Acute complex conditions exam 1

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Subjective pain assessment
N-normal O-onset P-precipitating/aggravating/relieving factors Q-quality R-region/radiation S-severity/other symptoms T-timing U-patient understanding/perception
Observable pain assessment
behavioral indicators
pain assessment tools
FLACC (infants) CPOT (clinical care plan observation tool) Wong Baker faces tool
pain assessment importance
self reporting, alternate communication methods, observable behavioral, physiological indicators
5 components of pain
sensory, affective, cognitive, behavioral, physiological
Types of pain
acute chronic nociceptive: somatic,visceral neuropathic: peripheral, central
nociception of pain
transduction, transmission, perception, modulation
pain assessment limitations
inability to respond, language barrier, altered loc, delirium, neonates, cultural influences, lack of knowledge, beliefs and attitudes about pain, addiction and tolerance, respiratory depression
Pain Pharmacology
opioid agonists: morphine, fentanyl nonopioids: acetaminophen, nsaids, ketorolac
pain prevention measures
•Physical techniques -Heat or Cold -Massage •Cognitive-behavioral techniques -Relaxation -Distraction -Music therapy •Movement therapy -Yoga •Biologically based therapies Aromatherapy
Subjective Renal Assessment
•Renal-focused health history •Urinary output and symptoms (FHP: elimination) •Medications •Nephrotoxic (NSAIDS, diuretics, etc.) •Surgeries •Functional Health Patterns •Elimination •Sleep-Rest •Reproductive/sexuality
Objective Renal Assessment
Inspection •Weight, general appearance Palpation •Costovertebral Angle Tenderness •Bladder Documentation •Normal physical assessment •Assessment abnormalities
Acute kidney injury
-Ranges from slight deterioration to severe impairment -Rapid loss of kidney function with: •Rise in serum creatinine and/or reduction in urine output •Elevated BUN and K+ •Azotemia—accumulation of nitrogenous waste products -High mortality rate; other life-threatening conditions
types of acute kidney injury
Prerenal Intrarenal Postrenal
Pre-renal kidney injury
-Interruption of blood flow to the kidneys -Hypotension, shock
Pre-renal Pathophysiology
•factors that reduce systemic circulation causing reduction in renal blood flow which leads to oliguria •Severe dehydration, heart failure, decreased CO •Autoregulatory mechanisms attempt to preserve blood flow •Prerenal azotemia results in i urine output
intrarenal Acute kidney injury
Occurs as a result of direct damage to the kidney from lack of oxygen (acute tubular necrosis). ■ Causes ☐ Physical injury - trauma ☐ Hypoxic injury - renal artery or vein stenosis or thrombosis ☐ Chemical injury - acute nephrotoxins (e.g. antibiotics, NSAIDs, contrast dye, heavy metal, blood transfusion reaction) ☐ Immunologic injury - infection, vasculitis, acute glomerulonephritis ■ Nursing Care ☐ Assess for oliguria or anuria. ☐ Assess for edema and manifestations of heart failure or pulmonary edema. ☐ Restrict fluid intake as prescribed. ☐ Review laboratory values for elevated potassium, low calcium levels. ☐ Monitor for ECG dysrhythmias and changes (tall T waves). ☐ Assess for flank pain, nausea, and vomiting. ☐ Assess for lethargy, tremors, and confusion. ☐ Monitor daily weights.
