Goya-Critical Care

Front 1

Describe the indication for and goals of mechanical ventilation

Back 1

A. Primary indicators
1. Inadequate spontaneous ventilation-pH reliable index (respiratory acidosis)
2. Hypoxemia w/ supplemental high flow O2
PaO2 <60mmHg or (SpO2 < 90%) w/ FiO2 >50%
note-arterial blood gas results indicate respiratory failure
CNS, muscular, obstruction, lung defects are all indicators
B. clinical indicators:
a. Respiratory assessment
i. respiratory rate >35bpm
ii. Minute ventilation <3lpm or >20lpm
iii. Negative inspiratory force <-25 cm H2O
iv. Vital capacity <10 ml/kg
b. Gas exchange
i. PaO2 <60mmHg w/ FiO2 >50%
ii. PaCO2 >50mmHg (acute) and pH < 7.25
C. goals
1. Adjust alveolar ventilation (pH, PaCO2)
2. Improve oxygenation-assess w/ pulse oximetry
3. Decrease work of breathing (WOB)

Front 2

Describe negative pressure veltilation

Back 2

Mimics spontaneous ventilation-negative pressure applied to chest wall increases volume of thoracic cage; negative intrathoracic pressure gradient causes air to enter lungs
No need for artificial airway
Used for chronic care of patients with neuromuscular disorders (ALS, MS)
Examples: iron lung, pulmowrap, chest cuirass

Front 3

Describe positive pressure ventilation

Back 3

Air applied under positive pressure at patient’s airway, forcing gas flow into lungs
Intrathoracic pressure changes are opposite of spontaneous breathing; venous return may be impeded (patient may require IV volume support)
Intrathoracic pressure remains positive throughout respiration; gas flow takes path of least resistance, is distributed to non-dependent, less-perfused lung regions-->Ventilation/ perfusion mismatch
ventilation parameters
a. FiO2-titrate with pulse oximetry goal: <50% (try to get as close to 21% as possible)
b. Rate: 10-20 bpm
c. Tidal volume (VT): 6-10ml/kg (5-6 is normal resting VT)

Front 4

Describe assist/control ventilation

Back 4

Breaths delivered at clinician-set parameters:
1. Tidal volume
2. Flow rate and pattern
3. Back-up respiratory rate (if machine doesn't sense patient inspiratory effort w/in the set time, will deliver full VT breath)
note-full VT w/ every breath (patient or machine initiated)
Advantages-provides full ventilatory support; patient controls rate of breathing
Disadvantages-settings may not match patient’s ventilatory demands; as spontaneous breaths increase, minute ventilation increases proportionately; can result in hyperventilation (set high respiratory rate and minute ventilation alarms)

Front 5

Describe Synchronized Intermittent Mandatory Ventilation (SIMV)

Back 5

Combination of machine and spontaneous breaths; mandatory breaths delivered when patient effort is sensed (synchronized); patient determines tidal volume and rate of spontaneous breaths
note-not every spontaneous breath will yield full VT; machine will kick in when patient effort is sensed w/in set rate parameters (ex. if machine is set for 10bpm, and patient breathes 20bpm, machine will assist 10/20 of those breaths)
Advantages-synchronized breaths improve patient comfort; reduces competition b/t patient and ventilator; hyperventilation less of a concern compared to A/C
Disadvantages-may not be enough support if set rate or VT too low (increases WOB)

Front 6

contrast volume vs pressure control ventilation

Back 6

A. Volume Ventilation (more common)
1. Volume delivery constant
2. Inspiratory pressure varies
3. Inspiratory flow constant
4. Inspiratory time determined by set flow and VT
B. Pressure Ventilation
1. Volume delivery varies
2. Inspiratory pressure constant
3. Inspiratory flow varies
4. Inspiratory time set by clinician
5. flow delivery is decelerating

