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287 Cards in this Set
- Front
- Back
- 3rd side (hint)
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List some emergency department conditions for which hyperbaric oxygen therapy (HBO) is an appropriate tx modality? (7)
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1. CO poisoning
2. gas gangrene 3. necrotizing fasciitis 4. acute traumatic peripheral ischemia 5. decompression sickness 6. air-gas embolism 7. Exceptional blood loss anemia p. e-1 |
- Table 18.1 indicates the following:
1. Air-gas embolism 2. Decompression sickness 3. CO poisoning 4. Crush injury, compartment syndrome, acute traumatic ischemias 5. Exceptional blood loss anemia 6. Delayed radiation injury (osteo and soft tissue) 7. Skin grafts and flaps 8. Thermal burns 9. Arterial insufficiencies (enhancement of healing in selected problem wounds, central retinal artery occlusion) 10. Necrotizing soft tissue infections 11. Clostridial myositis and monecrosis (gas gangrene) 12. Osteomyelitis (refractory) 13. Intracranial abscesses |
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What is the name/concept of single patient HBO units?
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Monoplace chamber
p. e-1 |
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What is the name/concept of numerous patient chamber for HBO unit?
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Multiplace chamber
p. e-1 |
- this also allows an assistant to enter the chamber
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How is atmospheric pressure measured, ie. 1 atmosphere of pressure is equal to what (3 units provided in the reading)
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- 14.7 pounds per sq inch
- 760 mmHg - 760 Torr |
When all pressures to which a person is exposed are summed up the result is called atmospheres absolute.
* HBO therapy is the application of pressures >1 atmosphere absoluate (ATA) to an environment of 100% oxygen. |
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In dive medicine, it is customary to refer to pressure in terms of feet of seawater. Explain.
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One atmosphere is equal to 33 ft (10 meters) of seawater. Therefore, at a depth of 33 ft, a diver is exposed to 2 atmospheres- one from the atmosphere above and one from the additional atmosphere below.
p. e-1 |
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What is the law that indicates that the total pressure of a mixture of of gases is equal to the sum of the partial pressures of each of the individual gases.
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Dalton's Law.
p. e-1. |
Ex. The air we breathe is mixed gas: 21% oxygen, 78%nitrogen, 1% mixed. Total pressure of air: 760 mmHg. therefore the partial pressure of nitrogen is: 760 mmHg x 0.78= 593mmHg. As the total pressure of the gas increases, so to does it's partial pressure.
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What law states that the partial pressure of gas dissolved in a liquid is proportional to the pressure exerted on that gas.
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Henry's Law.
p. e-1 |
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T/F: 3 ATA of pressure in HBO is high enough to sustain basal metabolic function in the complete abscence of Hgb.
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True
p. e-1 |
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Assuming gases are kept at a constant temperature. Which law states that the volume of gas is inversely proportional to the pressure exerted on it?
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Boyles law
p.e-1 |
in short: as the pressure increases, the volume decreases and vice versa
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What states that the gases will move from an area of high concentration to an area of low concentration?
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Law of mass action
p. e-1 |
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What are the two basic effects of HBO on tissues?
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1. Effects related to the increase in PO2.
2. Effects related to the mechanical forces of the pressure itself. p. e-2 |
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Why does HBO improve oxygen delivery to hypoxic tissues. (an unlikely question, but serves to explain well)
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Hyperoxygenated plasma can transport oxygen to areas inaccessible to RBC's, delivering oxygen to relatively hypoxic tissues. Oxygen dissolved in plasma can be delivered to the tissues at a distance of at least 3-4 times that delivered by hgb. RBC's become more pliable and can enter compromised microvascular circulation more efficiently. Which increases oxygen deliery.
p, e-2 |
In HBO vasoconstriction occurs, but not in hypoxic tissues- allowing for this delivery.
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What effect does HBO have on gas bubbles?
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Decreases the size of gas bubbles. (Boyles law)
e-2 |
Remember: the volume of the gas is inversely proportional to the pressure exerted on it.
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By what mechanism does Cyanide lead to severe tissue hypoxia in eventually lactic acidosis?
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CN binds to the mitochondria in the cell, inhibitiing oxydative phophorylation.
p. e-3 |
Read section on CO and CN poisoning...
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What is the most important first step tx in Necrotizing Fasciitis?
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First line tx: immediate and aggressive surgical debridement and abx.
p. e-3 |
If you did not get this one, you need to be smacked in the head with a tack hammer!
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When is HBO appropriate for NF tx?
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It is an adjunct to surgery and abx
p. e-3 |
Do not delay surgery for this.
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What the heck is Clostridium?
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Gram positive, spore forming anaerobe. naturally exists in soil, humans, and animal GI tracts
p. e-3 |
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What is Gas Gangrene?
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a clostridial myonecrosis
p. e-3 |
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What is the MC cause of spontaneous gas gangrene?
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Clostrium Septicum
- this can occur in otherwise healthy individuals, however, it is MC in those w/hx of colon CA. p. e-3 |
- it is aerotolerant!
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What organism is MC implicated in gas gangrene, up to 80-90%.
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Clostridium Perfringens
p. e-3 |
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T/F: Gas gangrene, as a gas producing organism, is evident > 50% of the cases and therefore plain film x-rays are of great benefit in determining the existence of this...ie. x-rays are very reliable.
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False. No very reliable. gas is not evident on at least 50% of plain films.
p. e-3 |
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T/F: Unlike necrotizing fasciitis, which requires early surgery, gas gangrene can be treated with HBO prior to surgery.
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True
p. e-3 -esp in those who are too ill to handle surgery |
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What is the term (and what are the injury types) for those injuries that share a common pathophysiology: ischemia and hypoxia at an injury site, a gradient injury, and potential for self-perpetuation.
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Acute Traumatic Peripheral Ischemia:
1. thermal burns 2. frost bite 3. threatened flaps/grafts 4. replantation of avulsed extremities and digits p. e-4 |
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What factors can often plan a role in the decision to use HBO?
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1. severity of the injury
2. host factors p. e-4 |
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What is the definitive tx for decompression sickness?
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HBO
p. e-4 - the cable company can totally give you a good deal! |
Hyperbaric oxygen (therapy)
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You are wanting to provide HBO for a patient that you suspect has DCS. What must be done prior to this?
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CXR.
Why? |
To r/o PTX. If a PTX is present it must be treated first.
p. e-4 |
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What is the MC cause of Cerebral Air Gas Embolism?
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Iatrogenic introduction of air into the circulation.
p. e-5 |
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As little as how many mL's of blood air foam entering the brain can be fatal?
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0.5 mL
p. e-5 |
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You are working on a rig off the coast. A diver is delivered to you after a rapid ascent to surface. This guy has an AMS and right sided hemiparesis. What do you immediately recongize as the problem?
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cerebral air gas embolism
p. e-5 |
Same can occur following a central line placement.
place pt in Left lateral decubitus, high flow oxygen, hemodynamic support...p. e-5 |
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What is the only definitive tx for acute arterial embolism?
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Hyperbaric chamber
p. e-6 |
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What are some absolute contraindications to hyperbaric oxygen therapy?
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1. Untreated PTX
2. Bleomycin 3. Cisplatin/Carboplatin 4. Doxorubin 5. Disulfiram p. e-6 |
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T/F: High levels of O2 given for 90-120 minutes under hyperbaric conditions, at 2.0 to 2.4 ATA, and even daily up to 6 weeks are not harmful to the lungs.
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True
p. e-6 |
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T/F: CNS toxicity can develop when patients breathe 100% O2 at pressures > 2.0 ATA. (HBO tx)
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True
p. e-6 |
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T/F: Occular damage, myopia, from HBO tx is irreversible.
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False
MC resolves w/in 6 weeks p. e-6 |
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What does beneficence mean?
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doing good
p. 97 |
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What does nonmaleficence mean?