Postrenal acute kidney injury
occurs with urinary tract obstructions that affect the kidneys bilaterally •Caused by mechanical obstruction of outflow which results reflux into renal pelvis, impairing kidney function
Acute kidney injury phases
Initiation - initial cause leading to oliguria Oliguria - metabolic waste products build up due to lack of excretion Diuresis - beginning recovery, lab values stabilize Recovery - renal function recovers, may take several
RIFLE classification
•Risk (R) - elevated creatinine 1.5 x baseline or GFR dec 25%; 0.5ml/kg/hr x6h •Injury (I) - serum creatinine 2 x baseline or GFR dec 50%; 0.5ml/kg/hr x12h •Failure (F) - creatinine 3 x baseline or GFR dec 75%; <0.3ml/kg/hr x 24h •Loss (L) - persistent kidney injury >4 weeks •ESRD/ESKD(E) - outcome >3 months
AKI findings
•Oliguria or anuria •Tachycardia •Hypertension or hypotension •Bibasilar crackles •Irritability, drowsiness, or confusion •Altered level of consciousness •Bleeding abnormalities, ecchymoses, and purpura •Dry, pruritic skin; maculopapular rash •Dry mucous membranes •Uremic breath odor •Seizures •Myoclonus •Retinopathy •Keratitis, iritis, and uveitis •Cardiac arrhythmias such as atrial fibrillation or a peaked T-wave from hyperkalemia •Limb ischemia or edema
AKi diagnostics
•Serum creatinine, BUN, electrolytes •Urinalysis •Renal ultrasound •Renal scan •CT scan •Renal biopsy
contrindications for contrast medium
•MRI or MRA with gadolinium contrast medium—may be fatal •Contrast-induced nephropathy (CIN) •Diabetics taking metformin: hold 48 hours before and after use of contrast medium; risk of lactic acidosis If contrast is needed for high-risk patients—use low-dose and o
renal replacement therapy
term used to encompass life-supporting treatments for renal failure. It includes: hemodialysis, peritoneal dialysis, hemofiltration and renal transplantation.
acute kidney injury nutrition
•Maintain adequate caloric intake •Primarily carbohydrates and # fat •Adequate protein to prevent breakdown •Restrict sodium, K+, phosphate •Calcium supplements or phosphate-binding agents •Enteral/parenteral nutrition if needed
acute kidney injury nursing process
Nursing diagnoses: •Electrolyte imbalance •Fluid imbalance •Risk for infection •Anxiety
acute care interventions
Acute care: •Strict intake and output •Daily weights •Assess for hypervolemia or hypovolemia •Assess for potassium and sodium disturbances •Meticulous aseptic technique •Careful use of nephrotoxic drugs
acute care evaluations
Evaluation outcomes are that the patient with AKI will: •Regain and maintain normal fluid and electrolyte balance •Adhere to the treatment regimen •Have no complications •Have complete recovery
kidney transplant
•Assess for rejection •Oliguria, edema, fever, inc. BP, weight gain, swelling/tenderness at site •Patient receiving cyclosporine may only show increased creatinine •Prevent infection •Monitor CBC and assess for s/s of infection •Patients receiving immunosuppressant drugs •Monitor urinary function •Living donor kidney functions immediately Deceased donor kidney may not function for 2-3 weeks
Movement of molecules from an area of higher concentration to an area of lower concentration.
active transport
the movement of materials through a cell membrane using energy
Diffusion of water through a selectively permeable membrane
hydrostatic pressure
the pressure within a blood vessel that tends to push water out of the vessel
osmotic pressure
pressure that must be applied to prevent osmotic movement across a selectively permeable membrane
decreased blood volume
An abnormally low amount of water in the body.
