Lecture 1 - stress, Drugs ICU Flashcards
Classes
Anti-dysrythmics
Vasopressors
Vasodilators
Inotropes
Sedatives/Paralytics/Analgesics
Standard of care drugs
Anti-dysrrhythmics
Amiodarone (Cordarone) – primarily rhythm control, ventricular
Diltiazem (Cardizem) – primarily rate control
Esmolol (Brevibloc)
Verapamil (Calan)
Labetolol (Normodyne)
Adenosine (Adenocard) – refractory SVT
Procainamide (Pronestyl)
Lidocaine (Xylocaine)
Vasopressors – Constrict the vasculature‘Clamp down’ – Goal is to increase Perfusion
Levophed (Norepinephrine)** (Largely most popular)
- Short half life
- Digital Ischemia
Vasopressin (Vasostrict, Pitressin, ADH) (Usually 2nd line agent)
- Vaso AND venoconstriction
- Not a catechol
- Long half life
- Digital Ischemia
Dopamine (Intropin)** (INCREASES MORTALITY IN SEPSIS and Cardiogenic shock)
Phenylephrine (Neo-synephrine)**
Pure vasoconstrictor**
Epinephrine (Adrenalin)
Peripheral pressors maybe/kinda should be used on ANY hypotensive patient.
Vasodilators
Nitroprusside (Nipride, Nitropress)
Nitroglycerin (Nitrol)
Hydralazine (Apresoline)
Labetolol (Normodyne)
Pulmonary artery selective dilators-
Remodulin
Sildenafil
Inotropic Agents – Increase contractility of the myocardium, may cause vasodilation as well
Primarily used for Cardiogenic shock-
- Dobutamine (dobutamine)* - shorter half life, easier to titrate
- Primacor (milrinone) – hypotensive issues, reallllllly long half life, accumulates with renal insufficiency
- Isoproterenol (Isuprel) – very chronotropic
- Lanoxin (digoxin)
Epinephrine (Adrenalin)** Hits everything
- B2 can increase lactate production
Sedatives/Paralytics/Analgesics
Sedatives
- Propofol
- Haldol
- Ketamine
- Benzodiazepines
- Versed (midazolam)
- Ativan (lorazepam)
- Valium (diazepam)
MISC
Precedex
Analgesics (mostly opioid)
- Dilaudid
- Morphine
- Fentanyl
Paralytics (NMBAs)
Non-depolarizing
- Nimbex (cisatracurium)
- Pavulon (pancuronium)
- Norcuron (vecuronium)
- Zemuron (rocuronium)
Depolarizing
- Succinylcholine
Standard of Care
DVT/PE prophylaxis
1) Heparin
-Naturally occurring
-Inactivates Xa and some others (9a, 12a, 13a) – More bleeding, monitored by aPTT (Clotting Time)
2) Low molecular weight heparin
-Fractioned version of heparin
-Only inactivates Xa
-More bioavailability/longer duration
-Issues with renal insufficiency
3) SCDs
GI prophylaxis
1) Proton pump inhibitors
- Omeprazole (Prilosec)
- Pantoprazole (Protonix)
2) H2 blockers
- Famotidine (Pepcid)
- Cimetadine (Tagamet)
3) Enteral feeding*
Bowel regimen
1) Colace
2) Senna
3) AMBULATION
Stress
Stimulus that causes disequilibrium between psychological and physiological functioning.
Activation of the hypothalamic–pituitary–adrenal axis.
Increase in catecholamine, glucocorticoid, and mineralocorticoid levels leads to a cascade of physiological responses.
Acute Stress Response:
Involves the stimulation of the sympathetic nervous system and activation of multiple neuroendocrine responses
Acute Stress Response: Phase 1
The first phase (ebb phase): Fight or Flight
- Increased heart rate and contractility, vasoconstriction, and increase in blood pressure
- Blood flow is redirected to vital organs.
- Pain sensations are temporarily attenuated.
- Body temperature and nutrient consumption fall.
- A sensation of thirst may be prominent.
- Increase in minute ventilation and respiratory rate, hyperglycemia, insulin resistance, and coagulopathies
Acute Stress Response: phase 2
The second phase (flow phase):
- Hyperdynamic state that results as the body compensates for the oxygen deprivation
- Characterized by multiple hormonal influences
- Pain and discomfort are now prominent.
- Movement is minimized to conserve metabolic costs.
- Prolonged activation of the stress response can lead to immunosuppression, adrenal insufficiency, hypoperfusion, tissue hypoxia, and eventual death.
- Adrenal Insufficiency may look like a recurrence of septic shock
Environmental Stressors in the Intensive Care Unit
Monitors, ventilators, IV pumps, noise from equipment, multiple staff members
Today, emphasis is on the patients’ and families’ needs.
More welcoming to visitors
Limiting noise
Lights and color
Windows and natural views, with calm colors
Anxiety
causes:
Threat of helplessness
Loss of control
Sense of loss of function and self-esteem
Failure of former defenses
Sense of isolation
Fear of dying and leaving loved ones
Fear of disability
Assessment of Anxiety
Physiological and behavioral indicators
Agitated behavior
- Increased blood pressure
- Increased heart rate
- Verbalization of anxiety
- Restlessness
Nursing Interventions
Creating a healing environment
Promoting rest and sleep:
- Provide quiet time.
- Eliminate pain.
- Position the patient for comfort with pillows.
- Minimize nursing care interruptions.
- Allow family to be with the patient.
- Fostering trust
- Providing information
- Allowing control
- Practicing cultural sensitivity
- Requires an open-minded and flexible nursing staff
- Reassurance
Restraints in Critical Care
Physical restraints
Chemical restraint
Alternatives to restraints
- Modifying patient environment
- Modifications to therapy
- Involvement of the patient/family in care
- Therapeutic use of self
Critical Care
Focus- both patients and family response to acute illness and includes prevention of complications, and promotion of meaningful recovery
- Functional change
- Behavioral change
- Trust
- Comfort
- Quality of Life
Post Intensive care syndrome
Aggregate cascade of problems negatively affecting the patients recovery, often causing caregiver role strain
- Psychological
- Physiologic
- Cognitive
Family Focused Care
- Method of care delivery that recognizes and respects the pivotal role of family
- Patient and family complete entity
- Support and communication with families
- Each patient and family are unique
Palliative Care
approach to care which focuses on improving the patients quality of life during life-threatening/chronic illness and should be inclusive of the patient’s family