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do no harm
p. 97 |
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Most codes of ethics address what 3- 7 features?
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1. beneficence
2. non-maleficence 3. respect for the patient: a. autonomy b. confidentiality c. honesty d. distributive justice e. respect for the law. p. 97 |
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What are the 5 factors predictive of improved outcomes after cardiac arrest?
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1. Witnessed arrest
2. brief down time and early ACLS 3. Ventricular arrythmias 4. Bystander CPR 5. Return of spontaneous circulation in response to ACLS protocols. p. 97 |
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What are the goals of resuscitive efforts?
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1. restore circulation
2. restore life p. 97 |
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How is futility defined?
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Any effort to achieve a result that is possible, but that reasoning or experience suggests is highly improbable and that cannot be systematically produced.
p. 98 |
More appropriate terms:
nonbeneficial ineffectual low likelihood of success READ THE STATEMENTS FROM AMA AND ACEP P. 98- which govern this action of futility of effort |
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Who has the final decision of whether CPR or other measures are taken to tx an individual?
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The physician: "the decision regarding CPR and its likelihood of benefit to the patient and the decisions to provide, limit or withhold resuscitive efforts are made by the EM Physician in the context of well-accepted research results, patient and family wishes and professional judgement.
p. 98 |
*Individual bias, such as resulting quality of life, etc. Should be avoided
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What are advanced directives?
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any proactive document stating the patients wishes in various situations should the patient be unable to do so.
p. 98 |
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What is a living will?
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Direction MC for someone terminally ill with specifications on resulting care.
p. 98 |
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What is the resource/legal mechanism granting a spokesman on a patients behalf should they become incapacitated?
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Durable power of attorney
p. 98 |
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CPR after defibrillation, why do we do that?
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most victims demonstrate asystole of PEA for several minutes following defibrillation. High quality CPR can convert nonperfusing rythms to perfusing rythms.
p. 67 |
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When finding a patient down, what is done prior to ventillations and chest compressions?
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Calling 9-1-1 or for help.
p. 67 |
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What can double or triple a person's chance of survival from v-fib?
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early (immediate bystander) CPR
p. 67 |
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What improves survival rates to 49-75% if in 3-5 minutes of victim collapse?
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CPR plus defibrillation
p. 67 |
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When performing CPR, why are dentures left in place if they fit properly?
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They form a better seal
p. 68 |
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What are the two MC causes of airway obstruction in CPR, when patient unresponsive?
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a. Tongue
b. epiglottis p.68 |
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T/F: In adults a blind finger sweep is acceptable, even if there is a risk of lodging/swelling, as this response is rare?
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False
- no longer recommended. p. 68 |
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What simple action can be the reason for spontaenous respirations in CPR?
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Opening the airway
p. 68 |
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T/F: Chest compressions alone can be effect if a rescuer is reluctant to perform mouth to mouth.
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True
p. 68 |
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T/F: In CPR, agonal respirations in an individual who just suffered cardiac arrest is adequate ventilation and may trigger stimulus necessary to provoke spontaneous ventillation.
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False
Agonal respirations are inadequate. Intermittent positive pressure ventilation w/oxygen enriched air should be done. p. 68 |
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Chest compressions (closed), what is the depth, rate?
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- depth: 4-5 cm
- approx 100 per minute p. 68 |
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Ventilations: 1. nonintubated 2. intubated
"talk to me" |
1. Non-intubated: 2 breaths per 30
2. Intubated 8-10 per minute...do not pause with Chest compressions p. 68 |
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What is the tidal volume in a NML perfusing individual? What is the ventilatory tidal volume in an individual who gets CPR?
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1. 8-10mL/kg
2. 6-7 mL/kg p. 69 |
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I don't really feel like this next one is a big deal question, but it's bolded...just read the statement...
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Rescue breaths w/an inspiratory time of 1 second each should be given at a rate of 8-10 per minute, w/a volume adequate to make the chest rise visibly (approx 6-7 mL/kg; 500-600 mL in adults). Supplemental O2 should be delivered as soon as possible.
p. 69 |
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Each resuce breath in CPR should be delivered over what duration?
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1 second
- class IIa rec. p. 69 |
- avoid hyperventilation
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What do you do for the patient you are going to provide mouth to mouth for but their mouth is jacked fromm maxillofacial trauma?
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Mouth to nose may be appropriate
p. 69 |
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Why is the heimlich maneuver effective?
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It creates an artificial cough- allowing expulsion of the FB.
p. 70 |
Blind finger sweeps are not recommended, but finger sweeps of visible matter is recommended.
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Where are abdominal thrusts performed in Heimlich Maneuver?
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Above umbilicus and below xiphoid process.
p. 70 |
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When are heimlich maneuver chest thrusts appropriate (what 2 patient types)
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- morbidly obese patient
- prego patient p. 70 |
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Adults, where is the most reliable and accessible location for pulse?
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Carotid
p. 71 |
Femoral as alternative.
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Explain Cardiac Pump Theory of closed chest compressions.
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Pressure transmitted to the heart, compressed between sternum and spine, increases pressure w/in the ventricles.
p. 71 |
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Explain Thoracic Pump Theory of closed chest compressions.
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compressions lead to increase in pressure through the thoracic cavity...
p. 71 |
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Explain Abdominal Pump Theory of closed chest compressions.
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Arterial and Venous components: - abdominal pressure leads to circulation in the vessls
p. 71 |
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T/F: Even if rescuer ventilations are not provided in CPR, chest compressions can be effective.
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True
p. 71 |
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When is open cardiac massage (open chest CPR) appropriate (6)?
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1. penetrating chest trauma
2. perioperative period before or after cardiothoracic surgery 3. cardiac arrest cause by hypothermia, pulmonary embolism, and pericardial tamponade, and abdominal hemorrhage 4. chest deformity in which closed chest CPR ineffective 5. penetrating abdominal trauma w/deterioration and cardiac arrest 6. blunt trauma w/cardiac arrest. p. 73 |
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What should be done during the initiation of resuscitation efforts (CPR)?
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Attempts should be made to determine if the patient has advance directives prohibiting CPR.
p. 73 |
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What is the leading cause of morbidity and mortality in both adults and children?
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acute brain injury
p. 98 |
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Explain reperfusion disease or the postresuscitation syndrome.
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Occurs when after both focal and global ischemia. For example, stroke causes a focal ischemia where as cardiac arrest and asphyxia result in global ischemia.
Cardiac arrest is the MC cause in adults, where as asphyxia is in children. |
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What is currently the most sensitive and specific clinical evaluation of irreversible brain damage following cardiac arrest?
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Failure to withdraw from a noxious stimuli 72 hours after resuscitation
p. 100 |
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What is the first priority in in cerebral resuscitation?
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Restore circulation, ventilation, and oxygenation. unless this is fixed, these derangements will produce further "secondary" brain injury.
p. 100 |
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in what time of return of spontaneous circulation (ROSC)following cardiac arrest can one begin ICED (induced cooling to eliminate deficits)?
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ROSC should occur in less than 1 hour
Figure 18-2, p. 100 |
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What are some contraindications for the use of ICED (induced cooling to eliminate deficits, for cerebral resuscitation) in someone who is witnessed cardiac arrest?
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- trauma
- sepsis - advanced dementia - active bleeding - CA w/brain met - DNR Figure 18-2, p. 100 |
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improvement in survival and neurologic outcome, following cardiac arrest, occurred when mild hypothermia was initiated when and continued for how long?
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When initiated at resuscitation efforts and continued for 12-24 hrs.
p. 101. |
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Cooling strategies are provided, for cerebral resuscitation efforts, both externally and invasively. The efficacy of hypothermia can be jeopardized by body's thermoregulatory mechanisms, which include (2):
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- shivering
- vasoconstriction - this can lead to increased myocardial demand as well as increase in ICP. p. 102 |
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What is the current recommendation of the AHA and international liason committee on resuscitation with regard to hypothermia?
