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Oxygen&Perfusion
F&E,Acid/Base Balance
| Question | Answer |
|---|---|
| Potassium = | 3.5-5.0 |
| Calcium = | 8.5-10.5 |
| Magnesium = | 1.8-2.7 |
| Hyperkalemia | High serum potassium caused by Massive intake Impaired renal excretion Shift from ICF to ECFCommon in massive cell destructionBurn, crush injury, or tumor lysis |
| Hyperkalemia Manifestations | Weak or paralyzed skeletal muscles Ventricular fibrillation or cardiac standstill Abdominal cramping or diarrhea |
| Hypokalemia | Low serum potassium caused by Abnormal losses of K+ via the kidneys or gastrointestinal tractMagnesium deficiencyMetabolic alkalosis |
| Hypokalemia Manifestations | Most serious are cardiac Skeletal muscle weakness Weakness of respiratory musclesDecreased gastrointestinal motility |
| Hypercalcemia | High serum calcium levels caused byHyperparathyroidism (two thirds of cases)Malignancy Vitamin D overdoseProlonged immobilizationBone metastases |
| Hypercalcemia Manifestations | Decreased memory Confusion Disorientation Fatigue Constipation |
| Hypocalcemia | Low serum Ca levels caused byDecreased production of PTHAcute pancreatitis Multiple blood transfusions AlkalosisDecreased intake |
| Hypocalcemia Manifestations | Positive Trousseau’s or Chvostek’s sign Laryngeal stridor Dysphagia Tingling around the mouth or in the extremities |
| Hypermagnesemia | High serum Mg caused byIncreased intake or ingestion of products containing magnesium when renal insufficiency or failure is present |
| Hypermagnesemia Manifestations | Lethargy or drowsiness Nausea/vomiting Impaired reflexes Respiratory and cardiac arrest |
| Hypomagnesemia | Low serum Mg caused by Prolonged fasting or starvation Chronic alcoholism Fluid loss from gastrointestinal tractProlonged parenteral nutrition without supplementationDiuretics |
| Hypomagnesemia Manifestations | Confusion Hyperactive deep tendon reflexes Tremors Seizures Cardiac dysrhythmias |
| Sodium | 135-148 |
| Hypernatremia | Elevated serum sodium occurring with water loss or sodium gain Causes hyperosmolality leading to cellular dehydration Primary protection is thirst from hypothalamus |
| Hypernatremia Manifestations | Thirst, lethargy, agitation, seizures, and coma Impaired LOC |
| Hyponatremia | Decreased serum sodium Results from loss of sodium-containing fluids or from water excess |
| Hyponatremia Manifestations | Confusion, nausea, vomiting, seizures, and coma |
| hypovolemia | Fluid volume deficit Abnormal loss of normal body fluids (diarrhea, fistula drainage, hemorrhage), inadequate intake, or plasma-to-interstitial fluid shiftTreatment: replace water and electrolytes with balanced IV solutions |
| hypervolemia | Fluid volume excess Excessive intake of fluids, abnormal retention of fluids (CHF), or interstitial-to-plasma fluid shiftTreatment: remove fluid without changing electrolyte composition or osmolality of ECF |
| Hypotonic | More water than electrolytes Pure water lyses RBCs Water moves from ECF to ICF by osmosisUsually maintenance fluids |
| Hypotonic Solutions | 1/2 NS(0.45% NaCl)Na 69.3mEqCl 69.3mEqpH 5.0 |
| Isotonic | Expands only ECF No net loss or gain from ICF |
| Isotonic Solutions | Lactated Ringer's(LR):Na 130mEq,Cl 109mEq,K 4mEq,Ca 3mEq,Lactate 28mEq,pH 6.5Normal Saline(0.9%), Na 154mEq,Cl 154mEq,pH 5.0D5W 50g dextrose, pH 4.5 |
| Hypertonic | Initially expands and raises the osmolality of ECF Require frequent monitoring of Blood pressure Lung sounds Serum sodium levels |