Front 7

Describe presssure control ventilation

Back 7

A. Uses
1. A/C-all breaths (machine and patient initiated) are time cycled and pressure limited
2. SIMV-only machine initiated breaths are time cycled and pressure limited; spontaneous breaths can be pressure supported
note-inspiratory time can be increased; increased I:E ratio-->increased oxygenation, pressure, and CO2 (harder to blow off)
B. Advantages-limits risk of barotrauma; recruits collapsed and flooded alveoli; improves gas distribution
C. Disadvantages-VT varies when patient compliance changes (i.e. ARDS, pulmonary edema); w/ increases in I-time, patient may require sedation and/or chemical paralysis
D. indications
1. Enhance patient/ventilatory synchrony (patient determines flow)
2. Lung protection-lower inspiratory pressure w/ decelerating flow can improve V/Q matching; adjusting I-time can improve oxygenation by increasing mean airway pressure (MAP)
2. Alveolar diseases that produce varying time constants (recruit alveoli by lengthening I-time)

Front 8

Describe pressure support ventilation

Back 8

A. definition
application of set positive pressure to spontaneous inspiratory effort; flow delivery is decelerating (requires intact respiratory drive)
spontaneous inspiratory effort assisted to preset pressure level; patient determines respiratory rate, inspiratory time, peak flow, and VT
B. Goals
overcome resistive work associated w/ artificial airway and circuit; improve patient/ventilator synchrony; augment spontaneous VT
C. Uses
Low level PSV: 5-10cm H2O PSV applied to spontaneous breaths during other ventilator modes (SIMV, PCV); decreases WOB (may be final level of support before extubation)
Max PSV-increased to level that augments spontaneous inspiratory efforts to yield tidal breaths of 10 ml/kg (meets total ventilatory needs of patient)
D. Advantages-patient controls rate, volume and duration of breaths; patient comfort; may overcome WOB
E. Disadvantages-may not be enough ventilatory support if patient condition changes; support level remains constant regardless of patient drive
F. Patient assessment-monitor exhaled VT; maintain system free of air leaks; monitor for increased RR with decreased VT

Front 9

Describe PEEP and CPAP

Back 9

A. PEEP (Positive end expiratory pressure)-application of constant, positive pressure; at end exhalation, airway pressure does not return to a 0 baseline
used w/ other mechanical ventilation modes (A/C, SIMV, PCV)
Increases functional residual capacity (FRC) and improves oxygenation; recruits collapsed alveoli; splints and distends patent alveoli; redistributes lung fluid from alveoli to perivascular space
B. CPAP (continuous positive airway pressure)-application of constant positive pressure throughout spontaneous ventilatory cycle; no mechanical inspiratory assistance provided (requires active spontaneous respiratory drive)
decreases WOB; VT and rate determined by patient; often final form of support before extubation
C. Indications (both PEEP and CPAP)-prevent and/or reverse atelectasis; improve oxygenation
D. Potential adverse effects (PEEP and CPAP)-decreased CO due to increase in positive intrathoracic pressure; barotrauma; ncreased intracranial pressure (ICP)

Front 10

describe sensitivity in mechanical ventilation

Back 10

Sensitivity setting establishes trigger variable, which determines when ventilator recognizes patient’s inspiratory effort
When patient effort is recognized, ventilator triggered to deliver breath; trigger can be a change in pressure or change in flow

Front 11

Describe potential complication of mechanical ventilation

Back 11

A. Ventilator malfunction-anually ventilate patient
B. Cardiovascular compromise/arrhythmias-onitor vital signs
C. Barotrauma-alveolar rupture due to overdistention (monitor PIP, breath sounds)
D. Infection-ET tube bypasses natural airway defense mechanisms-->nosocomial or aspiration pneumonia (good handwashing, provide mouth and tube care)
E. Psychological-patients may be extremely anxious and/or agitated; give consistent, calming explanations, offer reassurance; sedation, anti-anxiety agents
F. Pulmonary O2 toxicity (goal-FIO2 <50%; PaO2 >70%)
G. Positive fluid balance-monitor weight, peripheral edema, I/O, and breath sounds
H. Gastric distention-monitor bowel sounds, NG tube

Front 12

A 61-year-old woman presents to the ED with a complaint of shortness of breath for 24hrs. Upon arrival her vital were: Pulse 100 and regular, RR- 30, BP- 80/60, T-36C and oxygen saturation of 92% on 15L by face mask.
Her physical examination upon arrival reveals an obese, diaphoretic woman. She has decreased breath sounds in all lung fields and she is using her accessory muscles of respiration. Her cardiac exam is only remarkable for tachycardia.
Her past medical history is remarkable for diabetes, hypertension, COPD and, chronic renal insufficiency. She continues to smoke 1 pack per day for 30years.
Upon further questioning she tells you she has been having dysuria for the past 2 days.

