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Cardiology part 2
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- 2. Part 2: Assessmentand Management of the Cardiovascular Patient
- 3. Sections Assessment ofthe Cardiovascular Patient Management of Cardiovascular Emergencies Managing Specific Cardiovascular Emergencies
- 4. Assessment of the Cardiovascular Patient Scene Size-up and Initial Assessment Determine scene safety. Determine level of responsiveness. Airway. Breathing: Note breath sounds indicative of cardiovascular problems. Circulation: Note color, temperature, turgor, moisture, mobility, edema. Treat life-threatening problems.
- 5. Assessment of the Cardiovascular Patient Focused History Common Symptoms Chest Pain • OPQRST History of Pain Dyspnea • Onset • Duration • Provocation/palliation • Orthopnea Cough
- 6. Assessment of the CardiovascularPatient Other Signs and Other Signs and Symptoms Symptoms Level of Edema consciousness Headache Diaphoresis Syncope Restlessness and anxiety Behavioral change Feeling of impending Anguished facial doom expression Nausea and/or Activity limitations vomiting Trauma Fatigue Palpitations
- 7. Assessment of the CardiovascularPatient Allergies Medications Nitroglycerin, propranolol, digitalis, diuretics, antihypertensives, antidysrhythmics, lipid-lowering agents Nonprescription drugs • Cocaine • Antihistamines • Alcohol
- 8. Assessment of the CardiovascularPatient Past Medical History Cardiac history Heart problems Other medical problems Family cardiac history Modifiable risk factors for heart disease (smoking, etc.) Last Oral Intake Caffeinated beverages Events Preceding the Incident Stress, strenuous or sexual activity
- 9. Assessment of the Cardiovascular Patient Physical Examination Inspection Tracheal position Thorax Epigastrium
- 10. Assessment of the CardiovascularPatient Auscultation Breath Sounds • Adventitious Sounds Heart Sounds • Normal • Abnormal
- 11. Assessment of the CardiovascularPatient Auscultation Carotid Artery Bruit
- 12. Assessment of the CardiovascularPatient Palpation Pulse Thorax • Crepitus • Chest Wall Tenderness Epigastrium
- 13. Management of Cardiovascular Emergencies Basic Life Support Advanced Life Support ECG Monitoring Vagal Maneuvers Precordial Thump Pharmacological Management Defibrillation Synchronized Cardioversion Transcutaneous Cardiac Pacing Diagnostic (12-Lead) ECG
- 14. Management of Cardiovascular Emergencies Monitoring ECG in the Field Parts of the Defibrillator Monitoring Leads Lead II, MCL1 “Quick-Look” Paddles
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- 23. Management of Cardiovascular Emergencies Monitoring ECG in the Field Causes of Poor Signals Excessive hair, loose or dislodged electrode Dried conductive gel, poor placement, diaphoresis Patient movement or muscle tremor Broken patient cable or lead wire Low battery Faulty grounding Faulty monitor
- 24. Management of Cardiovascular Emergencies Vagal Maneuvers Indication Stable patient with symptomatic tachycardia Maneuvers Valsalva maneuvers Coughing Carotid Sinus Massage • Avoid in patients with a history of cerebrovascular or carotid artery disease, or patients with carotid bruits.
- 25. Management of Cardiovascular Emergencies Precordial Thump Indication Pulseless patient who has a witnessed arrest. Most effective when performed immediately after onset of VF. Not used in pediatric patients. Technique
- 26. Management of Cardiovascular Emergencies Pharmacological Management Antidysrhythmics Atropine Sulfate Lidocaine Procainamide Bretylium Adenosine Amiodarone Verapamil
- 27. Management of Cardiovascular Emergencies Sympathomimetic Agents Epinephrine Norepinephrine Isoproterenol Dopamine Dobutamine Vasopressin Drugs Used for Myocardial Ischemia Oxygen Nitrous Oxide Nitroglycerin Morphine Sulfate Nalbuphine
- 28. Management of Cardiovascular Emergencies Thrombolytic Agents Aspirin Alteplase Relteplase Other Prehospital Drugs Furosemide Diazepam Promethazine Sodium Nitroprusside
- 29. Management of Cardiovascular Emergencies Drugs Infrequently Used in the Prehospital Setting Digitalis Beta Blockers • Propranolol, metaprolol, labetalol Calcium Channel Blockers • Verapamil, nifedipine, diltiazem Alkalinizing Agents • Sodium bicarbonate
- 30. Management of Cardiovascular Emergencies Defibrillation Chest Wall Resistance Paddle pressure, paddle–skin interface, paddle surface area, number of previous countershocks, and inspiratory vs. expiratory phase at time of shock Success of Defibrillation Time until VF Condition of the myocardium Heart size and body weight Previous countershocks Proper paddle size, placement, interface, and pressure Properly functioning defibrillator
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- 38. Management of Cardiovascular Emergencies Emergency Synchronized Cardioversion Indications Unstable, tachycardic patient • Perfusing VT • PSVT • Rapid atrial fibrillation • 2:1 atrial flutter
- 39. Management of Cardiovascular Emergencies Procedure Similar to defibrillation. Premedicate the patient whenever possible. Turn on the synchronizer. Hold discharge buttons until countershock administered.
