Test 2 Flashcards
Pulmonary Embolism - PE
A collection of particulate matter that enters the venous system and lodges in the pulmonary vessels
Clinical Signs and Symptoms of a PE –
dependent upon number and size of emboli
Symptoms:
▪ impending doom – restlessness - apprehension
▪ dyspnea with …
▪ abrupt onset ▪ pleuritic chest pain ▪ tachycardia
▪ cough
▪ hemoptysis
Signs: ▪ tachypnea ▪ pleural friction rub ▪ S3 or S4 ▪ fever ▪ petechiae ▪ ↓SaO2 ▪ diaphoresis ▪ ST and T wave changes if severe
Priority Problems of a PE
▪ Hypoxemia r/t mismatch of perfusion and alveolar respiration
▪ Hypotension due to reduced forward flow of blood
▪ anxiety
▪ potential for bleeding due to anticoagulants
What is PaO2 and Fio2?
partial pressure arterial O2 (get this from your ABGs)
Fio2 = fraction of inspired o2 (A patient on room air = fio2 = .21)
Diagnosis of a PE:
▪ Abnormal ABG’s ▪ early respiratory alkalosis ▪ later respiratory acidosis see Fraction of Inspired oxygen (PaO2-FiO2) ▪ eventually metabolic acidosis
▪ Chest X-ray
Non specific x 24 hrs unless very large PE
▪CT Scan, MDCTA (very specific)
▪ TEE, Doppler ultrasound
▪Lung scan (ventilation/perfusion scan), pulm angiogram
Nursing Care for PE:
improve ventilation and perfusion, minimize risk of additional clot formation, prevent complications
▪ respiratory assessment
▪ administer O2 ▪ crackles
▪ cardiac assessment
▪ S3 S4
▪ anticoagulation medications
▪ IV heparin
▪ warfarin
▪ thrombolytic
▪ surgical management
▪ vena cava filter
Acute Respiratory Failure definition:
pulmonary system fails in one or both functions; oxygenation and CO2 elimination
Acute Resp. Failure
Ventilatory Failure
Oxygenation Failure
Combined Failure
Acute Respiratory Failure
▪ Clinically Defined
PaO2 < 60mmHg OR PaCO2 > 50mmHg
SaO2 < 90% with ABG pH < 7.30
▪ Manifestations often subtle at onset and
progress rapidly
Patient is always hypoxemic
what is V/Q?
“V” - ventilation-air that reaches the lungs
“Q” - perfusion-blood that reaches the lung
What is normal V and normal Q?
Normal V (ventilation) is 4 L of air per minute Normal Q (perfusion) is 5L of blood per minute. Normal V/Q ratio is 4/5 or 0.8.
When the V/Q is higher than 0.8, it means ventilation exceeds perfusion.
When the V/Q is < 0.8, there is a VQ mismatch caused by poor ventilation.
Ventilatory Failure:
normal perfusion & abnormal ventilation
▪ PaCO2 > 45mmHg in patients with otherwise healthy lungs
Oxygenation Failure:
normal ventilation with abnormal perfusion
What are possible causes of oxygenation failure?
Impaired diffusion at alveolar level Right to left shunt in pulmonary vessels Low O2 concentration atmospheric air Failure of Hgb to bind to Oxygen V/Q mismatch Acute Respiratory Distress Syndrome (ARDS) classic case
Combined Ventilatory & Oxygenation Failure:
Diseased bronchioles & alveoli (oxygenation failure)
-ex. Ephysema, asthma
Increased work of breathing leads to ineffective respiratory muscle function (ventilatory failure)
What are the CNS signs and symptoms of V/Q mismatch?
▪ Irritability
▪ Confusion
▪ Impending doom
▪ Somnolence
What are the respiratory signs and symptoms of V/Q mismatch?
▪ Dyspnea
▪ Increased Depth - hypoxemia
▪ Decreased Depth - hypercapnia
What are the cardiovascular signs and symptoms of V/Q mismatch?
▪ Tachycardia - early ▪ HTN - early ▪ Bradycardia - late ▪ Hypotension - late ▪ Arrhythmias
Acute Respiratory Distress Syndrome (ARDS):
syndrome of lung inflammation and injury, potentially fatal non-cardiac pulmonary edema. Often associated with acute lung injury (ALI)
Characteristics of ARDS?