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They recommend the use of therapeutic hypothermia to treat patients who remain comatose after resuscitation from cardiac arrest.
p. 102 |
*Class II recommendation
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How does lidacaine work? And to what antiarrythmic drug class is it associated?
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Lidocaine binds to fast moving sodium channels, preventing recovery after repolarization. It suppresses automaticity in the HIS Purkinje System and spontaneous deploarization of the ventricle during diastole. It favors this on ischemic cardiac tissue, with minimal effect on viable/NML cardiac tissue.
Class Ib antiarrythmic. p. 154 |
Has CNS effects: sedation, analgesia, and anticonvulsant effects.
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What are the first and second line treatments, in ACLS guidelines, for v-fib and pulseless v-tach?
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First line: Amiodorone
Second line: Lidocaine p. 155 |
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In who is lidocaine toxicity most likely (when infusion provided for the treatment of v-fib or pulseless v-tach)?
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1. Infusions longer than 24 hrs
2. patients with hepatic insufficiency 3. patients with renal insufficiency p. 155 |
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What are the symptoms associated with Lidocaine Toxicity? What is the common blood level associated with this?
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1. slurred speech
2. drowsiness 3. confusion 4. nausea 5. vertigo 6. ataxia 7. tinnitus 8. paresthesias 9. muscle twitching Levels > 5 mcg/mL (serious sxs >9 mcg/mL) P. 155. |
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What drug class are the following medications: procainamide, dispyramide, and quinidine.
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Class Ia
binds fast moving sodium channels in their inactive states and inhibit recovery after repolarization, in a time and volatage dependent manner. p. 155 |
Procainamide specifically: prolongs the action potential duration and reduces the speed of conduction. Causes prolongation of the PR, QRS and QT...
Procainamide also has anticholinergic properities to it. |
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What Class Ia Antirrhymic agent is used to: tx and prevent ventricular arrythmias (stable v-tach and wide complex tachycardia) and may also be used to convert SVT rythms: a-flutter, a-fib, WPW and PSVT?
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Procainamide
p. 155 |
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Which means of providing procainamide administration carries fewer side effects, bolus or continuous infusion?
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Continuous infusion
p. 155 |
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A patient was provided procainamide, and immediately became hypotensive- what likely led to this. Additionally, he was also noted to have QT prolongation- what should be done?
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1. Either a high dose or rapid infusion
2. stop the medication p. 155 |
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You ordered labs in your patient, following hx, PE, as well as medication profile. The labs were ANA, for SLE. What antiarrythmic caused this concern?
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Procainamide
p. 155 |
- can also cause agranulocytosis, leukopenia, bone marrow suppression, hypoplastic anemia, thrombocytopenia.
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You are finishing your shift in the ER and note that one of your doc friends is about to give procainamide to a kid in WPW. However, you viewed that chart, noting that the kid is on: zyrtec, singulair, physostigmine, flonase. NKDA. What do you do? Why?
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Stop him, and use another means where possible or at least identify that is the kid has Myasthenia Gravis, do not give!!! This is contraindicated 2/2 increased weakness.
p. 155 |
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What is the appropriate venue for a trial of Class Ic antiarrythmics?
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Inpatient only
p. 156 |
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What are the following with regard to class of antiarrhythmics as well as action: acebutol, atenolol, esmolol, and metoprolol?
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Class II
- cardioselective p. 156 |
making these a better choice for: asthma, COPD, and DM
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What is unique about the following B-blocking agents: acebutolol,carteolol,penbutolol, and pindolol?
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These beta-blocking agents actually have sympathomimetic activity. They occupy the beta receptors and produce very low stimulation- effectively blocking from higher stimulation.
p. 156 |
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Which betablocker agent also has alpha blocking capabilities?
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Labetalol
p. 156 |
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What is the quinidine effect, as it pertains to Betablockers?
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Membrane stabilization which results in a reduction of membrane permeability to fast inward channels (sodium ions). This can sometimes cause QRS widening.
p. 156 (see next card for the Betablockers MC implicated) |
-propranolol
-acebutol -alprenolol |
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All betablockers are used to tx HTN, except what two agents?
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Sotalol and esmolol
p. 156 |
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unless contraindicated, what oral agent MUST be administered with in 24 hrs of AMI (acute myocardial infarction)?
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Betablockers
p. 156 |
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What betablocking agent exhibits negative ionotropic and chronotropic effects as well as is short acting?
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Esmolol
p. 156 |
Onset of action:1-4 minutes
1/2 life: 9 minutes Complete reversal: 30 minutes |
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T/F: 90% of esmolol is excreted in the kidney's so caution is advised when dosing for renal patients.
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False: while 90% is eliminated in the Kidneys- renal or hepatic dosing is not required
p. 156 |
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What Betablocking agent has a 3:1 (oral) and 7:1 (parenteral) beta and alpha acting effects?
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Labetolol
p. 156 |
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How is labetolol eliminated?
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Predominantly by the liver
p. 156 |
Onset of action of labetolol: 2-5 min s/p IV, 20 min s/p oral.
Duration: 20min-2 hrs s/p IV, 8-24 hrs s/p oral |
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What betablocker is a wise choice for treating HTN in pts with myocardial ischemia, and has little effect on cerebral perfusion pressure or intracranial pressure and can be used in the patients with acute neurologic emergencies?
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Labetolol
p. 156 |
ALSO SAFE IN PREGNANCY!!!!!!!!
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How do you effectively increase the dose of labetolol?
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Double the dose (w/each increase, which is IV q 10 minutes)
p. 157 |
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Your colleage provided a treatment for a pts HTN, using labetolol infusion. As you walk by the room, the patient who is standing begins to collapse, immediately after rising. Your friend states that the patient did not listen to his instructions. What were they?
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To remain flat following IV infusion of labetolol for 3 hrs. As orthostatic HoTn could be impressive.
p. 157 |
Additionally, as a BOLD FACE note: Acute dosing of IV labetolol can lead to a "cumulative effect" because each dose will persist for 2-4 hrs.
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T/F: Vivid nightmares are associated with Labetolol.
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True: also, lightheadedness, drowsiness,dizziness, fatigue, and lethargy
p. 157 |
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What Betablocker: slows AV conduction, slows sinus conduction, decreases cardiac output, prevents exercise induced increase in BP, and decreases myocardial O2 demand. It is non-cardioselective and no sympathomimetic activity.
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Propranolol
p. 157 |
Used for a wide variety of SVT's, Propranolol has a low bioavailability when taken orally, but is dramatically increased IV (requiring 1/10 oral dose)
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T/F: Propranolol is less effective at ventricular arrhythmias than for Supraventricular arrythmias, but it can be used for V-tach's or ectopy 2/2 digoxin or catecholamine toxicity and polymorphic v-tach.
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True
p. 157 |
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What non-selective betablocker, which also has Class III antiarrhythmic effects on electrophysiology, and is only administered orally (in US)
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Sotalol
P. 157 |
- inhibits the response of adrenergic stimuli in the myocardium, bronchial, and vascular smooth muscle.
- onset of action: 2-3 hrs, duration of action: 24 hrs. |
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In a patient with NML renal fxn, what is the elimination 1/2 life of sotalol?
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7-18 hrs
p. 157 |
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Sotalol SE's are based on what?
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Dose related
p. 157 |
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What Class II drug can have proarrhythmic effects, particularly in patients w/torsades de pointes, prolonged QT intervals, hypokalemia, or those taking high doses of the drug.
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Sotalol
p. 157 |
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What drug is customarily classifed as a Class III drug but also exhibits Class I,II, and IV effects?
