Module - 7 - Environmental & Toxicological Emergencies Flashcards
1
Q
- You are transporting a thirty-eight-year-old man who is presented to the ER with a history of cocaine-induced tachycardia and is complaining of midsternal chest pain. Vital signs are as follows: temperature 101.2°F, BP 200/100, HR 140, RR 28, SaO2 97% on 2 liters/min of oxygen via nasal cannula. Which of the following medication is contraindicated for management of this patient?
A. Nitroglycerin
B. Morphine Sulfate
C. Metoprolol
D. Midazolam
A
- C: Beta blockers must not be used in the treatment of cocaine, amphetamine, or other alpha adrenergic stimulant overdose. The blockade of only beta receptors increases hypertension and reduces coronary blood flow, left ventricular function, cardiac output, and tissue perfusion by means of leaving the alpha adrenergic system stimulation unopposed. The appropriate antihypertensive drugs to administer during hypertensive crisis, resulting from stimulant abuse are vasodilators like nitroglycerin, diuretics like furosemide and alpha blockers like phentolamine. Although benzodiazepines and NTG are first-line agents in drug-induced acute coronary syndromes, cocaine-induced vasoconstriction also is reversed by phentolamine. Therefore, AHA 2005 Guidelines recommends phentolamine as a second-line agent. Cocaine stimulates both the peripheral and central adrenergic nervous system. The drug is metabolized by the liver and excreted by the kidney. With excessive or prolonged use of cocaine, the drug can cause itching, tachycardia, hallucinations, and paranoid delusions. Overdoses cause tachyarrhythmias and a marked elevation of blood pressure. Toxicity results in seizures, followed by respiratory and circulatory depression of medullar origin. This may lead to death from respiratory failure, stroke, cerebral hemorrhage, or heart failure. Cocaine is also highly pyrogenic because the stimulation and increased muscular activity cause greater heat production. Heat loss is inhibited by the intense vasoconstriction. Cocaine-induced hyperthermia may cause muscle cell destruction and myoglobinuria, resulting in renal failure. These can be life-threatening, especially if the user has existing cardiac problems.
2
Q
- You have been requested to transport a fifty-five-year-old mane with a history of CHF who is complaining of blurred vision and visual disturbances. The patient states that he has been seeing green and yellow halos for the last two days. The ECG on the monitor shows the following rhythm. The most likely cause for his visual disturbance is
A. Digitalis toxicity
B. MI
C. Pulmonary embolism
D. Retinal hemorrhage
A
- A: The pharmacological actions of digoxin usually results in ECG changes, including ST depression or T wave inversion, which alone may not indicate toxicity. PR interval prolongation, however, may be a sign of digoxin toxicity. Cardiac manifestations are the result of depression through the sinoatrial and atrioventricular nodes and alteration of impulse formation. An often described but rarely seen noncardiac symptom of digoxin toxicity is a disturbance of color vision (mostly yellow and green color) called xanthopsia. Treatment of digital toxicity includes supportive care, possible correction of electrolyte imbalance, or the administration of Fab fragments if conventional supportive care to life-threatening dysrhythmias and hyperkalemia fails. Fab fragments bind to digoxin, and the Fab-digoxin complex is excreted in the urine.
3
Q
- You have been requested to transport a twenty-year-old female with a history of acetylsalicylic acid poisoning two hours prior to your arrival at the sending facility. The patient is complaining of nausea, headache, and tinnitus. When evaluating her ABGs, you would expect which of the following acid-base disturbances to manifest in the early stage of poisoning?
A. Respiratory alkalosis
B. Respiratory acidosis
C. Metabolic alkalosis
D. Metabolic acidosis
A
- A: Salicylate toxicity initially manifests in an increased respiratory rate and hyperventilation. Blood gas analysis usually reflects respiratory alkalosis. Clinical manifestations of mild intoxication include headache, vertigo, tinnitus (ringing in the ears), mental confusion, sweating, and thirst. Severe intoxication produces similar symptoms combined with base/electrolyte imbalances. Patients are agitated, restless, and uncommunicative and may have seizures or become comatose. Noncardiac pulmonary edema is observed in severe poisoning, whereas bleeding diatheses are less common. Treatment involves gastric emptying, administration of oral-activated charcoal, and alkaline diuresis. The severely poisoned patient may require hemodialysis. Refer to the table for review of estimated dose ingested and toxic reaction.
4
Q
- All of the following muscle enzymes, if elevated, are a diagnostic hallmark in a heatstroke patient, except
A. SGOT and SGPT
B. Troponin 1 and 2
C. LDH
D. Creatinine phosphokinase
A
- B: The muscle enzymes, CPK or CK, SGOT, SGPT, and LDH in heatstroke are elevated in the tens of thousands ofdiagnostic hallmark of heatstroke. These enzymes are released by damaged muscle and levels above five times the upper limit of normal indicate rhabdomyolysis. Myoglobin has a short half-life and is, therefore, less useful as a diagnostic test in the later stages. Muscle breakdown occurs from direct thermal injury, clonic muscle activity, or tissue ischemia. CPK or CK levels greater than 20,000 are ominous and are indicative of later DIC, acute renal failure, and potentially dangerous hyperkalemia.
5
Q
- Defibrillation is usually not effective until the body core temperature is greater than
A. 25°C
B. 28°C
C. 30°C
D. 32°C
A
- C: If ventricular fibrillation (VF) is detected, emergency personnel should deliver three shocks to determine fibrillation responsiveness. If VF persists after three shocks, further shocks should be avoided until after rewarming to above 30°C (86°F). CPR, rewarming, and rapid transport should immediately follow the three defibrillation attempts. If core temperature is below 30°C (86°F), successful defibrillation may not be possible until rewarming is accomplished. If the patient fails to respond to initial defibrillation attempts or initial drug therapy, subsequent defibrillations or additional boluses of medication should be avoided until the core temperature rises above 30°C (86°F).
6
Q
- Which of the following rewarming techniques can best avoid the dangers of the afterdrop phenomenon when managing a hypothermic patient?
A. Passive external
B. Active internal
C. Passive internal
D. Active external
A
- B: The consensus is that the patient should be rewarmed as quickly as possible because the myocardium is refractory to therapy below 30°C. There are three techniques for rewarming: passive external, active external, and active internal. Only passive external, active external, and limited forms of active internal rewarming measures can be initiated in the prehospital environment. Afterdrop is a dangerous phenomenon that can occur in the initial stages of passive and active external rewarming. Afterdrop is defined as a decline of 1-2°C in the core body temperature when cool blood from the extremities moves to the core. Any action that moves blood rapidly from the extremities to the heart can cause afterdrop and precipitate ventricular fibrillation. Active internal rewarming delivers heat to the body core, thereby avoiding the dangers of afterdrop. The heart, lungs, and brain are warmed first and in turn rewarm of the rest of the body.
7
Q
- You are transporting a patient with history of seizures while on a camping trip in July. Her husband drove her to the closest ER for treatment. She has a history of cardiac heart failure and only takes furosemide daily. Labs reveal CK 27,000, LDH 800, BUN 34, CR 1.1, K 3.1, Hgb 15.3, Hct 44, CO2 16, and glucose of 62. The foley bag contains urine that appears dark greenish-brown in color with an output of less than 20 mL in the last hour. She is unresponsive with BP 100/40, HR 144, RR 32, and SaO2 94%. The decrease in urine output and abnormal urine character is most likely the result of which of the following?