▪ acute and refractory hypoxemia despite 100% FIO2 ▪ dyspnea ▪ decreased lung compliance ▪ alveolar collapse ▪ bilateral infiltrates “white out” → ▪noncardiac-associated bilateral pulmonary edema
Pathophysiology of ARDS:
activation of the systemic inflammatory response in response to direct or indirect lung injury
Phases of ARDS:
Phases: Early changes of SOB and increased HR Infiltrates, pulm. Edema Increasing hypoxemia (days 2-10) Pulmonary fibrosis
What are Direct Mechanisms of ARDS:
lead to alveolar inflammation and injury: ▪ aspiration ▪ inhalation injury ▪ contusion ▪ embolism ▪ radiation ▪ reperfusion injury ▪ oxygen toxicity
What are indirect Mechanisms of ARDS:
activation of SIR from outside the lung, tissue destructive cytokines travel to the lungs ▪ shock ▪ sepsis ▪ trauma ▪ pancreatitis ▪ drug overdose ▪ massive blood transfusion ▪ disseminated intravascular coagulopathy
Diagnosis of ARDS:
▪ Abnormal Chest X-ray
▪ Abnormal ABG’s
▪ Refractory hypoxemia
▪ despite supplemental O2
▪ Abnormal Pulmonary Function Tests
▪ ↓ compliance
▪ ↓ FRC
Nursing Priority of ARDS:
Early Recognition!
Collaborative management Support and improve oxygenation: ▪ mechanical ventilation ▪ positioning Medications & fluids Nutritional support Prevention of complications ▪ multi-organ system dysfunction/failure ▪ ventilator acquired pneumonia
How is lung cancer diagnosed and treated?
Diagnosis
∙ chest x-ray ∙ biopsy ∙ CT
∙ bronchoscopy ∙ thoracoscopy ∙ PET
∙ MRI
Treatment
∙ non-surgical - chemotherapy, radiation therapy, targeted therapy, photodynamic therapy
∙ surgical – removal of tumor, lobectomy, pneumonectomy
Cerebral Angiography
- Images of cerebral circulation
- Use: checks patency/adequacy of circ.
-Prep: good hydration
check circulation distal extremity
NPO
allergies
Post cerebral angiography
- keep leg straight
- observe site for hematoma
- check distal circulation
- neuro assessment
- pressure dressing
CSF normal findings
- Clear, colorless
- Normal pressure
- Few WBC
- No RBC
- Composition similar to plasma
Cerebral blood supply
brain receives 750 ml/min of blood = 20% of CO
Monro-Kellie Hypothesis
- The skull does not expand
- Within this closed system are 3 fluctuating components: blood (move into sinuses), brain (swell), CSF (shunted or absorbed quicker)
- If one component increases, one or both of the others decrease
Cerebrospinal Fluid
- Volume 120ml to 150ml
- Body produces about 500ml daily
- Cushions brain and spinal cord
- Absorbed through arachnoid villa
- Returned to systemic circulation by internal jugular
Cerebral Perfusion Pressure
- Changes in MAP or ICP affect CPP
- Normal MAP = 70 to 105 mmHg
- Normal ICP = 5 to 15 mmHg
- Normal CPP = 60 to 100 mmHg
*any increase/decrease in CPP means brain isn’t being adequately perfused
Autoregulation
- Ability of the brain to maintain cerebral blood flow despite changes in CPP
- Achieves this by altering diameter of arterioles (response to changes in cerebral environment)
- Autoregulation does not work if CPP < 50mmHg or > 150mmHg
Intracranial Pressure (ICP)
- Pressure exerted by brain tissue, CSF, blood against the inside of the skull
- Normal 5-15mmHg
- Prolonged elevation causes ischemia due to decreased cerebral blood flow
Cushing’s Triad
- Elevated SBP
- Widening pulse pressure- (normal =30-40mmHg)
- Bradycardia
- LATE sign of increased ICP
Herniation Syndromes
- Cingulate- lateral shift of 1 hemisphere
- Uncal- uncus of temporal lobe pushed over edge of tentorium
- Central- downward displacement of basal ganglia
- Cerebellar-cerebellar tonsils pushed toward through -foramen magnum
Guillian-Barre’ Syndrome
- Acute autoimmune disorder
- Destruction of myelin –impairs impulse conduction (communicate)
- Descending
- Affects respiratory function
- Ascending GBS
- Most common
- GBS “ground to brain symptoms”
Stages of Guillian-Barre’ Syndrome