Back 12

septic shock
anion gap metabolic acidosis

Front 13

Describe the different types of shock

Back 13

A. Hypovolemic shock-due to decreased circulating blood volume in relation to total vascular capacity; characterized by a reduction of diastolic filling pressures
B. Cardiogenic shock-due to cardiac pump failure related to loss of myocardial contractility/functional myocardium or structural/mechanical failure of cardiac anatomy; characterized by elevations of diastolic filling pressures and volumes
C. Extra-cardiac obstructive shock (Obstructive)-due to obstruction to flow in cardiovascular circuit; characterized by either impairment of diastolic filling or excessive afterload
D. Distributive shock-caused by loss of vasomotor control resulting in arteriolar/venular dilatation and/or shunt; characterized (after fluid resuscitation) by increased cardiac output and decreased SVR; example-septic shock (bacterial, fungal, viral, rickettsial)

Front 14

Describe the hemodynamics of hypovolemic shock

Back 14

i. CO (cardiac output)-decreased
ii. SVR (systemic vascular resistance)-increased
iii. PWP (pulmonary wedge pressure-indirectly measures left atrial pressure)-decreased
iv. EDV (end diastolic volume)-decreased

Front 15

Describe the hemodynamics of cardiogenic shock

Back 15

i. CO-decreased
ii. SVR-increased
iii. PWP-increased
iv. EDV-increased

Front 16

Describe the hemodynamics of obstructive shock

Back 16

i. CO-decreased
ii. SVR-increased
iii. PWP-increased (big increase in afterload)
iv. EDV
a. afterload-increased
b. preload-decreased

Front 17

Describe the hemodynamics of septic shock

Back 17

high CO
low SVR
low CVP (central venous pressure)

Front 18

Describe the causes and prognoses of the different typs of shock

Back 18

A. Hypovolemic shock-degree of volume loss determines response
10%-well tolerated (tachycardia)
20-25%-failure of compensatory mechanisms (hypotension, orthostasis, decreased CO)
>40%-associated w/ overt shock (marked hypotension, decreased CO, lactic acidemia)
B. Cardiogenic shock-#1 cause of in-hospital mortality (Q-wave MI); requires >40% loss of functional myocardium (single MI or cumulative damage); usually involves left main or LAD obstruction; RV infarction-less mortality
C. Obstructive-faster rates of development of obstruction to blood flow lead to more severe response (even compared w/ a larger obstruction obtained over a longer period of time); acute pulmonary emboli, tension pneumothorax and acute cardiac tamponade are common causes
D. distributive shock-loss of peripheral resistance and shunting (predominantly septic shock)

Front 19

Describe the SIRS-sepsis continuum

Back 19

A. Systemic Inflammatory Response Syndrome (SIRS)-2 or more of the following
i. T>38C or *<36C*
ii. HR>90
iii. *RR>20* (PaCO2<32)
iv. Leukocyte ct>12K, <4K or *>10%bands*
B. Sepsis-SIRS + infection
C. Severe sepsis
Severe Sepsis-presence of sepsis + organ hypoperfusion or dysfunction
Organ hypoperfusion-elevated lactic acid; oliguria; abnormal peripheral circulation; AMS
Organ dysfunction-ARF; ARDS; DIC; Delirium
D. Septic shock-sepsis + refractory hypotension (SBP<90; MAP<65; >40mmHg drop compared to baseline)

Front 20

Describe sepsis management

Back 20

A. Resuscitation-crystalloid or colloid fluids in 1st 6 hours (1000cc at a time); reduce fluids if increased CVP and no improvement in perfusion
note-quick resuscitation w/ a lot of fluids is critical for mortality
B. Antibiotics-broad-spectrum antibiotic w/in 1 hour recognition (critical!) of septic shock and sepsis; blood cultures before antibiotics (but don't wait for results); narrow antibiotic coverage from data
C. imaging studies-source control
D. Vasopressors/Inotropes
1. NE and DA most common (keep MAP >65)
2. Dobutamine-for decreased CO; SVO2 <70%
3. Epinephrine-1st alternative
E. Steroids-if refractory to vasopressors; Hydrocortisone >dexamethasone
F. blood products-transfuse if SVO2 <70%, Hb <6
G. mechanical ventilation-evidence of lung failure; give low VT, low pressure in ARDS

