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207 Cards in this Set
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2 indications to induce emesis if patient has ingested toxin
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• Patient is alert without neurologic signs and is able to vomit without high risk of aspiration
• It has been a relatively recent timeframe since ingestion (definitely not beyond 6hrs) |
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side effexts from giving hydrogen peroxide orally to induce emesis
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1. foaming at mouth
2. ulcers on tongue 3. gastric erosion or ulceration (the bubbling action of H2O2 lifts the mucosal layer) |
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How to dose hydrogen peroxide iver the phone
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• Dosages: never >3 tablespoons!
* <5lb: 1tsp * 5-10lb: 2tsp * 10-20lb: 1.3T * 20-30lb: 2T * 30-40lb: 2.7T * >40lb: 3T |
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Preferred drug for inducing emesis
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• Apomorphine = preferred option for dogs
• Can also dissolve a tablet and place liquid at ocular conjunctiva |
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Preferred drug for inducing emesis
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• Xylazine = preferred option for cats (but cats are much more difficult to get to vomit)
• Sedation may also occur |
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Why isn't morphine a good drug choice for inducing emesis
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it causes a massive histamine release
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3 drug types to consider when a patient ingests a toxin
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* Induce emesis: hydrogen peroxide, apomorphine, xylazine
• Activated charcoal: absorbs toxin • A cathartic (Sorbitol): helps material move through GI tract |
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Anecdote indicated for ethylene glycol
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• Fomepizole (4-MP)
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Anecdote indicated for organophosphate toxicity
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• Pralidoxime (2-PAM)
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Anecdote indicated for organophosphate pesticides, carbamate pesticides, any SLUDD condition
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Atropine
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Anecdote indicated for acetaminophen
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• N-acetylcysteine (acts as a liver protectant)
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Anecdote indicated for serotonin syndrome
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Cyproheptadine
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anecdote indicated for warfarin-type rat poison
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Vitamin K1 + phytonadione
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reversal for opioids
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• Naloxone
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Rodenticides anticoagulant types
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• 1st generation: Warfarin, Chlorophacinone, Diphacinone, Pindone
• 2nd generation (longer-acting): Brodifacoum, Bromadiolone, Difenacoum, Difethialone • If 1st generation, treat 2-3wks; if 2nd generation, treat 3-6wks |
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MOA of rodenticides
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• MOA: inhibits vitamin K epoxide reductase
(enzyme involved in recarboxylation (and recycling) of vitamin K * Vitamin K is necessary for production of clotting factors II, VII, IX, & X and proteins C&S |
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CS of rat poisoning
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1. Prolonged prothrombin time (PT) (>90sec): evident within 12-48hrs after ingestion
• Factor VII has the shortest half-life of the clotting factors affected 2. Internal hemorrhage causes external symptoms 3. Respiratory distress due to pleural hemorrhage 4. Cervical masses 5. Prolonged bleeding from wounds 6. Retroperitoneal bleeding, pericardial bleeding, uterine bleeding 7. Spontaneous bleeding is evident 3-7d after ingestion |
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good test to run initially when client brings in a possible exposure to rat poisoning
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PT (best time is at 48-72hrs after possible ingestion, since a delay will be evident but there will likely not be clinical bleeding yet)
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Treatment of KNOWN rat poisoning
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• Vitamin K1 orally BID
• If 1st generation, treat 2-3wks; if 2nd generation, treat 3-6wks |
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Treatment of SUSPECTED rat poisoning
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tell owner to return in 48-72hrs and test PT
• If normal PT: ingestion is unlikely, no further medication is required • If prolonged PT: proceed with treatment |
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Treatment of active bleeding from rat poisoning
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need to replace the clotting factors!!!