- Initial Period (1-4 weeks), Definitive symptoms begin
- Plateau Period (days to 2 weeks)
- Recovery Period (6 months to 2 yrs): Remyelinization , Axonal regneration
GB Plan of Care
- Diagnostic testing
- Priority nursing care: Respiratory care - priority, Pain management, Communication and emotional, Nutritional
- Involvement of family, other team members
- Education
- Medical treatments—plasmapheresis (take out antibodies and replace them with new ones, complications - bleeding, ecchymosis)
Treatment for GBS
-Plasmapheresis:
Removes circulating antibodies assumed to cause disease
Plasma selectively separated from whole blood; blood cells returned to patient without plasma
Plasma usually replaces itself, or patient is transfused with albumin
Early Signs of Intracranial Pressure
- change in mentation, may be subtle
- change in LOC
restlessness, fidgety, barely off normal
3. addition of other signs and symptoms pupil changes visual changes motor weakness of 1 or > limbs headache
Later signs of worsening intracranial pressure increase
All of the above plus:
- nausea, vomiting
- deteriorating LOC
- confusion
- papilledema
- hemiplegia
- decerebrate posturing
- decorticate posturing
Late Symptoms of increased Intracranial pressure
- Cushing’s reflex:
- Increased systolic blood pressure
- Increased pulse pressure
- bradycardia
Pathophysiology of SCI
- Injury interrupts blood supply - damage to blood vessels
- Clots accumulate in damaged vessels
- Chemical mediators produce ischemia
- Necrosis and neuron death occurs
- CPP may be decreased by neurogenic shock
Key Assessment Findings in SCI
- Neurological system- level of sensation, motor ability, breathing
- Cardiovascular system- neurogenic shock (lose sympathetic tone- vessels dilate=bp falls)
- Respiratory system- vent, deep breathing, RT, quad cough, incentive spirometry
- GI/GU systems- spinal shock= bowel sounds will be absent, distended abdomen, loss of emptying of bladder, urinary retention, UTI
Spinal Shock (Syndrome)
mainly a loss of reflexes, minutes within injury can last up to weeks, flaccid paralysis, loss of sensation, loss of motor response
temporary
drug Management of SCI
- steroids: decreases inflammation but decrease immune, prone for stress ulcers, elevated glucose
- dextran:expand plasma, increase cap blood flow to spinal cord
- atropine sulfate: bradycardia
- dopamine: elevate bp
- muscle relaxant: after shock has resolved
Priority Problems for Long-Term Management of SCI
- Difficulty breathing
- Impaired physical mobility (safety)
- Spastic or flaccid bladder and bowel
- Impaired adjustment
Autonomic Dysreflexia
- develops massive sympathetic discharge from kinked catheter, constipation
- severe HTN, hr drop, headache, nasal stuffiness, flushing
- first thing to do!!!!- raise the head of bed (to decrease hemorrhagic bleed in head)
- loosen tight clothing, assessing for cause, check for fecal impaction, urinary retention
antidote for heparin
protamine sulfate
antidote for warfarin
vitamin k
antidote for tpa
FFP
Medications for CO
Digoxin, inotropic (dobutamine, dopamine)
Right brain injury= left side of body is effected
Hemiplegia Impairment in creativity Confused on date time place Cannot recognize faces Loss of depth perception Trouble staying on topic Can’t see thing on left side- left side neglect Trouble with grooming Emotional unstable Impulsive Denial Not able to interpret nonverbal language
left sided brain injury
Right hemiplegia Aphasia- trouble formulating words and comprehending them Aware of limits Severe depression Trouble understanding written text Issues with writing - agraphia Impaired math Memory intact Trouble seeing on right side of body
Drug Therapy for strokes
Thrombolytics Anticoagulants Lorazepam, other antiepileptics Calcium channel blockers Stool softeners Analgesics (for pain) Antianxiety drugs
