Cardiovascular System II
Cardiovascular System II
Objectives • Present the clinical features and emergency management of cardiovascular disorders, including: – Diagnose and treat rhythm disturbances. – Detect and treat cardiomyopathy. – Treat shock. – Create differential diagnosis and management plan for syncope.
Case Study 1: “Not Breathing” A 10-day-old male infant is brought to ED for not breathing and color change. The child was 3 weeks premature, and was discharged from hospital 3 days ago with an apnea monitor. Decreased activity since discharge. Poor feeding today.
Instructor Information Begin discussion of assessment and management of a patient with cardiopulmonary failure.
The PAT is as follows: • Appearance: Abnormal • Breathing: Abnormal • Circulation: Abnormal
Vital signs include: • Heart rate: 220 bpm • Respiratory rate: 14 breaths/min • Blood pressure: 55/36 mm Hg • Weight: 3.5 kg (birth weight 3.7 kg) • Oxygen saturation: 88% on room air
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Initial assessment: • A: Patent without evidence of obstruction • B: Nonlabored but diminished respiratory rate • C: Mottled, cool, distal cyanosis, tachycardic and weak pulse • D: Weak cry, nonfocal exam • E: Normothermic, no evidence of trauma, fontanel flat
Detailed physical exam: • Head/Neck: No abnormalities • Heart: Tachycardia, no murmurs heard • Lungs: Decreased breath sounds • Abdomen: Liver 2 finger breadths below RCM • Neurologic: Weak cry, lethargic, poor interaction, responsive to pain and contact • Extremities: Cyanotic, cool upper and lower extremities
Key Questions What is your general impression of this patient? Categorize this patient into one of the following categories: • Stable • Respiratory Distress • Respiratory Failure • Shock • Primary CNS Dysfunction • Cardiopulmonary Failure/Arrest
Core Knowledge Points—General Impression Cardiopulmonary failure because all arms of the PAT are abnormal.
Patient appearance is lethargic but responsive, with inadequate respirations and tachycardia; mottling with distal cyanosis.
Key Questions What are your initial management priorities?
Critical Actions Check ABCs. Open airway. Give 100% oxygen by BMV, or perform endotracheal intubation.
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Check rhythm on cardiac monitor. Obtain vascular access. Obtain blood glucose prn. Check rectal temperature.
Core Knowledge Points—Tachyarrhythmias Tachyarrhythmias: • Wide complex – Ventricular tachycardia (rare rhythm in children but if wide need to consider of ventricular origin) – Supraventricular tachycardia (SVT) with aberrancy • Narrow complex – Sinus tachycardia (rates usually < 220) – SVT (Rates usually > 220)
Clinical features can be varied: • Palpitations in verbal children • Shock in any age • Generalized symptoms of malaise and weakness
Diagnostic studies may include: • Cardiac monitor, ECG, sepsis evaluation if young infant who has signs and symptoms suggestive of infection • Chest radiograph, echocardiogram
Management includes ABCs and stabilization.
Core Knowledge Points—Dysrhythmias The pediatric patient has 3 basic types of pathologic rhythm disturbances, which include fast pulse (tachyarrhythmia), slow pulse (bradyarrhythmia), and absent pulse (pulseless) (Table 4-3 in the APLS textbook). These can be further divided into 7 classifications based on their anatomic function.
Dysrhythmias may be the cause of impaired cardiac function leading to cardiac arrest.
Occult dysrhythmias (e.g., prolonged QT syndrome, Wolf-Parkinson-White syndrome, etc.) may present with intermittent severe symptoms (e.g., palpitations or sudden death).
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Clinical features—consider the following symptoms: • Intermittent, paroxysmal presence of symptoms • Dramatic onset and change in condition • Sudden onset of symptoms with little or no prodrome • Presentation of dysrhythmias can range from stable to cardiopulmonary arrest. — Infant or child may show subtle signs of major physiological derangement.
Core Knowledge Points—Distinguishing SVT from ST
Sinus Tachycardia (ST) Supraventricular Tachycardia (SVT) History Fever, sepsis, dehydration, Intermittent, paroxysmal in onset hemorrhage, hypovolemia, precedes ECG ST rate is less than 2x normal SVT rate at or greater than 2x normal rate rate for age. Rate varies with for age. Minimal or no rate change with activity. activity.
Supraventricular tachycardia (SVT) history is intermittent, paroxysmal, with sudden onset. Sinus tachycardia (ST) history suggests sepsis, dehydration, hemorrhage, hypovolemia.
SVT ECG steady rate at or greater than 2x normal rate for age. ST rate is less than 2x normal rate for age. Minimal or no rate change with activity with SVT.