Front 21

Describe management of the different types of shock

Back 21

A. Hypovolemic shock
i. rapid replacement of blood, colloid, or crystalloid
ii. dentify source of blood or fluid loss-endoscopy/ colonoscopy; angiography; CT/MRI scan
B. cardiogenic shock
i. LV infarction-intra-aortic balloon pump (IABP); cardiac angiography; revascularization (angioplasty/stent, coronary bypass)
ii. RV infarction-fluid and inotropes w/ PA catheter monitoring
iii. Mechanical abnormality-echocardiography; cardiac cath; corrective surgery
C. Obstructive shock
i. Pericardial tamponade-pericardiocentesis; surgical drainage (if needed)
ii. Pulmonary embolism-Heparin; CT angio; thrombolytics; embolectomy
D. Distributive (septic) shoc
i. identify site of infection and drain
ii. antimicrobial agents (key rules)<1 hour from suspicion
iii. ICU monitoring and support-fluids, vasopressors, inotropic agents
Goals:
i. ScV02 >70%
ii. CVP 8-10 or 12-15
iii. improving organ function
iv. decreasing lactate levels
v. MAP>65

Front 22

An 85-year-old man is brought to the ED from nursing home for a change in his mental status. Upon arrival, his vital signs revealed a RR of 30, heart rate of 90, T of 40C and an oxygen saturation of 88% on 5LPM by face mask. He is lethargic, has coarse rhonchi in all lung fields and the nurses are suctioning green mucus from her mouth. A grade 3/6 holosystolic murmur is heard throughout his precordium. His advance directive states he is a full code and you intubate him for respiratory failure

Back 22

ARDS

Front 23

Describe respiratory failure and abnormal gas exchange

Back 23

duration of failure-determines classification (acute vs chronic) and management
1. Failure to Oxygenation-PaO2 <60mmHg
2. Failure to Ventilation-PaCO2 >50mmHg
factors that determine effectiveness of gas transfer
1. Rate at which fresh air is supplied to alveoli (alveolar ventilation)
2. Degree of ventilation & perfusion matching in each gas-exchange unit
3. Extent that CO2 & O2 equilibrate b/t gas-exchange unit & capillary blood

Front 24

differentiate the gas exchange defects

Back 24

1. Hypoxemic Respiratory Failure (type 1 respiratory failure)-characterized by reduction in PaO2 w/ normal or reduced PaCO2
2. Hypercarbic Respiratory Failure (type 2)-reduction in alveolar ventilation (inadequate minute ventilation)-->hypercapnia & secondary hypoxemia
Mechanism-reduced Neural Input; mechanical impedence; elevated Dead Space Fraction
note-type 1 causes are mostly lung related; type 2 causes mostly CNS related (reduced central drive, impaired neuromuscular function)
3. Mixed Hypoxemic/ Hypercarbic (type 3)-progressive parenchymal lung disease (severity of hypoxemia not accounted for by degree of hypercapnia alone); hypoxemaia and hypercapnia; most common type; most patients need mechanical ventilation

Front 25

Describe the causes of hypoxemic repiratory failure

Back 25

1. ventilation-perfusion (V/Q) mismatch (most common)-disorders affecting airways, parenchyma or vasculature
In normal lung, V/Q are closely matched (ratio=1); V/Q mismatch alters ratio; improves w/ oxygenation
2. Shunt (2nd most common)-extreme type of V/Q mismatch; venous blood passes directly into arterial circulation w/out participating in gas exchange; oxygenation can't improve w/ supplemental O2 (bypasses gas exchange)
types of shunts-intracardiac; pulmonary vascular; pulmonary parenchymal (seen in ICU); systemic (sepsis is most common)
3. Decreased FiO2 (High Altitude)-barometric pressure decreases w/ increasing altitude & partial pressure of O2 decreases
4. Diffusion Abnormality-thickening of alveolar membrane or decreased transit time in pulmonary capillary bed impairs diffusion of O2

Front 26

Describe the Alveolar-arterial (A-a) gradient and its role in determining respiratory failure

Back 26

measures difference b/t alveolar concentration of O2 and arterial concentration of O2
A-a gradient=PAO2-PaO2
Normal gradient=age (years)/4 + 4
normal A-a gradient-extrapulmonary cause (type 2)
widened A-a gradient-pulmonary cause (types 1, 3)

Front 27

How do you differentiate b/t acute and chronic respiratory failure?

