McCann Paramedic Program: Cardiology Lecture 4-Specific Cardiac Conditions

1. Cardiovascular Emergencies
Part IV
Dale A. LeCrone Sr NRP
Instructor

2. • Coronary Artery Disease (CAD)
• Most common form of heart disease
• Leading cause of death in US adults
• Coronary Arteries
• Supply oxygen and nutrients to the myocardium
• If blocked the muscle supplied by it will be deprived oxygen (ischemia)
• If not unblocked quickly the muscle will die (undergo infarction)

3. • Affects the inner lining of the
aorta, cerebral and coronary
blood vessels
• Leads to narrowing of the
vessels and reduction of blood
flow through them

4. • Hypertension
• Cigarette smoking
• Diabetes
• High serum cholesterol
• Lack of exercise
• Obesity
• Family history
• Male gender

5. • Modifiable risk factors:
• Cigarette smoking
• Hypertension
• Serum cholesterol
• Lack of exercise
• Obesity
• Modification can make
a difference.

6. • Atherosclerosis a major
contributor
• Arterial bruits: “swishing” sounds
heard over carotid arteries
• Claudication: severe pain in calf
muscle
• Phlebitis: swelling and pain along
the veins
• Can lead to deep vein thrombosis
(DVT)

7. • Risk factors include:
• Oral contraceptives
• Smoking
• Recent surgery
• Trauma
• Extended immobilization
• Signs include:
• Pain
• Redness
• Swelling
• Warmth
• Tenderness in the extremity

8. • Clot development can lead to decreased blood flow.
• If dislodged (thromboembolism), may completely block a vessel
• Prehospital treatment includes supportive care.

9. • Prehospital treatment is limited, includes:
• Supplementary oxygen
• Obtaining IV access
• Possible aspirin administration

10. • Principle symptom of CAD
• Occurs when oxygen supply cannot meet demand
• Switch to anaerobic metabolism leads to CO2 and lactic acid accumulation
• If occurring at rest, CAD is more severe.

11. • Prinzmetal angina
• Caused by coronary artery vasospasm
• Causes chest pain at rest
• Increased risk of:
• Ventricular dysrhythmias
• Myocardial infarction
• Heart block
• Sudden death

12. • Stable angina
• Follows predictable, recurrent pattern
• Unstable angina
• More serious, higher level of obstruction
• Changes in frequency, severity, duration
• May begin during sleep or at rest
• Warning of impending MI

13. • Any group of clinical symptoms consistent with acute MI
• Patients should receive a 12-lead ECG.
• ST-segment elevation: “Q-wave AMI”
• No ST-segment elevation: unstable angina or a non-ST-segment elevation (UA/NSTEMI).
• ST-segment depression or no changes: angina

14. • Not all chest pain is from cardiac ischemia or injury
• Do a thorough physical exam.
• Assume chest pain is at least unstable angina or evolving AMI.
• Prehospital treatment should be the same for both.
When a patient with chest pain calls for an
ambulance, it means that the patient never had
chest pain before or that his or her chronic
chest pain has changed. Take all chest pain
complaints seriously.

15. • Pathophysiology
• Part of cardiac muscle is deprived of blood flow long enough that portions die
• Blood flow slowed by:
• Blood clot occlusion of coronary artery
• Coronary artery spasm
• Reduction of overall blood flow

16. • Pathophysiology (cont’d)
• Location and size depends on which artery is blocked and where
• Subendocardial myocardial infarction: only inner layer of muscle affected
• Transmural myocardial infarction: infarct extends through the entire wall
Subendocardial Transmural

17. • Pathophysiology (cont’d)
• Infarcted tissue is surrounded by a ring of ischemic tissue
• Deprived of oxygen but still viable
• Electrically unstable
• Most deaths from AMI are preventable.

18. • Symptoms
• Chest pain is the most common symptom.
• Patient often clenches fist when describing
• May radiate to arms, fingers, neck, jaw, upper back, or epigastrium.
• Sometimes mistaken for indigestion
• Not influenced by body movements

19. • Symptoms (cont’d)
• Patients with silent MI may present with:
• Sudden dyspnea
• Rapid progress to pulmonary edema
• Sudden loss of consciousness
• Unexplained drop in blood pressure
• Apparent stroke or simply confusion

20. • Symptoms (cont’d)
• Women more likely to present with:
• Nausea
• Lightheadedness
• Epigastric burning
• Sudden onset of weakness or tiredness
• Pain radiating down right side

21. • Assessment
• For history, ask usual questions, but also if any pain medication has helped.
• If nitroglycerin was taken and did not work:
• Patient may be having an AMI.
• Nitroglycerin may be stale.