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Amiodorone
P. 158 |
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How does amiodorone prolong atrial and ventricular repolarization (essentially impairing SA node fxn, depressing AV node conduction, etc)
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Inhibition of potassium channels.
p. 158 |
However, it also blocks fast moving sodium channels, decreases HR and AV node conduction via blockade of Beta-receptors as well as CCB
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What is the first line antiarrhythmic agent in ACLS pathways for pulseless VTach and VFib; and is even used in atrial arrhythmias in patients with significantly decreased EF (<40%).
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Amiodarone
P. 158 |
Oral Amiodarone: effective mgt in suppression and prevention of recurrent V-fib and V-Tach, a-fib, a-flutter, and Jxnal and wide complex tachycardias. (metabolized by liver, excreted by biliary excretion. 96% protein bound )
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What are the short term side effects of Amiodarone? What are the long term side effects of Amiodarone?
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Short Term: bradycardia, HoTn
Long Term: thyroid disorders, pulmonary fibrosis, skin discoloration, hepatic dysfunction, corneal infiltrates, and other conditions. p. 158 |
In fact, prior to long term tx, the patient needs ophthalmology and pulmonary function tests.
Adverse effects also include: asystole, cardiac arrest, shock; as well as: proarrhythmic activity and hepatotoxicity. |
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You are working in the ER and write an order for your patient, in stable, V-Tach to receive 150 mg Amiodarone. However, a colleague tells you that the patient cannot receive this 2/2 their allergy. What is it?
|
Iodine and/or shellfish.
Amiodarone contains 37.3% Iodine. p. 158 |
|
|
|
You write an order for amiodarone for a patient with coumadin. The patient is transferred to the floor. The attending on the ward asks where you went to medical school or even if you have the faintest idea what is about to happen to this patient in the next few days. Do you (have any idea)?
|
50% decrease in warfarin metabolism, which increases bleeding
p. 158 |
Amiodarone increases the serum concentration of many drugs: digoxin, procainamide, quinidine, theophylline. Coadministration with simvistatin can lead to rhabdomyolysis
|
|
|
What drug is a pure class III antiarrhythmic, w/o effects on conduction velocity?
|
Dofetilide
p. 158 |
Used to convert a-fib to NSR
Dofetilide prolongs QT/QTc interval w/o changing the QRS |
|
|
You have given a patient dofetilide, for conversion of their a-fib (tho IV is ideal, only oral is available), 2/2 to their symptoms. A colleague reports to you: "You can't do that dummy, he's on antacids". Another guy says, "You can't do that dummy, you do not have the credenitalling identifiing that you have received the special training"! Is any of this true?
|
1. No, GI absroption is great, even w/antacids
2. Yes, you are a dummy! Dofetilide can only be provided by someone having received appropriate training. p. 158 |
|
|
|
What BASELINE QTc interval makes Dofetilide contraindicated.
|
QTc interval longer than 440 ms.
p. 158 |
|
|
|
What QTc interval and CrCl while on therapy makes Dofetilide contraindicated?
|
QTc interval > 500 ms and CrCL <20 mL/min.
p. 159 |
If provided, the patients should be admitted to a hospital for continuous EKG monitoring as well as Renal checks.
|
|
|
What is the MC serious side effect of dofetilide?
|
QT prolongation, resulting in Torsades De Pointes.
p. 159 |
V-Tach is another serious SE.
MC adverse effects: Dizziness, HA, and CP |
|
|
What is Ibutilide? What is it used for?
|
1. Class III antiarrhythmic
2. conversion atrial fibrillation and atrial flutter p 159 |
|
|
|
Just a fact about diltiazem (didn't know how to word as a question)
|
Non-Dihydropyridine CCB, that slows AV node conduction, yet minimal systemic vasodilation and preferentially dilates the coronary arteries.
p. 159 |
|
|
|
T/F: It is same, sometimes, to use diltiazem in the tx of wide complex tachyarrhythmias (suggesting accessory pathway, WPW).
|
FALSE: DO NOT USE
p. 159 |
|
|
|
A patient is converted from IV to oral Diltiazem. How long does the patient remain on IV diltiazem prior to d/c?
|
1 Hour
to allow for peak response p. 159 |
- transient elevation in LFT's- will resolve with continued use
- Cimetidine: increases serum diltiazem, by inhibiting metabolism |
|
|
What Class IV antiarrhythmic has substantial inhibitory effects on cardiac conduction system (unlike others in this class)
|
- Verapamil
p. 160 |
|
|
|
What Class IV agent is as effective as Adenosine and Diltiazem at terminating narrow-complex PSVT and for controlling the ventricular response in a-fib/a-flutter?
|
Verapamil
p. 160 |
|
|
|
You administered verapamil to a pt in PSVT. Shortly after this administration, the patient goes into cardiac arrest and dies. You are told by the cardiologist that you had missed evidence of a dx that would have made verapamil contraindicated in this patient. What was the rhythm evidence and why is this bad?
|
WPW or Lown-Ganong-Levine syndrome
- the accessory pathway is the problem- becomes accelerated p. 160 |
|
|
|
What can be given to prevent, prophylactically, HoTn when giving verapamil?
|
Calcium Gluconate or chloride (500-1000mg)
p. 160 |
|
|
|
You are called by a Family Medicine guy, who noted at d/c from the ER you gave a patient a rx for immediately verapmil for their PSVT, to take qid. Wants to know what to do w/the extended release dosing. What do you tell him?
|
1. To take the dose of the qid meds, add them together, and give that in the extended concentration.
2. Get his crap together and learn to call the pharmacy for this kinda help- you have patients to see p. 160 |
|
|
|
Why do you want to be cautious when giving a CCB to a patient who is currently on a betablocker, any anti-HTN, as well as any other anti-arrhythmic med?
|
The effects are additive.
p. 160 |
|
|
|
What medication increases SA node automaticity and AV node conductionby blocking vagal activity and is termed a parasympatholytic?
|
Atropine
p. 160 |
|
|
|
What are the acceptable routes of administration for atropine?
|
-IM
-IV -ET tube -SC -IO p. 160 |
|
|
|
How much should the atropine dose be increased by when providing by ET Tube?
|
2-2.5 times the IV dose
p. 160 |
|
|
|
Is dilution of 1mg/mL atropine necessary when administered thru ET tube?
|
No, but 10 ML must be placed when providing 1mg/1mL.
p. 160 |
|
|
|
What dose of atropine will lead to a complete vagal blockade?
|
0.04mg/kg
p. 160 |
|
|
|
Dose of atropine <0.4mg and slowly administering therapeutic dose...what effect can this have on heart rate?
|
Reflex bradycardia, 2/2 to vagal stimulation
p. 160 |
|
|
|
You give a patient adenocard to slow the rate, nothing happens. Why?
|
Reentrant SVT not involving the AV node.
p. 160 |
Adenocard works on SA and AV node.
|
|
|
Is adenocard effective on anterograde conduction over accessary pathways in patients w/WPW?
|
No
p. 160 |
|
|
|
What medication in SVT has an onset of action w/20-30 seconds and duration of action that is 60-90 seconds?
|
Adenosine (adenocard)
161 |
|
|
|
T/F: a patient is provided adenocard for their SVT, and converts, but quickly returns w/to their presenting rhythm. This suggests failed tx.
|
False, this is common 2/2 to the short duration of action
p. 161 |
Contraindicated in those with II and III degree AV heart block, as well as sick sinus rhythm
|
|
|
What SE in asthmatics can occur with adenocard administration that improves w/standard therapy for this concern.?
|
Bronchospasm
p. 161 |
|
|
|
what syndrome of the heart will not receive Digoxin 2/2 to the risk, in a-fib/a-flutter, leadint to an extremely rapid ventricular rate and even v-fib?
|
WPW
- the accessory pathway p. 161 |
Digoxin
Onset of action: 5-30 minutes via IV, 30-120 minutes via oral. Duration of action: oral: 1.5-4 hrs IV; 2-6 hrs |
|
|
A patient comes in who has taken too much digoxin. No digibind available. You call toxicologist, who says to call the nephrologist for dialysis...what do you say?
|
"You know there is minimal benefit in doing this? Hemo-and peritoneal dialysis are ineffective at removing significant amts of dig!"
p. 161 |
You could also say, "Really? You've got to be kidding me? Are you a self respecting clinician? How are you able to look at yourself w/o getting sick?"