• Plasma (fresh, frozen, or cryo-poor) at 10mg/kg **best choice** • Whole blood • Autotransfusion |
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Bromethalin
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* A Neurotoxic rodenticide
• MOA: interferes with oxidative phosphorylation; undergoes rapid absorption and hepatic metabolism |
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CS of Bromethalin toxicity
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Clinical signs: progressive ataxia, weakness, paresis, seizures, coma, death (dose-dependent toxicity)
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Treatment of Bromethalin toxicity
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Treatment: no antidote; provide symptomatic therapy
* Early (peak conc. at 4hrs) aggressive decontamination: no emesis, but can use activated charcoal * Supportive care: IV fluids, O2 * Diazepam (for seizures) * Mannitol (for cerebral edema) |
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MOA of Cholecalciferol rodenticides
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• MOA: Vitamin D toxicosis thus causing increased body calcium
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CS of Cholecalciferol rodenticides
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• Clinical signs: vomiting (immediately); diarrhea, depression, PU/PD (12-24hrs); renal failure (3d)
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Treatment of Cholecalciferol rodenticides
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Treatment: dialysis; 0.9% NaCl + furosemide (saline diuresis)
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Amphetamines
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(stimulant drugs for ADHD)
• Drugs: amphetamine, Adderall, Vyvanse, Concerta, Focalin, Ritialin |
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MOA of Amphetamines toxicity
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MOA: alpha and beta adrenergic stimulation (mechanism not completely understood)
• Release of norepinephrine, inhibition of MAO and catecholamine reuptake which causes over-stimulation • Release of serotonin and dopamine |
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CS of Amphetamines toxicity
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• Profound tachycardia, arrhythmias; hypertension
• Tremors, restlessness, anxiety, seizures • Hyperthermia (>106°F is a danger level!), coagulation defects secondary to hyperthermia • Decontamination: induce emesis if <6hrs and have control of airway |
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Treatment of Amphetamines toxicity
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Treatment: supportive care for clinical signs
• Main goals: prevent hyperthermia and prevent tachycardia • Fluid therapy (monitor electrolytes and urine output) • Anti-arrhythmic drugs (beta blockers: propranolol PO, esmolol CRI) • Urine acidifiers: ascorbic acid • Control muscle spasms (to prevent hyperthermia): methocarbamol, diazepam • Sedatives: Ace, Propofol |
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Common source of zinc toxicity
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pennies
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MOA of zinc toxicity
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• Source: pennies
• MOA: zinc is an essential metal involved in bone formation, immunity, keratogenesis, reproduction, growth, vision, wound healing, brain development, CNS function * Causes GI irritation and ulceration • Direct damage to RBC membrane à hemolysis • Liver, pancreatic, and renal failure |
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CS of zinc toxicity
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• Vomiting, diarrhea; dark urine and feces
• Pale mucus membranes, lethargy, depression, icterus |
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Treatment of zinc toxicity
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Treatment: Chelation therapy should not be started until object is removed
• Zinc is rapidly eliminated and may not require treatment after object removal • Calcium EDTA or D-penicillamine |
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Lab findings in zinc toxicity
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1. Heinz body anemia
2. Spherocytosis 3. Hemoglobinemia 4. Hemoglobinuria 5. Bilirubinemia |
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Toxic parts of sago palm
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Seeds, leaves, and pulp of cones are toxic
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MOA of sago palm
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MOA: affects liver; some effect on neuromuscular system and GI tract
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CS of Sago palm toxicity
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• Vomiting, anorexia, diarrhea to constipation, polydipsia, icterus
• Thrombocytopenia, high BUN/Creatinine, increased liver enzymes • Hepatic necrosis and fibrosis causes chronic liver disease |
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Treatment of sago palm toxicity
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• Supportive care and hospitalization
• Fluid therapy • GI protectants • Liver protectants: N-acetylcysteine, silimaryin, SAMe |
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What makes chocolate toxic
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methylxanthines (caffeine and theobromine)
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MOA of chocolate toxicity
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• Caffeine: increase cAMP which causes the release of catecholamines, increased muscular contractility, positive ionotrope + chronotrope
• Theobromine: unknown; related to adenosine receptors or reuptake of calcium which leads to cellular excitability |
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decontamination of chocolate
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• Induce emesis if alert and <1hr
• Follow with oral charcoal decontamination; repeat dosing up to 3d (undergoes enterohepatic recycling) • Urinary catheter to prevent reabsorption of metabolites |
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CS of choc toxicity
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• Vomiting
• Restlessness, hyperactivity, hyperthermia • Tachycardia, cardiac arrhythmias • Tremors, seizures • Can progress to weakness and coma |
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Treatment of choc toxicity
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• Supportive care with IV fluids (maintain perfusion), ECG and BP monitoring
• Lidocaine, if there is ventricular tachycardia • Diazepam for seizures |
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MOA of ethylene glycol toxicity
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• CNS depression, secondary to alcohol effects at brain
• Metabolism to glycoaldehyde, glycolic acid, glyoxylic acid, oxalic acid, malate, formate, glycine --> acidosis • Oxalic acid and calcium interaction à crystallization in renal tubules --> acute renal failure |