| Hypertonic Solutions | D5 1/2 NS(5%D,0.45%NaCl):50g dextrose,Na 69.3mEq,Cl 69.3mEq,pH4.0D10(10%D):100g dextrose,pH4.5 |
| Respiratory Acidosis | pH is down PaCO2 is up |
| Metabolic Acidosis | pH is down HCO3 is down |
| Respiratory Alkalosis | pH is up PaCO2 is down |
| Metabolic Alkalosis | pH is up HCO3 is up |
| CO2 | 35-44 |
| HCO3 | 22-26 |
| pH | 7.35-7.45 |
| BUN | 10-30mg/dl (1.8-7.1mmo/L) |
| Creatinine | 0.5-1.5mg/dl (44-133mmol/L) |
| CO2 | is an acid,Measured as partial pressure exerted by CO2 PaCO2 |
| HCO3 | bicarbonate is basic(alkaline)Binds with free H= to decrease concentration |
| Buffering systems | Activated in response to changes in acid/base balance Absorb excess acid or basePrevent significant changes in pHLocated in ECF and ICF compartments Function at different times |
| Compensation | Respiratory system compensates for changes in pH by increase or decreased respiration Renal system compensates for changes in pH by producing more acidic or more alkaline urine |
| Lungs compensate by regulating carbonic acid | Decrease carbonic acid by blowing off CO2 & leaving water H2CO3 - CO2 = H2O Response begins within minutes/hoursRespiratory rate will change Metabolic acidosis: RR ↑ Metabolic alkalosis: RR ↓ |
| Kidneys compensate by regulating HCO3 (bicarbonate) | Reabsorb bicarbonate or regenerate new bicarbonate from CO2 and waterH2O + CO2 = HCO3 + HCatalyzed by enzyme carbonic anhydraseH+ secreted by tubular cells and is buffered by dibasic phosphate (HPO4) and ammonia (NH3)Response begins within hours/d |
| Normal ratio for Kidney compensation | bicarbonate 20 : 1 carbonic acid |
| Role of K+ | H+ cannot be excreted w/o another +ion being retained,decreased pH=H+ leaves kidneys,K+stays(hyperkalemia),If H+stays,K+ must move out into ECF=hyperkalemia,Increased pH=retention of H+ & excretion of K+(hypokalemia) |
| Metabolic Acidosis pH < 7.35, HCO3 < 22, K > 5.5, PaCO2 N | Increased noncarbonic acids or decreased bicarbonate Diabetic ketoacidosisDiarrheaRenal failureShockSalicylate (acetylsalicylic acid) overdoseSepsis |
| Metabolic Acidosis Clinical manifestations | deep, rapid respirations (Kussmaul’s)Disorientation & comaVentricular dysrhythmiasLactic acidosis & hypotension |
| Metabolic Acidosis Compensation: | Increased respiratory rate Kidneys = H+ excretion & HCO3 retention K+ moves out of cell |
| Respiratory Acidosis pH<7.36, PaCO2>44mmHg, HCO3 N, K+>5.5 | Hypoventilation, may be r/t:Drug overdose Chest trauma Pulmonary edema Airway obstructionCOPDNeuromuscular disease |
| Respiratory Acidosis Clinical Manifestations | severe respiratory acidosis:Cyanosis, rapid and shallow breathing Diaphoresis, disorientationCO2 narcosis: HA, blurred vision, weaknessProlongedincreased intracranial pressure, dysrhythmiasPapilledema, peripheral vasodilation |
| Respiratory Acidosis Compensation | Increased respirations (gradual adaptation to increased CO2) Kidneys excrete H+ and retain HCO3K+ moves out of cells |
| Metabolic Alkalosis pH>7.45, PaCO2 N, HCO3>26, K+<3.5 | Excess loss of acid Loss of gastric secretions,Vomiting,Gastric suctioning Overuse of antacids or increased intake of bicarbonate K+ wasting diuretics H+ is excreted to balance K+ loss |
| Metabolic Alkalosis Clinical manifestations | apathy & mental confusion Shallow breathing Polyuria & polydipsia (hypokalemia)Volume depletion, lightheadednessSpastic muscles, weakness, cramps, paresthesiasDizziness, dysrhythmias |
