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Circulatory Shock & Electrolyte Disorders (Distributive (Septic…

- - - - Shock Tx
        
        Sustaining cardiac output
        
        Reducing workload and O2 needs of myocardium
        
        Increasing coronary perfusion
        
        Adjusting peripheral vascular resistance
        
        Monitor volume
        
        Tx Priorities
        
        Maintain BP, airway, breathing, & O2 (ABCs)
        
        Addressing underlying cause
        
        Fluid replacement
        
        Whole blood can be used if >30% lost
        
        Volume expanders (colloids, crystalloids)
        
        Main Drug Classes for Tx
        
        Inotropic Agents
        
        Catecholamines
        
        Vasodilators/Vasoconstrictors
        
        Colloids/Crystalloids
        
        Electrolytes
- - - - Tx
        
        Colloids
        
        Proteins/large molecules not filtered into interstitium at capillaries
        
        IV, create oncotic pressure from drawing interstitial fluid into vasculature --> ++plasma volume
        
        Protein-based
        - Serum albumin - Serum globulins - Plasma protein fraction
        
        Non-blood colloids
        - Dextran - Hetastarch
        
        Prototype Drugs: Human Serum Albumin
        
        Trade names
        
        Albuminar
        
        Alburex
        
        Plasbumin
        
        Tx uses
        
        Low plasma volume
        
        Hypovolemic shock
        
        Hypoproteinemia
        
        Mechanism
        
        IV --> osmotic gradient --> fluid from instertitium into vasculature --> ++intravascular volume --> ++BP
        
        S/E
        
        Allergic reaction (uncommon)
        
        Peripheral edema
        
        Pulmonary congestion*
        
        Clotting difficulties (blood dilution)
        
        Circulatory overload*
        
        Renal failure --> fluid overload*
      - Tx
        
        Crystalloids
        
        Solutions (usually isotonic) with physiological concentrations of electrolytes
        
        IV, replace lost fluid --> maintain BP, ++urine output
        
        Crystalloids can leave vasculature (unlike colloids)
        
        NS
        
        Dextrose 5%
        
        LR
        
        Hypertonic salines
- - - - Tx
        
        Balance between improving cardiac output & increasing coronary perfusion
        
        Balance between reducing pulmonary edema & maintaining BP
        
        Fluid volume --> optimal filling pressure & stroke volume
        
        Vasodilators
        - Nitroprusside - Nitroglycerin
        
        Arterial & venous dilation --> decreased venous return & reduction in arterial resistance
        
        Helps with coronary perfusion
        
        Contraindicated in hypotension
        
        Adrenergic Agonists
        - Dobutamine (Dobutrex, B1 agonist)
        
        Mostly beta agonist --> mostly inotropy than chronotropy, some vasodilation --> decreased afterload
        
        Phosphodiesterase Inhibitor
        - Milrinone (Primacor)
        
        Increases contractility (Ca2+ myocardial influx) --> decreased afterload, increased stroke volume
        
        Catecholamines
        - Epinephrine - Dopamine
        
        Positive inotropes (++contractility) - Caution (arterial constriction & ++HR)
        
        Organ failure d/t vasoconstriction
        
        Potent non specific adrenergic agonist
        
        ++CO, MAP, coronary flow
        
        Vasoconstrictors
        - Norepinephrine (Levophed) (A1, B1, B2) - Isoproterenol (Isuprel) (B1, B2) - Phenylephrine (Neosynephrine) (A1)
        
        Maintain BP when fluid replacement not enough
        
        A1 adrenergic receptors on arterioles
        
        Effects potent but short, with S/E of potential organ damage
        
        Last resort
- - - - Pathophysiology
        
        Inflammatory response from infection
        
        Mast cells + cytokines --> WBC, complement, platelets, NO
        
        Toxins from bacteria
        
        Vasodilation (histamines & systemic serotonin)
        
        Clotting (d/t endothelial injury + platelet activation)
        
        Inflammation & vascular permeability
        
        S/S
        
        Hypotension (+narrow pulse pressure)
        
        Abrupt changes in cognition or behaviour
        
        Warm, flushed skin** (unique to septic shock)
        
        Fever & ++WBC*
        
        Elevated lactate/metabolic acidosis
        
        Decrease in systemic vascular resistance
        
        Maldistribution of volume d/t ++vasodilation & plasma leakage
        
        Multiple Organ Dysfunction Syndrome (MODS)
        
        Presence of altered organ function in acutely ill patient, where homeostasis is insufficient without intervention
        
        End-result of severe sepsis
        
        Tx
        
        Antimicrobial Tx
        
        Broad spectrum --> focal
        
        Source control
        
        Isolation precautions
        
        O2 Tx
        
        Maintain >92% saturation (COPD = 90%)
        
        If continued...
        
