Exam 3 lecture 5 Flashcards
Define critical care. Where does it usually take place?
Care if patients with acute life threatening illness.
Usually takes place in specialized units such as the ICU, OR, emergency departments
What are some pharmacokinetic alterations in critically ill patients
- Oral absorption is impaired/unpredictable in critically ill patients
There are alterations in gastric emptying and gastric motility.
Many of the patients in ICU are on opioids, this alters patients PK - IV route (if available) used for treatment of critically ill patients
why do Alterations in drug distribution vary between different critically ill patient populations.
- Relates in part to fluid/hydration status
Hydrophilic drugs (aminoglycosides)- higher volume of distribution in critically ill surgical/trauma patients than in medical patients
- Alterations in plasma protein binding
- decreased albumin (decreased protein binding of many drugs)
-increased acute phase proteins (alpha-1 acid glycoprotein) (increased protein binding of drugs that bind alpha-1 acid glycoprotein
What is something to know about metabolism of drugs of critically ill patients
Hepatic enzyme expression and activity may be decreased in some critically ill patients.
How common is renal dysfunction in critically ill patients? Why? How do we detect changes in renal function? WHat disease states are associated with increased renal elimination?
Renal dysfunction is common in critically ill patients.
This could be due to shock, sepsis- related organ failure or nephrotoxic drugs.
You do not see changes in Scr immediately when some one has changes in renal function. Immediate changes could be seen by looking at I/O of urine.
Hemodialysis (HD) or continous renal replacement therapy is common in ICU so adjust drugs
burns and trauma are associated with increased renal elimination
What is sepsis? Mortality rate? what is it associated with? What are the causes and sites of infections? How to to resolve it?
Life threatening organ dysfunction caused by dysregulated response to infection (exaggerated immune response)
associated with immune dysregulation and coagulation and thrombosis leading to endothelial injury
High mortality rate (30%)
Can occur in response to any pathogen (bacterial most common) and site of infection (common; lungs, bloodstream, urinary tract)
No specific drug therapy. Antibiotic therapy (broad spectrum IV antibiotics), early detection and supportive therapy is critical
What is septic shock? symptoms? Treatment?
A subtype of sepsis associated with cardiovascular collapse (profound hypotension.)
Hypotension related to decreased vascular tone
Treated by
1. Fluids (crystalloids, colloids)
- Vasopressors (increase vascular tone, potentially cardiac output)
-goal mean arterial pressure (MAP) >65mmHg
- Norepinephrine is preferred vasopressor of choice (phenylephrine, epinephrine and dopamine used if it doesnt work)
- vasopressin may be added on
- dobutamine (inotrope) may be added on - corticosteroid (IV hydrocortisone) may offer mortality benefit if not responding to vasopressor
How common is respiratory failure for ICU admission? Causes?
respiratory failure/ mechanical ventilation is common reason for ICU admission
numerous causes. Airway compromise, hypoventilation, hypotoxic failure (poor air exchange), inability to protect airways
What is ARDS? Mortality rate? Triggers to ARDS? How to handle ARDS? WHat decreases mortality?
ARDS is a life threatening respiratory failure characterized by acute, diffuse inflammatory lung injury.
25-40% mortality
Triggers include Pneumonia, sepsis, trauma, aspiration, others
Often requires mechanical ventilation with sedation, potentially neuromuscular blockade
Corticosteroid may decrease mortality in severe ARDS
What is a mnemonic for general supportive care in hospitals
FAST HUGS BID
What does FAST HUGS BID stand for
F- feeding, fluids
A- Analgesia
S- Sedation
T- Thromboprophylaxis
H- HOB elevation
U- Ulcer (stress ulcer) prophylaxis
G- Glycemic control
S- Spontaneous awakening trial
B- Bowel regimen
I- Indwelling Catheters
D- delirium assessment
What are general supportive care points about “feeding” patients in ICU
Many ICU patients unable to take adequate oral intake. They may also have specialized nutritional requirements (liver failure, renal failure, increased caloric needs due to trauma, burn, surgery)
EN or PN are common (EN preferred if possible)
What are some general supportive care points to know about “fluids” in patients in ICU. WHat is the goal when giving fluids? What to monitor?
Consider maintenance and resuscitation via crystalloids, colloids and blood products.
goal is adequate resuscitation and meeting maintenance requirements without causing fluid overload.
Carefully monitor INs and OUTs (urine output is early indicator of renal dysfunction)
EXAM! What is the incidence of VTE (venous thromboembolism in medical ICU vs surgical setting? What are the risk factors for VTE?
up to 30% venous thromboembolism (VTE) incidence in medical ICU, upto 60-70% in surgical settings
Most critically ill patients have risk factors for VTE.
- immobility
- trauma, surgery, use of vascular catheters, sepsis, hypercoagulable states
- cancer, obesity, prior history of VTE
EXAM! What can complicate thromborpophylaxis as a general supportive care? Which ICU patients should and should not receive pharmacologic VTE prophylaxis
Can be complicated by underlying bleeding risks, active bleeding, need for invasive procedures, neuraxial anasthesia.
The majority of ICU patients should receive pharmacological VTE prophylaxis unless sufficiently mobile and very low risk OR contraindications to pharmacological prophylaxis
Exam! Agents that we have and use for thromboprophylaxis
UFH
LMWH (enoxaparin, dalteparin)
LMWH preferred over UFH
KNOW DOSING FOR THROMBOPROPHYLAXIS FOR EXAM
Just a note
UFH dosing and monitoring for thromboprophylaxis (exam)
5000 U Sq Q8h or Q12h
monitor; s/s of bleeding, CBC (platelets for HIT), no adjustment for renal dysfunction. no reason to measure APTT with prophylactic dose
Enoxaparin dosing and monitoring (exam)
30 mg SQ q12h, 40 mg Sq q24h (may dose base on anti- Xa activity in selected patients)
monitoring; s/s bleeding, CBC (platelets for HIT)
CrCl<30 ml/min; 30 mg SC q24h
what are SRMD? What is mortality rate? Risk factors?
Stress related mucosal damage (stress ulcers)
risk factors
- shock, coagulopathy, chronic liver disease
- Mechanical ventilation/respiratory failure
-others: Neurotrauma, burn injury, extracorporeal life support - drugs: Antiplatelet agents, anticoagulants, NSAIDs
What are our pharmacologic options for stress ulcer prophylaxis? when to d/c
- Histamine-2-receptor antagonists (H2RAs)
-PPIs
EN is also protective against stress ulcers, but can not be used as sole prophylaxis in high risk patients
discontinue SUP (stress ulcer prophylaxis) when risk factors no longer present
What are some H2RAs used for SUP? ROA? adverse effects?
Famotidine or ranitidine
Enteral or parenteral
Adverse- potential thrombocytopenia
PPI drugs? ROA? Risks associated with it?
Omeprazole, lansoprazole (-azole)
Enteral, Parenteral
Potential for increased risk of C diff, effects on mortality controversial
Summarize the following for SUP risk factors, When to dx, choice of PPI vs H2RA
PPI associated with lower incidence of clinically important bleeding, but are more likely to be associated with infectious complications
dx prophylaxis when risk factor is gone