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3 stages of ethylene glycol toxicity -CS
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1. Stage 1(<12hrs) = CNS depression for first 12hrs; ataxia, vomiting, PU/PD, hypothermia (cats)
--- See increased osmolality and osmolality gap & a high-gap metabolic acidosis ---See elevated lactate, hyperphosphatemia, hyperglycemia ---Can see calcium oxalate crystals in urine 2. Stage 2 (12-24hrs) = cardiopulmonary phase; tachycardia, tachypnea, vascular changes (↑ or ↓ BP) 3. Stage 3 (24-72hrs) = acute renal failure, azotemia |
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treatment for ethylene glycol toxicity
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Treatment (ASAP): ethanol or fomepizole (4-methylpyrazole) = competitive inhibitors of alcohol dehydrogenase
• Alcohol is cheaper initially, but can cause neurologic signs; 4-MP is cheaper in long run & safer for patient • Prognosis: grave for cats; poor to guarded in dogs |
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How to treat caustic chemical burns
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Treatment: lavage site for 20-30min
* Restore skin pH to normal (check skin pH with litmus paper or urinalysis strips) |
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How to treat a alkaline burn
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Alkaline burns: apply dilute acetic acid
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treatment of an acidic burn
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Acidic burns: sodium bicarb or MgOH solution
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Estimate the percentage of body that is burned: use the rule of nines (total = 99%)
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1. Each forelimb = 9%
2. Each rear limb = 18% 3. Neck + head = 9% 4. Thorax = 18% (each half is 9%) 5. Abdomen = 18% (each half if 9%) * Small burns tend to be over-estimated; large burns tend to be udner-estimated |
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CS of electric cord chewing
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See oral burns and non-cardiogenic pulmonary edema ( from severe systemic & pulm. hypertension)
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First degree burns
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superficial wounds that involve the entire epidermis
•Quite painful •Erythematous •Hair is still attached |
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Healing of First degree burns
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Expect healing within10d
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Second degree burns
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partial thickness wounds that involve epidermis and dermis (can be deep or superficial)
•+/- pain (painful at the edges of the burn wound) •See blistering, subcutaneous edema |
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Healing of Second degree burns
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Expect slower healing (requires removal of eschar)
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Third degree burns
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full thickness wounds that involve all skin layers including subcutaneous tissue
•Initially are painless at center of lesion, because area is devoid of nerves •Hairless (no hair root left); skin may be white or black |
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Healing of Third degree burns
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Healing of skin does not occur (indication for skin grafting)
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Prognosis of body burns
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depends on percentage of burn and severity of burn
* Poorer prognosis if concurrent smoke inhalation (Dermal burns cause sequestration of inflammatory cells in lungs) * Guarded to poor prognosis if >20-50% of body is covered with 2nd or 3rd degree burns |
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Complications of burn injuries
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1. Hypovolemia
2. Impaired myocardial contractility 3. Spread of inflammatory mediators from the burn wound 4. Hypermetabolic response 5. Resetting of thermoregulatory set point 6. Shift in utilization of amino acids |
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Hypovolemia and burn injuries
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Fluid losses occur at site of injury: burned tissue will sequester Na which draws water in from circulation causing tissue edema
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Small burns cause edema only at site of injury
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mediated by histamine --> increased capillary permeability
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Large burns cause edema throughout entire body, including healthy tissues
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mediated by histamine, bradykinin, reactive oxygen species (ROS), arachidonic acid metabolites --> systemic inflammation
1. Decreased arterial pressure (fluid loss as edema), ↑pulse rate, decreased cardiac output & stroke volume 2. Compensatory vasoconstriction (attempt to restore vascular functional balance) ↓blood flow to tissues 3. Altered coagulation 4. Decrease in immune competence 5. Metabolic response: acidosis, hyperventilation, decreased cell membrane potential; cellular accumulation of Na, Ca, and water; loss of cellular K |
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How burns cause Impaired myocardial contractility
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* Burned tissue releases myocardial depressant factors (TNFα, IL-1β, myocardial toxic factor)
* Any carbon monoxide (associated with the cause of burn) -->urther depression of CV status (inability to carry O2) * Failure of heart --> arrhythmias, cardiac arrest, poor perfusion, multi-organ dysfunction |
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Spread of inflammatory mediators from the burn wound
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(eschar is a significant source of inflammatory mediators)
* Removal of the eschar improves outcome of severe burns (this may require several procedures) * Fluid from burned tissue has been shown to cause immunosuppression and decreased cell-mediated immunity |
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Hypermetabolic response in burn victims
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* Mediated by ↑↑release of catecholamines -> ↑cardiac output, ↑O2 consumption, ↑glucose production, protein wasting
* This catabolic state can last for months, even if the burn heals/corrects * Catecholamine release is due to increased metabolism from the reset thermoregulatory set point and due to pain * Implications of intervention: animal has higher caloric requirements for months after burn injury |
