Alexander ch21 lecture

Copyright © 2017, 2012 Pearson Education, Inc. All Rights Reserved.
Advanced EMT
A Clinical-Reasoning Approach, 2nd Edition
Chapter 21
Cardiovascular
Disorders

• Applies fundamental knowledge to provide basic
and selected advanced emergency care and
transportation based on assessment findings for
an acutely ill patient.
Advanced EMT
Education Standard

1. Define key terms introduced in this chapter.
2. Explain the relationship between electrical and
mechanical events in the heart.
3. Describe the events in the normal function of the
cardiac conduction system.
4. Relate the waves and intervals of a normal
Lead II ECG to the physiologic events they represent.
Objectives (1 of 5)

5. Describe how myocardial ischemia and damage to
the cardiac conduction system can cause cardiac
arrhythmias.
6. Describe the roles of the heart and blood vessels in
maintaining normal blood pressure.
7. Explain the importance of early recognition of signs and
symptoms, and early treatment of patients with cardiac
emergencies.
Objectives (2 of 5)

8. Explain the pathophysiology of cardiovascular conditions
and emergencies.
9. Recognize both typical and atypical presentations of
cardiovascular emergencies.
10.Differentiate between patients with adequate perfusion
and patients with inadequate perfusion.
11.Explain the importance of managing the airway,
ventilation, and circulation in patients with cardiac
problems.
Objectives (3 of 5)

12.Explain the pharmacology and use of aspirin,
nitroglycerin, nitrous oxide, and oxygen in the treatment
of cardiovascular emergencies.
13.Given a series of scenarios, demonstrate the
management of a variety of patients with cardiovascular
emergencies.
14.Discuss the rationale for fibrinolytic therapy and
percutaneous coronary interventions (PCIs) in patients
with cardiac emergencies.
Objectives (4 of 5)

15.Decide when circumstances warrant requesting
paramedic assistance in caring for patients with
cardiovascular emergencies.
16.Describe the rationale for using CPAP in patients
with pulmonary edema.
Objectives (5 of 5)

• The cardiovascular system transports:
– Oxygen
– Chemical messages
– Nutrients
– Waste products to organs designed to eliminate
substances
• Anything that interferes with ability of heart and
blood vessels to transport blood to and from
tissues compromises body function.
Introduction (1 of 2)

• Advanced EMTs must
– Quickly recognize problem; provide prompt treatment.
– Understand anatomy and physiology of the heart and
pathophysiology of cardiovascular diseases.
 Recognize emergencies
 Treatment
 Transport
Introduction (2 of 2)

Think About It
• What specific questions should Will and Justin
ask to determine the problem?
• What treatments should the patient receive in
the prehospital setting?
• What are the considerations in deciding how to
transport the patient, and to what hospital?

Figure 21-2
Cross section of the heart.

• Heart in mediastinum; hollow, muscular organ with
four chambers
– Upper chambers—atria
– Lower chamber—ventricles
• Myocardium
– Middle layer that contracts due to electrical properties
• Endocardium
– Smooth inner layer; blood flows through
Anatomy and Physiology Review (1 of 5)

• Double-walled sac surrounds heart.
– Inner layer
 Epicardium or visceral pericardium
– Outer layer
 Pericardium
– Pericardial fluid
 Allows frictionless movement of heart

• Right atrium receives deoxygenated blood.
– From the systemic circulation via the superior and
inferior vena cava
• Left atrium receives oxygenated blood.
– From the lungs through the pulmonary vein
• Both atria contract at the same time.
– Forcing blood into the ventricles

• After a brief pause, both ventricles contract,
forcing blood into the pulmonary and systemic
circulation.
• Oxygenated blood leaves left ventricle.
– Through the aorta
• Deoxygenated blood leaves right ventricle.
– Enters pulmonary artery and travels to lungs

• Four valves maintain forward flow of blood
through heart .
– Aortic semilunar
 Between left ventricle and aorta
– Pulmonary semilunar
 Between right ventricle and pulmonary artery
– Bicuspid (mitral)
 Between left atrium and ventricle
– Tricuspid
 Between right atrium and ventricle

Figure 21-3
The coronary arteries.

Anatomy and Physiology Review—
Coronary Circulation (1 of 2)
• Left and right coronary arteries branch from aorta.
– Extend along surface of heart.
• Aortic valve opens during ventricular systole,
– Cusps cover opening of coronary arteries.
• During diastole
– Aortic valve closes, allowing blood from aorta to enter
coronary arteries.