abnormal increase in the volume of blood plasma in the body
Interprofessional Care
Many different professionals working together for the good of the patient
Hypotonic IV fluids
Treats intracellular dehydration Lower osmolarity than ECF 0.45% NS D2.545%NS
Isotonic IV fluids
• Normal Saline (0.9% NaCl) • Lactated Ringer (LR) • IV fluids are used to replace or maintain fluid
Hypertonic IV fluids
Used only when serum osmolarity is critically low Osmolarity higher than ECF D50W D10W D5NS D5W in 0.45% NaCl d5LR
Acid-Base Regulation
buffer systems respiratory mechanisms renal mechanisms
buffer system
A mixture of an acid and a base which resists changes in pH •Act chemically to change strong acids to weak acids or bind acids to neutralize them •Respiratory and renal systems need to be functioning adequately
respiratory system regulation
Respiratory center in medulla controls breathing Increased respirations lead to increased CO2 elimination and decreased CO2 in blood Decreased respirations lead to CO2 retention
Renal System Regulation
Conserves bicarbonate and excretes acid Three mechanisms for acid elimination Secrete free hydrogen Combine H+ with ammonia (NH3) Excrete weak acids
Acid-base alterations
•Imbalances occur when compensatory mechanisms fail •Classification of imbalances •Respiratory (CO2) or metabolic (HCO3) •Acidosis or alkalosis •Acute or chronic
arterial blood gases
clinical test on arterial blood to identify the levels of oxygen and carbon dioxide
Diabetes Ketoacidosis
•Caused by profound deficiency of insulin •Characterized by: Hyperglycemia, Ketosis, Acidosis, Dehydration •Precipitating factors: Illness, Infection, Improper insulin dosage, Unknown dx •Insulin deficiency: (Fig. 48-12 in the textbook) •Without treatment: •Severe depletion of sodium, potassium, chloride, magnesium, and phosphate •Acidosis à vomiting and further fluid and electrolyte losses •Hypovolemia followed by shock may cause renal failure, causing retention of ketones and glucose and further acidosis •Dehydration, electrolyte imbalance, and acidosis causes coma and if not treated, death
Hyperosmolar Hyperglycemic Syndrome (HHS)
A metabolic complication of uncontrolled type 2 diabetes, similar in severity to diabetic ketoacidosis but without ketosis and acidosis.
subjective respiratory data
•Respiratory history •Smoking/vaping history •Environmental exposures •Allergens •Chemicals Smoke
Objective Respiratory Assessment
•VS with pulse oximetry (consider perfusion) •Work of breathing •Adventitious lung sounds (Upper/lower) •Stridor •Wheeze •Crackles •Rhonchi Audible aeration
Respiratory Diagnostic Tests
•Radiology •X-ray •CT •MRI •V/Q Scan •Capnography •Bronchoscopy A/C/V Blood Gas
an inflammation in the lung caused by infection from bacteria, viruses, fungi, or parasites, or resulting from aspiration of chemicals
Pneumonia types
•Viral—most common •May be mild or life-threatening •Bacterial •May require hospitalization •Mycoplasma—atypical •Aspiration •Necrotizing •Opportunistic
pneumonia manifestations
•Cough: productive or nonproductive •Green, yellow, or rust-colored sputum •Fever, chills •Dyspnea, tachypnea •Pleuritic chest pain •Fine or coarse crackles •With consolidation: •Bronchial breath sounds •Egophony •Increased fremitus •With pleural effusion •Dullness to percussion
pneumonia complications
•Atelectasis •Pleurisy •Pleural effusion •Bacteremia •Pneumothorax •Acute respiratory failure •Sepsis/septic shock •Lung abscess •Empyema
Respiratory Nursing Diagnoses
•Impaired gas exchange •Impaired breathing •Fluid imbalance •Hyperthermia •Activity intolerance
Respiratory nursing implementation
•Monitor assessment parameters, provide treatment, and monitor response •Collaborate with respiratory therapy, PT •Collect specimens •Administer antibiotics •Oxygen, hydration, nutrition, breathing exercises, early ambulation, and positioning •Elevate head-of-bed 30 degrees and have sit up for all meals •Assist with eating, drinking, taking meds as needed •Assess for gag reflex •Monitor reflux and gastric residuals (NG tube) •Early mobilization •Cough and deep breathe, incentive spirometry •Twice-daily oral hygiene
Respiratory nursing care
•Effective respiratory rate, rhythm, and depth of respirations •Lungs clear to auscultation •Absence of infection
air in the pleural cavity caused by a puncture of the lung or chest wall
spontaneous pneumothorax
A pneumothorax that occurs when a weak area on the lung ruptures in the absence of major injury, allowing air to leak into the pleural space. •Risk factors: Tall, thin, male, family history, or previous spontaneous pneumothorax
latrogenic pneumothorax
caused by medical treatments, especially transthoracic needle aspiration
tension pneumothorax
a type of pneumothorax in which air that enters the chest cavity is prevented from escaping
blood in the pleural cavity
a condition marked by lymphatic fluid in the pleural space caused by a leak in the thoracic duct.
