Respiratory Interpretation of ABGs (compensated and uncompensated) and conditions that cause changes in ABGs - DONE Arterial Blood Gases - ABGs ● pH: 7.35-7.45 ● pCO2: 35-45mmHg ● pO2: 80-100 ● HCO3 (Bicarb):22-26mEq/L ● O2 Sat: >95% (96-100%) ● Acidosis: High CO2 (respiratory). Low Bicarb (metabolic) ● Alkalosis: Low CO2 (respiratory). High Bicarb (metabolic) ● ROME: Respiratory is Opposite / Metabolic is Equal ● Allen test needed to take ABG PCO2: 35-45mmHg ● Greater that 45 → respiratory acidosis ○ Causes: hypoventilation, COPD, pneumonia, pulmonary edema ● Less that 35 → respiratory alkalosis ○ Causes: hyperventilation (from anxiety), hyperthyroidism HCO3 (Bicarb):22-26mEq/L ● Kidneys regulate bicarbonate ● HCO3 less than 22 → metabolic acidosis ○ Causes: DM, sepsis, starvation, chronic diarrhea ● HCO3 greater than 26 → metabolic alkalosis ○ Caused by: vomiting, gastric suction, hypokalemia, antacid abuse Compensating: ● IF pH is in the normal range while CO2 or HCO3 is out of range → compensated ● IF pH is NOT in the normal range while CO2 or HCO3 is out of range → uncompensated ● Respiratory compensation takes place in seconds or minutes ● Metabolic compensation can take hours or days Partial or NO compensating: look at 2nd system to see if it within range or not ● IF 2nd system is within range → uncompensated ● IF 2nd system is out of range, and pH is out of range → partial compensation ABG calculator Ventilators. Knowledge of various modes and indications for use: A/C, SIMV, PEEP, CPAP, weaning, complications and alarms. Sedation (diprivan) and precautions - DONE Invasive Ventilation → Intubation: ● Intubation (endotracheal tube or nasotracheal tube) ● Short term ● Inserted by MD, NP, or paramedic ● Passed the vocal cords and sits 2cm above carina ● Document tube size and centimeters inserted ● Can cause trauma to teeth, oral and tracheal mucosa ● Care: ABGs, Vital signs, skin color, reposition in mouth every 12hrs, suction as needed ● Must check placement immediately after insertion: ○ CO2 detector, auscultate for breath sounds bilaterally, get chest x-ray Invasive Ventilation → Tracheostomy: ● Surgical incision into the trachea to establish airway ● Always have extra kit at bedside ● Long term ventilator support ● Humidify air, suction as needed, perform oral care, prevent infection ● Passy-Muir speaking valve: used to help clients speak Mechanical Ventilation: ● Needed for: apnea, acute respiratory failure, impending respiratory failure, anesthesia-induced hypoventilation, severe oxygen deficit ● Goals: ○ Support or manipulate gas exchange ○ Increase lung volume (relieve respiratory distress/failure) ○ Reduce or manipulate the work of breathing ○ Minimize cardiovascular impairment Ventilator settings: ● Tidal volume: 500-1000 ○ Amount of air pumped into the lungs with each stroke. ● FiO2: 40-100% ○ Percentage of air that is oxygen that the ventilator delivers ● Respiratory rate: 12-20 ● MV (minute volume): Tidal Volume x Respiratory Rate ● Pressure support: 5-15 ● Positive end expiratory pressure (PEEP): increases 5-15. ○ Pressure in the thoracic cavity to keep alveoli open (prevents alveolar collapse) ○ Blood returning to the heart is less. ○ Decreased cardiac preload. Also low blood pressure. Understand how changing the setting of the ventilator affect ABGs Types of Mechanical Ventilators: ● Volume cycled: delivers a pre-determines MINUTE VOLUME ordered by Dr. ○ Minute volume = breaths (RR) x tidal volume ○ Most commonly used in the acute care setting ● Pressure Cycled / Pressure control ventilation: deliver a set pressure ○ Commonly used for pediatrics and patients