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- 41. Management of Cardiovascular Emergencies Transcutaneous Cardiac Pacing Indications Symptomatic, unstable patients who do not respond to pharmacological therapy • Symptomatic bradycardias with high-degree AV blocks. • Atrial fibrillation with a slow ventricular response. • Other significant bradycardias, including asystole.
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- 49. Management of Cardiovascular Emergencies Carotid Sinus Massage Indications Paroxysmal supraventricular tachycardia in a stable patient. Complications Do not use in patients with a history of cerebrovascular or carotid artery disease. Do not use in patients having carotid bruits. Asystole, PVCs, VT, and VF may occur. Patient may experience bradycardia, nausea, and vomiting. Support and Communication
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- 58. Managing Specific Cardiovascular Emergencies Angina Pectoris Myocardial Infarction Heart Failure Cardiac Tamponade Hypertensive Emergencies Cardiogenic Shock Cardiac Arrest Peripheral Vascular and Other Cardiovascular Emergencies
- 59. Angina Pectoris Epidemiology& Pathophysiology Pathophysiology Angina occurs when the heart’s demand for oxygen exceeds the blood’s oxygen supply. Commonly caused by artherosclerosis. May also result from spasm of the coronary arteries (Prinzmetal’s angina). Stable vs. Unstable Angina Disease Progression Spectrum of coronary artery disease best referred to as acute coronary syndrome
- 60. Angina Pectoris Causesof Chest Pain Cardiovascular, including acute coronary syndrome, pericarditis, or thoracic dissection of the aorta Respiratory, including pulmonary embolism, pneumothorax, pneumonia, and pleural irritation Gastrointestinal, including cholecystitis, pancreatitis, hiatal hernia, esophageal disease, gastroesophageal reflux, peptic ulcer disease, and dyspepsia Musculoskeletal, including chest wall syndrome, costochondritis, acromioclavicular disease, herpes zoster, chest wall trauma, and chest wall tumors
- 61. Angina Pectoris FieldAssessment Signs of Shock Chest Discomfort Typically sudden onset, which may radiate or be localized to the chest. Patient often denies chest pain. Duration Episodes last 3–5 minutes. Pain relieved with rest and/or nitroglycerin.
- 62. Angina Pectoris Breathing History Past episodes of angina: • Episodes of angina that are increasing in frequency, duration, or severity are significant. ECG Do not delay scene time. 12-Lead ECG preferred: • Angina typically causes nonspecific ST changes.
- 63. Angina Pectoris Management Relieve anxiety: Place the patient in a position of physical and emotional comfort. Administer oxygen. Establish IV access. Monitor ECG. Consider medication administration: Nitroglycerin tablets or spray Nifedipine or other calcium channel blockers Morphine sulfate
- 64. Angina Pectoris SpecialConsiderations Patients with new-onset or crescendo angina often require hospitalization. Symptoms not relieved by rest, nitroglycerin, and oxygen may indicate an overall worsening of the disease or the early stages of a myocardial infarction. Patients may refuse transport after pain is relieved, even though the underlying problem is not addressed.
- 65. Myocardial Infarction Pathophysiology Death and necrosis of heart muscle due to inadequate oxygen supply. Causes may include occlusion, spasm, microemboli, acute volume overload, hypotension, acute respiratory failure, and trauma. Location and size dependent on the vessel involved.