        Fluid resuscitation
        
        NS 500 ml bolus & reassess
        
        Pediatrics: 20 ml/kg
        
        Adults: 30 ml/kg
        
        Adrenergic/Inotropes
        
        Titrate to get MAP >60 mmHg
        
        Norepinephrine (IV)
        
        Dopamine or Dobutamine (IV)
        
        Notes
        
        Dopamine (top choice)
        
        Non-selective adrenergic agonist
        
        Low doses --> renal vasodilation (preserve kidney fx)
        
        High doses --> too much vasoconstriction
        
        S/E Arrhythmias, cardiac stress, peripheral vasoconstriction
        
        Dobutamine
        
        B1 selective --> CO improved
        
        Note
        
        Rule of Thumb:
        
        Pediatric patients compensate well, then suddenly crash, with respiratory failure 1st
        
        Adults compensate less well, with cardiac failure 1st
        
        Complications
        
        Hypotension --> hypoxia --> hypoxemia --> overal ischemia...
        
        Renal failure
        
        Fx affected at 15-20 min of ischemia
        
        S/S: Oliguria
        - Tx: Inotropes, fluid resuscitation
        
        DIC
        
        Ongoing complement activated coagulation, inflammatory mediators, cytokines, NO damage + decreased fibrin synthesis d/t hepatic hypoperfusion --> widespread coagulation --> depletion of platelets & clotting factors --> risk of hemorrhage
        
        Tx (assess 1st):
        - Anticoagulants (inhibit Thrombin), Heparin - Blood products (whole blood, platelets, FFP, Vit.K)
        
        Metabolic acidosis (switched to anaerobic metabolism)
        
        Tx:
        
        Fix underlying issue
        
        Correct hyperkalemia
        
        Insulin (shifts K+ into cells)
        
        +O2 (decrease CO2)
        
        Sodium bicarbonate IV (temporary fix)
        
        Hyperglycemia (decreased glucose transport d/t cell metabolism alterations + sympathetic stimulation --> cortisol --> ++serum glucose)
        
        Tx:
        
        Insulin IV + NS enteral nutrition
        
        GI Ischemia (mucosal vasoconstriction)
        
        S/S: N&V, abdominal pain, later bowel necrosis + acute hemorrhage
        
        Tx:
        
        PPIs, H2 antagonists, sucralfate
        
        Antiemetics
        
        NG feeds
  - - - Pathophysiology
        
        Vascular stage
        
        IgE --> Mast Cell --> ++Histamine --> binds to H1 receptors on endothelial cells --> vasodilation + increased permeability + hemostasis (+risk of clotting) + fluid shifts
        
        Cellular stage
        
        Leukocytes (neutrophils) migrate to tissues
        
        Leukocyte activation & phagocytosis
        
        Secretion of enzymes & oxygen radicals --> eliminate microbe + oxidative stress, inflammation, & cellular injury
        
        Notes:
        
        Other vasodilators released:
        
        Nitric Oxide
        
        Binds with 'superoxide radicals' made by WBC --> potent toxic "reactive nitrogen" --> epithelial damage --> platelet activation --> ++ risk of clotting
        
        Systemic serotonin
        
        Massive fluid shifts --> up to 35% volume in 10 min
        
        S/S
        
        Early:
        
        Itching
        
        Flushed skin
        
        Urticaria
        
        Swelling
        
        Coughing, wheezing, tachypnea, SOB
        
        Later:
        
        Hypotension --> circulatory collapse
        
        Edema
        
        Cyanosis
        
        Sympathetic stimulation
        
        Clotting
        
        Tx
        
        Adrenergics:
        
        Epinephrine IM mid-anterior lateral thigh (vastus lateralis muscle)
        
        q5min x 3 dose maximum
        
        Airway & ventilation:
        
        Oxygen @ 15L by non-rebreather mask
        
        Intubation PRN
        
        Antihistamines:
        
        Benadryl (Diphenhydramine) IV
        
        Bronchodilators:
        
        Ventolin (Salbutamol) nebulizer
        
        Glucocorticoids:
        
        Hydrocortisone
        
        Methylprednisolone IV
        
        Prednisone PO (continued x 3 days)
        
        Stop causative agent:
        
        Stop infusion
        
        Application of ice to the site of causative agent
        
        If continued anaphylaxis...
        