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Resetting of thermoregulatory set point in burn victims
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* Burns cause thermoregulatory set point to be reset at higher level = more heat is required to remain at this point
* Animal must use energy to maintain higher temps = increased catecholamine release (vicious cycle) |
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Methods of intervention in Resetting of thermoregulatory set point in burn victims
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keep patient warm to conserve their energy, cover wounds, administer beta blockers
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Shift in utilization of amino acids in burn victims
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* Massive uptake of amino acids while systemic levels of amino acids are low
* Can lead to negative nitrogen balance |
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3 goals with burn victims
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Resuscitation + Analgesia + Topical cooling
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first measures when treating burn victims
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<2hrs since injury, use cool water compresses for 30min to stop the continuing thermal injury (↓extent of injury)
* Administer O2 if there is risk of smoke inhalation or in patients with extensive burns * Provide analgesia: opioids (oxymorphone, morphine, fentanyl) * If 2nd or 3rd degree burns, provide IV fluids |
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why dont you use ice on burns
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Don’t use ice—this will decrease/hinder perfusion
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WHy do you give IV fluids to 2nd or 3rd degree burn victims
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1. Extensive fluid loss due to edema at burn site and throughout body
2. Hypoalbuminemia decreases oncotic P 3. Incresed capillary permeability 4. Want to prevent renal failure by restoring circulating volume |
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Amount of fluids to give 2nd or 3rd degree burn victims
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o Shock doses of crystalloids in first hour (divide into 1/3 – ¼ increments, not given all at once)
-----Dogs: 90ml/kg/hr give 20-30ml/kg over 10-15min -----Cats: 45ml/kg/hr give 10ml/kg over 30min * After initial resuscitation, calculate CRI in relation to amount of burn: ---Dogs: 2-4ml/kg/hr x %total body surface area burned ---Cats: 1-2ml/kg/hr x %total body surface area burned * Give half of amount within 6hrs of injury * Always re-check fluid therapy at 4-6hrs later; the goal is 0.5-1ml/kg/hr urine production |
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Why Avoid colloids and aggressive fluid therapy in first 12-24hrs after extensive burns
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Vascular leakage + aggressive fluids could cause more subcutaneous and pulm. edema
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Appropriate methods of debridement of burn wounds
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1. surgical excision
2. soaking in isotonic saline for 30min and trimming the separate tissue * It’s important to remove eschar early to increase chance of recovery |
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when not to use silvadene on a burn wound
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(-) not for use in patients with liver or kidney failure
(-) may cause transient leukopenia (indication to terminate treatment) |
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Why dont you use NSAIDs in burn victims
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negative effect on platelets and GI mucosa (contribute to ulceration in GI tract)
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The worst thermal injuries occur at ...
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the upper airway
* Causes mucosal edema & swelling, progressive over 1st 24hrs |
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Smoke particles interfere with normal physiologic mechanisms
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1. Inactivates surfactant --> atelectasis
2. Impairment of function of alveolar macrophages 3. Inhibit mucociliary clearance --> decreased particulate removal --> bacterial pneumonia |
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Dermal burns increase the morbidity associated with smoke inhalation!!!
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activation of neutrophils to lungs = increased inflammatory response = lung dysfunction
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Heat stroke
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Heat stroke is defined as a patient with a core body temperature of 106 or above and concurrent evidence of neurologic dysfunction (seizures, obtundation, coma, ataxia).
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Heat exhaustion
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Heat exhaustion is defined as a patient with a core body temperature 103 and 106 and mild signs of dizziness, increased thirst, fatigue, and malaise.
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2 types of heat stroke
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1. Classic or Non-exertional heat stroke: is heat stroke secondary to exposure to high environmental heat.
2. Exertional heat stroke: is heat stroke secondary to strenuous exercise. |
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Hyperthermia
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Hyperthermia refers to a rise in body temperature above the hypothalamic set point due to impaired (laryngeal paralysis, drugs) or overwhelmed (exertion, concurrent disease (heart disease, obesity, laryngeal paralysis) heat-dissipating mechanisms
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Pyrogenic hyperthermia
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FEVER
refers to a rise in body temperature secondary to resetting of the hypothalamic temperature point. |
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Things to help you diagnose heat stroke
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1. a recent weather change, either a dramatic rise in temperature or humidity
2. an acute, definitive change from the pet’s normal behavior 3. pet was found trapped in a hot, non-circulating area or was outside all day |
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Acclimatization
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Acclimatization is a physiologic process that improves a body’s response to high heat by increasing the effectiveness of internal heat dissipating mechanisms.
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How long does it take a body to acclimate to weather changes?
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7-14 days
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Heat stroke occurs due to an imbalanced response to heat stress in what 3 things?
