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HA EXAM #2 copy

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
● 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
● 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
● 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
● 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
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
○ 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
Cardiac output: HR x SV
Know your drip calculations - DONE
Medication Calculations
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
Drug solution mL ​ x dose ordered x ​ 60 minutes​= _______mL/hr
Drug mcg
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
● 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
● Folic acid, pyridoxine (Vit 6), and vitamin B12