22. • Other symptoms include:
• Diaphoresis
• Dyspnea
• Anorexia, nausea, vomiting, belching, hiccups
• Profound weakness, dizziness, palpitations
• Feeling of impending doom

23. • Take note of:
• Patient’s general appearance
• Patient’s state of consciousness
• Pale, cold, and clammy skin
• Vital signs
• Left-sided heart failure signs
• Right-sided heart failure signs

24. • Typical signs include:
• Apprehension
• Ashen-gray pallor
• Cold, wet skin
• Rapid pulse rate
• Decreased blood pressure from decreased CO
• Increased blood pressure from pain and anxiety

25. • Start treatment at once for a middle-aged or older patient with chest
pain.
• Treatment goals:
• Limit size of infarct.
• Decrease fear and pain.
• Prevent serious cardiac dysrhythmias.

26. • Place patient at physical and emotional rest.
• Stress response can make damaged heart race
• Can place peripheral circulation in a state severe vasoconstriction
• Heart pushed faster, works harder from afterload

27. • Cycle can be interrupted by education programs
• To begin treatment, place patient in a semi-Fowler position.
• Do not allow patient to get on stretcher alone.

28. • Treat (MONA) in following order:
• Oxygen (SPO2 <94%)
• Aspirin
• Nitroglycerine
• Morphine

29. • Give nitroglycerin if BP is adequate.
• Do not mix with PDE-5 inhibitors.
• Place 0.4-mg under tongue.
• Do not give with hypotension or bradycardia.
• Repeat every 3 to 5 minutes, up to three doses.

30. • Morphine sulfate may be given by IV.
• 2- to 4-mg doses as needed
• Do not give if patient has/is:
• Low blood pressure
• Dehydrated
• AMI involving the heart’s inferior wall
• Some protocols prefer fentanyl.

31. • Perform cardiac monitoring.
• Document the initial rhythm.
• Place anterior chest leads.
• A monitor with audible beeps for each QRS complex is helpful.
• Keep cardiac drugs close at hand.

32. • Record vital signs.
• Measure blood pressure at least every
5 minutes.
• Measure pulse rate.

33. • History and secondary assessment
• Find out if patient:
• Has history of cardiac disease
• Takes any heart medications
• Has had a previous heart attack or heart surgery
• Obtain more details about current symptoms and any relevant past medical
history.

34. • Transport the patient.
• Once stable, transport in semi-Fowler position
• Use safe and appropriate transport.
• If serious dysrhythmia develops, consider stopping and treating immediately.

35. • Most AMIs occur from thrombus formation at a preexisting
atherosclerotic plaque site.
• Thrombus prevents blood flow
• Reperfusion attempts to restore circulation
• Be alert for good candidates.
• Know which hospitals have capabilities.
• Provide early notification to ED.

36. • Fibrinolysis
• Designed to dissolve occluding blood clot
• If given within 30 to 60 minutes of onset, may abort MI altogether
• Decreased mortality rates when given in the field to patients with STEMI

37. • Fibrinolysis (cont’d)
• Agent activates body’s internal system for dissolving clots
• May lead to bleeding.
• To determine appropriate candidates:
• Be certain patient is experiencing an AMI.
• Exclude high-risk patients.

39. • Fibrinolysis (cont’d)
• Convert clot-dissolving enzyme from plasminogen to plasmin
• Alteplase (tissue plasminogen activator)
• Streptokinase
• Reteplase (recombinant tissue)

40. • Fibrinolysis (cont’d)
• A prehospital fibrinolytic program should have:
• Well-established protocols
• Checklists
• Experience in ACLS
• Communication with receiving institution
• Medical director with training and experience

41. • Percutaneous coronary intervention (PCI)
• Alternative to fibrinolysis
• Devices are passed through a 2-mm diameter catheter through a peripheral
artery.
• Recanalizes and keeps open a blocked artery

42. • Occurs when the heart cannot pump fast or powerfully enough to
empty its chambers
• Blood backs up into systemic or pulmonary circuit, or both
• May develop in situations besides AMI

43. • Pathophysiology
• Left ventricle most commonly damaged
• Right side continues to pump normally.
• Left side cannot keep up, and pressure increases.
• Serum is forced into alveoli and forms a pulmonary edema.

44. • Pathophysiology (cont’d)
• Oxygenation becomes impaired.
• To compensate:
• Respiratory rate increases (tachypnea).
• Cyanosis may occur.
• Cheyne-Stokes respirations may present.

