infection
WBC + band neutrophils
Immature neutrophils that indicate new infection
WBC + basophils
Increase during the healing process and allergic response
WBC + eosinophils
Increase during an allergic and parasitic condition
WBC + lymphocytes
-Occurs in chronic and acute viral infections
-Play a major role in B and T cells
-Decrease in numbers during steroid therapy
WBC + monocytes
-Second line of defense against bacterial infections and foreign substances (macrophages)
-Stronger than neutrophils and can ingest larger particles of debris
Monocytes respond..
Late during the acute phase of infection and inflammatory process and continue to function during the chronic phase of phagocytosis
Nursing interventions of aWBC
-Monitor trends of values, S&S of an infection such as increased temperature, tachycardia, edema, redness or wound drainage
-Monitor for S&S of allergies, such as tearing, runny nose or rash
-Monitor for S&S of healing
Coagulation
Determines blood viscosity
Prothrombin time (INR)
0.9-1.1
Activated partial prothromboplastin time (PTT)
Lab value is specific to the area of intervention
D-dimer
<0.3mmol/L
PT/INR
-Taken pre-op to identify coagulation levels
-If the pt is taking coumadin, they will require routine blood levels to maintain blood consistency
PTT
Blood test used to monitor PTT levels for IV heparin therapy
D-dimer
-Occurs through fibrinolysis
-Measures the amount of fibrin degradation and confirms the presents of fibrin
-Used to diagnose PE, DIC and DVT
Nursing interventions for aCoagulation
-Monitor for of bleeding
-Educate your pt on bleeding risks, bruising and petechiae associated with medication therapy such as coumadin
-Educate your patients on the rationale for frequent blood work
Kidney function + Cr
-By-product of muscle catabolism
-Filtered by the glomeruli and excreted in the urine
-Indicator of renal disease
-Not influenced by diet or fluid intake
Low levels of Cr indicate…
Pregnancy, eclampsia or small muscle mass
High levels of Cr indicate…
RF, CHF, shock, SLE, cancer, leukemias, diabetic neuropathy, rhabdomyelosis, HTN & AMI
Drugs influencing Cr levels
Ancef, gentamicin, barbituates & amphotericin B
BUN
-End product of protein metabolism
-Excreted by the kidneys
-Correlates with Cr increase or decrease
Etiology of decreased BUN levels
Severe liver damage, low-protein diet, overhydration, malnutrition (-ve nitrogen balance) & IV fluids (glucose)
Drugs that cause decreased BUN levels
Phenothiazines
Etiology of elevated BUN
Dehydration, high protein intake, DM, GI bleed, low renal blood supply & licorice
Drugs that cause elevated BUN
-Nephrotoxic drugs
-Hydrochlorothiazide, edecrin, lasix, abx, gentamicin, methicillin, vancomycin, methyldopa, propranolol, morphine & lithum
GFR
-Estimation of how well blood passes through the filters in the kidney
-Calculated value is based on the age & Cr level
-<60 ml/min indicates kidney damage
Diabetes (hemoglobin A1C)
-Glucose molecule is attached to hemoglobin A1
-Calcultates the average blood glucose level within last 3 months
-Elevated levels above 8% indicate uncontrolled diabetes
Slide 56&57
Thyroid stimulating hormones (T3)
-More short acting and more potent than T4
-Secreted in response to thyroid- stimulating hormone from the pituitary gland and the thyroid-releasing hormone from hypothalamus
-Used for diagnosing hyperthyroidism
Thyroid stimulating hormone (T4)
-Secreted by the thyroid gland
-More concentrated than T3
-PKU test in newborns
-Used to measure how well the thyroid gland is functioning and if tumors are present
Nursing diagnosis of shock
-Ineffective peripheral tissue perfusion, risk for decreased cardiac tissue perfusion, ineffective cerebral tissue perfusion, and risk for impaired liver function
-Anxiety r/t threat of death & threat to current status
Planning stage of shock + goals
-Restoration of adequate tissue perfusion
-Normal BP >65 mm Hg
-Return/recovery of organ function
-Progression toward further complications r/t prolonged states of hypoperfusion
Collaborative care & successful management of shock includes
-Identification of patients at risk for shock
-Integration of the patient’s history, physical examination, and clinical findings to establish a diagnosis
-Interventions to control or eliminate the cause of decreased perfusion
-Protection of target and distal organs from dysfunction
-Provision of multisystem supportive care
Emergency management of shock
Patent airway & O2 delivery
Cornerstoe of therapy for septic, hypovolemic & anaphylactic shock is…
-Volume expansion; isotonic crystalloids (NS) for fluid resuscitation
Volume expansion
If the patient does not respond to 2 to 3L of crystalloids, blood administration and central venous monitoring may be instituted
Complications of fluid resuscitation
-Hypothermia & coagulopathy