SVT characteristics (versus sinus tachycardia): • Heart rate is >2 times normal rate for age. • Rhythm is steady. • P waves are absent. • History is not suggestive of volume depletion or sepsis.
Core Knowledge Points—Diagnostic Studies Radiology studies include chest radiographs; it is important to look for signs of structural congenital heart disease, congestive heart failure (due to a prolonged dysrhythmia), or signs of infection (pneumonia).
Laboratory tests should ALWAYS include a blood glucose check to exclude hypoglycemia in any child with abnormal mental status.
Differential diagnoses may include: • Hypoglycemia
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• Sepsis • Hyperthyroidism • Volume depletion • Catastrophic illness, e.g., CNS, GI trauma (abuse) • Metabolic disease
Critical Actions Manage ABCs. Get baseline ECG. Obtain vascular access. For SVT (see AHA algorithm): • Vagal maneuvers for stable SVT • Adenosine: 100 mcg/kg bolus, increase to 200 mcg/kg (maximum first dose is 6 mg, maximum second and subsequent doses 12 mg) – given for stable SVT if unresponsive to vagal maneuvers or for unstable SVT if IV access is immediately available. • Cardioversion for unstable SVT (poor perfusion) • Procainamide or amiodarone to be considered if possible of ventricular origin; that is QRS >0.08 seconds • Digoxin to slow rate if cardioversion unsuccessful • Cardiology consultation
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The PALS algorithm for tachycardia (sinus tachycardia, SVT, and ventricular tachycardia) with POOR PERFUSION is shown below:
Tachycar dia Managem ent
Management is driven by presence or absence of poor perfusion.
Sinus tachycardia is not an arrhythmia but its etiology must be determined.
Provide ventilation and oxygenation for all patients in cardiopulmonary arrest, as the primary etiology is often respiratory failure.
Patients such as this should be transported to a pediatric referral center after stabilization. Transport issues include: • ALS transport with monitoring and IV access • Treatment plan for possible en route for recurrence – including potential for cardioversion • Consult the accepting pediatric cardiologist
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Documentation considerations include: • Always try to get baseline 12-lead ECG before and after cardioversion. • Treatment record from prehospital and ED care • Emergency Medical Treatment and Active Labor Act (EMTALA) compliance
Risk management considerations include: • Always check blood glucose. • Assure rapid triage of infants in distress. • Do not hesitate to cardiovert when child is unstable.
Reversible non-cardiac causes of dysrhythmias: Four H’s: • Hypoxemia • Hypovolemia • Hypothermia • Hyper/Hypokalemia and metabolic disorders
Reversible non-cardiac causes of dysrhythmias: Four T’s: • Tamponade (cardiac) • Tension pneumothorax • Toxins/poisons/drugs • Thromboembolism
Case Development ECG reveals SVT. Infant receives BMV ventilation. Preparations made to cardiovert but rapid IV access is obtained. Adenosine 100 mcg/kg IV push is given followed by normal saline bolus (flush). Sinus rhythm returns. BMV is discontinued as infant’s condition stabilized. 100% oxygen nonrebreather mask is placed. Sinus rhythm returns. ECG does not show early repolarization (e.g., WPW).
Case Study 2: “Unresponsive Episodes” 2-year-old girl passed out eating cereal; awoke after 5 minutes. She was stiff with eyes rolled back for approximately 5 minutes. Minimal period of sleepiness, now awake and alert; no retractions; skin color is normal.
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Instructor Information Begin discussion of assessment and management of a patient with syncope.
The PAT is as follows: • Appearance: Normal • Breathing: Normal • Circulation: Normal
Initial assessment: ABCDEs: Normal.
Vital signs include: • Heart rate: 120 bpm • Respiratory rate: 24 breaths/min • Blood pressure: 80/60 mm Hg • Temperature: 37.7°C • Weight: 12 kg • Oxygen saturation: 99%
Focused history: • Three similar episodes; two associated with “temper tantrums.” • PMH: Negative • FH: Negative for sudden death
Key Questions What is your general impression of this patient?
Categorize this patient into one of the following categories: • Stable • Respiratory Distress • Respiratory Failure • Shock • Primary CNS Dysfunction • Cardiopulmonary Failure/Arrest
Core Knowledge Points—General Impression The patient presents with syncope and normal appearance on exam. She is in no distress and the exam is normal. Her history, however, is concerning and ominous.
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Key Questions What are your initial management priorities?