- 66. Myocardial Infarction Transmuralvs. Subendocardial MIs. Effects of a Myocardial Infarction Dysrhythmias Heart Failure Ventricular Aneurysm Goals of Treatment Pain Relief Reperfusion
- 67. Myocardial Infarction FieldAssessment Breathing Signs of Shock Chief Complaint Typically related to chest pain. Evaluate using OPQRST: • Discomfort > 30 minutes. • Radiation to arms, neck, back, or epigastric region. Patients may minimize symptoms. Feelings of “impending doom.”
- 68. Myocardial Infarction OtherSymptoms Nausea and vomiting Diaphoresis Myocardial Infarctions & the ECG Diagnostic ECGs: • 12-lead ECGs • S-T segment • Pathological Q waves Dysrhythmias: • Asystole, PEA, VF, VT. • Dysrhythmias are the leading cause of death in MI.
- 69. Myocardial Infarction ReperfusionScreening Reperfusion of ischemic/injured tissue. Time from onset to treatment < 6 hours. Absence of history that would exclude thrombolytics. Transport Rapid transport indicated when acute MI suspected
- 70. Myocardial Infarction Management Prehospital Administer oxygen. Establish IV access. Consider medication administration: • Aspirin • Morphine sulfate • Promethazine • Nitroglycerin • Nitrous oxide • Nubain • Antiarrhythmia medication as indicated
- 71. Myocardial Infarction Monitor ECG. Rapid transport as indicated. Avoid patient refusals if possible. Identify candidates for thrombolytic therapy. In-Hospital: Diagnostic ECGs. Enzyme levels. Risk assessment. Treatment: • Cardiac catheterization, PTCA, and CABG.
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- 73. Heart Failure Left Ventricular Failure Pathophysiology Results in increased back pressure into the pulmonary circulation.
- 74. Heart Failure Right Ventricular Failure Pathophysiology Results in increased back pressure into the systemic venous circulation. Pulmonary Embolism
- 75. Heart Failure CongestiveHeart Failure Pathophysiology Reduction in the heart’s stroke volume causes fluid overload throughout the body’s other tissues. Manifestation
- 76. Heart Failure FieldAssessment Pulmonary Edema: Cough with copious amounts of clear or pink-tinged sputum. Labored breathing, especially with exertion. Abnormal breath sounds, including rales, rhonchi, and wheezes. Pulsus paradoxus and pulsus alternans. Paroxysmal Nocturnal Dyspnea (PND) Medications: Diuretics. Medications to increase cardiac contractile force. Home oxygen.
- 77. Heart Failure MentalStatus Mental status changes indicate impending respiratory failure. Breathing Signs of labored breathing. Tripod positioning. “Number of pillows.” Skin Color changes. Peripheral and/or sacral edema.
- 78. Heart Failure Management General management: Avoid supine positioning. Avoid exertion such as standing or walking. Maintain the airway. Administer oxygen. Establish IV access. Limit fluid administration.
- 79. Heart Failure MonitorECG. Consider medication administration: Morphine Nitroglycerine Lasix Dopamine/dobutamine Promethazine Nitrous oxide Avoid patient refusals if at all possible.
- 80. Cardiac Tamponade Epidemiology& Pathophysiology Pathophysiology Result of fluid accumulation between visceral pericardium and parietal pericardium. Increased intrapericardial pressure impairs diastolic filling. Typically worsens progressively until corrected. Epidemiology Acute onset typically the result of trauma or MI. Benign presentations may be caused by cancer, pericarditis, renal disease, and hypothyroidism.
- 81. Cardiac Tamponade FieldAssessment Patient History Determine precipitating causes. Patient relates a history of dyspnea and orthopnea. Exam Rapid, weak pulse Decreasing systolic pressure Narrowing pulse pressures Pulsus paradoxus Faint, muffled heart sounds Electrical alternans
- 82. Cardiac Tamponade Management Maintain airway. Administer oxygen. Establish IV access. Consider medication administration: Morphine sulfate Nitrous oxide Furosemide Dopamine/dobutamine
- 83. Cardiac Tamponade RapidTransport Pericardiocentisis Pericardiocentisis is the definitive treatment. Insertion of a cardiac needle and aspiration of fluid from the pericardium. Procedure should be performed only if allowed by local protocol. Procedure should be performed only by personnel adequately trained in the procedure.