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1. thermoregulation
2. acute phase response 3. heat adaptation |
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body has 4 ways to lower its temperature
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1. radiation
2. conduction 3. evaporation 4. convection |
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Radiation
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Radiation is the release of heat from the body directly into the environment no surface contact is required.
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Conduction
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Conduction is the transfer of heat between 2 objects in direct contact with each other. It is partially determined by the thermal conductivity of the surface (for example metal is a great conductor). Conduction occurs when the animal is in direct contact with a surface (i.e. a cold steel table).
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Evaporation
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Evaporation is the release of heat as liquid water is converted into water vapor. This is the most effective way for humans, dogs, and cats alike to dissipate excessive body heat and is accomplished by panting and sweating (the skin of humans and only the foot pads of dogs). Minimal evaporation occurs above a humidity level of 70%.
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Convection
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Convection is heat dissipation when relatively cool air passes over the body (i.e. fan or a cool summer breeze).
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A common cellular response to heat stress
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the production of heat shock proteins
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This is the most effective way for humans, dogs, and cats alike to dissipate excessive body heat
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evaporation
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acute phase response and heat stroke (3)
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The acute phase response protects against heat stress and injury and promotes repair by a complex coordinated interaction between the endothelium, white blood cells, and epithelial cells.
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What is released during heat stress that helps control levels of inflammatory cytokines, keeping them in check?
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IL-6, an anti-inflammatory cytokine
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3 causes for multi-organ dysfunction and failure in heat stroke
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1. increased acute phase protein response
2. impaired heat-shock protein response 3. damaged gastrointestinal tract |
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heat stroke: kidneys
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Renal tubular necrosis from a direct thermal insult, hypoxia from decreased perfusion, and thrombosis all lead to ARF.
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heat stroke: Central Nervous System (CNS):
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* cerebral edema, also the Purkinje cells are very sensitive to thermal injury
* ataxia and dysmetria early. * CNS dysfunction from decreased cerebral perfusion pressure (CPP), decreased cerebral blood flow (CBF), and neuronal necrosis. *** The decreased CBF is from a combination of microthrombi and decreased perfusion from loss due to increased capillary permeability. |
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heat stroke: muscles
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Degeneration & necrosis lead to rhabdomyolysis & myoglobinuria.
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heat stroke: cardiac
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1. Increased output failure
2. myocardial necrosis 3. hemorrhage 4. arrhythmias from hyperkalemia (from muscle necrosis). |
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heat stroke: GI
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Due to decreased perfusion we can see ischemic ulceration and bacterial translocation. Bacterial translocation can lead to sepsis.
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heat stroke: liver
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* hepatocellular necrosis & cholestasis from reticuloendothelial system (RES) damage.
* elevated ALT - are either from direct thermal injury to hepatocytes or from decreased liver perfusion. |
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heat stroke: lungs
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In the pulmonary endothelium vascular endothelial damage causes increased permeability, which leads to pulmonary edema.
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heat stroke: coagulation
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* DIC is common since the endothelial cell is very susceptible to thermal injury. Subsequent activation of platelets and clotting cascade occurs.
* Increased fibrinolytic activity may contribute to coagulation changes. Platelet dysfunction and increased vascular permeability lead to petechiae. * Also see drop in platelets from bone marrow insult several days after event. |
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heat stroke: metabolites
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1. hypoglycemia (from increased use, decreased liver production or sepsis)
2. hyperkalemia (from muscle necrosis, and respiratory alkalosis) or hypokalemia (from metabolic acidosis and vomiting). |
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heat stroke: bone marrow
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Also increased nucleated red blood cells from heat damage to bone marrow. These decrease within 12 hours after treatment.
* Also see drop in platelets from bone marrow insult several days after event. |
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easiest way to diagnose bone marrow damage from heat in a suspected heat stroke victim
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A blood smear can check for nRBCs
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when do you Stop active cooling
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at 103F (39C) because temperature will continue to fall and we need to avoid shivering associated with undershooting the normal temperature.