I prefer the first response. But you roll how you want |
|
|
T/F: Digixin reduces hospital stays as well as mortality associated w/CHF.
|
False.
Reduction in hospital stays yes, but does nothing for mortality p. 161 |
|
|
|
What effect do the following medications have on digoxin levels: Amiodarone, verapamil, nifedipine, diltiazem, felcainide, quinidine, erythromycin, and tetracycline?
|
Increases serum levels
p. 161 |
read dig section p. 161
|
|
|
What agent is MC associated with GI sxs, also has toxicity sxs reported as: MS changes, confusion, HA, drowsiness, anorexia, N/V, weakness, visual changes, delirium and seizures.
|
Digoxin
p. 161-162 |
|
|
|
Potassium levels in serum can have adverse effect on Digoxin, how so?
|
Hypokalemia can increase dig toxicity
Dig toxicity can increase serum potassium p. 162 |
DigiFab or DigiBind
|
|
|
What medication is used in refractory torsades de pointes and temproary control of refractory symptomatic bradycardia?
|
Isoproterenol
p. 161 |
- antiarrhythmic, stimulates beta adrenergic receptors. (epocrates) |
|
|
T/F: Magnesium is indicated for torsades de pointes and refractory V-Tach/V-Fib regardless of the prearrest Magnesium level.
|
True
p. 161 |
|
|
|
What drug is a sympathomimetic drug that exerts potent inotropic and mild chorotropic activities. Posesses increase in myocardial contraction, systemic vasodilation, and minimal changes in HR. Doses up to 20 mcg/kg/min will increase CO, decrease PVR, and decrease pulm occlus pressure. Yet, > 20 mcg/kg/min will increase HR and induce arrhythmias.
|
Dobutamine
p. 162 |
|
|
|
What Vasopressor does NOT require a central line access to use? (i.e. can be given peripherally)
|
Dobutamine
p. 162 |
indicated for short term + ionotropic support for the tx of cardiovascular decompensation, 2/2 vent dysfxn or low output HF
|
|
|
What vasopressor agent is the preferred agent for the tx of: shock w/depressed cardiac output (despite LV filling pressure) and cardiogenic shock?
|
Dobutamine
p. 163 |
|
|
|
What are the effects of dopamine at low doses, 0.5-5.0 mcg/kg/min?
|
- vasodilation of:
Renal Arteries Mesenteric Arteries Coronary Arteries Cerebral Arteries p. 163 |
|
|
|
What are the effects of dopamine at doses: 5.0-10.0 mcg/kg/min?
|
improved myocardial contraction, improved cardiac output, increase SA node conduction.
p. 163 |
|
|
|
What two agents are considered first line vasopressors in septic shock?
|
Dopamine and Norepinephrine
p. 163 |
|
|
|
What medication is clinically indicated for: MI, trauma, HF, and renal failure when fluid resuscitation is unsuccessful or not appropriate?
|
Dopamine
p. 163 |
* Use the lowest dose of dopamine to maintain desired Blood Pressure. MC: 3-20 mcg/kg/min
|
|
|
What should be done when pressor extravasation occurs?
|
Infiltrate the effected area as soon as possible with 5-10 mg of Phentolamine (Regitine)
p. 163 |
|
|
|
Who is dopamine contraindicated in?
|
Patients with Pheochromocytoma and Tachyarrhythmia
p. 163 |
|
|
|
What endogenous catecholamine and non-selective alpha and beta adrenergic agonist is used for: anaphylactic shock, as a bronchodilator in acute asthma, and myocardial stimulant in cardiac arrest.
|
Epinephrine
p. 163 |
|
|
|
T/F: Epinephrine not only bronchodilates, but also antagonizes the effects of antihistamines.
|
True
p. 163 |
|
|
|
What is the epinephrine dose in asthma, of 1:1000 solution, SC?
|
0.3-0.5 mg q 20-30 minutes. Max of three administrations.
p. 163 |
|
|
|
What is the epinephrine dose in bradycardia and HoTn, of 1:10000 solution, IV?
|
2-10 mcg/min
p. 163 |
|
|
|
T/F: In ACLS the dose of epinephrine is 1 mg q 3-5 minutes , IV or IO of the 1:1000 solution is appropriate.
|
False, it is a 1:10,000 solution.
|
Do not give more than this: it can be harmful
|
|
|
What agents produce ionotropic effects by inhibition of phosphodiesterase, which is responsible for the degredation of cAMP- which increases intracellular calcium. and thus myocardial contractility and force of contractions.
|
Milrinone and Inamrinone
p. 164 |
|
|
|
What medications are used for SHORT term management of decompensated congestive heart failure. However, 2/2 to their adverse SE's should only be used if refractory or intolerant of conventional therapy.
|
Milrinone and Inamrinone
p. 164 |
|
|
|
A friend is getting ready to treat a known CHF patient, refractory to pressor agents administered. He orders Inamrinone + D5NS. What is the problem?
|
Inamrinone can only be diluted in 0.45% or 0.9% saline. Dextrose eliminate the drugs activity.
Milrinone however, can work with any: saline or dextrose. p. 164 |
|
|
|
What is the other name for norepinephrine?
|
Levophed.
p. 164 |
|
|
|
How does norepi differ from epinephrine?
|
Norepinephrine has no effect on Beta-2 receptors
p. 164 |
|
|
|
What drug is contraindicated in: HoTn resulting from cyclosporine or halogenated hydrocarbon anesthesia, uncorrected blood deficits, or in mesenteric or peripheral vascular thrombosis.
|
Norepinephrine
p. 164 |
|
|
|
What drug is structurally similar to epinephrine, except, that it stimulates alpha receptors with minimal to no effect on beta receptors.
|
Phenylephrine (Neo-Synephrine)
p. 164 |
|
|
|
Why is Neo-Synephrine not ideal in severe HoTn patients?
|
It works by peripheral vasoconstriction and therefore has no impact on Stroke Volume
p. 164 |
|
|
|
Why do you not give neo-synephrine to bradycardia patients?
|
because it can cause more severe reflex bradycardia
p. 164 |
- also avoid in narrow angle closure glaucoma
|
|
|
What drug class intensifies the effects of Neo-Synephrine?
|
MAOI's.
p. 164 |
*Truly, does anyone use these anymore?
|
|
|
During resuscitation, of pulseless V-Tach abd V-Fib, vasopressin may be used in addition to epinephrine, why?
|
For its vasopressor effects as a non-adrenergic vasoconstrictor.
p. 165 |
|
|
|
What are the four contraindications to IO placement indicated in the book?
|
1. Overlying infection
2. Exposed bone 3. Underlying fracture 4. Structural bone disorders (osteogenesis imperfecta) p. 215 |
|
|
|
What is the principle of IO access for fluids and medications?
|
Fluids and medications administered into the non-collapsible bone sinuses rapidly enter the central circulation.
p. 215 |
|
|
|
Though IO is appropriate for all ages, why is it a principle mgt strategy in children?
|
2/2 to their higher percentage of red bone marrow and relatively thin bone cortex
p. 215 |
|
|
|
T/F: All the following agents can be given successfully by IO: paralytics, anticonvulsants, analgesics, benzodiazepines, vasopressors (such as epinephrine), and blood products.
|
True- the infusion rates are comparable for IV and IO. In fact, any medication that can be given IV can be given IO
p. 215 |
|
|
|
Prior to giving medications through the IO needle, what must be done and why?
|
- confirm appropriate placement of the needle. THis needs to be done to ensure that extravasation into the tissues does not occur- this is toxic.