A. CHF secondary to an acute MI
B. Disseminated intravascular coagulation
C. Rhabdomyolysis secondary to heatstroke
D. Acute renal failure secondary to furosemide toxicity
A
- C: Rhabdomyolysis is a common condition which complicates a variety of genetic and acquired diseases. It is characterized by muscle cell necrosis and release of muscle cell components into the circulation, most notably creatinine phosphokinase (CPK), also known as creatinine kinase (CK) and myoglobin. Other muscle enzymes that can be elevated are SGOT, SGPT, and LDH. The primary mechanism through which muscle damage occurs in rhabdomyolysis is sarcoplasmic calcium overload, leading to activation of degradative enzymes. This may occur secondary to a number of processes, including ATP depletion and increased intracellular sodium concentration and direct sarcolemmal injury. The complications of rhabdomyolysis can be potentially life threatening and include cardiac arrest and myoglobinuric acute renal failure. Prompt action must be taken to prevent these complications in a patient with rhabdomyolysis, most importantly aggressive intravenous volume replacement. Hyperthermia is an elevated body temperature due to failed thermoregulation. Hyperthermia occurs when the body produces or absorbs more heat than it can dissipate. When the elevated body temperatures are sufficiently high, hyperthermia is a medical emergency and requires immediate treatment to prevent disability and death. The most common causes are heat stroke and adverse reactions to drugs. Heat stroke is an acute condition of hyperthermia that is caused by prolonged exposure to excessive heat or heat and humidity. The heat-regulating mechanisms of the body eventually become overwhelmed and unable to effectively deal with the heat, causing the body temperature to climb uncontrollably. Hyperthermia is a relatively rare side effect of many drugs, particularly those that affect the central nervous system. Malignant hyperthermia is a rare complication of some types of general anesthesia.
8
Q
- Which of the following blood transfusion reaction can occur within minutes of administration?
A. Hemolytic
B. Anaphylactic
C. Febrile
D. Circulatory overload
A
- A: Acute hemolytic reaction has the shortest onset and is considered a medical emergency. It results from rapid destruction (hemolysis) of the donor red blood cells by host antibodies, usually related to ABO blood group incompatibility—the most severe of which often involves group A red cells being given to a patient with group O type blood. Properdin then binds to complement, C3, in the donor blood, facilitating the reaction through the alternate pathway cascade. The most common cause is clerical error (i.e., the wrong unit of blood being given to the patient). The symptoms are fever and chills, sometimes with back pain and pink or red urine (hemoglobinuria). The major complication is that hemoglobin released by the destruction of red blood cells can cause acute renal failure. The most important step in treating a presumed transfusion reaction is to stop the transfusion immediately (saving the remaining blood and IV tubing for testing) and to provide supportive care to the patient. More specific treatments depend on the nature and presumed cause of the transfusion reaction.
9
Q
- You are transporting a forty-year-old mane with history of esophageal varices. The sending physician has ordered a unit of PRBC’s transfusion to be infused during transport. Transport time to the receiving facility is approximately 20-30 minutes. The patient should be monitored for which of the following during transport?
A. Volume overload
B. Citrate toxicity
C. Vaso-occlusive crisis
D. Hemolytic reaction
A
- D: Acute hemolytic reaction can occur within minutes of the transfusion. The most common immediate adverse reactions to transfusion are fever, chills, and urticaria. The most potentially significant reactions include acute and delayed hemolytic transfusion reactions and bacterial contamination of blood products. During the early stages of a reaction, it may be difficult to ascertain the cause. Citrate is the anticoagulant used in blood products. It is usually rapidly metabolized by the liver. Rapid administration of large quantities of stored blood may cause citrate toxicity, resulting in hypocalcaemia and hypomagnesemia when citrate binds calcium and magnesium. This can result in myocardial depression or coagulopathy. Patients most at risk are those with liver dysfunction or neonates with immature liver function having rapid large volume transfusion.
10
Q
- What condition would you suspect with the following 12-lead ECG?
A. Hypokalemia
B. Cardiac tamponade
C. Digitalis toxicity
D. Tricyclic antidepressant toxicity
A
- D: TCAs exert a quinidinelike cardiac action that depresses conduction velocity, prolonged QT interval, QRS interval widening, right bundle-branch block, and first-degree heart block are common findings. More than fifty medications, many of them common, can lengthen the Q-T interval in otherwise healthy people and cause a form of acquired long QT syndrome known as drug-induced long QT syndrome. Medications that can lengthen the Q-T interval and upset heart rhythm include certain antibiotics, antidepressants, antihistamines, diuretics, heart medications, cholesterol-lowering drugs, diabetes medications, as well as some antifungal and antipsychotic drugs. An easy way to assess for a prolonged QT interval is to measure the Q-T interval from the beginning of the QRS complex to the end of the T wave. If the length measures greater than 50% the width of an R-R interval, the Q-T interval is prolonged.
11
Q
- The treatment for acetaminophen poisoning is
A. Normal saline
B. N-acetylcysteine (NAC)
C. Sodium bicarbonate IV drip
D. Pyridoxine
A
- B: N-Acetylcysteine (NAC); trade name Mucomyst, Acetadote is FDA approved to reduce the extent of liver injury after acetaminophen overdose. The primary toxic effect of acetaminophen is hepatotoxicity caused by the formation of the toxic metabolite N-acetyl-p-benzoquinonimine. Acute ingestion of 200 mg/kg in children or 6.5 grams in adults of acetaminophen may cause hepatotoxicity. Chronic ingestion of acetaminophen often occurs in adults with ongoing pain syndromes or children with febrile illnesses and can also result in hepatoxicity if the recommended daily dose is exceeded. The decision to initiate antidotal therapy following acute ingestion is based on the serum acetaminophen concentration. The Rumack-Matthew nomogram compares the acetaminophen concentration with the time since ingestion to provide guidance on which patients should be considered for antidotal therapy. The nomogram cannot be used to evaluate chronic ingestions. Oral administration is often limited by nausea and vomiting, which results in delayed or ineffective administration of NAC. Intravenous administration of NAC results in 100% bioavailability. Adverse events associated with IV NAC administration include anaphylactoid type reactions such as flushing, urticaria, rash, hypotension, and bronchospasm. NAC can minimize liver toxicity associated with acetaminophen and should be administered within 8-10 hours of an acute exposure when possible.