• Blood flows through coronary veins,
– Empties into right atrium
• Ischemia
– Any obstruction to coronary blood flow deprives
affected area of oxygen.
– Leads to pain; injury of myocardial cells; infarction,
or death, of that portion of myocardium
Coronary Circulation (2 of 2)

• Blood vessels
– Known as vasculature
• Three types of vessels
– Arteries, veins, capillaries
• Arteries: thick-walled vessels
– Carry higher-pressure blood leaving heart
• Arterioles: smallest arteries
– Smooth muscle tissue, allowing them to constrict
and dilate
Anatomy and Physiology Review—The
Vascular System and Blood (1 of 5)

• Capillaries
– Microscopic blood vessels; single cell-layer thick;
diameter wide enough for red blood cells in single file
• Veins
– Contain valves that prevent backflow of blood
– Sytemic circulation: through aorta to body, and back
to heart through vena cava

• Systemic circulation
– Closer to surface of body are peripheral circulation;
sacrificed during shock
– Hepatic portal system
– Bronchial arteries

• Central circulation
– Blood in large arteries and supply of blood to internal
organs
• Pulmonary circulation
– Pulmonary veins
– Pulmonary arteries

Figure 21-5
Components of the blood.

• Blood
– Plasma
– Red blood cells
– White blood cells
– Platelets

• Perfusion
– Adequate blood pressure
 Mean arterial pressure
 Stroke volume
 Cardiac output
 Systemic vascular resistance
Anatomy and Physiology Review—Perfusion,
Cardiac Output, and Blood Pressure (1 of 2)

• Systolic blood pressure
– Normal range 100 to 140mmHg
• Diastolic blood pressure
– 60 to 90 mmHg
• Hypertension
• Hypotension
Anatomy and Physiology Review—Perfusion,
Cardiac Output, and Blood Pressure (2 of 2)

Figure 21-7
The cardiac conduction system.

Cardiac Electrophysiology
• Electrical activity of cardiac cells leads to
mechanical contraction of cardiac muscle.
• Electrical activity conducted to surface of skin;
detected by electrodes
– Electrocardiogram (ECG) series of waves

Cardiac Electrophysiology (1 of 5)
• Types of cardiac cells
– Pacemaker cells
 Automaticity
– Conductive and contractile cells
 Mechanical contraction
– Electrical stimulus begins at sinoatrial (SA) node.

• Electrical impulse through heart based on flow
of ions through channels in cell membranes
– Positively charged ions (in cardiac function)
 Sodium, potassium, and calcium
– Negatively charged ion (in cardiac function)
 Chloride

• Depolarization
– Positively charged ions flow to a less positive area until
the difference between the two becomes zero.
• Repolarization
– Difference in charges is restored.
– ATP required
• Waves on ECG represent depolarization and
repolarization.

Figure 21-10
Relationship of cardiac electrical activity and ECG waves.

• SA node
– 60 to 100 bpm
• AV node
– 40 to 60 bpm
• His-Purkinje (ventricles)
– 20 to 40 bpm

Figure 21-12
Normal sinus rhythm originates in the SA node. It is regular at a rate of 60 to 100 per
minute. The P wave is upright, with a P–R interval of 0.12 to 0.20 seconds. There is the
same number of P waves as QRS complexes. The QRS wave is less than 0.12 seconds.

• Electrocardiogram (ECG)
• Cardiac monitoring
• Waveforms
– P wave
– P–R interval (PRI)
– QRS complex
– T wave

• Electrical activity does not give information about
the strength of cardiac contractions.
• Despite critical decreases in cardiac output,
organized electrical activity can appear on the
ECG.
• What other information should you be looking for
in the assessment?
Think About It

• Clinical reasoning
– Develop list of differential diagnoses and field
impressions.
– Chief complaint
– Obtain history.
– Vital signs
– Perform physical exam.
General Assessment
of Cardiovascular Complaints

• Assess airway
– Need for assisted ventilation and oxygen
• If unresponsive patient pulseless
– Begin resuscitation.
– Apply automated external defibrillator (AED).
– Perform cardiopulmonary resuscitation (CPR).
• Responsive patient with signs of hypoxia or poor
perfusion needs oxygen
General Assessment of Cardiovascular
Complaints (1 of 3)