p. 215 |
|
|
|
Why may there be a delay in onset when comparing IO and IV medications in the delivery of medications for IO administration?
|
Because the medications must pass through the marrow to be absorbed.
p. 215 |
|
|
|
Bone marrow aspirate. When drawing for hematology: Hgb, Leukocyte, HCT, and Plts. What is equivalent and what is interpreted with caution?
|
Only Hgb is reliable- use caution in all others
p. 216 |
|
|
|
Bone marrow aspirate. When drawing for Sodium, Chloride, glucose, bilirubin, bicarb, urea, and creatinine...is this reliable or is caution needed?
|
Reliable
p. 216 |
|
|
|
Bone marrow aspirate. When drawing for venous gas: PH, pCO2, and pO2. Reliable or observe with caution?
|
PH is reliable, however, interpret pCO2 and pO2 w/caution.
p. 216 |
|
|
|
Bone marrow aspirate. When drawing for transfusion preparation: ABO, Rh typing, and Leukocyte activity...is this reliable or risky?
|
All are reliable.
p. 216 |
|
|
|
Most of the IO insertion devices are permissable for placement where?
|
1. Proximal Tibia
2. Distal Tibia 3. Proximal Humerus p. 217 |
Extremities: Distal femur (non-peds); proximal and distal tibia, proximal humerus, sternum.
|
|
|
There is only one adjustable needle, pediatric IO device. The adjustable depths are based on what?
|
Patients age.
p. 217 |
- distal femur not approved by FDA
- proximal humerus- not recommended prior to 5 y/o |
|
|
What is the MC site of IO insertion?
|
Proximal Tibia
p. 217 |
|
|
|
When inserting needle for IO placement into the proximal tibia, in a child why is it important that the placement be 2 cm inferior to the tibial tuberosity?
|
To avoid physeal plate injury
p. 217 |
|
|
|
Why, if you should elect to perform an IO insertion into the distal tibia, should ot be superior to the medial malleolus?
|
To avoid the saphenous vein
p;. 217 |
|
|
|
Where is the saphenous vein located (important to remember for when inserting an IO into the distal tibia)?
- and because it is a bold part in the reading. |
The saphenous vein is located 2 cm anterior and 2 cm superior to the medial malleolus.
p. 217 |
|
|
|
You have a friend who is getting ready to place an IO using a drill- what do you tell him about it?
|
- find landmarks
- place drill needle perpendicular to the skin - do NOT start and stop the drill as the needle passes through the skin- this causes painful twisting of the skin - Once decrease in resistance, release trigger. Needle should stand on own. - Attach 5-10 cc syringe and remove blood/marrow - Flush site (should flush easy) - palpate site to ensure no infiltration p. 217 |
|
|
|
What is the MC complaint when placement IO?
|
Pain during insertion and infusion
p. 217 |
|
|
|
How many attempts can be made on each bone for the placement of the IO?
|
1 attempt per bone is recommended.
- risk of soft tissue fluid accummulation is a risk in the setting of multiple attempts. p. 217 |
|
|
|
When should IO needles be removed?
|
- as soon as definitive vascular access is obtained
p. 218 |
|
|
|
T/F: After removing IO needles, you should apply a pressure bandage and abx ointment.
|
False.
-simple bandage appropriate. Abx and pressure dressing are not necessary. p. 218 |
|
|
|
While central access is generally regarded as safe. What is associated with higher complications in children <1 y/o, <10 kg in weight or <75 cm in height?
|
>6 F size catheter
p. 218 |
- 5F in term, neonates and infants
- 3F in preterm (<36 weeks) |
|
|
True/False: Large volume resuscitation is an indication for Central Access.
|
False.
p. 218 |
|
|
|
What are some complications of IO infusion (8)?
|
1. Pain
2. Infx (cellulitis,osteomyelitis) 3. Local Hematoma 4. Fluid Extravasation 5. Growth Plate Injury 6. Fracture 7. Air or Fat Microemboli 8. Compartment Syndrome p. 220 |
|
|
|
What are the indications for pediatric central venous access (5)?
|
1. Inability to obtain peripheral access
2. Need for invasive hemodynamic monitoring 3. Administrative or caustic or hypertonic solutions 4. Need for long term vascular access 5. Need for transvenous pacemaker placement p. 220 |
|
|
|
What are the complications of pediatric central venous access (12)?
|
1. PTX
2. Thoracic Duct injury 3. Arterial Puncture 4. Cardiac Tamponade 5. Air Embolism 6. Arrhythmia 7. Incorrect Position 8. Hemothorax 9. Subcutaneous Hematoma 10. Neuropathies 11. Death 12. Infection (highest in femoral sites) p. 221 |
|
|
|
What is associated with higher complication ratings in central line placement?
|
1. Multiple attempts
2. Subclavian approach p. 221 |
|
|
|
When performing a subclavian central line, why us the right preferred over the left?
|
The dome of the right lung is lower than the left.
p. 221 |
|
|
|
What maneuvers in children will enhance the internal jugular vein, when beginning central line?
|
- trendelenburg
- liver compression - valsalva -p. 221 |
Valsalva is the single most beneficial maneuver.
|
|
|
What is the central line location most ideal in code situation?
|
- femoral line
p. 222. |
|
|
|
You obtain an x-ray following a right inguinal central line. The x-ray shows distal curling on the abdominal/chest film. What happened?
|
The central line is in the hepatic vein.
p. 222 |
|
|
|
What is a probable- useful central access in the first week and sometime up to the second week of life?
|
umbilical vein
p. 222 |
|
|
|
Umbilical vein, what catheter size is used in term and what size is used for preterm infants?
|
- 5.0 F term
- 3.5 F pre-term p. 222 |
|
|
|
What are some complications of umbilical vein cannulation?
|
1. Thrombosis
2. Embolism 3. Vessel perforation 4. Infx 5. Tissue Ischemia and damage 6. Hepatic necrosis 7. Hydrothorax 8. Cardiac arrhythmias 9. Pericardial effusions and tamponade 10. Erosion of the atrial and ventricular walls. p. 222 |
|
|
|
What is Ohm's Law equation(the pressure between two points in the vessel)?
|
change in pressure=Q x R
where Q is blood flow and R is resistance to flow p. 232 |
measurement of systemic vascular resistance or total peripheral resistance (TPR)
|
|
|
When performing hemodynamic monitoring, why is measurement of arterial pressure so important?
|
- hypotension implies tissue hypoperfusion
p. 232 |
|
|
|
When considering hemostatic monitoring, what is always pathologic and reflects a failure of NML circulatory homeostatic mechanisms?
|
Hypotension
p. 233 |
|
|
|
T/F: Normotension always reflects adequate cardiovascular stability.
|
False
p. 233 |
Even in profound shock, a person can be normotensive 2/2 TPR, w/CO remaining grossly inadequate.
|
|
|
What is the maximum pressure during ventricular ejection?
|
Systolic pressure
p. 233 |
|
|
|
What is the lowest pressure in the blood vessels between heartbeats during ventricular filling as stored arterial blood runs into the periphery.
|
Diastolic pressure
p. 233 |
|
|
|
Palpation of certain pulses: radial, femoral and carotid, should yield a minium systolic BP. What are they?
|
- radial: 80 mmHg
- femoral: 70 mmHg - carotid: 60 mmHg p. 233 |
|
|
|
In the hypotensive patient, non-invasive blood pressure measurements can underestimate systolic pressure by more than _____mmHg.
|
30
p. 233 |
Therefore, intra-arterial blood pressure monitoring provides more accurate assessment of cardiovascular instability during resuscitation.
|
|
|
What is the AHA and ACC recommendations for hemodynamic monitoring in refractory shcok receiving vasoactive agents?