Core Knowledge Points—Syncope Syncope in young children is a serious symptom. Life-threatening causes must be eliminated. A differential diagnosis is critical: • Seizure • Cardiac • Breath-holding spell
Clinical features include: • Loss of consciousness • Lasted only a few minutes • Minimal or no postictal state • No stigmata of seizure: Urinary incontinence, bitten tongue, witnessed tonic- clonic activity.
Core Knowledge Points—Diagnostic Studies Radiology studies may include: • Chest radiograph offers little. • CT or MRI may be indicated if seizures are considered.
Laboratory studies often are normal, but if patient has abnormal mental status or concerning history, may include: • Electrolytes • CBC with differential • Ca++, Mg++, PO4
Obtain an ECG as this will assist the physician in determining potential life-threatening cardiac causes of syncope.
Core Knowledge Points—Prolonged QT Ten percent present with seizures. Fifteen percent of patients with prolonged QTc die during their first episode of arrhythmia and 30% of these deaths occur during the first year of life.
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Core Knowledge Points—Cardiac Causes of Syncope Also consider in differential:
• Hypertrophic cardiomyopathy — Formerly called IHSS (idiopathic hypertrophic subaortic stenosis) — Syncope with exercise — At risk for sudden death — Positive family history — Non-specific murmur — ECG can show non-specific findings. — CXR is non-diagnostic. — Echocardiogram is diagnostic.
• Chronic cardiomyopathy — Chronic CHF
• Dysrhythmias
Cardiac arrhythmias should be considered in all patients presenting with brief, nonspecific changes in level of consciousness: • Fainting, syncope, seizures, breath-holding, apparent life-threatening events
Family history may be positive for sudden, unexplained deaths prior to 55, fainting episodes, or unexplained accidents.
Episodes associated with exercise are particularly concerning. No further exercise until cleared by a cardiologist.
Cardiac causes of syncope can present as a collapse rhythm.
Epinephrine 0.01 mg/kg (0.1 mL/kg 1:10,000) IV or IO • 0.1 mg/kg (0.1 mL/kg 1:1000) tracheal tube
Anti-arrhythmic includes amiodarone, lidocaine and magnesium.
Reversible causes include the 4 H’s (hypoxemia, hypovolemia, hypothermia, Hyper- /hypokalemia) and the 4 T’s (tamponade, tension pneumothorax, toxins, thromboembolism).
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Pulseless Arrest*
VF/VT Not VF/VT
Shock x 3 Vasopressor
Vasopressor CPR x 3 min (Drug - Shock)
Shock *CPR and seek reversible causes throughout Anti-arrhythmic
Case Development This patient has prolonged QT syndrome. She is at risk for fatal dysrhythmia (ventricular tachycardia or ventricular fibrillation). She needs to be admitted/transferred to a pediatric cardiology center for cardiology evaluation.
This child is hospitalized. She is monitored and confirmed to be at risk for dangerous dysrhythmia. She is discharged on medications shown to decrease her risk of ventricular tachycardia/ventricular fibrillation (e.g., β blockers). She is a candidate to receive an AICD (automatic implantable cardiac defibrillator) when she gets older.
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Case Study 3: “Chicken Pox” A 6-month-old boy present with chicken pox lesions that began 3 days ago. The lesions are spreading and there are more scabs today. He has had a fever since yesterday, and it is higher today. Today, his skin appears to be red. He is fussy and not feeding well.
Instructor Information Begin discussion of assessment and management of the patient in compensated shock.
The PAT is as follows: • Appearance: Normal/Abnormal – he is fussy, which may be an early sign of shock or CNS condition. • Breathing: Normal. • Circulation: Normal.
Vital signs include: • Heart rate: 160 bpm – tachycardia is seen in many conditions, but there is concern in a patient with infection that it could be a sign of shock • Respiratory rate: 40 breaths/min – without retractions, may indicate metabolic acidosis • Blood pressure: 79/56 mm Hg – blood pressure is normal, so this is not decompensated shock • Temperature: 39°C • Weight: 8.1 kg • Oxygen saturation: 98% on room air
Initial assessment: • A: Patent without evidence of obstruction • B: Normal • C: Generalized red erythroderma, warm, tachycardic (febrile) • D: Nonfocal exam, irritable • E: Many impetiginous scabs, pustules and vesicles; some with surrounding cellulitis
Detailed physical exam: • Head/Neck: No abnormalities except for skin • Heart: Tachycardic, no murmurs heard • Lungs: Clear breath sounds
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• Abdomen: Normal except for skin • Neurologic: Alert, subdued, no meningismus • Skin: Many vesicles, scabs, pustules; some with surrounding cellulitis. Generalized warm erythroderma. Capillary refill 2 seconds.