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four poisonous snakes of North America
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1. cottonmouth or water moccasin
2. rattlesnakes 3. copperheads 4. coral snakes |
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Snake bite order of severity of clinical signs
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rattlesnake (most severe), water moccasin (intermediate), and copperheads (least severe)
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CS of a snake bite
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the clinical signs can be delayed for up to 8 hours
1. Swelling of the area around the bite can progress for up to 36 hours 2. Painful 3. hypotension 4. hypersalivation 5. muscle twitching can be seen. 6. bites to the muzzle or neck can cause swelling severe enough to interfere with breathing. |
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main function of venom
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to immobilize the victim and predigest tissue
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4 ingredients present in venom
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1.Phospholipase A
2.Hyaluronidase 3.Collagenase 4.Crotalase |
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Phospholipase A
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Phospholipase A, which uncouples oxidative phosphorylation, releases histamine, kinnins and serotonin, and disrupts cell membranes
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Hyaluronidase
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Hyaluronidase, which breaks down connective tissue allowing venom to spread through the tissues
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Collagenase
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Collagenase, which breaks down collagen, facilitating spreading of the venom
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Crotalase
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Crotalase, a thrombin like enzyme, a fibrinogen clotting enzyme that can lead to consumption of fibrinogen and DIC-like clinical signs
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ORGAN SYSTEMS AFFECTED BY VENOM (5)
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1.Respiratory
2.Coagulation 3.Renal 4.Endothelial Cells/interstitium 5.Hemodynamic |
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Venom: Respiratory system
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* direct swelling of the upper airways can cause hypoxemia and complete occlusion of the airway
* Some venom contains a neurotoxin, which causes central respiratory depression. * the damage to the endothelium can cause leaky capillaries in the lungs and contribute to pulmonary edema. * A neuromuscular blockade can occur with Mojave toxin and affect ventilation. |
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Venom: Coagulation
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* The coagulation system is activated whenever there is endothelial cell damage
* Crotalid venom causes a syndrome similar to disseminated intravascular coagulation (DIC) through crotalase * Snake venom possesses several proteins that activate both the pro-coagulant, anti-coagulant, and fibrinolytic systems. * there are platelet aggregators and inhibitors of platelet aggregation. |
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Venom: Renal
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– myoglobin from muscle damage (rhabdomyolysis) can cause renal failure and hypovolemia can cause acute tubular necrosis.
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Venom: Endothelial Cells/interstitium
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Crotalid venom damages capillary endothelial cells via polypeptides present in the venom. This causes swelling and death of the endothelial cells leading to “leaky vessel” syndrome.
Blood leaks out leading to loss of protein, red blood cells, and edema. Clinically we see peripheral edema and petechiae and ecchymosis. |
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Venom: Hemodynamic
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The combination of vasodilation (histamine, bradykinin), and loss from increased vascular permeability cause massive decreases in cardiac output and hypovolemia that can cause further progression of organ dysfunction.
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test that can differentiate DIC from venom-induced coagulopathy.
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D-dimer
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the only anti-dote to envenomation
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Antivenin
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an indicator of envenomation on a blood smear
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echinocytes (an indicator of envenomation, if present, but absence cannot be used to rule it out, and thought to be seen only with rattlesnake bites)
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Diphenhydramine and snake bites
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Diphenhydramine is only used for an allergic reaction to antivenin and has no effect on the venom itself.
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Right-sided heart failure think
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ascites (dogs), pleural effusion (cats
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Left-sided heart failure think
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pulmonary hypertension
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Pale mucus membranes + good CRT
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suggests low PCV
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CRT
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CRT—indicates peripheral perfusion
CRT >2sec indicates a profound decrease in cardiac OUTPUT |
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If dog enters clinic with ascites, look at jugular
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* jugular distension indicates disease in chest
* normal jugular (no distension) indicates disease process in abdomen |
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jugular distension AND HEART DZ
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Jugular vein tells us about the right heart; distension indicates increased pressure in right atrium
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Right heart failure causes fluid where?
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in belly of dogs and fluid in chest of cats
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Left apical impulse—indicates
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mitral valve (left heart)
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Right apical impulse—indicates
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tricuspid valve (right heart)
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Thrill (cardiac)
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•Thrill = palpable manifestation of a murmur
* Presence of a thrill indicates at least a 5/6 murmur * Thrill at time of beat indicates a systolic murmur |
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Deficits in femoral pulses indicate what?