with ARDS Ventilator Modes: ● Assist/Control Mode (A/C): machine does all the work ○ Very sick patient (stay sedated) ○ Most patients will be placed on this mode initially ● Synchronized Intermittent Mandatory Ventilation (SIMV): “weaning off” ○ Synchronized to the machine and patient ○ Encourage patient to breathe more frequently on their own ○ Encourages early extubation ○ Patient must expend the energy to breathe extra ○ IF patient does not breathe, a breath will be delivered ● CPAP (on a ventilator): Patient is doing all the work, ventilator is just the back up ○ Continuous positive airway pressure to prevent alveolar collapse ○ Patient must be breathing on their own Ventilator Alarm ● Find the problem ● High pressure alarm: ventilator is encountering resistance when delivering breath ○ Patient trying to take off the tube ○ Patient biting down the tube ○ Patient is coughing ○ Secretions or mucus in the airway ● Low pressure alarm: it is too easy for the oxygen to go thru, check for leaks ○ Patient is disconnected ○ Pneumothorax ○ Developing ARDS ○ Stiffening of the lungs related to scarring or ischemia ● High Inspiratory Rate: patient is breathing rapidly due to pain or agitation (using too much energy, change settings) ● Low Minute Volume: ventilator could not deliver preset volume ○ Most common cause: tube got disconnected ○ If patient is talking, there there is an air leak ● IF you do not know the cause → disconnect from the ventilator, ambubag with 100% O2 and call for help Anesthetic and analgesia: ● Propofol (Diprivan) drip is often used but it is expensive. (Anesthetic, NOT analgesic) ● Fentanyl and Versed drips are a good combo for pain relief ETT care, precautions, criteria for extubation****** Trach care and precautions********** Chest tubes and pleurovacs care, maintenance, and troubleshooting - DONE Chest Tube ● Needed when the pleural space fills with air, blood, or serous fluid ● Becomes increasingly difficult for the lung to expand → eventually collapses ● AIR: ○ Sterile procedure, position patient in high fowler’s (air rises) ○ Inserted into 2nd or 3rd intercostal space, mid clavicular line anteriorly ● Fluid: ○ Sit on the side of the bed and lean on several pillows (fluid sinks) ○ Inserted midaxillary line 4th intercostal space or lower ● Lots of bubbles - problem with equipment. If proximal tube is clamped and bubbling continues, then it is the equipment ● A few bubbles - could be still pneumothorax. If proximal tube is clamped and bubbling stops, then it is the lungs ● Put the tube in sterile water if the patient is disconnected. ● Chest tube assessment: STOP. Site. Tubing. Output. Patency ● Post open-heart surgery → document drainage Q15min ● IF drainage is >200mL/hr → notify doctor immediately ● NEVER clamp it, even for ambulating or transport Subcutaneous Emphysema: ● When air leaks from the pleural space into the subcutaneous tissues ● The patient looks like the “Michelin Man” ● The tissue crackles to the touch Heimlich Valve: ● Rubber one-way valve ● Attached at the end of a chest tube to allow air to escape BUT not re-enter ● Used for pneumothorax patients with NO drainage of fluid ● Patient can go home with the valve on Recognizing airway and chest conditions, causes, treatments, hypoxia, obstructions, rib fractures, surgeries, ARDS, respiratory failure. - DONE ARDS: acute respiratory distress syndrome - damage to the alveoli from a condition ● Diffuse alveolar capillary damage that allows leakage of fluid from the vascular space into interstitium and alveoli preventing gas exchange ● Oxygen enters without a problem. Oxygen is being shunted ○ Shunt: percentage of blood that has not been oxygenated while in the pulmonary circulation and not enters the left side of the heart without oxygen ● No gas exchange, lungs infiltrated with puss ● Give small tidal volumes ● Use pressure control mode - Patient is totally sedated and intubated ● Positioning is important (PRONE positioning improves gas exchange and recruits alveoli) ● PEEP is very important to keep alveoli open ARDS causes: ● Genetic predisposition ● Aspiration of gastric fluids ● Infectious pneumonia ● Toxic inhalation ● Severe acute respiratory syndrome (SARS) coronavirus ● Sepsis, burns, trauma, acute pancreatitis, venous air embolism ARDS - Oxygenation and Ventilation: ● Refractory hypoxemia (hallmark of ARDS) ● Goal is to optimize oxygen delivery - Pressure controlled ventilation ● Fluid management (need to control pulmonary edema without dehydrating the patient) ● Use positive inotropic agents (strengthen heart contraction) and vasoconstrictors ● May need ECMO (extra corporeal membrane oxygenation) ● Use low tidal volumes and frequent breaths ● Permissive hypercapnia ARDS - Nutritional support: High carbohydrates avoided to prevent carbon dioxide production Pneumothorax, hemothorax, pulmonary embolism, tension pneumothorax - DONE Tension pneumothorax: ● As the fluid or air builds up in the pleural space, the lung on the affected side collapses ● The increases pressure in the thoracic cavity causes the heart and trachea to shift away from the accumulated air or fluid (mediastinal shift) ● Medical emergency - PEA (pulseless electrical activity, AKA cardiac arrest) Causes of Air/Fluid in the Pleural Space: ● Surgical procedure involving the thorax ● Accidental puncture of the pleura during surgery ● Pneumothorax caused by central line insertion ● High ventilator pressures leading to pneumothorax Pulmonary embolism: thrombus migrates to the pulmonary arteries ● Virchow’s triad: venous stasis, hypercoagulability vein wall damage ● Causes: Immobility, heart failure, dehydration, atrial fibrillation ● Hypoxic. Dyspnea or sustained hypotension without other explanation ● Sustained sinus tachycardia without explanation ● Sudden death event if embolus is large ● Pleuritic chest pain, cough, pain, (feeling of impending doom) PE - Diagnostic ● VQ scan - ventilation/perfusion scan (fastest) ● CT angiogram (most accurate). With contrast show vasculature PE - Management: ● Heparin and TPA (keep in mind TPA contraindications) ● Treat at least 5 days of IV heparin, bridge with warfarin ● Continue oral anticoagulants for 3-6 months ● Prevention: early ambulation post-op, low molecular weight heparin, sequential compression devices (compression socks) ● Placement of vena cava filter to catch emboli (consider risks for clots on device) ● Prevent DVT. If DVT - diagnostic: ultrasound ● INR → 2-3 on warfarin Pneumonia, status asthmaticus - DONE Ventilation: movement of air that requires energy Perfusion: blood flow passing by the alveoli allowing for gas exchange. Commonly affected by pulmonary emboli Pneumonia: Inflammatory response to invasion of microorganisms. Aspiration can cause pneumonia ● Walking pneumonia: responds well to ABX, younger patients, no cor morbidities ● Hospital acquired pneumonia: happened in the hospital, or contact in the hospital within the last 3 months ● Ventilator acquired pneumonia: ○ Keep HOB up 30 degrees ○ Reposition every 2hrs (helps pulmonary drainage of secretions) ○ Mouth care at least every 4 hrs ● Community acquired pneumonia: assisted living, college dorms, and jails Pneumonia - Aspiration: ● Causes: alcohol abuse, depressed respirations