Key Questions What is your general impression of this patient?
Categorize this patient into one of the following categories: • Stable • Respiratory Distress • Respiratory Failure • Shock • Primary CNS Dysfunction • Cardiopulmonary Failure/Arrest
Core Knowledge Points—General Impression Compensated shock • Tachycardia and mild change in appearance (fussy) • Possible septic shock as varicella lesions with signs of secondary infection (Staph aureus, group A strep) • Erythroderma: Scarlet fever versus toxic shock
Key Questions What are your initial management priorities?
Critical Actions Provide supplemental oxygen. Obtain vascular access. Determine rapid glucose. Begin fluid resuscitation at 20 mL/kg – 160 mL normal saline. CBC, blood culture, other optional labs IV antibiotics Repeated assessment for signs of shock
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Also important to continue assessment to determine if scarlet fever or toxic shock For toxic shock: • IV fluid infusion • Start infusion of dopamine. • Consider dobutamine infusion.
Core Knowledge Points—Shock Shock is inadequate tissue perfusion (delivery of oxygen and nutrients) to meet the metabolic demands of the body.
Types of shock include: • Hypovolemic • Cardiogenic • Distributive • Septic
Compensated: • Vital organs continue to be perfused by compensatory mechanisms. • Blood pressure is normal.
Decompensated: • Compensatory mechanisms are overwhelmed and inadequate - hypotension, high mortality risk.
Aggressive treatment of early shock: • Halts progression to decompensated shock
Clinical features: • Apnea, tachypnea, respiratory distress • Skin: Pale, cool, delayed capillary refill. Warm shock will appear normal. • Lethargic, weak, orthostatic weakness • Tachycardia, hypotension
Specific types of shock: • Distributive shock: Neurologic deficits (spinal cord injury); anaphylaxis (urticaria, allergen trigger, wheezing) • Septic shock: Petechiae, erythroderma
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Core Knowledge Points—Hypovolemic Shock Fluid loss: • Diarrhea, vomiting, anorexia, diuresis • Hemorrhage
Resuscitation: • Fluid replacement • Normal saline or lactated Ringer’s 20 mL/kg bolus infusions, reassess, repeat as needed • Blood transfusion for excessive hemorrhage
Core Knowledge Points—Cardiogenic Shock Poor myocardial contractility or impaired ejection: • Cardiomyopathy, congenital heart disease, myocarditis, tamponade, congestive heart failure, dysrhythmia, septic shock, drugs (e.g., thiopental)
Resuscitation: • Fluid bolus (10 mL/kg) and reassess • Inotropes, pressors (e.g., dopamine, dobutamine, epinephrine)
Core Knowledge Points—Distributive Shock Inappropriate vasodilation with a maldistribution of blood flow: • Anaphylactic shock, spinal cord injury, septic shock • “Warm shock”
Resuscitation: • Vasoconstrictors (e.g., epinephrine) • Anaphylaxis treatment • Spinal cord injury treatment • Sepsis treatment
Core Knowledge Points—Septic Shock Elements of distributive shock and cardiogenic shock: • Inappropriate vasodilation with a maldistribution of blood flow • Myocardial depression
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Resuscitation: • Fluid bolus • Pressors and inotropes • Antibiotics (expect possible deterioration initially due to toxin release)
Case Development Labs drawn. IV fluids given with decrease in heart rate to 120 bpm IV antibiotics given Patient admitted and discharged 4 days later
Option for prolonged observation in ED monitoring for deterioration in vital signs and clinical status. • Benign observation period suggests scarlet fever. • Worsening suggests possible toxic shock. • Toxic shock: Similar to septic shock requiring fluids, pressors, inotropes, ICU monitoring
Early recognition and treatment of compensated shock may prevent progression to decompensated shock. • Identifying early compensated shock is difficult.
Decompensated shock has a poor prognosis.
Core Knowledge Points—Emergency Information Form Overall, parents of patients with underlying cardiac disease should receive information about their child’s disease, treatment, and how to reach primary care (PCP) and specialty physicians.
Ideally parents of children with cardiac disease should carry an updated emergency information form (EIF) when seeking emergency care. This form provides immediate pertinent medical information. A medical ID bracelet is also useful.
Available from ACEP and AAP.
The EIF should be updated by the patient’s primary care physician and specialists.
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The Bottom Line • Obtain rapid history and assess children in shock or respiratory distress for cardiac disease including postsurgical complications. • Utilize the EIF to gather information, contact specialists, and guide therapy. • Echocardiography and cardiology consultation for definitive diagnosis and cardiac function determination.
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