45. • Pathophysiology (cont’d)
• Fluid leaks into the lungs’ interstitial spaces, causing pressure and creating:
• Wheezing and crackles
• Foamy, blood-tinged sputum
• Work of breathing increase
• Dyspnea and hypoxemia
• Release of epinephrine
• Increased oxygen demand

46. • Pathophysiology (cont’d)
• Sympathetic nervous system response produces vasoconstriction
• Clinical symptoms include:
• Elevated blood pressure
• Sweating and pale, cold skin
• Confusion or disorientation

47. • Assessment
• Signs and symptoms:
• Extreme restlessness and agitation
• Severe dyspnea and tachypnea
• Tachycardia
• Crackles and wheezes
• Frothy pink sputum

48. • Assessment (cont’d)
• ECG may show cannon atrial waves:
• Pulsations seen in jugular veins
• Caused by pressure surge through venous system
• Often with fluid overload and heart failure

49. • Management
• Prehospital treatment aimed at:
• Improving oxygenation
• Decreasing workload of heart by reducing preload
• Administer 100% oxygen by demand valve or bag-mask device.
• If cannot tolerate, use nonrebreathing mask

50. • Management (cont’d)
• Monitor respiratory status.
• Sit the patient up with the feet dangling.
• Start a saline lock or an IV line
• Attach monitoring electrodes for dysrhythmias.

51. • Management (cont’d)
• Pharmacologic therapy (check local protocols)
• Nitroglycerin (vasodilator)
• Furosemide (diuretic)
• Morphine sulfate (vasodilator)
• Bronchodilators
• Pressor (ordered by physician if transport is long)

52. • Management (cont’d)
• Transport patient sitting with legs dangling.
• May receive pacemaker
• Left-ventricular assist device (LVAD)
• Can support body while waiting for a donor heart
• Tube draws blood into the device’s pump
• Oxygen-rich blood is sent to the aorta.

53. • Usually results from left-sided heart failure
• As blood backs up, right side has to work harder
• Increases systemic vein pressure
• Edema occurs.
• Causes fluid in the peritoneal cavity which results in abdominal distention
(ascites)

54. • Can improve left-sided heart failure
• Decrease in output may decrease preload.
• May lessen pulmonary congestion
• Treatment includes:
• Make the patient comfortable.
• Monitor.
• Treat signs of left-sided failure.

55. • Pathophysiology
• Occurs when excessive fluid accumulates within the pericardium
• Limits heart’s ability to fully expand
• If not treated, cardiac filling reduces enough to stop blood circulation.

56. • Assessment
• Can result from
• Tumors
• Pericarditis
• Chest trauma
• MI (rare)
• Signs and symptoms:
• Dyspnea and weakness
• SV decrease
• Distended jugular vein
• Beck’s triad

57. • Assessment (cont’d)
• ECG of limited value, but may show:
• Electrical alternans and pulsus alternans
• Pulsus paradoxus
• Difficult to distinguish between cardiac tamponade and tension
pneumothorax

58. • Management
• Pericardiocentesis to withdraw fluid
• As little as 50 mL may cause improvement.
• May not be allowed by paramedics because of risk
• If not, transport quickly, giving supportive care.

59. • Pathophysiology
• Occurs when heart cannot pump sufficient blood volume to maintain tissue
perfusion
• May occur after resuscitation.
• Symptoms include:
• Difficulty breathing
• Extreme fatigue
• General malaise

60. • Assessment
• Signs/symptoms similar to other shock types:
• Confusion or comatose
• Restless and anxious
• Rapid and shallow respirations
• Racing and thready pulse

61. • Assessment (cont’d)
• BP falls to less than 90 mm Hg systolic
• May be higher with preexisting hypertension
• Goal is to treat before shock become irreversible.

62. • Management
• Improve oxygenation and peripheral perfusion without adding work for the
heart
• Secure airway and administer 100% oxygen.
• Place patient in supine position; if pulmonary edema, place in semi-Fowler’s position.

63. • Management (cont’d)
• Start an IV line at keep-vein-open rate.
• Physician may order a trial of fluids.
• Rapidly infuse 100 to 200 mL of saline,
• Monitor pulse, blood pressure and LOC.
• Obtain a 12-lead ECG.

64. • Management (cont’d)
• Paramedics may administer vasopressor drugs.
• Dopamine maintains renal perfusion best.
• Requires careful titration and frequent monitoring
• Transport immediately to a hospital.

65. • Aneurysm: dilation or pouching
out of a blood vessel
• At greatest concern are those that
involve the aorta.

66. • Pathophysiology
• Waves of blood pound against the aortic walls.
• Produces degenerative changes in the media of the aorta
• “Unglues” the layers of the aortic wall

67. • Pathophysiology (cont’d)
• May lead to a disruption of the underlying intima and tearing in areas of
greatest stress:
• Ascending aorta just distal to aortic valve Descending aorta just beyond takeoff point of
left subclavian artery

68. • Pathophysiology (cont’d)
• Dissection often begins after intima is torn.
• Aortic valve: coronary blood flow will be affected.
• Takeoff point of the left common carotid or left subclavian artery: arterial blood flow will
be affected.