- 84. Hypertensive Emergencies Hypertensive Emergency Causes Typically occurs only in patients with a history of HTN. Primary cause is noncompliance with prescribed antihypertensive medications. Also occurs with toxemia of pregnancy. Risk Factors Age-related factors Race-related factors
- 85. Hypertensive Emergencies Field Assessment Initial Assessment Alterations in mental state Signs & Symptoms Headache accompanied by nausea and/or vomiting Blurred vision Shortness of breath Epistaxis Vertigo Tinnitus
- 86. Hypertensive Emergencies History Known history of hypertension Compliance with medications Exam BP > 160/90 Signs of left ventricular failure Strong, bounding pulse Abnormal skin color, temperature, and condition Presence of edema
- 87. Hypertensive Emergencies Management Maintain airway. Administer oxygen. Establish IV access. Consider medication administration: Morphine sulfate Furosemide Nitroglycerin Sodium nitroprusside Labetalol
- 88. Cardiogenic Shock Pathophysiology General Inability of the heart to meet the body’s metabolic needs. Often remains after correction of other problems. Severe form of pump failure. High mortality rate. Causes Tension pneumothorax and cardiac tamponade. Impaired ventricular emptying. Impaired myocardial contractility. Trauma.
- 89. Cardiogenic Shock FieldAssessment Initial Assessment Chief Complaint Chief complaint is typically chest pain, shortness of breath, unconsciousness, or altered mental state. Onset may be acute or progressive. History History of recent MI or chest pain episode. Presence of shock in the absence of trauma.
- 90. Cardiogenic Shock MentalStatus Restlessness progressing to confusion Airway and Breathing Dyspnea, labored breathing, and cough PND, tripod position, accessory muscle retraction, and adventitious lung sounds ECG Tachycardia and atrial dysrhythmias Circulation Hypotension Cool, clammy skin
- 91. Cardiogenic Shock Management Maintain airway. Administer oxygen Identify and treat underlying problem. Establish IV access. Consider medication administration: Vasopressors Other meds
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- 93. Cardiac Arrest SuddenDeath Causes Electrolyte or acid–base imbalances Electrocution Drug intoxication Hypoxia Hypothermia Pulmonary embolism Stroke Drowning Trauma End-stage renal disease and hyperkalemia
- 94. Cardiac Arrest FieldAssessment Initial Assessment Unresponsive, apneic, pulseless patient ECG Dysrhythmias History Prearrest events Bystander CPR “Down time”
- 95. Cardiac Arrest Management Resuscitation Return of Spontaneous Circulation Survival Role of Basic Life Support General Guidelines Manage specific dysrhythmias. CPR. Advanced airway management. Establish IV access.
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- 99. Cardiac Arrest PostresuscitationManagement Manage dysrhythmias and problems as presented. Be alert for PEA. Transport rapidly: • Take care to protect intubation and IV access. Withholding Resuscitation Rigor mortis Dependent lividity Decapitation, decomposition, incineration Valid advanced directive
- 100. Cardiac Arrest TerminatingResuscitation Indications for termination of resuscitation • Patient over 18 years old. • Cause is presumed cardiac in origin. • Successful endotracheal intubation. • ACLS standards applied throughout the arrest. • On-scene effort > 25 minutes, or four rounds of drug therapy. • ECG remains asystolic or agonal. • Blunt trauma victims presenting with or developing asystole.
- 101. Cardiac Arrest TerminatingResuscitation Contraindications to termination of resuscitation: • Patient under 18 years old. • Arrest is of a treatable cause. • Present or recurring VF/VT. • Transient return of a pulse. • Signs of neurological viability. • Witnessed arrest. • Family or others opposed to termination of resuscitation. Always follow local protocols related to termination of resuscitation. Support the family or others after termination of resuscitation. Coordinate with law enforcement as required.
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- 104. Peripheral Vascular andOther Cardiovascular Emergencies Atherosclerosis Pathophysiology Progressive degenerative disease of the medium-sized and large arteries. Results from the buildup of fats on the interior of the artery. Fatty buildup results in plaques and eventual stenosis of the artery. Arteriosclerosis Claudication
- 105. Peripheral Vascular andOther Cardiovascular Emergencies Aneurysm Pathophysiology Ballooning of an arterial wall, usually the aorta, that results from a weakness or defect in the wall Types Atherosclerotic Dissecting Infectious Congenital Traumatic
- 106. Peripheral Vascular andOther Cardiovascular Emergencies Abdominal Aortic Aneurysm Often the result of atherosclerosis Signs and symptoms • Abdominal pain • Back/flank pain • Hypotension • Urge to defecate
- 107. Peripheral Vascular andOther Cardiovascular Emergencies Dissecting Aortic Aneurysm Caused by degenerative changes in the smooth muscle and elastic tissue. Blood gets between and separates the wall of the aorta. Can extend throughout the aorta and into associated vessels.