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Deficits indicate arrhythmias
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The vast majority of murmurs are
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systolic
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grading murmurs
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1 = can hear it if very experienced & in perfect listening conditions
2 = soft focal murmur with no radiation 3 = obvious murmur with mild radiation (1-2 rib spaces away); vet students can hear it! 4 = loud murmur with diffuse radiation but no thrill 5 = loud murmur with thrill 6 = thrill, and can hear it even with stethoscope not in contact with chest wall |
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Why Look at pulmonary parenchyma & vasculature on rads
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to evaluate edema, effusion, distension of vessels
* Used to evaluate left sided pressures in dogs & cats (distension of vessels indicates higher pressures) * indicates right-sided function in cats (pleural effusion in a cat indicates right-sided failure) o Evaluate heart size |
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Vertebral heart score
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measure the long axis (carina to apex) and short axis (perpendicular to long axis, just ventral to caudal vena cava), place each of these lines at cranial edge of T4, and count # vertebral bodies
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VHS normals in dog and cat
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Normal in dog: <10.5-11.0; Normal in cat: <8.0
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what do ECGs tell us
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Tells us about rate & rhythm, electrical conductivity of heart
Allows us to completely characterize any arrhythmias |
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BNP
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BNP = peptide hormone released by left ventricle in response to wall stretch or stress
•Can be secreted by a dilated heart or a heart under conditions of hypertension •Secreted during heart failure |
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#1 congenital heart disease in dogs
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Patent ductus arteriosus (PDA)
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Subaortic stenosis (SAS)—common in
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large breeds
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Pulmonic stenosis (PS)—common in
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small breeds
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Bichon, Poodle, Maltese: commonly diagnosed with
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PDA
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Labrador Retriever: commonly diagnosed with
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tricuspid valve dysplasia
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Bull Terrier commonly diagnosed with
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: mitral valve dysplasia
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Golden Retriever, Boxer, Newfoundland: commonly diagnosed with
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SAS
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Canine Subvalvular Aortic Stenosis (SAS)
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More common in large breeds (Golden Retriever, Boxer, Newfoundland)
* Pathology: narrowing of passage just below the aortic valve; thickened wall of chamber |
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PE & auscultation: Canine Subvalvular Aortic Stenosis (SAS)
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systolic murmur at left base (cranial to the mitral valve at apex of heart)
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Pulmonic stenosis affects
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Affects the right heart and its function: right ventricle normally has to generate 20-30mmHg of pressure, but has to work harder to generate enough P to force blood through stenosed valve = hypertrophy of right ventricle
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PE & auscultation: Pulmonic stenosis
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systolic murmur at left cardiac base
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continuous murmur (“washing machine”) that intensifies in systole
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Patent ductus arteriosus (PDA)
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Patent ductus arteriosus (PDA)
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Pathophysiology: direct communication between the pulmonary artery and descending aorta
* Left-to-right shunt: oxygenated blood flows back through heart; increase in volume flowing through pulmonary vasculature |
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•ECG Impulse begins at ?
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SA node
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P wave:
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depolarization of atrium
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PR interval:
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atrial depolarization and conduction through the AV node
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QRS complex:
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depolarization of ventricles
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Q wave (any negative deflection before R):
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1st phase of ventricular depolarization; forces are directed left to right
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R wave (tallest positive deflection):
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2nd phase of depolarization
•Ventricles depolarize from endocardium to epicardium •Usually the largest peak in Lead II (MEA +60°): forces directed right to left; LV is larger than RV |
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S wave (any negative deflection after R):
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final phase of depolarization; involves basal regions of free walls & septum;
impulse is directed towards the right ventricle |
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ST segment:
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isoelectric period after depolarization
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T wave:
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repolarization of ventricles; variable direction of impulse and the subsequent orientation of wave
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Limitations to ECGs
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ECGs indicate electrical conductivity, but do not indicate cardiac function as a pump
These are not diagnostic for chamber enlargement |
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normal mechanism for initiating cardiac contraction
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Sinus rhythm =
- Mechanism: heart beats originate in sinus (SA) node This is the only “normal” rhythm in cats; this is one of the “normal” rhythms in dogs |
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Sinus tachycardia
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•Rhythm: regular sinus rhythm (minimal R-R interval variation) + ↑ HR (>160bpm in dog; >240bpm in cat)
•Mechanism: beat originates in sinus node, but at a faster rate of impulses/signals than normal |
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Sinus bradycardia -#1 rule out?