69. • Pathophysiology (cont’d)
• Stanford classification
• Type A (ascending aorta) requires surgery.
• Type B can be handled medically.

70. • Pathophysiology (cont’d)
• DeBakey classification:
• Type I: ascending aorta, aortic arch,
and descending aorta
• Type II: ascending aorta
• Type III: descending aorta distal to
left subclavian artery

71. • Assessment
• Typical patient:
• Man with chronic hypertension
• Pregnant patient
• Younger patient with Marfan syndrome
• Chief complaint: sudden chest pain

72. • Assessment (cont’d)
• May be difficult to
distinguish between
AMI and dissecting
aneurysm

73. • Assessment (cont’d)
• Signs and symptoms depend on location and extent of dissection:
• Innominate artery: difference in blood pressure in both arms
• Left common carotid artery: symptoms of stroke
• Ostia: compromised coronary blood

74. • Assessment (cont’d)
• Distention of descending aorta usually in older patients
• Pain likely less severe
• Dissection usually proceeds distally.
• Lower extremities affected

75. • Management
• Provide adequate pain
relief.
• Calm the patient.
• Administer 100% oxygen.
• Insert IV line, and give
crystalloid solution.
• Obtain an ECG strip.
• Administer IV morphine
sulfate.
• Transport immediately.

76. • Pathophysiology
• Expanding aneurysm: aneurysm gets larger
• Produces symptoms by compressing adjacent structures
• Rupture is imminent.

77. • Assessment
• As it expands, symptoms begin:
• Sudden onset of abdominal or back pain
• Urge to defecate
• Physical findings:
• Pulsatile mass palpable in the abdomen
• Possible normotensive, signs of shock developing

78. • Management
• Administer supplemental oxygen.
• Consider pneumatic antishock garment.
• Transport without delay.
• Insert IV line and give normal saline or lactated Ringer’s.

79. • Pathophysiology
• High BP affects nearly 60 million Americans.
• BP at rest is greater than 140/90 mm Hg.
• Persistent elevation is indicative of hypertensive disease, which can:
• Significantly shorten a life span
• Predispose to other medical problems

80. • Assessment
• Symptoms include:
• Headache, dizziness, weakness
• Epistaxis
• Tinnitus
• Blurred vision

81. • Management
• Acute elevation of blood pressure with evidence of end-organ damage
• Left-sided heart failure
• Dissecting aortic aneurysm

82. • Management (cont’d)
• Hypertensive encephalopathy signaled by:
• Sudden rise in BP greater than 200/130 mm HG
• Determining factor is when mean arterial pressure exceeds 150 mm Hg
• MAP = DBP + 1/3 (SBP – DBP)

83. • Management (cont’d)
• First noticeable symptoms:
• Severe headache
• Nausea
• Vomiting
• Followed by
• Seizures
• Mental status alterations
• Focal neurologic signs

84. • Management (cont’d)
• Treatment goal: lower BP in gradual controlled manner in a 30- to 60-minute
period
• If within 20 to 30 minutes of hospital:
• Provide supportive treatment only.

85. • Management
• If long transport time, initiate drug therapy:
• Labetalol: slow IV push at 20 mg, or by IV drip
• Nitroglycerine: 0.4 mg sublingual
• Check blood pressure every 3 to 5 minutes.

86. • Endocarditis
• Infection of inner lining of the
heart
• Characterized by endocardium
inflammation
• Caused by staphylococcal or
streptococcal infection

87. • Endocarditis (cont’d)
• Highest risks
• Patients with prosthetic heart valves
• Intravenous drug abusers
• Comes from other locations through bloodstream

88. • Endocarditis (cont’d)
• If untreated, can:
• Cause large growths on valve leaflets
• Damage or destroy heart valves
• Treatment:
• Antibiotics
• Surgery in severe cases

89. • Pericarditis
• Acute inflammation of
pericardium
• Red and swollen pericardial sac
• Buildup in fluid in pericardial sac
• Sharp, stabbing chest pain
• Treatment: nonsteroidal anti-
inflammatory drugs or antibiotics

90. • Myocarditis
• Inflammation of myocardium from infection or traumatic injury
• Signs and symptoms:
• Chest pain
• Dysrhythmia
• Heart failure
• Sudden cardiac arrest

91. • Rheumatic fever
• Inflammatory disease caused by streptococcal bacteria
• Causes mitral valve stenosis and ensuing heart complications

92. • Scarlet fever
• Caused by Streptococcus pyogenes
• Signs and symptoms:
• Sore throat
• Fever
• Rash
• “Strawberry tongue”
• Treatment includes antibiotics