12
Q
- Antidote for Coumadin overdose is
A. Protamine sulfate
B. Glucagon
C. Vitamin K, FFP
D. Physostigmine
A
- C: The antidote for an overdose with warfarin (Coumadin) is vitamin K. In severe cases, blood or plasma transfusions can be given to help reverse a Coumadin overdose. In all cases, the patient should be evaluated for bleeding (including less obvious internal bleeding) and appropriate measures should be taken to control the bleeding. Warfarin is prescribed to people with an increased tendency for thrombosis or as secondary prophylaxis in those individuals that have already formed a blood clot (thrombus). Warfarin treatment can help prevent formation of future blood clots and help reduce the risk of embolism. Heparin is generally used for anticoagulation for the following conditions: acute coronary syndrome (NSTEMI), atrial fibrillation, deep-vein thrombosis, pulmonary embolism, cardiopulmonary bypass for heart surgery, ECMO circuit for extracorporeal life support. Antidote dosage for heparin reversal is Protamine Sulfate 1 mg IV for every 100 IU of active heparin. In patients who are allergic to fish, it can cause significant histamine release, resulting in hypotension and bronchoconstriction, and also causes pulmonary hypertension. Infusion should be slow to minimize these side effects. In large doses, Protamine Sulfate itself has some anticoagulant effect. Lab value monitoring will include coagulation studies. The prothrombin time (PT) and its derived measures of prothrombin ratio (PR) and international normalized ratio (INR) are measures of the extrinsic pathway of coagulation. They are used to determine the clotting tendency of blood, in the measure of warfarin dosage, liver damage, and vitamin K status. The reference range for prothrombin time is usually around 12-15 seconds; the normal range for the INR is 0.8-1.2. PT measures factors I, II, V, VII, and X. It is used in conjunction with the activated partial thromboplastin time (aPTT), which measures the intrinsic pathway.
13
Q
- Treatment of Digitalis toxicity would include all of the following, except
A. Digibind
B. TCP
C. Magnesium
D. Beta-blockers
A
- D: The administration of beta-blockers or calcium channel blockers, which also reduce heart rate, are contraindicated in digitalis toxicity. Digoxin toxicity is a poisoning that occurs when excess doses of digoxin (digitalis) are consumed acutely or over an extended period of time. Digoxin toxicity is often divided into acute or chronic. The theraputic level for digoxin is 0.5-2.0 ng/mL. Low potassium levels predispose to digitoxicity and dysrhythmias. The classic dysrhythmia is a paroxysmal atrial tachycardia with block. Symptoms include fatigue, nausea, vomiting, changes in heart rate and rhythm, loss of appetite (anorexia), diarrhea, visual disturbances (yellow or green halos around objects), confusion, dizziness, nightmares, agitation, and/or depression. The primary treatment of digoxin toxicity is digoxin immune Digoxin (Digibind) should not be given if the apical heart rate is below 60 beats per minute. Other treatments that may be tried to treat life-threatening dysrhythmias until digoxin immune fab is acquired are Magnesium, phenytoin, and lidocaine. Atropine is also used in cases of bradydysrhythmias. In severe cases, hemodialysis may be required to reduce the levels of digoxin in the body.
14
Q
- When managing a patient with an electrical injury, with the presence of hemochromogen, you should maintain a minimum urine output of
A. 30-50 mL/hr
B. 50 mL/hr-100 mL/hr
C. 1-2 mL/kg/hr
D. 100 mL/hr
A
- D: It is essential to maintain higher rates of urinary output because hemoglobinuria and myoglobinuria are common with electrical injuries. The fluid resuscitation must be based on actual urine flow. A minimum of 50-100 mL/hour of urine output must be maintained; however, in the presence of urinary hemochromagen, the fluid volume must sufficient quantity to maintain a minimum urine output of 100 mL/hr. Lopez, Orchid Lee (2011-02-15). Back To Basics: Critical Care Transport Certification Review (pp. 279-280). Xlibris. Kindle Edition.
15
Q
- The drug of choice for a patient exhibiting signs and symptoms of malignant hyperthermia is
A. Anectine
B. Sodium bicarbonate
C. Dantrolene
D. Glucagon
A
- C: The current treatment of choice is the intravenous administration of dantrolene (Dantrium), the only known antidote, discontinuation of triggering agents, and supportive therapy directed at correcting hyperthermia, acidosis, and organ dysfunction. Dantrolene is a muscle relaxant that appears to work directly on the ryanodine receptor to prevent the release of calcium. Treatment must be instituted rapidly on clinical suspicion of the onset of malignant hyperthermia. Malignant hyperthermia (MH) is a rare life-threatening condition that is triggered by exposure to certain drugs used for general anesthesia (specifically all volatile anesthetics), nearly all gas anesthetics, and the neuromuscular blocking agent succinylcholine. In susceptible individuals, these drugs can induce a drastic and uncontrolled increase in skeletal muscle oxidative metabolism, which overwhelms the body’s capacity to supply oxygen, remove carbon dioxide, and regulate body temperature, eventually leading to circulatory collapse and death if not treated quickly. Malignant hyperthermia develops during or after receiving a general anesthetic, and symptoms are generally identified by operating department staff. Characteristic signs are muscular rigidity, followed by a hypercatabolic state; with increased oxygen consumption, increased carbon dioxide production (hypercapnea, usually measured by capnography), tachycardia (fast heart rate), and an increase in body temperature (hyperthermia) at a rate of up to ~2°C per hour, temperatures up to 42°C (108°F) are not uncommon. Rhabdomyolysis (breakdown of muscle tissue) may develop as evidenced by red-brown discoloration of the urine and cardiological or neurological evidence of electrolyte disturbances.