|
- Invasive Monitoring
- artline: which provides measurement of: MAP, pulse pressure and CO and access for repeated sampling. p. 233 |
REVIEW TABLE 34-3: USES FOR ATERIAL CATHERIZATION IN THE ED...THIS IS A MUST, BUT TOO INVOLVED FOR THIS.
|
|
|
What are the potential sites for art line placement? Which is the MC? Which is most Ideal for codes- in a pinch and for CPR?
|
- axillary, brachial, dorsalis pedis, ulnar, tibial, tibial posterialis, and temporal, femoral, and radial arteries
MC: Radial CPR/Code: Femoral p. 233 |
|
|
|
Which site is preferred for the measurement of invasive BP monitoring and aortic pressure in the presence of vasoconstriction?
|
Femoral artery.
p. 233 |
|
|
|
What is the greatest risk in emergency with femoral art line placement?
|
Pseudoaneurysm and Retroperitoneal Hematoma from artery trauma
p. 234 |
|
|
|
T/F: Optimal MAP varies depending on the underlying cause of the hemodynamic instability.
|
True
p. 234 |
|
|
|
T/F: In distributive shock, such as refractory septic shock, increasing MAP > 65 mmHg w/fluids and vaspressors increases oxygen delivery. In addition, this improves indices of organ perfusion: such as oxygen consumption, venous oxygen saturation, lactic acidosis, UOP, capillary blood flow, and gastric mucosal pCO2
|
False
p. 234 (see next slide) |
This does not improve indices of organ perfusion, such as oxygen consumption, venous oxygen saturation, lactic acidosis, UOP, capillary blood flow, and gastric mucosal pCO2
|
|
|
The Role of BP on Hemodynamics: What is the ACC and AHA recommended goal for systolic BP in those with MI?
|
100 mmHg
p. 234 |
|
|
|
The Role of BP on Hemodynamics: A Systolic BP < _____ is an independent predictor of increased morbidity and mortality in TBI pts.
|
< 90 mmHg
p. 234 |
|
|
|
The international Consensus Conference recommends a target MAP of ____ in uncontrolled hemorrhage due to trauma, MAP of ____ for traumatic brain injury, and MAP ______ for all other forms of shock.
|
40 mmHg
90 mmHg > 65mmHg p. 234 |
|
|
|
What is an indicator of central blood volume?
|
CVP
p. 234 |
|
|
|
What are the 6 listed contributors to central venous pressure provided?
|
1. central venous blood volume
2. compliance of the central compartment 3. Tricuspid valve disease 4. Dysrhythmia 5. Reference level of transducer 6. Intrathoracic pressure p. 235 |
|
|
|
What is the MC complication of central line placement shared by IJ, Subclavian and femoral lines?
|
Arterial puncture
p. 235 |
|
|
|
What is an acceptable non-invasive way to estimate right atrial pressure when invasive monitoring is not available?
|
Observation of the internal jugular venous pulsation
p. 235- nxt slide important |
Sternal angle is approximately 5 cm above the atria...so add 5 to the est value from sternal angle.
Ex: pulsation is 4.5 cm above the sternal angle when the patient is 45 degrees indicates a CVP of >9.5 cm H2O. |
|
|
When using the U/S device to assess CVP, if the jugular vein is distended larger than the adjacent common carotid artery when viewed in the transverse plane w/the patient in the semi upright position, the CVP is >_____cm H2O.
|
10
p. 236 |
A nearly completely collapsed internal jugular vein on the transverse view in the supine position indicates a very low CVP.
|
|
|
What is the NML CVP in a healthy individual (as a general rule, excluding additional factors)
|
0-10 mmHg
p. 236 |
|
|
|
What CVP in a critically ill patient, in general, should prompt fluid resuscitation (with careful monitoring)
|
< 4 mmHg
p.236 |
|
|
|
Explain the "5-2" rule as an estimation in the ED of volume status.
|
After initial CVP measurement, infuse 250mL NS IV over 15 minutes (10-20cc/kg bolus). An increase in CVP>5 mmHg indicates volume overload and d/c of fluid. An increase of CVP of 2 mmgHg or less indicates low volume and justifies a second fluid challenge.
p. 236 |
However, remember the septic shock literature CVP goal: 8-12mmHg
|
|
|
When do you measure CVP?
|
At the end of expiration (both spontaneous respiratory and ventilated patients)
p. 236 |
|
|
|
What is the ideal indicator of oxygen delivery and tissue perfusion?
|
Cardiac Output
p. 237 |
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While hemodynamic parameters of BP, CVP, and CO serve as serrogates for tissue oxygenation and perfusion, what 2 things are better measurements?
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Venous Oxygen Saturation and Serum Lactate measures are better measures of oxygen saturation.
p. 239 |
* Read "optimal cardiac output and determing fluid responsiveness" pp. 238-239
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What is the measure of monitoring that assess tisue oxygen extraction and the balance between oxygen delivery and oxygen consumption.
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Venous Oxygen Saturation
p. 239 |
* NML oxygen extraction is 25-35%, resulting in venous oxygen delivery ~ 70%. Anything less supports poor delivery or greater consumption.
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What devices are used to assess Smvo2 and Scvo2?
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Smvo2- pulmonary artery catheter
Scvo2- central line p. 239 |
Smvo2- measures oxygen consumption of the entire body
Scvo2- measures oxygen consumption of the upper portion of the body and not the coronary sinus. - review table 34-7, p. 239 |
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Other than shock, what other factors contribute to elevations in lactate? (10)
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1. seizures
2. DKA 3. Malignancy 4. thiamine deficiency 5. malaria 6. HIV 7. CO poisoning 8. Cyanide poisoning 9. Mitochondrial Myopathies 10. Drugs: metformin, zocor, lactulose, antiretrovirals, niacin, isoniazid, and linezolid. p. 239 |
2/2 to impaired hepatic clearance, liver dz patients will also have more elevations than non-liver dz patients in serum lactates.
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FYI Card: Hemodynamic Monitoring truths
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- Tachycardia is Never a good thing
- Hypotension is always pathologic - CVP is only elevated in dz - There is no such thing as a NML cardiac output - Peripheral edema is only of cosmetic concern p. 240 |
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Serum lactate levels are predictors of mortality. Levels > 4 mmol/L, even in normotensive patient for ____hrs predicts high mortality rates, >90%. Clearance as early as 6 hrs, associated w/increased survival at 60 days.
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24 hrs.
* in TICU...following trauma, this would be trended q 6 hrs to predict mortality. (by some) p. 240 |
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What are the 5 pacemaker types?
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Transcutaenous, transvenous, transesophageal, epicardial, and permanent.
p. 241 |
- all generators are external, except epicardial- which can be internal or external, and permanent which is internal only.
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T/F: When performing cardiac pacing on a patient, it is paramount to safety to disengage the machine/pacing when performing CPR.
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False- there is little risk for injury.
p. 241 |
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T/F: the same pads and electrodes are used for pacing, cardioversion, and defibrillation in the newer defibrillation units.
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True
p. 241 |
If the units require different devices: Place defibrillator paddles 2-3 cm from the pacer pads
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When performing pacing, what is the difference between asynchronous and synchronous pacing.
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Asynchronous: delivers an electrical impulse at a set interval w/o regard for inherent cardiac pacemaker activity
Synchronous: (Safer)- pacing impulse is delivered only if intrinsic electrical complex is not sensed at a present interval p. 241 |
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What is the most commonly encountered difficulty with transvenous pacing?
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Securing venous access and not placing the distal electrode into the right ventricle.
p. 242 |
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You are preparing transvenous pacing in a patient requiring emergency pacing for hemodynamically unstable bradycardia. Asynchronous or synchronous?
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Asynchronous setting (sensitivity off)
p. 242 |
Transvenous pacing is optimal in Urgent, not emergent settings.
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You have a patient that just went into cardiac arrest, you decide needs paced. What form of pacing is appropriate?
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Transcutaneous
p. 242 |
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Where is the generator placed for permanent pacers?