Fluid resuscitation in pediatrics
Fluid resuscitation= 20 mL/kg of isotonic crystalloid/bolus
Primary goal of drug therapy in shock is
-Correction of decreased tissue perfusion
Adrenergic drugs for increasing tissue perfusion
Dobutamine, dopamine, E & NE
Vasodilator goal & drugs in increasing tissue perfusion
-Achieve/maintain a MAP of >65mmHg
-Alpha-adrenergic agonists & nitroglycerin
Vasoactive medications (adrenergic-agonists) effects
-Have a variety of effects on the alpha- and beta-adrenergic receptors
-Effects are related to the specific dose of the adrenergic drug
Common vasoactive medications (adrenergic-agonists)
Dobutamine, dopamine, E & NE, midodrine hydrochloride and phenylephrine hydrochloride
Maintenance dose of dobutamine hydrochloride
-2-15mcg/kg/min; acts on B1 more than B2
High dose of dobutamine hydrochloride
40mcg/kg/min; acts on B2 more than A1
Dopamine hydrochloride low dosage
0.5-3mcg/kg/min; dopaminergic
Dopamine hydrochloride moderate dose
3-10mcg/kg/min; B1 &A1
High dose of dopamine hydrochloride
> 10mcg/kg/min
Epinephrine hydrochloride (adrenalin chloride) low drug dose
1-4mcg/min; B1 more than B2 and A1
Epinephrine hydrochloride (adrenalin chloride) high dose
4-40mcg/min; A1 more than or equal to B1
Slide 69
Vasoactive drugs adverse effects + CNS
Headache, restlessness, tremors, nervousness, dizziness and insomnia
Vasoactive drugs adverse effects +CV
Chest pain, vasoconstriction, HTN, tachycardia (positive chronotropy), fluctuations in BP, and palpitations or dysrhythmias
Vasoactive drugs adverse effects +GI
Anorexia, dry mouth, N/V
Vasoactive drug nursing considerations
-Ideally, administer through a central line rather than a peripheral IV
-High rate of extravasation
-Carefully monitor VS, pt will typically be in the ICU
Nutrition + shock
-Enteral nutrition within the first 24 hours
-Initiate parenteral nutrition if enteral feedings contraindicated or fail to meet at least 80% of caloric requirements
-Monitor protein, nitrogen, BUN, glucose & electrolytes
Health promotion in shock management
-Identify pt at risk
Health promotion in shock management
-Identify pt at risk: Elderly, debilitating illness, immunocompromised & surgical or trauma pts
-Preventing shock: Monitor fluid balance to prevent hypovolemia and handwashing to prevent infection
Nursing role with patients in shock
-Monitor ongoing physical & emotional status
-Planning & quickly implementing nursing interventions
-Evaluate the pt response to therapy
-Provide emotional support
-Collaborating with other members of the health team
Acute intervention of pt in shock
Neuro, CV, resp, renal, temperature & skin changes, GI, hygiene and emotional support/comfort
Cardiogenic shock oxygenation
Supplemental O2, intubation
Cardiogenic shock circulation
Blood flow restored with thrombolytics, angioplasty with stent implantation, coronary revascularization, decreased workload of the heart with circulatory devices such as IABP & VAD
Cardiogenic shock drug therapies
Nitrates, inotropes (dobutamine), diuretics (furosemide), B-adrenergic blockers (contraindicated with rEF)
Cardiogenic shock supportive therapies
Correction of dysrhythmias
Hypovolemic shock oxygenation
Supplemental O2
Hypovolemic shock circulation
Fluid volume restored, rapid fluid replacement with large-bore IV, peripheral IV, end points of fluid resuscitation such as CVP of 15mmHg & PAOP of 10-12mmHg
Hypovolemic shock drug therapies
No specific drug therapies
Hypovolemic shock supportive therapies
-Cause corrected (ie. Bleeding or GI losses)
-Warmed fluids used
Septic shock oxygenation
Supplemental O2 or intubation
Septic shock circulation
Aggressive fluid resuscitation, end points of fluid resuscitation accomplished such as CVP of 15mmHg and PAOP of 10-12mmHg
Septic shock drug therapies
GOES w/ card 168
Antibiotics, vasopressors (dopamine), inotropes (dobutamine), anticoagulants (LMWH)
Septic shock supportive therapies
Cultures before antibiotics, monitor temperature, maintain glucose, stress ulcer prevention
Neurogenic shock oxygenation
Patency of airway, supplemental O2 & intubation
Neurogenic shock circulation
Fluids administered with caution
Neurogenic shock drug therapies
Vasopressors (phenylephrine), atropine (for bradycardia)
Neurogenic shock supportive therapies
Minimize spinal cord trauma & monitor temperature
Anaphylactic shock oxygenation
Patent airway, supplemental O2 & intubation
Anaphylactic shock circulation
Aggressive fluid resuscitation with colloids
Anaphylactic shock drug therapies
Antihistamine (diphenhydramine), epinephrine with nebulizer, bronchodilators with nebulizer (albuterol), and corticosteroids if hypotension persists
Anaphylactic shock supportive therapies
Remove noxious stimuli, avoid known allergens, premedicate according to prior hx of sensitivity