        Fluid resuscitation
        
        NS 500 ml bolus & reassess
        
        Pediatric: 20 ml/kg
        
        Adult: 30 ml/kg
        
        Positioning
        
        Supine, legs elevated --> core circulation
        
        Trendelenburg position
- - - - Sodium (Na+)
        
        Na+ Fx
        
        Controls & regulates volume of body fluids
        
        Major determinant of ECF volume
        
        Chief electrolyte of ECF, but influences ICF
        
        Generation & transmission of nerve impulses
        
        Eliminated mainly by kidneys
        
        Conserved by kidneys (aldosterone)
        - Normal range: 135-145 mEq/L
        
        Hyponatremia Pathophysiology
        
        Na+ loss from intravasculature
        
        Decreases osmolality of ECF
        
        Water moves into interstitial space, then into cells
        
        Extracellular compartment is depleted of water
        
        Cells swell --> clinical symptoms
        
        S/S
        
        N/A
        
        Headache
        
        Confusion
        
        Drowsiness/fatigue
        
        Restlessness/irritability
        
        Muscle weakness, spasms, cramps
        
        Seizures, coma
        
        Tx
        
        <135 mEq/L
        
        Caused by dilution of plasma or sodium loss
        - Give Na+ via IV - D5NS
        
        - Prototype Drug: Sodium Chloride
        
        Tx uses
        
        Hyponatremia
        
        Mechanism
        
        Replacement solution for lost sodium
        
        S/E
        
        Hypernatremia
        
        Lethargy, confusion, restlessness
        
        Muscle tremor or rigidity
        
        HTN/Hypotension (if fluid overload)
        
        Pulmonary edema
        
        Hypernatremia Pathophysiology
        
        Na+ increased in intravasculature
        
        Increased osmolality of ECF
        
        Water leaves interstitial space & cells
        
        Cells shrink
        
        Suppression of aldosterone --> Na+ excreted in urine
        
        Tx
        
        More than >145 mEq/L
        
        Often d/t kidney disease or excessive sodium intake
        
        Most common electrolyte imbalance in hospital
        
        Restrict salt intake
        - 0.45% NS - Diuretics
      - Potassium (K+)
        
        K+ Fx
        
        Major cation of the ICF
        
        Main regulator of cellular enzyme activity & and cell water content
        
        K+ & Na+ have inverse relationship (More K+ = Less Na+, and vice-versa)
        
        Vital for nerve impulse transmission (particularly in the nerves, heart, skeletal, intestinal, and lung)*
        
        Cellular metabolism and excitation
        
        Assists in acid-base balance by exchanging with H+
        
        Excreted mainly by kidneys
        
        Conserved by sodium pump & kidneys when low
        
        Aldosterone triggers K+ excretion in urine*
        
        Normal range: 3.5-5.0 mEq/L
        
        Causes of Hypokalemia
        
        Decreased intake
        
        Increased loss (GI, diuretics, trauma, burns)
        
        Shift into cells
        
        ++Aldosterone
        
        ++Diuretics
        
        Pathophysiology
        Low ECF K+ --> Increase in resting membrane potential --> cell less excitable
        
        S/S
        
        GI tract
        
        Anorexia
        
        N&V
        
        Abdominal distention
        
        CNS
        
        Lethargy
        
        Diminished reflex
        
        Confusion
        
        Mental depression
        
        Muscles
        
        Weakness
        
        Flaccid paralysis
        
        Weakness of respiratory muscles
        
        Respiratory arrest
        
        CV system
        
        Decrease in standing BP
        
        Dysrhythmias
        
        Myocardial damage
        
        Cardiac arrest
        
        ECG changes
        
        Long PR
        
        Depressed ST
        
        Low T
        
        Prominent U
        
        Kidneys
        
        Decreased function to concentrate waste
        
        Water loss & thirst
        
        Kidney damage
        
        Tx
        - KCL (IV or PO)
        
        1 more item...
        