from medication, sleep apnea, GERD, and bacteria from dental plaques ● Physical findings: ○ Hypoxemia, dyspnea, fever, chills ○ Dullness with percussion, decreased breath sounds, crackles ○ Myalgia, and confusion on elderly patients ○ Egophony: tennessee increased ○ Bronchophony: kentucky increased ○ Fremitus: tactile is increased (99) Pneumonia - Diagnosis: ● Chest x ray ● Blood culture (which organism) ● CBC - complete blood count ● ABG - arterial blood gases ● Sputum culture and sensitivity Pneumonia - Management: ● Antibiotics, IV fluids, cortisone ● Supportive therapy: oxygen, mechanical ventilation, pulmonary toilet ● Prevention: ○ Pneumonia Vaccine needed to patients older than 65 ○ Flu shot for patients younger than 65 Asthma: ● Chronic inflammatory disorder of the airways, reversible ● Inflammation causes obstruction in the airways (bronchoconstriction) ● Inflammation causes increased mucus production ● Treatment can be to avoid triggers ○ Allergens, exercise, air pollutants, respiratory infections ○ Drugs, foods, GERD, psychological or emotional stress Asthma - Manifestations: ● Attacks can be gradual or sudden ● Wheezing, dyspnea, chest tightness ● Cough, hypoxemia ● Treat with: Short acting beta agonist (albuterol). Rinse mouth after using inhaler (thrush) ● ALWAYS bronchodilator first, THEN steroid ● Albuterol side effects: hypertension, tachycardia, and tremors Status Asthmaticus: ● Severe, life threatening, acute episode of airway obstruction ● Intensified once it begins, often does not respond to common therapy ● Patient can develop pneumothorax and cardiac/respiratory arrest ● Treatment → Intubate, IV fluids, potent systemic bronchodilator, steroids, epinephrine, and oxygen Diagnostic Tests (CXR, V/Q scar, bronchoscopy) significance and nursing care pre and post procedure*************** Shock: Stages of shock: signs and symptoms in each stage. All the different types of shock – know each type of shock, its common causes, signs and symptoms, how we treat it, nursing care, labs, medications, etc Vasoactive drips – drug of choice for each shock such as levophed for septic etc. Shock: Impaired tissue perfusion ● Not a disease process, it is caused by previous conditions ● Decreased tissue perfusion and impaired cellular metabolism ● Imbalance between oxygen supply and demand ● Low blood flow: ○ Cardiogenic (post MI) ○ Hypovolemic (trauma or hemorrhage) ● Distributive shock: vasodilation (hallmark), fluid leaks out of vessels, blood circulation is slower ○ Septic ○ Anaphylactic ○ Neurogenic Stages of SHOCK: ● Compensatory phase: subtle changes (irritability, changes in heart rate and BP) ● Progressive phase: increased symptoms (patient will have physical manifestations) ● Irreversible phace: death is probable (MOD - multi organ dysfunction). NOT reversible Shock - in the Emergency Room: ● Check Lactate ● ABG: check how severe the acidosis is ● Establish 2 large bore IVs or central line ● Have O neg blood available. Transfuse is more than 30% of blood has been lost ● Control any bleeding Compensatory Mechanisms in Shock ● SNS activation: ○ Sympathetic nerves and adrenal medulla stimulated ○ Epinephrine and norepinephrine are released ○ Vasoconstriction, ↑ myocardial contractility, ↑ heart rate ● Endocrine response ○ Decreased arterial pressure ○ Stimulated posterior pituitary to secrete ADH ○ Vasoconstriction leading to ■ ↑ SVR (systemic vascular resistance aka afterload) ■ ↑ blood pressure ■ ↑ preload ● Renin-Angiotensin Activation ○ Decreased renal perfusion and increased sympathetic stimulation ○ Releases renin to stimulate angiotensin I ○ Angiotensin I → Angiotensin