16
Q
- You are transporting a sixty-five-year-old man who was brought to the emergency department with a history of alcoholism. The staff reports that the patient was found in an alley unresponsive and hypothermic. From the following 12-lead ECG, you would expect the patient’s body temperature to be at approximately
A. 36°C
B. 34°C
C. 30°C
D. 25°C
A
- C: Hypothermia, defined as core body temperature
17
Q
- You have been requested to transport a twenty-year-old female from an ICU with a history of TCA overdose two hours prior to your arrival at the sending facility. Your cardiovascular assessment of the patient would most likely include all of the following with this type of toxicity, except
A. Early sinus bradycardia
B. QRS
C. Prolonged QT and PR interval
D. Early tachycardia
A
- A: Sinus tachycardia is the most common cardiac disturbance seen following TCA overdose. TCAs remain widely prescribed for depression and an increasing number of other indications, including anxiety disorders. TCA overdose is a significant cause of fatal drug poisoning. The severe morbidity and mortality associated with these drugs is well documented due to their cardiovascular and neurological toxicity. Additionally, it is a serious problem in the pediatric population due to their inherent toxicity and the availability of these in the home when prescribed for bed wetting and depression. An overdose on TCA is, especially, fatal as they are rapidly absorbed from GI tract in the alkaline conditions of the small intestines. As a result, toxicity often becomes apparent in the first hour after an overdose. However, symptoms may take several hours to appear if a mixed overdose has caused delayed gastric emptying. Many of the initial signs are those associated to the anticholinergic effects of TCAs such as dry mouth, blurred vision, urinary retention, constipation, dizziness, emesis, tachycardia, mydriasis (pupil dilation), fever, and flushing (skin redness). Treatment depends on severity of symptoms and can include the administration of IV fluids, and pressor agents (alpha-adrenergic agents are preferred). GI decontamination may be helpful within the first several hours postingestion because TCAs can slow gastric emptying through the anticholinergic activity. Activated charcoal reduces the absorption of TCAs. It may also be beneficial in cases of multi-substance ingestion. It should be administered only in patients who are able to protect the airway. If there is a metabolic acidosis and/or ECG changes present (prolonged QT interval, QRS widening), infusion of sodium bicarbonate is recommended. Physostigmine is not an antidote to cyclic antidepressant poisoning and should not be used on these patients. Commonly known TCAs, among others, are amitriptyline (Elavil, Tryptizol, Laroxyl); doxepin (Adapin, Sinequan); imipramine (Tofranil, Janimine, Praminil); nortriptyline (Pamelor, Aventyl). The toxic effects of tricyclics are results of the following four main pharmacologic properties: 1. Inhibition of norepinephrine and serotonin reuptake at nerve terminals 2. Anticholinergic action 3. Direct alpha-adrenergic blockade 4. Membrane-stabilizing effect on the myocardium by blocking the cardiac myocyte fast sodium channels
18
Q
- The most critical goal and life-saving measure in heat illness is
A. Cooling the patient to rapidly decrease body temperature
B. Administering large amounts of fluids and inotropic agents to correct dehydration and hypotension
C. Immediate endotracheal intubation to prevent aspiration
D. Administering H2 blockers, mannitol and sodium bicarbonate to prevent acute renal failure and gastrointestinal bleeding
A
- A: Cooling can be accomplished by first removing the patient from the hot environment. The transport team should remove the patient’s clothing and wet down the patient. Covering the patient with cool fluid and increasing the movement of air over the patient enhance heat loss by increasing the evaporative gradient. The transport team should open the windows of the ambulance or make use of the air circulation of helicopter rotors during transport to further increase air movement over the patient. Controversy surrounds the question of which method is ideal for cooling the patient with heatstroke. Several methods are considered to be of therapeutic benefit. Packing the patient in ice and immersing the body in cold water are historic methods of cooling. Other therapies involve the use of room-temperature water evaporated from the patient’s skin surface by circulating air from a fan. The field treatment measure of ice packs placed in areas of maximum heat transfer (neck, axillae, and inguinal areas) may also be continued with caution. Cooling measures are ceased when body core temperature reaches 39°C (102°F). Refractory hyperthermia will require move-invasive methods. Iced-water gastric lavage, iced peritoneal lavage, hemodialysis, and cardiopulmonary bypass have been used as end attempts in severely refractory hyperthermia.
19
Q
- A scuba diver descended to a depth of ninety-nine feet. The scuba diver is under an ambient pressure of how many ATA?
A. 1
B. 2
C. 3
D. 4
A
- D: Atmospheric pressure is the force per unit area exerted against a surface by the weight of air above that surface in the earth’s atmosphere. A column of air one square inch in cross-section, measured from sea level to the top of the atmosphere, would weigh approximately 14.7 lbs per square inch (psi) or 760 mmHg (torr), which is defined as 1 atmosphere of pressure (ATM). Because the density of water is uniform throughout, the proportional relationship of pressure and depth remains constant; pressure increases 1 ATM for every thirty-three-foot column of seawater. At the given depth underwater, the total pressure will be the sum of the barometric pressure exerted by the column of air above plus the hydrostatic pressure exerted by the column of water. This is the concept of absolute pressure or atmospheres absolute (ATA). Therefore, a scuba diver at a depth of thirty-three feet will experience an ambient pressure of 2 ATM absolute pressure, or 2 ATA (air column plus water column).
20
Q
- The most common type of decompression sickness typically seen diving emergencies is
A. Musculoskeletal
B. Pulmonary
C. Arterial gas embolism
D. Cutaneous
A
- B: Decompression illness (DCI) describes a collection of symptoms arising from decompression of the body. DCI is caused by two different mechanisms, which result in overlapping sets of symptoms. The two mechanisms are the following: Decompression Sickness (DCS), which results from gas dissolved in body tissue under pressure, precipitating out of solution and forming bubbles on decompression. It typically afflicts scuba divers on poorly managed ascent from depth or aviators flying in inadequately pressurized aircraft. Arterial gas embolism (AGE), which is gas bubbles in the bloodstream. In the context of DCI these may form either as a result of precipitation of dissolved gas into the blood on depressurization, as for DCS above, or by gas entering the blood mechanically as a result of pulmonary barotrauma. Pulmonary barotrauma is a rupturing of the lungs by internal overpressurization caused by the expansion of air held in the lungs on depressurization such as a scuba diver ascending while holding the breath or the explosive decompression of an aircraft cabin or other working environment. Immediate treatment of DCS and AGE are to establish basic and advanced life-support measures, place the patient in left lateral decubitus position (Durante position) has been recommended to minimize further passage of air emboli to the brain and transport to the closest hyperbaric treatment facility for recompression. Patients should be transported in an aircraft with cabin pressurized to 1 ATA. If the aircraft cannot be pressurized to 1 ATA, such as a helicopter, it should be flown at the lowest and safest altitude possible, preferably below 1,000 feet above sea level.
21
Q
- Situations that involve a right shift in the oxygen-hemoglobin dissociation curve are all of the following, except
A. Alkalosis
B. Hypercapnia
C. Hyperthermia
D. Increased level of 2,3-DPG
A
- A: The oxygen-hemoglobin dissociation curve illustrates the relationship between hemoglobin saturation and PaO2. This curve depicts the ability of hemoglobin to bind and release oxygen into the tissues. Various physiologic states change the relationship between hemoglobin saturation and PaO2.
22
Q
- Gases in the lungs of a scuba diver expand as ambient pressure decreases during ascent best describes which gas law?
A. Henry’s
B. Dalton’s
C. Graham’s
D. Boyle’s
A
- D: As a diver descends from or ascends to the water’s surface the effect of increasing ambient pressure on the scuba diver involve an understanding of the behavior of gases under conditions of varying pressure and volume. The following table is a brief description of the primary gas laws of diving.
23
Q
- You are transporting a patient who you note has tea-colored urine in small amount in the foley catheter bag. The nurse reports that his output is only 50 mL in the last twenty-four hours. What treatment would you expect to initiate during the two-hour flight?
A. Rapid fluid resuscitation, sodium bicarbonate drip, and consider Lasix and mannitol
B. Rapid fluid resuscitation, potassium replacement therapy, and aggressive pain management
C. Fluid restriction, sodium bicarbonate drip, and consider Lasix and mannitol
D. Fluid restriction, potassium replacement therapy, and aggressive pain management
A
- A: The main goal of treatment is to treat shock and preserve kidney function. Initially this is done through the administration of generous amounts of intravenous fluids, usually saline. This will ensure sufficient circulating volume to deal with the muscle cell swelling (which typically commences when blood supply is restored) and to prevent the deposition of myoglobin in the kidneys. Amounts of six to twele liters over twenty-four hours are recommended. While many sources recommend mannitol, which acts by osmosis to ensure urine production and may prevent heme deposition in the kidney, there are no studies directly demonstrating its benefit. Similarly, the addition of bicarbonate to the fluids is intended to improve acidosis and thereby prevent cast formation in the kidneys, but there is limited evidence that it has benefits above saline alone. Furosemide, a loop diuretic, is often used to ensure sufficient urine production.