| Metabolic Alkalosis Compensation | Decreased respiratory rate to retain CO2Kidneys retain H+ and excrete HCO3K+ moves into cells |
| Respiratory Alkalosis pH 7.44 or >, PaCO2<36mmHg, HCO3 N, K+<3.5 mEq/L | Hyperventilation, may be r/t Anxiety High altitude Pregnancy Fever Hypoxia Excessive tidal volume in ventilated patients Initial stage of pulmonary embolus |
| Respiratory Alkalosis Clinical manifestations | CNS irritabilityLight-headedness, circumoral numbnessParesthesias Numbness, prickling, tinglingAltered consciousnessCramps, carpopedal spasm |
| Respiratory Alkalosis Compensation | Decreased respiratory rate; Increased H+ excretion and HCO3 retention by kidneysK+ moves out |
| Respiratory problem = respiratory imbalance | COPD Pneumonia Pulmonary embolus Respiratory failure |
| Non-respiratory problem = metabolic imbalance | Diabetic ketoacidosis Renal failure Diarrhea Vomiting |
| Diuretic Drugs | Drugs that accelerate the rate of urine formation Result: removal of sodium and water |
| Carbonic Anhydrase Inhibitors (CAIs) | Diuretic Drugs acetazolamide (Diamox) methazolamide dichlorphenamide |
| Carbonic Anhydrase Inhibitors (CAIs) Mechanism of Action | The enzyme carbonic anhydrase helps to make H+ ions available for exchange with sodium and water in the proximal tubulesCAIs block the action of carbonic anhydrase, thus preventing the exchange of H+ ions with sodium and water |
| Carbonic Anhydrase Inhibitors (CAIs) Mechanism of Action | Inhibition of carbonic anhydrase reduces H+ ion concentration in renal tubulesAs a result, there is increased excretion of bicarbonate, sodium, water, and potassiumResorption of water is decreased and urine volume increased |
| Carbonic Anhydrase Inhibitors (CAIs) Indications | Glaucoma Edema Epilepsy High altitude sickness |
| Carbonic Anhydrase Inhibitors (CAIs) Adverse Effects | Metabolic acidosis Anorexia Hematuria Photosensitivity Melena Hypokalemia Drowsiness Paresthesias Urticaria |
| Loop Diuretics | bumetanide (Bumex)ethacrynic acid (Edecrin)furosemide (Lasix) |
| Loop Diuretics Mechanism of Action | Act directly on the ascending limb of the loop of Henle to inhibit chloride and sodium resorption Increase renal prostaglandins, resulting in the dilation of blood vessels and reduced peripheral vascular resistance |
| Loop Diuretics Effects | Potent diuresis and subsequent loss of fluid Decreased fluid volume causes: Reduced BP Reduced pulmonary vascular resistance Reduced systemic vascular resistance Reduced central venous pressure Reduced left ventricular end-diastolic pressure |
| Loop Diuretics Effects | Potassium and sodium depletion |
| Loop Diuretics Indications | Edema associated with HF or hepatic or renal diseaseControl of HTNIncrease renal excretion of Ca in patients with hypercalcemiaCertain cases of HF resulting from diastolic dysfunction |
| Loop Diuretics Adverse Effects | CNS:Dizziness,HA,tinnitus,blurred vision,GI:N/V,diarrhea,Hematologic: Agranulocytosis,neutropenia, Thrombocytopenia,Metabolic: Hypokalemia,hyperglycemia, hyperuricemia |
| Osmotic Diuretics | mannitol (Osmitrol) |
| mannitol (Osmitrol) | Works in the proximal tubulePulls water into the renal tubules from the surrounding tissues Inhibits tubular resorption of water and solutes, producing a rapid diuresis |
| mannitol (Osmitrol) | Increases glomerular filtration and renal plasma flow—helps to prevent kidney damage during acute renal failureReduces excessive intraocular pressure |