II (by angiotensin converting enzyme ACE) ○ Arterial constriction stimulates adrenal cortex to release aldosterone ○ Kidney keeps sodium and water → increase preload Systemic Inflammatory Response Syndrome (SIRS) ● Suspected with any patient with shock or risk for shock ● Often with septic shock, BUT can happen in any type of shock ● Massive systemic unregulated inflammatory response ● Treat like septic shock Hypovolemic Shock: ● Low preload → low cardiac output → low MAP → low tissue perfusion → MODS ● Control the hemorrhage (infuse with colloids and crystalloids) ● Modified trendelenburg to increase blood return to the heart ● Replace fluids and blood, maybe give vasoconstrictor ● Monitor vital signs, urinary output ● Elevate lower extremities ● Monitor for pulmonary edema Hypovolemic shock patient manifestations: ● Change in LOC ● Tachycardia, tachypnea ● Cool clammy skin ● Hypotension ● Decreased urine output Cardiogenic shock: NOT volume issue. PUMPING issue ● Impaired tissue perfusion - heart is not pumping ● The problem is pump failure - trying to reduce the workload of the heart ● Systolic dysfunction (left ventricle): MI, blunt trauma, pulmonary HTN ● Diastolic dysfunction (less ventricular filling): cardiac tamponade, cardiomyoppathy ● Goal: to ↑ contractility while ↓ workload of the heart ● Vasodilators (nitroglycerin) or Nipride (strong, need monitoring) ● Dobutrex/Dobutamine or Milrinone (increase contractility) ● Balloon pump in left ventricle to assist the heart ● NO trendelenburg. Elevate HOB to relieve pulmonary symptoms ● IF too much fluid - give diuretics (BUT this is NOT a volume issue) ● Mechanical intervention → VAD (ventricular assist device) or IABP IABP - Intra Aortic Balloon Pump ● Balloon inserted into the aorta through the femoral artery ● The balloon inflates and deflates to ↑ blood flow and ↓ workload of the left ventricle ● Patient is on bed rest Septic (low BP) ● Systemic inflammatory response to infection (elevated WBCs) ● Severe sepsis: organ dysfunction ● Septic shock: presence of sepsis combined with hypotension despite fluid resuscitation ● Treat with Norepinephrine (levophed) Potent vasoconstrictor ● Check ABGs and lactic acid often. Intubation is usually required ● Monitor blood glucose every hour (stress will cause hyperglycemia) ● Patient must have fluid replacement → to maintain CVP normal ● Patient is extremely vasodilated, ↓ SVR, ↓ BP, ↓Cardiac output, ↑ HR ● DIC: patient prone to bleeding because all the clotting factors are used. ○ Treat with HEPARIN → stops microvascular clotting → Stops DIC Anaphylactic (multiple transfusions) ● Life threatening response to an allergen (most common is insect bites) ● Massive release of histamine → massive vasodilation and bronchoconstriction ● Treat with epinephrine (vasoconstricts, bronchodilators, and ↑ HR and contractility ● Protect the airway (priority) Laryngeal edema Neurogenic (spinal cord injury, opioid overdose) LOW AND SLOW ● Decreased venous return (preload), blood pools on the periphery ● Sympathetic response is not working, parasympathetic dominates → bradycardia ● MASSIVE vasodilation ● ↓Preload → ↓cardiac output → organ damage ● Decrease in CVP, PAOP/WEDGE pressure, SV, BP ● Cause: injury/disease of spinal cord ● Treat with: Dopamine, Epinephrine, Norepinephrine (levophed), Atropine (like sinus bradycardia treatment) Pulmonary artery catheter(Swan-Ganz catheter): ● Monitors pressure in the chambers of the right side of the heart and pulmonary artery, displayed on the heart monitor ● CONSENT is needed ● Used to measure the Wedge pressure/PAWP (intravascular fluid status) ● Gives