24
Q
- Your head-injured patient is hypothermic. In what direction does the oxyhemoglobin dissociation curve shift to?
A. Up
B. Down
C. Right
D. Left
A
- D: Hypothermia causes the oxygen-hemoglobin dissociation curve to shift to the left. Remember everything that is low is left.
25
Q
- Poisoning of the cytochrome oxidase enzyme system may cause
A. Histotoxic hypoxia
B. Hypemic hypoxia
C. Hypoxic hypoxia
D. Stagnant hypoxia
A
- A: Histotoxic hypoxia interferes with the utilization phase of respiration because of metabolic poisoning or dysfunction. Cyanide, sulfide, azide, and carbon monoxide all bind to cytochrome oxidase, thus competitively inhibiting the protein from functioning, which results in chemical asphyxiation of cells. Methanol [methylated spirits] is converted into formic acid, which also inhibits the same oxidase system.
26
Q
- Two types of drug poisoning that cause hallucinations are
A. Cocaine and PCP
B. PCP and lysergic acid diethylamide
C. LSD and benzodiazapines
D. Methamphetamine and LSD
A
- B: Lysergic acid diethylamide (LSD) is the most potent hallucinogen known. Phencyclidine (PCP), also known as angel dust and other street names, is a recreational, dissociative drug formerly used as an anesthetic agent, exhibiting hallucinogenic and neurotoxic effects. Patients may become hostile, beligerent, and destructive. A common neurologic sign of PCP intoxication is nystagmus. Extreme caution should be taken during transport; use of ear protection, sedation, and restraints may be necessary prior to transport. In extreme situations, sedation and neuromuscular blocking agents, with airway control, may be necessary to safely transport these patients.
27
Q
- You have been requested to a farming area to transport a forty-year-old man involved in a plane crash. On arrival, the patient is complaining of shortness of breath with increased salivation and blurred vision. Vital signs are BP 100/58, HR 50, RR 36, SaO2 92%. Management of this patient would include all of the following, except
A. Diazepam
B. Atropine
C. Sodium thiosulfate
D. Pralidoxime
A
- C: Many organophosphates are potent nerve agents, functioning by inhibiting the enzyme action of acetylcholinesterase (AChE) in nerve cells. They are one of the most common causes of poisoning worldwide and are frequently intentionally used in suicides in agricultural areas. The effects of organophosphate poisoning are recalled using the mnemonic SLUDGE (salivation, lacrimation, urination, defecation, gastrointestinal motility, emesis). These side effects occur because of the excess acetylcholine (AcH) that results from blocking acetylcholinesterase (enzyme responsible for the breakdown of AcH). In addition, bronchospasm, blurred vision, and bradycardia may result. Treatment includes the administration of Atropine (drying effect) and the antidote is pralidoxime (2-pam). Pralidoxime reversibly binds to the enzyme acetylcholinesterase, competing with organophosphate binding. Since barbiturates are potentiated by the anticholinesterases, they should be used cautiously in the treatment of seizures; diazepam is the recommended drug of choice.
28
Q
- One of the major organs that must be functional if heat is to be dissipated is the
A. Skin
B. Hypothalamus
C. Kidney
D. Liver
A
- A: One of the major organs that must be functional if heat is to be dissipated is the skin. The primary mechanism for heat dissipation is the evaporation of sweat. Vasodilation maximizes the cooling surface and greatly decreases peripheral vascular resistance.
29
Q
- ARDS and DIC are a result of what in the hyperthermic patient?
A. Temperature increase
B. Lysosomal enzymes
C. Release of sodium
D. Retention of potassium
A
- B: Muscle damage is evidenced by rhabdomyolysis. Elevated creatine phophokinase (CPK) values are a diagnostic hallmark of heatstroke because of the rhabdomyolytic process. The release of destructive lysosomal enzymes occurs as a result of extensive muscle damage, which can lead to ARDS, DIC, and ATN.
30
Q
- The antidote for ethanol toxicity is
A. Dextrose
B. Sodium Bicarbonate
C. Fomepizole
D. Naloxone
A
- C: Ethylene glycol is an organic compound widely used as an automotive antifreeze. In its pure form, it is an odorless, colorless, syrupy, sweet-tasting liquid. The major danger is due to its sweet taste. Because of that, children and animals are more inclined to consume large quantities of it than they are other poisons. The primary source of ethylene glycol in the environment is from run-off at airports where it is used in de-icing agents for runways and airplanes. Upon ingestion, ethylene glycol is oxidized to glycolic acid which is, in turn, oxidized to oxalic acid, which is toxic. This and its toxic byproducts first affect the central nervous system, then the heart, and finally the kidneys. Ingestion of sufficient amounts can be fatal if untreated. Serum blood levels guide treatment for ethylene glycol ingestion. Ethanol IV administration blocks the conversion of ethylene glycol to its toxic form. Fomepizol (Antizol) is an antidote for ethanol toxicity, which prevents the formation of toxic metabolites.
31
Q
- Digitalis toxicity can easily be exacerbated by
A. Acute MI
B. Electrolyte abnormalities
C. Undiagnosed diabetes
D. Beta-blockers
A
- D: A group of medicines extracted from foxglove plants are called “digitalin.” The use of digitalis purpurea extract containing cardiac glycosides for the treatment of heart conditions is used to increase cardiac contractility (positive inotrope) and as an antiarrhythmic agent to control the heart rate, particularly in atrial fibrillation. Digitalis is often prescribed for patients in atrial fibrillation, especially if they have been diagnosed with CHF. Digitalis works by inhibiting sodium-potassium ATPase. This results in an increased intracellular concentration of sodium, which in turn increases intracellular calcium by passively decreasing the action of the sodium-calcium exchanger in the sarcoplasmic reticulum. The increased intracellular calcium gives a positive inotropic effect. Digitalis poisoning can cause heart block and either bradycardia or tachycardia, depending on the dose and the condition of the patients heart. The classic drug of choice for VF (ventricular fibrillation) in the emergency setting, amiodarone, can worsen the dysrhythmia caused by digitalis; therefore, the second-choice drug lidocaine is more commonly used.
32
Q
- All of the following medications are classified as calcium channel blockers, except
A. Diltiazem
B. Calan, Isoptin
C. Nicardipine
D. Metoprolol
A
- D: Metoprolol is classified as a beta-blocker, which blocks the action of endogenous catecholamines (epinephrine and norepinephrine) in particular, on β-adrenergic receptors, part of the sympathetic nervous system, which mediates the “fight or flight” response. There are three known types of beta receptors, designated β1 (one heart), β2 (two lungs) and β3 receptors. β1-adrenergic receptors are located mainly in the heart and in the kidneys. β2-adrenergic receptors are located mainly in the lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle, and skeletal muscle. β3-adrenergic receptors are located in fat cells. Some beta-blockers such as, labetalol and carvedilol, exhibit mixed antagonism of both β—and α1-adrenergic receptors, which provides additional arteriolar vasodilating action. Calcium channel blockers are a class of drugs and natural substances that disrupt the calcium (Ca2+) conduction of calcium channels.
33
Q
- A patient presenting with a complaint of tinnitus and flulike symptoms will most likely have which of the following diagnosis?