Complaints (2 of 3)
• Onset
• Provocation
• Quality
• Radiation
• Severity
• Time
• Symptoms
• Allergies
• Medications
• Past history
• Last oral intake
• Events

Complaints (3 of 3)
• Chest pain
• Dyspnea
• Heaviness
• Pressure/
discomfort
• Indigestion
• Abdominal
pain
• Back pain
• Headache
• Visual
disturbances
• Palpitations
• Syncope
• Altered
mental status
• Nausea;
vomiting
• Cardiac arrest

Acute Coronary Syndromes (1 of 19)
• Insufficient supply of oxygen to heart
– Unstable angina
– Acute myocardial infarction
– Sudden cardiac arrest

Figure 21-15
Development of atherosclerosis. (A) Damage to the endothelium of the tunica intima.
(B) Formation of a fatty streak. (C) Development of plaque with a fibrous cap narrows the
artery lumen. (D) Rupture of the plaque and platelet aggregation occlude the artery.

• Atherosclerosis
– Genetics
– Inflammatory response
– Smoking
– Diabetes
– Hypertension

• Atherosclerosis—development
– Disruption of endothelium of tunica intima
– Damaged endothelial layer allows lipids to enter
and accumulate in tissues beneath intima; seen as
“foreign invader.”
– Plaque narrows coronary artery lumen.
– Rupture of plaque leads to acute myocardial
infarction (AMI).

• Angina pectoris
– Chest pain occurs when myocardial oxygen demand
higher than amount of oxygen that diseased coronary
arteries can supply.
– Pain retrosternal; “pressure” or “tightening”; radiates to
neck, jaw, left arm
– Nausea, vomiting, pallor, diaphoresis, and dyspnea
sometimes occur.

• Angina pectoris (continued)
– Stable angina
 Recurrent chest pain
 Comes only during exercise or stress; resolves with rest or
nitroglycerin
– Unstable angina
 Occurs at rest
 Decrease in oxygen supply; without prompt treatment,
progresses to AMI

Figure 21-18
Myocardial infarction results in death of the affected heart muscle.

• Acute myocardial infarction
– Fibrous plaque of coronary artery disease ruptures;
damaged blood vessel initiates body’s clotting cascade
– Further narrows or completely obstructs artery;
myocardial cells deprived of oxygen begin to die
– Usually occurs at rest; pain similar to that of angina
pectoris

• Signs and symptoms of myocardial infarction
– Classic response
 Chest pain; described as discomfort, ache, pressure
– Silent MIs
– Typical signs and symptoms

Figure 21-19
The signs and symptoms of angina pectoris and AMI are similar. Differentiating between
them in the prehospital setting is difficult, but both the pain of angina and of AMI are treated
the same way.

• Atypical presentations of ACS
– Anginal equivalents
 Atypical chest pain
 Pain in back, arms, or jaw
 Indigestion or abdominal discomfort
 Nausea and vomiting
 Faintness or fainting
 Weakness

• Assessment and management of ACS
– Suspect that any patient with chest pain or chest
discomfort is experiencing ACS.
– Nearly any type of dispatch could result in a patient
with a cardiovascular emergency.
 Do not let dispatch for chest pain limit your thinking about
problems other than ACS.

• Assessment and management of ACS (continued)
– General appearance, age; obtain chief complaint
– Determine immediate life threats.
– Assess airway, breathing, and circulation.
– Suspected ACS with dyspnea, indications of heart
failure, signs of hypoxia, administer oxygen to maintain
an SpO2 of 95% or greater

– Patients with myocardial ischemia have increased
risk of cardiac arrest.
– AED ready for operation at all times
– Secondary assessment: focused history, vital signs,
focused assessment
– Use mnemonic OPQRST.

– Past medical history, SAMPLE history
– Additional symptoms
– Risk factors:
 Hypertension, diabetes, high lipid levels, obesity, smoking,
previous history/family history of CAD

– Blood pressure, heart and respiration rates, pulse
oximetry
– Systolic blood pressure of 90 mmHg required to
administer nitroglycerin.
– May experience dysrhythmia, bradycardia, tachycardia,
irregular pulse
– Cardiac patients can deteriorate quickly.