continuous cardiac output reading (used when titrating inotropes) ● Measures pressure in right atrium, pulmonary artery, and SVR ● Central venous pressure (CPV): 4-10mmHg ○ Measures pressure of blood returning to the right side of the heart. ○ IF Low → fluids are low. IF High → fluids are too high ● ● ○ Confirms if a patient is volume depleted Pulmonary artery occlusive pressure (Wedge pressure) PAWP: 6-12mmHg ○ Fluid status of the left side of the heart. High → left sided HF patient. ○ IF Low → fluids needed Cardiac output: 4-8L/min Systemic vascular resistance (afterload): 800-1200 dynes/sec/cm^-5 ○ Low when vessels are dilated. ○ Increased when vessels are constricted. Stroke volume (SV): 60-150mL/beat Mean arterial pressure (MAP): 80-100mmHg (perfusion issues below 70) ● ● ● ● ● Inotropic: affect contractility. Ex: Dopamine Chronotropes: affect heart rate. Dromotropic: affect the speed of impulse conduction through the heart Alpha 1 receptors: in the heart Alpha 2 receptors: in the lungs ● ● ● Hemodynamic parameters of the various shock states—understand the concept and what the nurse should do when those values are abnormal. “Hemodynamics” or “Hemodynamic parameters,” = heart rate, blood pressure, CVP, PAWP, cardiac output, cardiac index, SVR, mean arterial pressure, BNP. BNP → best HF measure (>100 puts you at risk for HF) (Give Natrecor or Primacor) MAP calculation - DONE Mean arterial pressure → >70 is good Normal MAP: 80-100mmHg. 70mmHg is acceptable. If less than 70, kidneys are not being perfused properly Systolic + (2xDiastolic) = MAP 3 Cardiac output: HR x SV Know your drip calculations - DONE Medication Calculations MCG/KG/MIN Solution mLs x 60 minutes x Patient’s weight (kg) x ORDER (mcg/kg/min)= ______mL/hr mcg in solution 1 hour MCG/KG/MIN Given rate → order Drug mcg in solution x ml/hr infusing (given) = ______mcg/kg/min Solution mL x 60 x kg MCG/MIN (DISREGARD WEIGHT) Drug solution mL x dose ordered x 60 minutes= _______mL/hr Drug mcg 1hr MCG/MIN Given rate → order mL/hr (given) x mcg in the bag = _______mcg/min mL in bag 60 min DIC definition, diagnosis, treatment modalities Disseminated Intravascular Coagulation ● Abnormally initiate and accelerated clotting ● Uses up all available clotting factors and platelets → hemorrhage ● Always and underlying cause ● D-Dimer is ordered (positive if in DIC) ● Patient at risk for tissue necrosis and organ failure due to impaired perfusion ● Causes: shock, septicemia, transfusion reaction, OB conditions ● Treatment: ○ Treat underlying cause (if known) ○ Replace clotting factors IF actively bleeding ■ Fresh frozen plasma ■ Platelets ■ Cryoprecipitate ○ Heparin : to prevent more clots from forming Hypothermia care - DONE Induced Hypothermia Therapy - Post Cardiac Arrest ● Reduce the risk of ischemic injury to the brain after a period of insufficient blood flow ● 32-34 C (90-93 F) - CODE ICE ● Used to prevent brain damage ● Patient must be intubated, sedated, and paralysis ● For 24hrs → rewarmed SLOWLY Acute Tubular Necrosis ● Nephrotoxicity from contrast dye ● Usually mild and reversible ● 4 phases: ○ Onset: initial injury to kidney cells, determine the cause, prevent progression ○ Oliguric or nonoliguric ■ Oliguric: <400mL/day. Watch for fluid overload. Higher mortality → might need dialysis. ■ Nonoliguric: not in fluid overload, treat with fluid restriction. ○ Diuretic: 1-2 weeks. Output gradually increases. Possible hypokalemia ○ Recovery: creatinine and BUN drop. Takes up to a year. Renal – know patho, causes, treatment, normal GFRs etc Acute renal failure (pre-renal, intra-renal, post-renal – causes / treatment