A. Acetominophen overdose
B. Beta-blocker overdose
C. Salicylate overdose
D. Magnesium toxicity
A
- C: The main undesirable side effects of aspirin are gastrointestinal ulcers, stomach bleeding, and tinnitus, especially in higher doses. In children and adolescents, aspirin is no longer used to control flulike symptoms or the symptoms of chickenpox or other viral illnesses because of the risk of Reye’s syndrome. Aspirin overdose can be acute or chronic. In acute poisoning, a single large dose is taken; in chronic poisoning, higher than normal doses are taken over a period of time. Toxicity is managed with a number of potential treatments, including activated charcoal, intravenous dextrose, normal saline, sodium bicarbonate, and dialysis.
34
Q
- Which of the following lab test is typically ordered four hours postingestion of acetaminophen overdose?
A. BUN
B. Liver function
C. Electrolytes
D. Coagulation
A
- B: The most effective way to diagnose aceteminophen poisoning is by obtaining a blood acetominophen level. A drug nomogram developed in 1975, called the Rumack-Matthew nomogram, estimates the risk of toxicity based on the serum concentration of acetominophen at a given number of hours after ingestion. Use of a timed serum paracetamol level plotted on the nomogram appears to be the best marker, indicating the potential for liver injury. Acetominophen level drawn in the first four hours after ingestion may underestimate the amount in the system because acetominophen may still be in the process of being absorbed from the gastrointestinal tract. Therefore, a serum level taken before four hours is not recommended. The toxic dose of acetominophen is highly variable. In adults, single doses above 10 grams or 200 mg/kg of bodyweight, whichever is lower, have a reasonable likelihood of causing toxicity. In children acute doses above 200 mg/kg could potentially cause toxicity. Damage to the liver, or hepatotoxicity results not from Tylenol itself but from one of its metobolites, N-acetyl-p-benzoquinonemine (NAPQI). NAPQI depletes the liver’s natural antioxidant glutathione and directly damages cells in the liver, leading to liver failure. Treatment is aimed at removing the acetominophen from the body and replacing glutathione. Activated charcoal can be used to decrease absorption of acetominophen if the patient presents for treatment soon after the overdose; the antidote N-acetylcysteine (NAC) acts as a precursor for glutathione, helping the body regenerate enough to prevent damage to the liver. A liver transplant is often required if damage to the liver becomes severe.
35
Q
- Antidote that can be administered for benzodiazepine overdose is
A. Naloxone
B. Romazicon
C. Deferoxamine
D. Fomepizole
A
- B: Flumazenil (also known as trade names Anexate, Lanexat, Mazicon, Romazicon) is a competitive benzodiazepine receptor antagonist that can be used as an antidote for benzodiazepine overdose. It reverses the effects of benzodiazepines by competitive inhibition at the benzodiazepine binding site on the GABA receptor. Flumazenil is very effective at reversing the CNS depression associated with benzodiazepines but is less effective at reversing respiratory depression. There are many complications that must be taken into consideration when used in the acute care setting. Its use, however, is controversial as it has numerous contraindications. It is contraindicated in patients who are on long-term benzodiazepines, those who have ingested a substance that lowers the seizure threshold, or in patients who have tachycardia, widened QRS complex, anticholinergic signs, or a history of seizures. Due to these contraindications and the possibility of it causing severe adverse effects, including seizures, adverse cardiac effects, and death, in the majority of cases, there is no indication for the use of flumazenil in the management of benzodiazepine overdose as the risks generally outweigh any potential benefit of administration. It also has no role in the management of unknown overdoses. Additionally, if full airway protection has been achieved, a good outcome is expected and therefore, flumazenil administration is unlikely to be required.
36
Q
- Iron poisoning can be managed with
A. Naloxone
B. Romazicon
C. Deferoxamine
D. Fomepizole
A
- C: The specific antidote for moderate to severe cases of iron poisoning is deferoxamine, a chelator that binds the ferric ion and forms a ferrioxamine complex, a water-soluble compound that is excreted in the urine (thereby reducing the iron load). Serious iron poisoning usually causes symptoms within six hours of the overdose. The symptoms of iron poisoning typically occur in five stages. In stage 1 (within 6 hours after the overdose), symptoms include vomiting, vomiting blood, diarrhea, abdominal pain, irritability, drowsiness, unconsciousness, and seizures. Deferoxamine mesylate, for injection, is an iron-chelating agent, available in vials for intramuscular, subcutaneous, and intravenous administration. Deferoxamine mesylate is contraindicated in patients with severe renal disease or anuria, since the drug and the iron chelate are excreted primarily by the kidney. Excretion of the resulting ferrioxamine complex results in pink-red urine that is classically called “vin-rosé urine.”
37
Q
- A patient presenting with ethylene glycol ingestion would present with the following signs and symptoms, except
A. Nystagmus
B. Elevated anion gap
C. Seizures
D. Metabolic alkalosis
A
- D: Symptoms of ethylene glycol poisoning usually follow a three-step progression, although poisoned individuals will not always develop each stage. Other laboratory abnormalities may suggest poisoning, especially the presence of a metabolic acidosis, particularly if it is characterized by a large anion gap. Large anion gap acidosis is usually present during the initial stage of poisoning.
38
Q
- What assessment when managing a patient with iron ingestion would indicate that the treatment is effective?
A. Urine output appears pink in color
B. Increased level of consciousness
C. Appearance of tea-colored urine output
D. Improvement of metabolic acidosis
A
- A: Excretion of the resulting ferrioxamine complex results in pink-red urine that is classically called “vin-rosé urine.”
39
Q
- The administration of Romazicon can cause which of the following adverse reactions?
A. Respiratory depression
B. Seizures
C. Hypotension
D. Tachycardia
A
- B: Romazicon has the possibility of causing severe adverse effects including seizures, adverse cardiac effects, and death. In the majority of cases, there is no indication for the use of flumazenil in the management of benzodiazepine overdose as the risks generally outweigh any potential benefit of administration. Additionally, if full airway protection has been achieved, a good outcome is expected and therefore, flumazenil administration is unlikely to be required.
40
Q
- Which of the following conditions is commonly associated with ethanol intoxication?
A. Hyperthermia
B. Hypoglycemia
C. Esophageal varices
D. Increased thiamine production
A
- B: Alcohol and hypoglycemia are the two things that really do not go together. Sometimes people with hypoglycemia or “low blood sugar” are mistaken for drunks. This is because their reaction to sugar and alcohol can be very similar. The high sugar content of some alcoholic drinks alone can cause blood sugar to drop so fast that they appear intoxicated. This is because over consumption of sugar causes the pancreas to release insulin into the blood stream. Because insulin has a much longer half-life (the time of a substance to reduce itself by half) than sugar, the insulin will remain longer in the blood than the sugar. Wernicke-Korsakoff syndrome is a neurological condition, caused by an acute deficiency of the vitamin thiamine, often related to acute and chronic alcohol use. Symptoms include confusion, profound short-term memory loss, incoordination, and abnormalities of eye movement (gaze palsies). Excessive prolonged use of alcohol can damage the stomach lining (gastritis), esophagus (esophageal varices), liver (liver failure, cirrhosis), pancreas (pancreatitis), and heart (cardiomyopathy). Ethanol enhances cutaneous blood flow, which causes heat loss through vasodilation.