Back 27

Acute Respiratory Failure-elevated PaC02 w/ normal HCO3; change of 10mm Hg of PaCO2 will change pH by 0.08
Chronic-elevated PaCO2 w/ elevated HCO3 (renal compensation); change of 10mm Hg of PaCO2 will change pH by 0.04

Front 28

describe the acute lung injury and ARDS continuum

Back 28

A. Acute lung injury-acute & persistent lung inflammation w/ increased vascular permeability; widespread, bilateral radiographic infiltrates; PaO2/FiO2 ratio <300
B. Acute respiratory distress syndrome (ARDS)-acute lung injury w/ worse hypoxia (PaO2/FiO2 ratio <200)
most patients require mechanical ventilation
pathological feature-diffuse alveolar damage (DAD)
causes-sepsis (most common); infection (most common cause outside hosptial)

Front 29

Describe the chest x-ray fidings and pathologic staging of ARDS

Back 29

A. Chest x-ray
Early-CXR may be normal (transient)
Patchy or homogeneous diffuse, bilateral infiltrates that may coalesce (white out); diffuse alveolar infiltrates may clear leaving interstitial, then fibrotic pattern; may clear w/ minimal residual
B. pathologic stages
1. Exudative (initial) Stage-characterized by diffuse alveolar damage
2. Proliferative-resolution of pulmonary edema & proliferation of type 2 alveolar cells
3. Fibrotic-obliteration of normal lung architecture, diffuse fibrosis & cyst formation

Front 30

Describe the clinical features of ARDS

Back 30

A. Early
Pulmonary dysfunction develops w/in 24-48hrs after inciting event (rapidly worsening tachypnea, dyspnea, hypoxemia requiring high O2)
Physical exam-cyanosis, tachycardia, tachypnea & diffuse rales
CXR-diffuse alveolar infiltrates
note-patients usually symptomatic at presentation
B. subsequent course-
Oxygenation improves over several days (patient remains on ventilator); poor lung compliance, high minute ventilation requirements, hypoxemia
CXR-becomes less opaque, interstitial infiltrates remain
Fibrosis may occur along w/ lung cyst

Front 31

Describe mechanical ventilation treatment of ARDS

Back 31

mainstay treatment; allows time for treatment of underlying cause & evolution of healing process
1. Lung Protective Ventilation
hallmark of ARDS is decreased lung compliance; patchy in distribution (different areas of lung are hyperinflated, hypoinflated & normal)
Ventilation w/ small tidal volumes & limited airway pressures can reduce overdistention; VT should be 6 cc/kg of ideal body weight (know height); pressure control can also be used to control overdistension
2. PEEP
used to improve oxygenation by preventing premature collapse of alveoli; ARDS patients need combination of PEEP & increased Fi02
reduces intrapulmonary shunts & improves arterial oxygenation; increases V/Q relationship
Adverse effects-decreased CO; increased lung volume & stretch during inspiration-->increases risk of barotrauma

Front 32

Describe steroid treatment and prognosis for ARDS

Back 32

A. glucocorticoids (for inflammation)
Steroids started <7 days of illness improved
Steroids started >14 days had increased mortality
note-early glucocorticoid treatment is key; indicated in sepsis treatment
B. prognosis-mortality at 50%
majority of deaths due to sepsis or multiorgan dysfunction (not respiratory failure)
Factors predicting risk of death-chronic liver disease, nonpulmonary organ dysfunction, sepsis, & advanced age

Front 33

After 3 days on mechanical ventilation, he develops sudden hypotension (80/60), tachycardia (120/min), high respiratory rate of 28/min and he is noted to be desaturating to 85% on FiO2 of 80%. His physical examination reveals some subcutaneous emphysema along his right chest and neck. His trachea is deviated to the left and there is decrease breath sounds on his right chest. His heart sounds appear to be muffled

Back 33

pneumothorax

Front 34

Describe a spontaneous pneumothorax and its etiology

Back 34

primary pneumothorax-usually occurs w/out precipitating event in person w/out clinical lung disease
secondary-complication of underlying disease (ARDS)
caused by rupture of subpleural emphysematous blebs located at apices of lungs; attributed to congenital abnormalities & inflammation of airways; strong association b/t primary spontaneous pneumothorax (PSP) & cigarette smoking
Patients are tall & thin; increase in length of chest may contribute to formation of subpleural blebs; gradient highest at apex (alveoli more distended)