chest tubes
hollow drainage tubes that are inserted into the chest to drain air, blood, pus, or fluid that has collected inside the pleural space/cavity
pulmonary embolism
clot or other material lodges in vessels of the lung
pulmonary embolism manifestations
•Depend on type, size, and extent of emboli: •Dyspnea most common (85%); mild-moderate hypoxemia •Other: tachypnea, cough, chest pain, hemoptysis, crackles, wheezing, fever, tachycardia, syncope, pulmonic heart sound •Massive PE: change in mental status, hypotension, impending doom, death
pulmonary embolism complications
•Pulmonary infarction •Occlusion of medium or large-sized vessel, inadequate collateral blood flow, and preexisting lung disease results in alveolar necrosis and hemorrhage which may results in abscess and pleural effusion •Pulmonary hypertension •Results from hypoxemia associated with massive (greater than 50%) or recurrent emboli •Right ventricular hypertrophy
pulmonary embolism diagnostics
D-dimer, spiral CT scan, ventilation perfusion scan
Normal Sinus Rythym (NSR)
ECG of a healthy heart shows an organized, uniform rhythm called normal sinus rhythm (NSR)
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Sinus Bradycardia
<60 normal sinus rhythm
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Sinus Tachycardia
>100 bpm
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Paroxysmal SVT
Intermittent SVT. Due to rapid atrial depolarization that overrides SA node (stress, over exertion, caffeine)
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Atrial Flutter
irregular beating of the atria; often described as "a-flutter with 2 to 1 block or 3 to 1 block"
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atrial fibrillation
occurs when the normal rhythmic contractions of the atria are replaced by rapid irregular twitching of the muscular heart wall
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Junctional Rhythm
the SA node is nonfunctional, P waves are absent, and heart is paced by the AV node at 40-60 beats/min
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Bundle Branch Blocks
- QRS is *prolonged/wide*
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premature ventricular contractions
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Ventricular Tachycardia
a very rapid heartbeat that begins within the ventricles
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Ventricular Fibrillation
the rapid, irregular, and useless contractions of the ventricles
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absence of contractions of the heart
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potassium and the heart
in charge of myocardial contraction. affects rate of ventricular depolarization normal level: 3.5-4.5 mEq/L
How to calculate HR on an EKG
▪Number of QRS complexes in 6 seconds and multiply by 10
Restoration of normal heart rhythm by electrical shock
application of an electric shock to the myocardium through the chest wall to restore normal cardiac rhythm
Dysrhythmia assessment findings
-irregular rate/rhythm, tachy, brady -decreased or increased BP -decreased O2 sat -pain: chest, neck, shoulder, back, jaw, arm -dizziness, syncope -dyspnea -extreme restlessness, anxiety -decreased level of consciousness, confusion -feeling of impending doom -numbness/tingling of arms -weakness and fatigue -cold, clammy skin -diminished peripheral pulses -diaphoresis -pallor -palpitations -n/v
Dysrhythmia Nursing process
ASSESSMENT -Health history -Medications (medications that may affect the heart) -Lab values (INR, PTT, aPTT, assess for anemia,) -Look for physical signs of diminished CO (especially changes in LOC), fluid retention (e.g., JVD [jugular vein distention, crackles, and wheezes], rate and rhythm of apical AND peripheral pulses, extra or abnormal heart sounds DIAGNOSIS -Decreased CO related to inadequate ventricular filling or altered heart rate -Anxiety related to fear of the unknown outcome of altered health state -Deficient knowledge about the dysrhythmias and its treatment POTENTIAL COMPLICATIONS -Cardiac arrest -HF -Thromboembolic event, especially with atrial fibrillation
EKG placement