options) Pre-renal causes: ● ↓ kidney blood supply (perfusion) ● ↓ cardiac output (heart failure, MI, cardiogenic shock, dysrhythmias) ● Dehydration (hemorrhage, third spacing, hypovolemia) ● Renal artery stenosis or thrombosis. Sepsis Pre-renal treatment: ● Increase IV fluids ● Usually fluid challenge of 250 cc NSS ● Look for increased urinary output and no crackles in the lungs ● Increase cardiac output ● Watch for changes in BNP ● Optimize cardiovascular function with medications and other therapies ● Treat any cardiac rhythm disturbances ● Monitor use of ACE inhibitors and NSAIDs (can make worse) ● Monitor BUN, creatinine, GFR Intra-renal causes: ● Directly affect kidney tissue itself ● Acute tubular necrosis (ATN) ● Acute glomerulonephritis (AGN) ● Drug-related causes ( medications such as aminoglycosides) ● Damage from hemolysis during a transfusion reaction ● Nephrotoxicity (ATN) from contrast dye Increased risk in patients with: ○ Diabetes mellitus ○ Fluid volume deficit ○ Multiple myeloma Intra-renal treatment: ● Hydration ● acetylcysteine (Mucomyst) before and after contrast Post-renal patho: ● Obstruction to urinary flow ● Urine backs up into kidney ● Both kidneys must be obstructed for failure to occur (one kidney can function well on its own) ● If relieved, great increase in urinary flow Post-renal causes: ● Kidney obstructions ○ Kidney stones ○ Tumors ● Outflow tract obstructions ○ Ureter stones ○ Tumors (benign prostatic hypertrophy, prostate cancer) Post-renal treatment: ● Relieve the obstruction by mechanical or surgical methods ● Watch for post-obstructive diuresis and resultant fluid volume deficit Chronic renal failure - unlike ARF, it is NOT reversible even with treatment 2 major causes of CRF: ● Hypertension: Causes glomerular capillaries to become thickened and stenotic ○ Blacks 8x more likely ● Diabetes Mellitus: microvasculature of the kidney is damaged 3 types of CRF: ● Decreased renal reserve: ○ Loss of kidney function by 40-50%. ○ Slight elevation in BUN and creatinine ● Renal insufficiency: ○ 60-80% of renal function is lost ○ Azotemia, electrolyte imbalances, anemia ○ Fatigue, polyuria, nocturia ● End-stage renal disease (ESRD): ○ Renal function <85% ○ Elevated BUN and creatinine ○ High potassium and phosphorus ○ Low calcium. ○ Dialysis needed or death will result. CRF concerns: ● Pulmonary edema ● Hypertension, hyperkalemia and pericarditis (from high levels of circulating nitrogenous waste) ● Metabolic acidosis Hemodialysis - removal of soluble substances and water from the blood by diffusion ● Patient MUST be STABLE ● Care of hemodialysis access site ○ Arteriovenous (AV) fistula or graft for long term use ○ Hemodialysis catheter, dual or triple lumen, or AV shunt for temporary access ○ Assess for adequate circulation. Hear a bruit, feel a thrill ○ Complications: thrombosis, infection, aneurysm, ischemia, heart failure ● Dietary restrictions on hemodialysis: Fluid, Phosphorus, Potassium, Protein, nitrogen Peritoneal Dialysis ● Allows for exchange of wastes, fluids, and electrolytes in the peritoneal cavity. ● Not recommended for patients with extensive abdominal surgeries ● FILL → DWELL(time fluid remains in the peritoneal cavity) → DRAIN ● Patients can do it on their own. No needle sticks ● Better blood pressure control ● Fewer dietary restrictions and fluid restrictions ● Complications: ○ Peritonitis (infection of the peritoneal cavity) ○ Exit site/tunnel infections Continuous Renal Replacement Therapy (CRRT): ● Slow dialysis ● Done by a trained ICU nurse ● For critical patients. Depending on vitals, machine may only be circulating blood ● Hemodynamically unstable patient (low vital signs) Care of AV fistulas ● No blood pressure on arm with fistula ● Must auscultate bruits and feel thrills ● Do not flush or aspirate from it ● Takes 3-6 months to mature for dialysis use Renal calculi ● Pain (renal colic) and hematuria, Oliguria ● Diagnosis ○ X-ray Renal ○ Ultrasonography ○ Blood work ○ Stone analysis: strain all urine and save stones ● Treatment ○ Opioid analgesics, NSAIDS (Toradol,Nexcede) ○ Thiazide diuretics ○ Allopurinol (uric acid reducer) ○ Lithotripsy (shock wave) ○ Ureteroscopy ○ Percutaneous ureterolithotomy / nephrolithotomy Urinary tract infections ● Lower UTI: bladder and urethra ● Upper UTI: ureter and kidneys ● Contributing factors ○ Urethrovesical reflux (backflow of urine) ○ Uropathogenic bacteria ○ Women - shorter urethra ● Signs and symptoms ○ Pain in the suprapubic, pelvic and back, burning and pain upon urination, frequency, nocturia, incontinence, hematuria ● Interventions ○ Proper care for catheters ○ Good hygiene wipe front to back ○ Increase fluids ○ Avoid coffee, tea, citrus, spices, cola and alcohol ○ Meds: antibiotics, analgesics, antispasmodics (reduces muscle spasms) Make sure you know your labs, medications and blood products. You should be familiar with normal electrolyte values, CBC, PT, PTT, lactic acid, Na, K+, Phos, Ca+, Creat, BUN, GFR Electrolytes values ● Na+ (sodium): 135-145 ● K+ (potassium): 3.5-5.0 ● Ca++ (calcium): 8.4-10.6 ● Mg++ (magnesium): 1.3-2.1 ● PO4 (Phosphate): 3.0-4.5 ● ● ● ● ● ● ● ● ● ● ● ● Red blood cells: White blood cells: 4,000 - 11,000 Platelets: 150,000 - 400,000 PT: 10-14 seconds ○ IF high, use vitamin K ○ FASTER → use FFP (fresh frozen plasma) INR: normal 0.8-1.2 / therapeutic 2-3 aPTT: 25 - 40 seconds Glomerular Filtration Rate (GFR): 125ml/min is normal Albumin: 3.5-5 ○ Volume expander (colloid) ○ Keep fluid in intravascular space ○ If low, fluid leak into 3rd spacing → edema Lactic acid: byproduct of anaerobic metabolism. ○ Tested for sepsis ○ 2-3 → monitor ○ >3 must be treated Crystalloid: Normal saline and LR Colloids (volume expander): albumin Packed red blood cells EKG changes, Symptoms of high and low electrolytes ● Hypernatremia: Dehydration, confusion, stupor, seizure, coma ● Hyponatremia: Muscle twitching, weakness, hypotension, tachycardia ● Hyperkalemia: Muscle weakness and flaccid paralysis, ECG: Tall peaked T waves or tented T waves, widened QRS complex, prolonged PR interval, flattened or absent P waves, depressed ST segment. ● Hypokalemia: hypotension, cardiac arrest. Metabolic alkalosis. ECG: flattening and inversion of T waves and depressed ST segment ● Hypocalcemia: lengthened QT interval, prolonged ST segment. ● Hypercalcemia: signs of heart block, and shorten QT interval ● Hypomagnesemia: dysrhythmias, vasodilation and hypotension ● Hypermagnesemia: heart block, bradycardia, widened QRS, and prolonged QT interval ● Hypophosphatemia: Muscle weakness, tremor, paresthesia, tissue hypoxia, seizures, weak pulse, hyperventilation, dysphagia ● Hyperphosphatemia: Tetany, and seizures, flaccid paralysis and muscle weakness Hormonal regulation of kidneys ● Antidiuretic hormone: water retention ● Aldosterone hormone: sodium and water retention ● Renin: stimulates release of angiotensin I (starts RAAS) ● Calcitriol: increases intestinal absorption of calcium ● Erythropoietin: stimulate bone marrow to produce RBC in situations like bleeding, anemia, and hypoxemia Medications for anemia ● Iron supplements ● Erythropoietin-stimulating agents (ESA): erythropoietin or darbepoetin, can cause hypertension ● Folic acid, pyridoxine (Vit 6), and vitamin B12