        Causes of Hyperkalemia
        
        Excess intake
        
        Dietary intake
        
        Parenteral administration
        
        Decreased loss
        
        K+ sparing diuretics
        
        Renal failure
        
        Adrenal insufficiency
        
        K+ shift out of cells
        
        Extensive injury (eg: crushing)
        
        Metabolic acidosis
        
        Pathophysiology
        
        High ECF K+ --> decrease resting membrane potential --> cell less excitable
        
        S/S
        
        GI tract
        
        Diarrhea
        
        Colic
        
        N/V
        
        CNS
        
        Numbness
        
        Paresthesias
        
        Muscles
        
        Early: Irritability
        
        Late: Weakness --> flaccid paralysis
        
        CV system
        
        Conduction disturbances
        
        Ventricular fibrillations
        
        Cardiac arrest
        
        ECG changes
        
        Low P wave
        
        Long PR
        
        Wide QRS
        
        Peaked T
        
        Kidneys
        
        Oliguria --> anuria
        
        Tx
        - Kayexalate (Sodium polystyrene sulfonate) (PO powder)
        
        Active in large intestine
        
        Leaches out K+
      - Calcium (Ca2+)
        
        Ca2+ Fx
        
        Most abundant electrolyte
        
        99% in bones
        
        Ca2+ and (Phosphate) P3- have inverse relationship*
        
        Nerve impulse
        
        Clotting
        
        Muscle contractions & other cell activity
        
        Needed for Vit.B12 absorption and use
        
        Necessary for strong bones & thickness of cell membranes
        
        Use is stimulated by Vit.D
        
        Real excretion, feces, bile, perspiration, and digestive secretions
        
        RDA
        
        1g for adults
        
        Higher for children, pregnant, lactating women, older adults, post-menopausal
        
        Normal value
        
        Total: 2.10-2.50 mmol/L
        
        Ionized: 1.15-1.35 mmol/L
        
        Hormonal Control Systems
        
        3 main organs to maintain Ca2+ levels
        
        Small intestine (absorb)
        
        Bones (storage)
        
        Kidney (homeostasis)
        
        PTH (increase serum concentration)
        
        Stimulates active Vit.D
        
        Mobilize calcium & phosphate from bones into serum
        
        Affects kidneys to excrete extra phosphate (prevents excess phosphate)
        
        Increases renal reabsorption of Ca2+
        
        Calcitonin (decrease serum concentration)
        
        Decrease renal reabsorption
        
        Inhibition of bone reabsorption
        
        Vit.D
        
        Facilitate Ca2+ absorption in small intestine
        
        Causes of Hypocalcemia
        
        Decreased ionized Ca2+ (large transfusion with citrated blood)
        
        Kidney disease
        
        Dietary deficit
        
        Decrease in GI and bone absorption
        
        Pathophysiology of Hypocalcemia
        
        Ca2+ line pores of cell membranes (especially neurons)
        
        Ca2+ & Na+ repel each other
        
        In hypocalcemia, blocking effect is minimized
        
        Easier Na+ influx --> easier depolarization --> increased excitability of nervous system --> spasms, tingling (convulsions & tetany if severe)
        
        Skeletal, smooth, & cardiac muscle fx all affected by overstimulation
        
        S/S
        
        Bones
        
        Osteoporosis --> fractures
        
        CNS
        
        Tingling--> convulsions
        
        Muscles
        
        Muscle spasm --> tetany
        
        CVS
        
        Dysrhythmias--> cardiac arrest
        
        Other
        
        Abnormal deposits of Ca2+ in body tissues
        
        1 more item...
        
        Causes of Hypercalcemia
        
        Loss from bones
        
        Immobilization
        
        Carcinoma with bone metastases
        
        Multiple myeloma
        
        Excess intake
        
        Dietary or antacids
        
        Increase in bone-mobilizing hormones
        
        ++PTH, ++Vit.D, steroid therapy
        
        S/S
        
        Bones
        
        Bone pain --> Osteoporosis --> fractures
        
        CNS
        
        Decreased deep-tendon reflexes --> lethargy --> coma
        
        Muscles
        
        Muscle fatigue (hypotonia) --> decreased GI motility --> constipation
        
        CVS
        
        Depressed activity --> dysrhythmias --> cardiac arrest
        
        Kidneys
        
        Stones --> kidney damage
        
        N&V
        
        Assessment Tips
        
        Trousseau's Sign
        
        BP cuff --> hand/arm spasms
        
        Chvostek's Sign
        
        Tap facial nerve (XII) --> twitch
        
        ECG Changes
        
        ST prolonged and rounded
        
        Note: Hyper-K+ affects height of ST wave, Ca2+ affects width
      - Phosphorus (P3-)
        