white= on right snow over grass = White over green smoke over fire = black over red chocolate good for heart = brown by heart
which is the most common lead
2 and v4
subjective cardiac assessment
•Sxs: sob, fatigue, dizziness, syncope, edema, palpitations, weakness, malaise, nausea •Hx: cardiac disease, diabetes, htn, strep infection, tobacco/drug use •Medications •Functional health pattern changes
Objective cardiac assessment
•Vital signs •Inspection: edema, cyanosis, jvd •Palpation: pulses, cap refill, edema •Auscultation: bruits, murmurs, heart sounds
Cardiac Diagnostic Tests
ECG Echocardiography Coronary angiography Cardiac Catheterization -Hemodynamic Monitoring Radionuclide tests -MUGA scan -Thallium imaging -PET scan
Non-modifiable risk factors for CAD
Age Gender Ethnicity Family history Genetic predisposition
Modifiable risk factors for CAD
Smoking, HTN, DM, obesity, diet, activity level, hyperlipidemia
Stable angina
chest pain that occurs when a person is active or under severe stress
care for stable angina
•increase O2 supply •To optimize myocardial perfusion: •oxygen •Nitrates •b-blockers •Calcium channel blockers
Acute coranary syndrome (ACS)
•Prolonged ischemia; not immediately reversible; includes: •Non-ST elevation acute coronary syndrome •Unstable angina and non-ST segment elevation myocardial infarction (NSTEMI) ST-segment-elevation myocardial infarction (STEMI)
MI signs and symptoms
PULSE: Persistent chest pains Upset stomach Lightheadedness Shortness of breath Excessive sweating
MI sequelae
•Dysrhythmias •Heart failure •Cardiogenic shock •Muscle dysfunction/rupture •pericarditis
cardiac catheterization
thin, flexible tube is guided into the heart via a vein or an artery
CABG (Coronary Artery Bypass Graft)
Open heart surgery involving arterial bypass using a transplanted vein
high WBC means
low Hgb means..
anemia This could be indicative of a GI bleed
High Hgb indicates
low WBC count
may indicate viral infections, pneumonia, autoimmune diseases, or cancers
High Hct indicates..
Low Hct indicates
anemia, blood loss
high plt count indicates
blood clots can form in your blood vessels.
Low plt count indicates
less than 150,000 platelets per microliter is lower than normal. When you have a low platelet count, you may have trouble stopping bleeding. Bleeding can happen inside your body, underneath your skin, or from the surface of your skin.
BMP tests for
Na, K, BUN, Creat, Gluc, HCO3-, Cl-
BMP indications
may be used to check the health of your kidneys, the status of your electrolyte and acid/base balance, as well as your blood glucose level - all of which are related to your body's metabolism.
high BNP indicates
congestive heart failure
the examination of urine to determine the presence of abnormal elements
Tropinin I and t
Cardiac troponin I appears to be a more specific marker of risk of composite cardiovascular disease and coronary heart disease, whereas cardiac troponin T is more strongly associated with risk of non-cardiovascular disease death
Creatine Kinase-Muscle Breakdown. High --> heart damage
D-dimer test
high--> must rule out PE If a D-Dimer is ordered it means the physician is considering a Pulmonary Embolism as one of their Differential Diagnoses (DDx). D-Dimer is a protein that is excreted by clots of blood. The amount of D-Dimer circulating in the body can be measured. If the D-Dimer is negative, a PE can be excluded from the DDx: Negative D-Dimer = No PE If the D-Dimer is positive it does not necessarily mean there is a PE. It only means the pt must be ruled out for a PE: they must receive a CTA Chest or VQ scan.
Arterial Blood Gases pH 7.35- 7.45 HCO3 (Bicarbonate) normal values 22-26 mEq/L PaCO2 ( CO2 or carbon dioxide content) 35-45 mm Hg PaO2 (oxygen saturation in arteria blood)- 80-100 mm Hg
electromagnetic waves with wavelengths shorter than ultraviolet rays, but longer than gamma rays
CT scan
a series of x-ray photographs taken from different angles and combined by computer into a composite representation of a slice through the body
an ultrasonic diagnostic procedure used to evaluate the structures and motion of the heart
ultrasound of the heart
V/Q scan
ventilation-perfusion scan - radioactive test of lung ventilation and blood perfusion throughout the lung capillaries (lung scan)