Front 35

Describe the clinical manifestations of a spontaneous pneumothorax

Back 35

A. presentation
Usually develops at rest (<10% occur during exercise); peak age is early 20s
Chest pain & dyspnea are major symptoms; chest pain is acute and localized to side of pneumothorax; larger the pneumothorax, the more symptomatic
B. physical exam-decreased chest excursion on affected side; diminished breath sounds; hyperresonant percussion
C. CXR
Presence of visceral-pleural line (most common
Deep sulcus sign
Hydropneumothorax (air-fluid interface)
Tension Pneumothorax (trachea deviation away)
D. arterial blood gas
Hypoxemia-common due to V/Q abnormalities (mismatch)
Acute respiratory alkalosis may be present-pain, anxiety contribute to hyperventilation-->hypocapnea and hypoxemia-->alkalosis

Front 36

Describe some non-invasive treatment for a spontaneous pneumothorax

Back 36

A. goals
1. remove air from pleural space
2. decrease likelihood of recurrence (50% w/in 2 years, usually on same side)
B. observation-air w/in pleural space reabsorbs at 1.25% of volume of hemithorax/day (O2 administration enhances reabsorption); recommended if pneumothorax <15%
C. simple aspiration-initial treatment for most PSP >15%
Air manually w/drawn from needle in 2nd intercostal space until no more air can be aspirated; if no resistance appreciated after 4L has been aspirated, assume persistent leak (Tube Thoracostomy indicated)

Front 37

Describe more invasive procedures to treat spontaneous pneumothorax

Back 37

A. Tube thoracostomy-for unstable patients, failure of simple aspiration or patients recurrent spontaneous pneumothorax; doesn't reduce
incidence of recurrence
B. Tube thoracostomy w/ pleurodesis agent- for recurrence of pneumothorax (sometimes for secondary pneumothorax); tetracycline or *Talc* are preferred agents; procedure is painful; patients should be premedicated w/ narcotics and short acting benzodiazepines
C. Video-assisted thoracoscopy (VATS)-effective treatment for spontaneous pneumothorax & prevents recurrence
Bullae best treated w/ wedge resection via endoscopic stapler; instillation of talc slurry
Recommended if:
1. lung remains unexpanded after 3-5 days of tube thoracostomy
2. bronchopleural fistula persist after 3 days
3. recurrent pneumothorax after chemical pleurodesis

Front 38

Describe what secondary spontaneous (SSP) and tension pneumothoraxes are

Back 38

A. SSP-occurs as a complication of underlying lung disease (COPD is most common); persistent air leaks more common & tend to persist longer compared w/ PSP
B. Tension pneumothorax-when intrapleural pressure exceeds atmospheric pressure throughout expiration
One way valve mechanism is present; during inspiration, air leaks into pleural space; during expiration, communication is occluded (air comes in, none goes out); results in compression of intravascular vessels w/in chest (life threatening)

Front 39

Describe the presentation and treatment of a tension pneumothorax

Back 39

A. presentation
Patients appear profoundly distressed w/ rapid labored breathing, cyanosis, marked tachycardia & diaphoresis; suspect in any patient w/ known pneumothorax who suddenly deteriorates or after any procedure known to increase risk
B. treatment
Medical emergency; supplemental O2 to prevent hypoxemia
Large bore needle placed into pleural cavity to immediately decompress lung (relieve pressure)
Tube thoracostomy

Front 40

53y/o woman had sudden onset of dyspnea 1 hour ago. She had undergone total hip arthroplasty 48hrs earlier. She is otherwise healthy except for controlled hypertension. She has a 20 pack-year smoking history

Back 40

pulmonary embolism

Front 41

Describe the etiology and risk factors of a pulmonary embolism (PE)

Back 41

A. Etiology
90% originate from deep venous thrombosis (DVT) in lower extremities (femoral vein)
If DVT is prevented-->PEs are prevented
B. risk factors-immobilization, recent surgery, hormones, genetics, heart problems, trauma