41
Q
- Pralidoxime chloride is administered in the management of
A. Heparin overdose
B. Organophosphate exposure
C. Iron ingestion
D. Cyanide toxicity
A
- B: The mainstays of medical therapy in organophosphate (OP) poisoning include Atropine, pralidoxime (2-PAM, Protopam), and benzodiazepines. Pralidoxime is a nucleophilic agent that reactivates the phosphorylated AChE by binding to the OP molecule. Used as an antidote to reverse muscle paralysis, resulting from OP AChE pesticide poisoning but is not effective once the OP compound has bound AChE irreversibly (aged). Current recommendation is administration within forty-eight hours of OP poisoning. Because it does not significantly relieve depression of respiratory center or decrease muscarinic effects of AChE poisoning, administer Atropine concomitantly to block these effects of OP poisoning. Signs of atropinization might occur earlier with addition of 2-PAM to treatment regimen. 2-PAM administration is not indicated for carbamate exposure since no aging occurs.
42
Q
- Antidote for heparin overdose is
A. Vitamin K
B. Fresh frozen platelets
C. Protamine sulfate
D. Protopam chloride
A
- C: Protamine sulfate is a drug that reverses the anticoagulant effects of heparin by binding to it.
43
Q
- Normal BUN is
A. 0-10
B. 6-23
C. 15-35
D. 35-45
A
- D: BUN:creatinine ratio is usually >20:1 in prerenal and postrenal azotemia, and <12:1 in acute tubular necrosis.
44
Q
- Elevated BUN can indicate all of the following, except
A. Dehydration
B. Intra-abdominal hemorrhage
C. Renal failure
D. Cerebral vascular accident
A
- D: Increased BUN levels suggest impaired kidney function. This may be due to acute or chronic kidney disease, damage, or failure. It may also be due to a condition that results in decreased blood flow to the kidneys, such as CHF, shock, stress, recent MI, or severe burns, conditions that cause obstruction of urine flow or dehydration. BUN concentrations may be elevated when there is excessive protein breakdown (catabolism), significantly increased protein in the diet, or gastrointestinal bleeding (because of the proteins present in the blood).
45
Q
- A patient exposed to organophosphates can present with the following clinical signs/symptoms, except
A. Salivation
B. Defecation
C. Mydriasis
D. Pulmonary edema
A
- C: Many organophosphates are potent nerve agents, functioning by inhibiting the action of acetylcholinesterase (AChE) in nerve cells. They are one of the most common causes of poisoning worldwide, and are frequently intentionally used in suicides in agricultural areas. The effects of organophosphate poisoning are recalled using the mnemonic SLUDGE (salivation, lacrimation, urination, defecation, gastrointestinal motility, emesis). These side effects occur because of the excess acetylcholine that results from blocking acetylcholinesterase. In addition, bronchospasm, blurred vision, and bradycardia may result. Another mnemonic is DUMBBELSS, which stands for diarrhea, urination, miosis, bradycardia, bronchoconstriction, excitation (as of muscle in the form of fasciculations and CNS), lacrimation, salivation, and sweating.
46
Q
- A patient presenting with tachycardia, pale skin, a change in behavior, and diaphoresis is most likely experiencing which of the following?
A. Insulin shock
B. Diabetic ketoacidosis
C. Alcohol intoxication
D. Renal failure
A
- A: Hypoglycemic (insulin shock) symptoms and manifestations can be divided into those produced by the counter-regulatory hormones (epinephrine and glucagon) triggered by the falling glucose, and the neuroglycopenic effects produced by the reduced brain sugar.
47
Q
- Organophosphate exposure causes the overproduction of the neurotransmitter acetylcholine by
A. Deactivation of the acetylcholinesterase enzyme, which is responsible for the breakdown of acetylcholine
B. Blocking the vagus nerve
C. Increasing adrenergic stimulation
D. Activation of the acetycholinesterase enzyme, which is responsible for the production of aceylcholine
A
- A: The primary mechanism of action of organophosphate pesticides is inhibition of carboxyl ester hydrolases, particularly acetylcholinesterase (AChE). AChE is an enzyme that degrades the neurotransmitter acetylcholine (ACh) into choline and acetic acid. ACh is found in the central and peripheral nervous system, neuromuscular junctions, and red blood cells (RBCs). Organophosphates inactivate AChE by phosphorylating the serine hydroxyl group located at the active site of AChE. The phosphorylation occurs by loss of an organophosphate leaving group and establishment of a covalent bond with AChE. Once AChE has been inactivated, ACh accumulates throughout the nervous system, resulting in overstimulation of muscarinic and nicotinic receptors. Clinical effects are manifested via activation of the autonomic and central nervous systems and at nicotinic receptors on skeletal muscle. Organophosphates can be absorbed cutaneously, ingested, inhaled, or injected. Although most patients rapidly become symptomatic, the onset and severity of symptoms depend on the specific compound, amount, route of exposure, and rate of metabolic degradation.
48
Q
- Management of cyanide toxicity includes all of the following, except
A. Amyl nitrate
B. Sodium nitrate
C. Protopam chloride
D. Sodium thiosulfate
A
- C: Pralidoxime chloride (2-PAM, protopam) is a nucleophilic agent that reactivates the phosphorylated AChE by binding to the OP molecule.
49
Q
- Which medication will require the addition of sodium thiosulfate in the infusion bag to prevent thiocyanate toxicity?
A. Neseritide
B. Nitroglycerin
C. Nicardipine
D. Nitroprusside
A
- D: Sodium nitroprusside is an antihypertensive agent used frequently in the critical care setting. Recently, the Food and Drug Administration (FDA) published a report that led to a labeling change, emphasizing the pharmacokinetics of nitroprusside with metabolism to highly toxic cyanide. Although evidence validates that cyanogenesis occurs with nitroprusside administration, prevention and treatment of cyanide poisoning is rarely instituted in clinical practice. Simultaneous infusion of thiosulfate with nitroprusside provides the sulfur donor necessary to prevent cyanide accumulation. Cyanide combines with thiosulfate to form the less toxic sodium thiocyanate, which is then excreted. A 10:1 ratio of nitroprusside to thiosulfate in the infusion eliminates the possibility of cyanide intoxication without altering the efficacy of nitroprusside.