| mannitol (Osmitrol) Indications | Used in the treatment of patients in the early, oliguric phase of ARF To promote the excretion of toxic substances Reduction of intracranial pressure Treatment of cerebral edema NOT indicated for peripheral edema |
| mannitol (Osmitrol) | Crystalizes,so always use a filter! Give w/blood. Never give to someone who is dehydrated or has liver failure,or Heart failure! Emergency Drug! IV ONLY! |
| Potassium-Sparing Diuretics | amiloride (Midamor)spironolactone (Aldactone)triamterene (Dyrenium)Also known as aldosterone-inhibiting diuretics |
| Potassium-Sparing Diuretics Mechanism of Action | Work in collecting ducts and distal convoluted tubulesInterfere with sodium-potassium exchangeCompetitively bind to aldosterone receptorsBlock the resorption of sodium and water usually induced by aldosterone |
| Potassium-Sparing Diuretics Drug Effects | Prevent potassium from being pumped into the tubule, thus preventing its secretionCompetitively block the aldosterone receptors and inhibit its actionThe excretion of sodium and water is promoted |
| Potassium-Sparing Diuretics Indications spironolactone and triamterene | Hyperaldosteronism Hypertension Reversing the potassium loss caused by potassium-losing drugs Certain cases of heart failure |
| Potassium-Sparing Diuretics Indications amiloride | Treatment of heart failure |
| Potassium-Sparing Diuretics Adverse Effects | CNS:Dizziness, headache,GI: Cramps, nausea, vomiting, diarrhea, Urinary frequency, weakness **hyperkalemia** |
| spironolactone adverse effects | Gynecomastia Amenorrhea Irregular menses Postmenopausal bleeding |
| Thiazide diuretics | hydrochlorothiazide (Esidrix, HydroDIURIL)chlorothiazide (Diuril)trichlormethiazide (Metahydrin) |
| Thiazide-like diuretics | chlorthalidone (Hygroton) metolazone (Mykrox, Zaroxolyn) |
| Thiazide and Thiazide-like Diuretics Mechanism of Action | Inhibit tubular resorption of Na, Cl, and K ions Action primarily in the distal convoluted tubuleResult: water, Na, and Cl are excreted K is also excreted to a lesser extent Dilate the arterioles by direct relaxation |
| Thiazide and Thiazide-like Diuretics Drug Effects | Lowered peripheral vascular resistanceDepletion of sodium and water (and potassium) |
| Thiazide and Thiazide-like Diuretics Precautions | Thiazides should not be used if creatinine clearance is less than 30 to 50 mL/min (normal is 125 mL/min)Metolazone remains effective to a creatinine clearance of 10 mL/min |
| Thiazide and Thiazide-like Diuretics Indications | Hypertension (one of the most prescribed group of drugs for this)Edematous statesIdiopathic hypercalciuriaDiabetes insipidus HF due to diastolic dysfunctionAdjunct drugs in treatment of edema r/t HF,hepatic cirrhosis, corticosteroid or estrogen therapy |
| Thiazide and Thiazide-like Diuretics Adverse Effects | CNS:Dizziness, headache, blurred vision, paresthesias, decreased libido,GI:Anorexia, nausea, vomiting, diarrhea,GU:Impotence,Integumentary:Photosensitivity, urticaria,Metabolic: Hypokalemia,glycosuria, hyperglycemia, hyperuricemia |
| Nursing Implications when administering diuretics… | Check for allergies,edema,CHF,LOC,head injury,Glsgocoma scale,Fluid Volume Status,Weight,V/S,Assess for disorder,take Lasiks in A.M.,monitor electrolytes,Diabetic pts on Thyazides monitor glucose, monitor I/Os. |
Created by:
LauraHall
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