Collaborative care of cardiogenic shock
-Restore blood flow to the myocardium by restoring the balance between 02 supply & demand
-Thrombolytic therapy, angioplasty with stenting, emergency revascularization and valve replacement
Collaborative care of cardiogenic shock cont’d
-Hemodynamic monitoring drug therapy (e.g., diuretics to reduce preload)
-Circulatory assist devices (e.g., intra-aortic balloon pump or ventricular assist device)
Collaborative care of hypovolemic shock
-Management focuses on stopping the loss of fluid and restoring the circulating volume
-Fluid replacement is calculated using a 3: 1 rule (3 ml of isotonic crystalloid for every 1 ml of estimated blood loss)
Collaborative care of septic shock
-Fluid replacement to restore perfusion; hemodynamic monitoring
-Vasopressors (NE)
-Vasopressin (ADH) for patients resistant to vasopressor therapy
Collaborative care of septic shock cont’d
-IV corticosteroids for patients who require vasopressor therapy, despite fluid resuscitation, to maintain adequate BP
-Antibiotics after cultures are obtained
Collaborative care of septic shock cont’d (2)
-Glucose levels <10 mmol/L
-Stress ulcer prophylaxis with histamine (H2)-receptor blockers
-DVT prophylaxis with low-dose unfractionated heparin or LMWH
1 hour bundle for initial resuscitation for sepsis & septic shock
-Initiate bundle
1. Measure lactate level (remeasure if it is >2mmol/L)
2. Obtain blood cultures
3. Administer broad-spectrum antibiotics
4. Begin rapid administration of 30ml/kg crystalloid for hypotension or lactate >=4mmol/L
5. Apply vasopressors if hypotensive during or after fluid resuscitation to maintain MAP of >=65mmHg
Vasoactive agent management
-Use NE as first-line vasopressor
-Target MAP of 65mmHG (for pt w septic shock)
Slide 86&87
Collaborative care of neurogenic shock in a spinal cord injury
-Spinal stability
-Tx of the hypotension & bradycardia with vasopressors & atropine
-Fluids used cautiously as hypotension generally is not r/t fluid loss
-Monitor for hypothermia
Collaborative care of anaphylactic shock
-Epinephrine & diphenhydramine
-Maintain patent airway with nebulized bronchodilators & endotracheal tube OR cricothyroidotomy if necessary
Collaborative care for anaphylactic shock cont’d
-Priority is airway
-Aggressive fluid replacement
-IV corticosteroids if significant hypotension persists after 1 to 2 hours of aggressive therapy
Disseminated intravascular coagulation (DIC) is always caused by…
-An underlying disease or condition which must be tx for it to be resolved
Rapidly occuring DIC
-DIC that evolves rapidly (over hours/days) causes primarily bleeding
-Diagnosed by demonstrating thrombocytopenia, an elevated PTT, PT & d-dimer (or serum fibrin degradation products), and a decreasing plasma fibrinogen level
Tx of DIC
Correction of the cause and replacement of platelets, coagulation factors (in FFP), and fibrinogen (in cryoprecipitate) to control severe bleeding
Expected outcomes of DIC includes
Verbalization of fears or anxiety
Tx of systemic inflammatory response syndrome (SIRS)
-Prevention & tx of infection
-Maintenance of tissue oxygenation
-Nutritional & metabolic needs
-Support of failing organs (ARDS, DIC, RF)
ARF
Acute respiratory failure
ARF & ARDS
Pt requires intubation with PEEP
Nursing diagnosis of ARF/ARDS
-Impaired gas exchange
-Ineffective airway clearance
Respiratory failure diagnostic studies
-Hx & physical assessment
-ABG analysis, chest x-ray, CBC, sputum/blood cultures, electrolytes, ECG, urinalysis
-Ventilation/perfusion (V/Q) lung scan
-Pulmonary artery catheter in severe cases
ARF nursing diagnosis
-Impaired gas exchange
-Ineffective airway clearance
-Ineffective breathing pattern
-Risk for fluid volume imbalance
Planning/goals of ARF tx
-ABG values within patient’s baseline
-Breath sounds within patient’s baseline
-No dyspnea or breathing patterns within patient’s baseline
-Effective cough and ability to clear secretions
ARF prevention
-Thorough hx & physical assessment to identify at-risk patients
-Early recognition of respiratory distress
ARF respiratory therapy
-O2 to correct hypoxemia
-Mobilization of secretions
-Positive-pressure ventilation (PPV)
-Non-invasive PPV: Bi-PAP or CPAP
ARF drug therapy
-Bronchodilators -Relief of bronchospasm
-Corticosteroids -Reduction in airway inflammation
-Diuretics, nitrates if HF present -Reduction in pulmonary congestion
Diuretics, nitrates if HF present -Reduction in pulmonary congestion
+ ARF
-IV antibiotics
-Benzodiazepines +/or narcotics
ARF + medical supportive therapy
-Tx the underlying cause
-Maintain adequate CO & hemoglobin concentration
ARF + nutritional therapy
-Maintain protein and energy stores
-Enteral or parenteral nutrition
-Nutritional supplements
ARDS + COVID
Prone positioning