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Into the side of the patients Non-Dominant hand (MC left pec)
p. 242 |
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What is used to define the features of permanent pacemaker?
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5 letter code
p. 242 |
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What are the five letters of the Pacemaker, how do they define type?
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1. The first letter defines the chamber(s) in which pacing occurs
2. The second letter defines the chamber(s) where the sensing occurs 3. T/I/D? 4. The fourth letter defines the presence or absence of adaptive rate mechanism 5. Defines if multi-site pacing is present (rarely used) |
1. A-atrium, V- Ventricle, D-dual chamber (or A and V)
2. The letters are the same as the first letters. 3. I- indicates inhibition of output pulse, causing pacemaker to recycle timing. T- triggered response to sensed event, D means both. 4. Rate modulation: R. MC: VVIR or DDDR (5 letter missing, not commonly used) |
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How far should defibrillator paddles be placed from a pulse generator in permanent pace maker patient?
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10 cm
p. 242 |
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How far should the pacing wire be placed in transvenous pacing?
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10 cm
p. 243 |
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Pacing spikes and a wide QRS complex are found in what lead when looking to reflect capture?
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V1
p. 243 |
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Transvenous pacing. How many mA of energy should be placed on the output dial?
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5
p. 243 |
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Pacemaker malfunction of a permanent pacemaker can be broken down into 5 summarized reasons?
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1. problems with the pocket
2. problems with the leads 3. failure to pace 4. failure to sense 5. malfunction causing overpacing or runaway pacing p. 244 |
examine the pocket and check the device itself and a CXR for lead placement and/or disruption.
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What is the treatment of choice for sudden cardiac death, reducing mortality from 30-45% to <2% every year?
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IMplantable cardioverter-defibrillators. ICD's
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Life span of the device ~ 8 years
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What is the leading cause of death in patients with ICD's?
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CHF
p. 244 |
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The MC reason an ICD patient reports to the ER is 2/2 concerns for a delivered shock.
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-False sensing
-Unsustained tachyarrhythmia -ICD-pacemaker interactions -Component failure p. 246 |
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When an ICD patient reports to the ED for evaluation, what is important to obtain from hx? *(5)
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1. number of shocks delivered
2. what the patient was doing at the time of the shocks 3. any prodromal sxs or postshock trauma. Also, focus on the following: 4. Anti-arrhythic drug changes 5. focus on detailed Physical Exam- Vital signs, cardiovascular status, generator pocket site, search body for trauma p. 244 |
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When evaluating an ICD patient, get an EKG. However, when interpreting the EKG what needs to be remembered about the ST segment depression and elevation?
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- if due exclusively to a shock, will resolve w/in 15 minutes.
p. 244 |
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You evaluate a patient with an ICD and determine that they have received numerous shocks for an otherwise stable rhythm. What should you do?
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Deactivate the ICD, by placing a magnet over the device.
Reenabling can be done by removing the magnet. However, after removal of the magnet: the patient needs to be evaluated by a cardiologst. p. 244 |
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You are performing CPR on a patient with an ICD. Are paddles placed over the generator?What happens of the generator fires while performing CPR?
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- No the paddles are not placed over the generator
- If the ICD fires while performing CPR, it does not cause harm p. 246 |
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Defibrillation and Cardioversion...what is the difference.
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Defib: The therapeutic use of electricity to terminate a non-perfusing rhythm.
Cardioversion: the therapeutic use of electricity to terminate a still perfusing rhythm. p. 246 |
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What are the contrindications for the use of defibrillator?
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1. asystole
2. PEA 3. NSR/SR 4. conscious patient with a pulse 5. Where danger to operator or others is a risk p. 246 |
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When is cardioversion indicated?
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- hemodynamically unstable patient w/Vtach, SVT, A-fib, A-flutter
p. 246 |
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When performing defibrillation it is imperative to ensure that a shock is truly indicated. ______artifacts and _____leads can lead to misinterpretation of the rhythm.
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Movement (artifacts)
Loose (leads) p. 247 |
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You are instructing a class on the use of AED. What is important to remind them to do prior to analysis (transport, etc)?
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-cease all movement, even transport to analyze- as this can lead to artifact.,
p. 247 |
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What does "synchronized" cardioversion mean?
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means that the electric current will be timed with the patient's intrinsic R wave, thus minimizing the risk of v-fib induction.
p. 247 |
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Prior to cardioversion/defibrillation, what should be removed from the patient to prevent burns?
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-Nitro paste
-metallic objects ALSO: remove direct flowing oxygen to prevent fire ignition. p. 247 |
VERY important: Avoid long pauses in CPR when defibrillating.
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Using the algorithm put forth by International liason comittee, after you have initiated CPR and provided shock, and begin CPR again- how many cycles must be performed prior to next "jolt".
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5 cycles of 30-2 compressions ro breaths.
p. 249 |
Random: defibrillation is asynchronized and cardioversion is synchronized.
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Internal defibrillation- this requires what be applied to the paddels and what are the joules set to?
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- saline applied
- 10 J p. 249 |
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When cardiac tamponade occurs, following worsening pericardial effusion, what needs to be done when this results on hemodynamic compromise?
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- Pericardiocentesis
p. 250 |
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T/F: The cause of pericardial effusion can be determined following a pericardiocentesis.
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True
- the fluid removed can be analyzed. p. 251 |
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T/F: During an acute, rapidly expanding pericardial effusion, stroke volume will increase w/removal of even a small amount of fluid (<50cc) from the pericardial sac.
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True
p. 251 |
read pathophysiology- p. 251
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What group of individuals makes up the greatest number of pericardial effusions leading to hemodynamic compromise?
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Oncology patients
p. 251 |
other conditions:
- infx (viral/bacterial, etc) - radiation exposure - TB - renal failure - autoimmune dz - drugs that induce lupus like syndrome - hypothyroidism - ovarian hyperstimulation - idiopathic |
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What are some of the common sxs a patient with cardiac tamponade may posses? What about a trauma patient?
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- dyspnea/tachypnea, CP (often pleuritic), chest fullness, Nausea, esophageal pain, abdominal pain from hepatic and visceral congestion.
Also, lethargy, fever, weakness, fatigue, anorexia, palpitations and shock. - some patients may not tell you these sxs (trauma), but instead will become confused, AMS, shock. p. 251 |
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What is the most sensitive PE finding for cardiac tamponade?
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Pulsus Paradoxus >10mmHg
p. 251 |
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The combination of pulsus paradoxus plus the presence of Beck's triad sxs should prompt what action?
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bedside u/s to search for pericardial effusion
p. 251 |
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What disoders can lead to pulsus paradoxus?
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- anything that increases intrathroacic pressure.
- COPD - obesity - tense ascites - severe asthma - CHF - mitral stenosis - massive PE p 251 |
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You have a patient with PEA. They do not have HoTn or PTX. What else could it be?
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Cardiac Tamponade
p. 251 |
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What is the MC U/S finding of cardiac tamponade?
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Right Sided heart collapse.
p. 251 |
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When preparing to perform the pericardiocentesis on a patient who has cardiac tamponade, you decide to give a bolus of NS. A colleague asks why...
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"because this acts a temporizing measure, filling the right vent with volume".
p. 252 |
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How long after operations and penetrating trauma can patients develop tamponade?
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2 weeks or more
p. 252 |
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A patient has a cardiac tamponade and needs to have the tension released, however, she is getting ready to go to surgery. MC you would not delay surgical intervention, but in this case you did, why?
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It would have had to be because she became hemodynamically compromised and on the verge of cardiac arrest.
p. 252- this is the only acceptable reason to delay definitive care. |
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If the patient has a small pericardial effusion, how does laying in the left decubitus position help?
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1. move the fluid to the dependent apex of the heat
2. moves the left lung out of the way, allowing more exposure of the heart p. 253 |
p. 253-255- read the procedure step by step...
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