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hypothermia
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Sinus arrhythmia
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• irregular sinus rhythm that originates in SA node
•Rhythm: HR varies with respiration - ↑HR during inspiration and ↓HR during expiration - R-R variation >10% •Normal in dogs, particularly brachycephalic breeds |
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Wandering atrial pacemaker
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•Mechanism: represents a shift in pacemaker discharge within atrium
- Usually associated with high vagal tone and sinus arrhythmia •Rhythm: regularly regular rhythm •Morphology: variable P wave height •Normal in dogs |
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pause in SA node activity
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Sinus arrest
leads to no P waves; usually followed by ventricular escape beat |
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Atrial (supraventricular) premature contractions (APC’s)
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•Mechanism: abnormal beat that originates prematurely in atria or AV junction
- Atrial disease •Rhythm: irregular rhythm; see non-compensatory pauses with premature QRS complexes •Morphology & conduction: normal-appearance QRS; P wave may be negative, positive, biphasic, or hidden |
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Drugs that will cause Atrial (supraventricular) premature contractions (APC’s)
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Drugs (digoxin, general anesthesia)
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most common supraventricular arrhythmia in the dog
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Atrial fibrillation
Significance: very bad cardiac disease -Atrial enlargement -Atrial disease -Pericardial disease |
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Atrial fibrillation
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* Mechanism & rhythm: irregularly irregular rhythm that originates from atria
* Morphology & conduction: no P waves, upright & narrow QRS complexes (usually) |
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Tx for Atrial fibrillation
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want to reduce the heart rate
*Diltiazem (calcium channel blocker), digoxin |
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Sick sinus syndrome common in
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Mini Schnauzers
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Sick sinus syndrome
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Cause/mechanism: co-existing AV nodal disease
•Rhythm: short or long pauses of sinus arrest +/- ventricular escape beats - Bradycardia-tachycardia episodes - See inappropriate rate for current level of patient activity |
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tx for Sick sinus syndrome
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atrial pacemaker, if patient is symptomatic
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Ventricular premature complexes (VPCs)
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•Mechanism: beats originating prematurely from an ectopic focus in ventricles
•Morphology: wide, bizarre QRS complexes + T-waves in opposite direction as QRS •Conduction: atrioventricular dissociation; compensatory pause; special conduction system not used |
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Cardiac causes for VPCs
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CHF, infarction, neoplasia, pericarditis, cardiomyopathy, traumatic myocarditis, inherited, Boxers (Arrhythmogenic Right Ventricular Cardiomyopathy)
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Non cardiac causes for VPCs
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2°: changes in autonomic tone, hypoxia, anemia, uremia, sepsis, GDV, pancreatitis, viral, neoplasia
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Drug causes for VPCs
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Drugs: digitalis, epinephrine, anesthetics
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Ventricular tachycardia
>100bpm with regular rhythm |
•Mechanism: rapid series of ventricular ectopic beats (may have an underlying sinus rhythm)
- AV dissociation: no relationship between P waves and QRS; P waves may sometimes be absent •Morphology & conduction: wide QRS complex (looks like VPCs); AV dissociation •Significance: serious hemodynamic effects |
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Ventricular escape rhythm/beat
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•Mechanism: beats originating from subsidiary pacemaker other than sinus node, that occur after a pause (originate from ventricular pacemaker site); represent a protective mechanism in heart
•Rhythm: usually escape with a low HR, after a longer-than-normal pause •Morphology & conduction: P waves may be absent or may be present but not associated with QRS complex; QRS morphology can be normal or similar to ventricular origin beat |
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AV blocks =
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when conduction of sinus beat is delayed or discontinued at AV junction, leading to a prolonged PR interval or P waves without associated QRS complexes
electrical signal does not use the special conduction system (not a sinus beat) |
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First degree AV block
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= prolonged PR interval with a normal rate & rhythm
• P wave is normal; QRS morphology is normal or aberrant • Causes: AV node fibrosis, drugs (atropine), hyperkalemia, high vagal tone |
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Second degree AV block
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= one or more P waves are not conducted
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Second degree AV block- 2 types
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Type I: progressive prolongation of PR interval until P wave is not conducted
Type II: intermitted P waves without associated QRS complexes |
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Third degree AV block =
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P waves and QRS complexes not associated in any way
•Atria and ectopic ventricular pacemaker are independent = slow, regular escape beats and rate Dog: <65bpm Cat: 100-120 bpm •Variable QRS morphology •Cause: AV nodal disease; correction requires a pacemaker |
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Atropine response test for AV blocks
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block vagal tone to further evaluate degree/cause of AV block; differentiate vagally-mediated and non-vagally-mediated causes of bradycardia
•If 1st degree block = ECG returns to normal •If 2nd degree block = may or may not return to normal (depends on cause) •If 3rd degree block no change in ECG |
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Bundle branch block =
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complexes originate with P wave, followed by wide QRS complex, due to delayed or blocked conduction through one of the ventricles
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mean electrical axis
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•MEA = direction that electrical activity is conducting within the heart
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Right axis shift:
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•S wave in Lead II is deeper than R is tall, and the QRS complex is negative
***Indicates right ventricular enlargement **** In Texas, a common cause of this is Heartworm Disease |
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Increased P wave duration
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left atrial enlargement
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Increased R amplitude in Lead II
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left ventricular enlargement
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Increased P amplitude
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right atrial enlargement
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No P waves:
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atrial fibrillation, atrial standstill, sinus arrest
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P waves without a QRS:
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AV block (1st, 2nd, or 3rd degree)
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