- 108. Peripheral Vascular andOther Cardiovascular Emergencies Acute Pulmonary Embolism Pathophysiology Blockage of a pulmonary artery by a blood clot or other particle. The area served by the pulmonary artery fails. Signs and Symptoms Dependent upon size and location of the blockage. Onset of severe, unexplained dyspnea. History of recent lengthy immobilization.
- 109. Peripheral Vascular andOther Cardiovascular Emergencies Acute Arterial Occlusion Pathophysiology Sudden occlusion of arterial blood flow due to trauma, thrombosis, tumor, embolus, or idiopathic means. Frequently involves the abdomen or extremities. Vasculitis Pathophysiology Inflammation of the blood vessels. Commonly stems from rheumatic diseases and syndromes.
- 110. Peripheral Vascular andOther Cardiovascular Emergencies Noncritical Peripheral Vascular Conditions Peripheral Arterial Atherosclerotic Disease Can be acute or chronic. Often associated with diabetes. Extremities exhibit pain, coldness, numbness, and pallor. Deep Venous Thrombosis Blood clot in a vein. Typically occurs in the larger veins of the thigh and calf. Swelling, pain, and tenderness, with warm, red skin. Varicose Veins Dilated superficial veins, common with pregnancy and obesity.
- 111. Peripheral Vascular andOther Cardiovascular Emergencies General Assessment and Management of Vascular Disorders Assessment Initial Assessment Circulatory Assessment • Pallor • Pain • Pulselessness • Paralysis • Paresthesia
- 112. Peripheral Vascular andOther Cardiovascular Emergencies Chief Complaint • OPQRST Physical Exam • Prior history of vascular problems • Differences in pulses or blood pressures Management Maintain the airway. Administer oxygen if respiratory distress or signs of hypoperfusion present. Consider administration of analgesics. Transport rapidly if signs of hypoperfusion present.
- 113. Cardiology Assessment ofthe Cardiovascular Patient Management of Cardiovascular Emergencies Management of Specific Cardiovascular Emergencies
Editor's Notes
- #75 Cor pulmonal heart disease caused by pulm disease, and pumln htn result from COPD
- #76 Manifestation – pulm edema
- #85 Hypertensive Emergency Life threatening elevation in blood pressure Usually occurs in poorly controlled or untreated Rapid increase in diastolic pressure (>130mmHg) Hypertensive Encephalopathy Headache Nausea Vomiting Alt ment Blindness Muscle triches Inability to speak Paralysis Left vetricular failure Pulmonary edema Stroke (hemorraghic and ischemic) Kidney damage Toxemia of pregnancy (preeclampsia) Occurs in 5% of pregnancies >140/90 Hypertension is sign not cause Risk of abruptio placentae, eclampsia (coma and seizures) and death
- #86 Field Assessment Initial Assessment Focused History History of poorly controlled or untreaded Htn s/s of hypertensive encephalopathy c/c headache, nausea and/or vomiting, blurred vision, SOB, epistaxis and vertigo (dizziness), tinnitis, alt ment, unconscious or seizing. Physical Exam Pulmonary edema with left ventricular failure Pulse bounding and strong BP >160/90 (not emergent, must have s/s) Edema (pitting or nonpitting) Motor/sensory deficits in parts of boy or one side
- #88 Management POC (protect airway prn) O2 IV Monitor Place pregnant pts on left side In the past we used calcium channel blockers such as nifedipine (procardia) however rapid decrease in BP can be harmful Loop diuretics to reduce preload and afterload may be used such as lasix Morphine and NTG Contact medical direction in severe cases especially if htn encephalopathy is present Advise pts who refuse tx of serious complications such as stroke seizures pulmonary edema and kidney damage
- #105 Arteriosclerosis – thickening loss of elasticity and hardening of walls from calcium deposits. Claudation – charlie horse in calfs, lack of blood flow on exertion