Front 42

Describe how a patient initially presents w/ a pulmonary embolism

Back 42

A. History & Physical-nonspecific for PE; dyspnea, pleuritic chest pain, tachypnea (rapid breathing) most common symptoms
note-can have same findings in sepsis, but 48 hours post surgery is too soon
B. CXR-usually normal (can't exclude PE)
C. EKG-usually normal or nonspecific changes; *S1Q3T3* & right axis deviation can indicate right heart compromise and massive PE

Front 43

Describe non-imaging tests used if patient has suspected PE

Back 43

A. arterial blood gas (ABG)-hypoxemia or a widened A-a gradient is common finding (young patients w/out lung disease can have normal PaO2 (and A-a gradient)
B. D-dimer-specific degradation product released into circulation when fibrin undergoes fibrinolysis
Highly sensitive but nonspecific screening test (elevated levels can be seen in many other conditions); *role of D-dimer is to rule out PE*

Front 44

Describe how to test for a deep vein thrombosis

Back 44

PEs often occur in setting of overt or occult DVT; diagnostic tests confirming presence of DVT is useful strategy to help identify possible PE
diagnosis of DVT can't be made reliable on history or physical exam
doppler ultrasound-noninvasive; detects 90% of clotted iliac, femoral, & popliteal veins; limited by obesity, edema, & tenderness, as well as cast or immobilization devices; interpret w/ caution when attempting to diagnosis a recurrent DVT

Front 45

Describe imaging tests used to diagnose PE

Back 45

A. spiral CT-*diagnostic modality of choice;* allows direct visualization of emboli and detection of parenchymal abnormalities
intraluminal defects in main or lobar pulmonary arteries have positive predictive value for PE
B. pulmonary angiogram-gold standard (not test of choice though); diagnosis of PE is ID of intravascular filling defect or abrupt cutoff
Limitations-invasive; accessibility; interpretations
Complications: <5% morbidity w/ selective angiography; Death <3%; hypotension, bronchospasm, pulmonary edema, anaphylaxis, arrhythmia
note-because of invasivness and complications, only due this test as a last resort (if still not sure of the diagnosis)

Front 46

Discuss initial anticoagulant therapy for PE

Back 46

Goal of treatment-prevent further embolization or DVT
*low molecular weight heparin (LMWH)*-fragments of degraded standard heparin (just as effective)
advantages-don't need to measure PTT; less bleeding; given subcutaneously
*Treatment of choice* for outpatient DVT and uncomplicated PEs in association w/ Coumadin

Front 47

Describe long-term anti-coagulation therapy for PE

Back 47

coumadin-inhibits vitamin K factors (II, VII, IX, X, protein C)
Dosage titrated to maintain international normalized ratio (INR) 2-3 (reduces recurrence by 90%)
Antithrombotic effect delayed 72-96 hrs (LMWH therapy must overlap); Heparin, LMWH & Coumadin can be started on same day
Duration of treatment-dependent on predisposing risk factors for DVT
Major transient risk factor-3 months of therapy (Trauma, Post surgery); once patient is fully ambulatory
idiopathic emboli: 6-12 months
high-risk thrombophilia-indefinite therapy
risks-deficiency of antithrombin, protein C or S; factor V Leiden; advanced cancer; recurrent episodes of idiopathic thromboemboli

Front 48

Describe critical life-saving measures used in the treatment of PEs

Back 48

A. thrombolytic therapy
tPA-ctivates plasminogen resulting in clot lysis; perfusion improved, but higher risk of bleeding
useful in treatment of massive or life-threatening PEs, hemodynamic compromise (most life-saving process of PE treatment)
B. embolectomy-rarely indicated; reserved for pts w/ documented massive PE, who are in refractory shock (only done in a few locations)

Front 49

Describe prophylactic measures taken to prevent PE

Back 49

risk factors for PE-older age (>75yrs); recent surgery or trauma (hip or knee); immobility or paresis
A. non-pharmacologic, non-invasive
Early ambulation & movement; graduated compression stockings & pneumatic compression devices
useful in high risk for bleeding w/ anticoagulation (recent GI bleed, hemorrhagic stroke, recent CNS surgery, thrombocytopenia)
B. pharmacological-LMWH (enoxaparin is most common)
C. surgical-inferior vena cava interuptions
indications-contraindication or complication w/ anticoagulation; recurrence of PE despite adequate anticoagulation
note-hasn't been shown to improve morbidity or mortality