        P3- Fx
        
        ~85% contained in bone
        
        Major role in bone formation
        
        Metabolic processes (ATP, enzymes for glucose, fat, protein)
        
        Necessary component of cell parts, in nucleic acids of DNA/RNA & phospholipids of membrane
        
        Acid-base buffer in ECF & renal excretion of H+
        
        O2 delivery depends on ATP
        
        Needed for normal function of WBC & platelets
        
        Causes of Hypophosphatemia
        
        <2.5 mg/dL
        
        Alcoholism
        
        Refeeding of patients after starvation
        
        Heat stroke
        
        Respiratory alkalosis
        
        Hyperventilation
        
        DKA
        
        Hepatic encephalopathy
        
        Major burns
        
        Hyperparathyroidism
        
        Low magnesium
        
        Low K+
        
        Diarrhea
        
        Vit.D deificency
        
        Diuretics & antacid use
        
        S/S
        
        Confusion
        
        Muscle weakness
        
        Tissue hypoxia
        
        Muscle & bone pain
        
        Increase susceptibility to infection
        
        Bruising & bleeding from platelet dysfunction
      - Magnesium (Mg2+)
        
        Mg2+ Fx
        
        Mostly within body cells: heart, bone, nerve and muscle tissues
        
        Second most important cation in the intracellular fluid
        
        Metabolism of carbohydrates and nitrogen, protein and DNA synthesis, DNA and RNA transcription, and translation of RNA
        
        Maintains normal intracellular levels of potassium, helps maintain electric activity in nervous tissue membranes and muscle membranes*
        
        Absorbed in the intestines and excreted by the kidneys
        
        Normal value: 1.5-2.5mEq/L (one third of the amount bound to plasma proteins)
        
        Hypomagnesemia Causes
        
        Decreased intake (malnutrition, starvation)
        
        Impaired GI absorption
        
        Malabsorption syndrome
        
        Alcohol withdrawal syndrome
        
        Hypercalcemia
        
        Excretion of Mg2+ by GI tract
        
        Diarrhea
        
        Draining GI fistula
        
        Excessive excretion
        
        ++Aldosterone
        
        Large urine losses
        
        Pathophysiology
        
        Hypercalcemia --> Excretion of Mg2+ by GI tract
        
        Mg2+ --> inhibits PTH transport --> decreased Ca2+ being released from bone --> possible Ca2+ deficit
        
        S/S
        
        Mental changes
        
        Agitation
        
        Depression
        
        Confusion
        
        CNS
        
        Convulsions
        
        Paresthesia
        
        Tremor, ataxia
        
        Muscles
        
        Cramps
        
        Spasticity
        
        Tetany
        
        CVS
        
        Tachycardia
        
        Hypotension
        
        Dysrhythmias
        
        Frequently associated hypokalemia
        
        Intracellular Mg2+ --> inhibition of renal outer medullary potassium (ROMK) channels --> ++ K+ excretion
        
        Hypermagnesemia Causes
        
        Rare in normal renal fx
        
        May occur from Mg2+ replacement
        
        May occur when MgSO4 (magnesium sulfate) is administered to prevent preeclampsia seizures
        
        Pathophysiology
        
        Renal fail/++IV Mg2+/decreased GI elimination and/or absorption --> ++Mg2+ --> altered electrical conduction --> slowed HR & AV block & diminished reflexes, drowsiness, lethargy --> Severe Respiratory Depression --> Respiratory arrest may occur + vasodilation (redness & warmth) from cardiac effects
        
        Prototype Drug: Magnesium Sulfate
        
        Tx uses
        
        Severe hypomagnesemia
        
        Catharsis of colon
        
        Anticonvulsant in patients with eclampsia & preeclampsia
        
        Mechanism
        
        Replacement solution for lost magnesium
        
        S/E
        
        Hypermagnesemia
        
        Sedation & confusion
        
        Diarrhea
        
        Flushing of skin
        
        Intense thirst
        
        Muscle weakness
        
        Serious: Neuromuscular blockade, respiratory paralysis, heart block, circulatory collapse