50
Q
- Your patient ingested an unknown toxin. The electrocardiogram recorded on ER admission shows a minimally irregular wide-QRS tachycardia with a long QT interval. The most likely cause is
A. TCA overdose
B. Early digitalis overdose
C. Calcium channel blocker overdose
D. Beta-blocker overdose
A
- A: Tricyclic antidepressants, (commonly called TCAs) have been prescribed since the 1950s for depression. Examples of TCAs are imipramine (Tofranil), amitriptyline (Elavil) and nortriptyline (Pamelor). Sinus tachycardia, the result of anticholinergic effects, often occurs with therapeutic doses of tricyclic antidepressants and has been a poor marker for serious toxicity. In a small study of patients with an acute overdose of tricyclic antidepressants, QRS prolongation, probably a manifestation of the quinidinelike effects of the drugs, was a better predictor of seizures and ventricular arrhythmias than was a serum drug level. Sodium loading may be the most important factor in the reversal of the symptoms of cyclic antidepressant toxicity. Prolonged QRS is most often the indication for serum alkalinization in TCA toxicity. Although beta-blockers were once contraindicated in CHF, as they have the potential to worsen the condition, studies in the late 1990s showed their positive effects on morbidity and mortality in CHF. Bisoprolol, carvedilol, and sustained-release metoprolol are specifically indicated as adjuncts to standard ACE inhibitor and diuretic therapy in CHF. Beta-blockers are primarily known for their reductive effect on heart rate, although this is not the only mechanism of action of importance in CHF. Beta-blockers, in addition to their sympatholytic B1 activity in the heart, influence the renin/angiotensin system at the kidneys. Beta-blockers cause a decrease in renin secretion, which, in turn, reduce the heart oxygen demand by lowering extracellular volume and increasing the oxygen-carrying capacity of blood. Beta-blockers’ sympatholytic activity reduce heart rate, thereby increasing the ejection fraction of the heart despite an initial reduction in ejection fraction. Glucagon has been used in the treatment of overdose. Glucagon has a positive inotropic action on the heart and decreases renal vascular resistance. It is, therefore, useful in patients with beta-blocker cardiotoxicity. Cardiac pacing should be reserved for patients unresponsive to pharmacological therapy. The most widespread clinical usage of calcium channel blockers is to decrease blood pressure in patients with hypertension, with particular efficacy in treating elderly patients. With a relatively low blood pressure, the afterload on the heart decreases; this decreases the amount of oxygen required by the heart. Calcium channel blockers, frequently, are used to control heart rate, prevent cerebral vasospasm, and reduce chest pain due to angina pectoris. Most calcium channel blockers decrease the force of contraction of the myocardium. Calcium channel blockers work by blocking voltage-gated calcium channels in cardiac muscle and blood vessels. This decreases intracellular calcium, leading to a reduction in muscle contraction. In the heart, a decrease in calcium available for each beat results in a decrease in cardiac contractility. It is because of the negative inotropic effects of most calcium channel blockers that they are avoided (or used with caution) in individuals with cardiomyopathy. Many calcium channel blockers also slow down the conduction of electrical activity within the heart by blocking the calcium channel during the plateau phase of the action potential of the heart. This results in a negative chronotropic effect, resulting in a lowering of the heart rate and the potential for heart block. The negative chronotropic effects of calcium channel blockers make them a commonly used class of agents in individuals with atrial fibrillation or flutter in whom control of the heart rate is an issue. Treatment of calcium channel blocker toxicity involves intravenous calcium, atropine, fluids, insulin, and inotropes. Insulin is required because, at high doses, calcium channel blockers block the effect of insulin.
51
Q
Cocaine OD considerations
A
- Cocaine stimulates both the peripheral and central adrenergic nervous system.
- Beta blockers must not be used in the treatment of cocaine, amphetamine, or other alpha adrenergic stimulant overdose.
- The appropriate antihypertensive drugs to administer during hypertensive crisis, resulting from stimulant abuse are vasodilators like nitroglycerin, diuretics like furosemide and alpha blockers like phentolamine.
- Overdoses cause tachyarrhythmias and a marked elevation of blood pressure. Toxicity results in seizures, followed by respiratory and circulatory depression of medullar origin.
- Cocaine is also highly pyrogenic because the stimulation and increased muscular activity cause greater heat production.
- Heat loss is inhibited by the intense vasoconstriction.
- Cocaine-induced hyperthermia may cause muscle cell destruction and myoglobinuria, resulting in renal failure.
52
Q
xanthopsia
A
An often described but rarely seen noncardiac symptom of digoxin toxicity is a disturbance of color vision (mostly yellow and green color)
53
Q
Digoxin toxicity ECG findings
A
- The pharmacological actions of digoxin usually results in ECG changes, including ST depression or T wave inversion, which alone may not indicate toxicity.
- PR interval prolongation, however, may be a sign of digoxin toxicity.
- Salvador Dali’s Mustache
54
Q
Salicylate toxicity
Ingested ranges:
Tx
A
- initially manifests in an increased respiratory rate and hyperventilation, usually reflecting respiratory alkalosis
Ingested amounts (mg/kg)
<150 No toxic reaction expected
150-300 Mild to moderate toxic reaction
300-500 Serious toxic reaction
>500 Potentially lethal toxic reaction
- involves gastric emptying, administration of oral-activated charcoal, and alkaline diuresis, severe toxicity may require hemodialysis.
55
Q
muscle enzymes examined in presence of heatstroke
A
CPK or CK, SGOT, SGPT, and LDH in heatstroke are elevated in the tens of thousands
- These enzymes are released by damaged muscle and levels above five times the upper limit of normal indicate rhabdomyolysis.
- Myoglobin has a short half-life and is, therefore, less useful as a diagnostic test in the later stages.
- Muscle breakdown occurs from direct thermal injury, clonic muscle activity, or tissue ischemia.
- CPK or CK levels greater than 20,000 are ominous and are indicative of later DIC, acute renal failure, and potentially dangerous hyperkalemia.
56
Q
Medication and electrical therapy in pt with core
<86˚F ≈ 30˚C
A
If patient’s core temp is <86˚F ≈ 30˚C
- 3X initial defibrillation attempts, if VF persists withold electrical and medication therapy until after passively warmed to >86˚F ≈ 30˚C
57
Q
Afterdrop is
A
- a dangerous phenomenon that can occur in the initial stages of passive and active external rewarming.
- Afterdrop is defined as a decline of 1-2°C in the core body temperature when cool blood from the extremities moves to the core.
- Any action that moves blood rapidly from the extremities to the heart can cause afterdrop and precipitate ventricular fibrillation.
- Active internal rewarming delivers heat to the body core, thereby avoiding the dangers of afterdrop.
58
Q
Passive external
A
Used in mild hypothermia and when the patient can generate heat by shivering and vasoconstriction.
The patient is placed in a warm environment, covered with blankets and allowed to rewarm naturally.
59
Q
Active external
A
Involves:
- placing heat on the external surface of the body
- thermal blankets,
- heat pack to the groin,
- neck,
- axillary areas.
60
Q
Active internal
A
Includes:
- heated oxygen,
- IV fluids,
- hemodialysis,
- peritoneal dialysis,
- gastric
- cardiopulmonary bypass.
81
Q
Temperatures and progression of ECG ∆’s
A
In the initial stages of hypothermia
<95°F (35°C) sinus tachycardia develops due to stress
<90°F (32°C) sinus bradycardia with progressive prolongation of the PR interval, QRS complex, and Q-T interval.
86°F (30°C), atrial ectopic activity is often noted and can progress to atrial fibrillation.
- 80% of patients have Osborn waves (J waves)
<86°F (30°C), progressive widening of the QRS and prolonged Q-T interval increases the risk of ventricular fibrillation.
When the temperature drops to 60°F (15°C), asystole.
