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
what are some points to know about glycemic control when relating to general supportive care? What is hyperglycemia associated with? Causes? target BG?
hyperglycemia is associated with increased OCU mortality.
Multifactorial causes (not limited to patients with underlying diabetes). underlying stress, TPN
Specific target controversial (balance between risk of hypo and hyperglycemia)
general target BG- 144-180
When to initiate insulin in general supportive care
Insulin > 180
- sliding scale
-continous infusion
- electronic glucose management systems
- avoid long acting insulin in unstable patients
What are the two types of neuromuscular blocking agents
Depolarizing
Nondepolarizing
What is an example of a depolarizing agent
Succinylcholine
What does succinylcholine look like? What function does this play? onset and duration? elimination?
Physically resembles Ach. So it can bind and activate Ach receptors. This leads to sustained depolarization of neuromuscular junction so muscle contraction can not occur. It is also hydrolyzed much more slowly compared to Ach.
1 minute onset and 3-5 min duration.
Elimination- Rapidly hydrolyzed in serum by the enzyme pseudocholinesterase
What is the use of succinylcholine
rapid sequence intubation (RSI)
used for placement of endotracheal tube. Permits complete airway control and simplifies visualization of vocal cords. Can cause initial muscle contraction.
How can we avoid the initial muscle contraction seen in succinylcholine
may pre administer defasciculating dose of non depolarized NMBA imediately prior to succinylcholine
NOT used fot sustained muscular blockade
adverse effects of succinylcholine? CI?
APNEA
Muscle contractions/fasciculations
hyperkalemia (arrythmia)
CI- Major burns, crash injury and upper motor neuron disease
How do non depolarizing NMBAs act? What are the 2 general classes? DO they cause initial fasciculation
competitively block action of Acg (do NOT activate receptors). They do not cause initial fasciculations. They are competitive.
2 general classes
- aminosteroidal
- benzylisoquinolinium
What are reversal agents for non depolarizing NMBAs
Acetylcholinesterase inhibitors
indications of NDNMBAs? DOes everyone on mechanical ventilator need to be on paralytic?
- May use for immediate/sustained paralysis
Not everyone on mechanical ventilator needs to be on paralytic. Some patients, especially those with ARDS may need paralytic. (acute respiratory distress).
In ARDS patients, it is recommended to administer as a continuous infusion rather than intermittent bolus dose.
- Operative setting (muscle relaxation)
- can be used in RSI
- if contraindication to succinylcholine (e.g burns)
- fast acting agent (rocriyonum) - Manage increased Intracranial pressure (ICP)
- Therapeutic hypothermia (NDNMBAs used to prevent/treat shivering)
ADRs of NDNMBAs
- paralysis of respiratory muscles/apnea
- safeguard to prevent unplanned extubation
- safeguard to prevent errors (naarcan vs norcuron) - inadequate pain and sedation
- NMBAs do NOT provide any analgesia, sedative or anxiolytic effect
- patient still feel pain and anxiety, however unable to communicate
- assessment of pain and sedation is difficult
- patients must be optimized on sedative and analgesic drugs (ideally prior to initiation of NMBA) - Prolonged paralysis/muscle weakness.
- pharmacokinetic effected accumulation possible pharmacodynamic effects
- risk increased with prolonged NMBA administration.
- drug holidays may decrease incidence
What are some additional miscellaneous ADRs of NDNMBAs? Drug I/a?
- related to immobility
- DVT prophylaxis
- use ocular lubricants
Drug i/a- corticosteroids and NMBAs