– Assess breath sounds.
– Crackles (rales) in lungs indicate acute heart failure
with pulmonary edema.
– Definitive interventions aimed at reopening blocked
artery in hospital
 Transport without delay.

• ACS treatment
– Administer oxygen as indicated.
– Administer aspirin.
– Start IV; listen to lung sounds before administering fluid
bolus.
– Give nitroglycerin, analgesic.

Table 21-1 (1 of 2)
ACS Medications
Medication Indications Contraindications
Dosage and
Administrati
on
Side
Effects
Additional
Information
Aspirin Chest pain
suggesting
angina
pectoris or
AMI
Inability to maintain airway,
known allergy, peptic ulcer
disease, asthma
162–325 mg,
given in
chewable form
Few
associated
with single
dose in ACS;
may cause
abdominal
pain
Reduces mortality
associated with AMI and
reduces rate of
reinfarction and stroke by
inhibiting platelet
aggregation.
Nitroglycerin Chest pain
suggesting
angina
pectoris or
AMI; signs
and
symptoms of
left-sided
heart failure
with
pulmonary
edema
Hypotension (systolic BP
<90–100 mmHg, according
to protocol); heart rate <50
or >100; patient has taken
maximum dose prior to
your arrival; patient has
recently taken a drug used
for erectile ysfunction (e.g.
sildenafil [Viagra], tadalafil
[Cialis], vardenafil [Levitra])
0.4 mg
administered
sublingually by
tablet or
metered-dose
spray; may be
repeated every
five minutes to a
total of three
dosages, as
long as systolic
BP remains 90–
100 mmHg or
greater
Hypotension,
headache,
flushed skin
Obtain venous access
first, if possible.
Nitroglycerin is converted
to nitric oxide in the
bloodstream, which
signals smooth muscle
cells to relax. Dilation of
coronary arteries
improves myocardial
perfusion. Dilation of
systemic vasculature
reduces myocardial
workload.

Table 21-1 (2 of 2)
ACS Medications
Medication Indications Contraindications
Dosage and
Administration
Side
Effects
Additional
Information
Nitrous oxide Chest pain Patients who cannot
follow instructions, or
who are intoxicated with
alcohol or Drugs
Self-administered:
Patient holds the
mask and inhales.
Accompanying
altered mental status
limits patient’s ability
to continuously self-
administer. Effects
last two to five
Minutes
Decreased
level of
responsive
ness
Use in a well-ventilated
area
Oxygen SpO2 < 4% None in the emergency
setting
2–15 L/min,
administered by nasal
cannula,
nonrebreather mask,
or bag-valve-mask
device
May dry
mucous
membranes
; few side
effects in
acute
setting
Oxygen is combustible.

• ACS treatment (continued)
– Monitor ACS patient closely.
– Reevaluate status of airway, breathing, oxygenation.
– Check pulse for changes in rate, rhythm, or strength;
assess vital signs.
– Reassess level of discomfort and response to
treatment.

• Sudden cardiac death and cardiac arrest
– Lethal cardiac dysrhythmias can occur as first
indication of CAD.
– Ventricular fibrillation
 No cardiac output; patient unresponsive and pulseless
 Only way to reverse is electrical defibrillation.

(continued)
– Automated external defibrillators (AEDs)
 Apply only to unresponsive and pulseless patients.
 Detects ventricular tachycardia and ventricular fibrillation
– Defibrillating patient who is in ventricular tachycardia
with pulse may result in ventricular fibrillation.

(continued)
– Asystole
 Absence of cardiac electrical activity; results in cardiac arrest;
chances of survival slim
– Causes of cardiac arrest other than ACS
 Trauma, stroke, toxins, environmental exposure, metabolic
imbalances

Table 21-2
Possible Causes of Cardiac Arrest
• Hypoxia
• Hypovolemia
• Hydrogen ion (acidosis/alkalosis)
• Hypo- or hyperkalemia (potassium)
• Hypoglycemia
• Hypothermia
• Toxins/tablets (poisoning/overdose)
• Tension pneumothorax
• Tamponade (cardiac tamponade)
• Thrombosis (coronary, pulmonary, cerebral)
• Trauma

Figure 21-24
Left-sided heart failure.

Figure 21-25
Right-sided heart failure.

Heart Failure (1 of 10)
• Heart cannot pump enough blood to meet
metabolic demands of body or it can only do so
when venous pressure is high.
• Heart failure is an end-stage result of many
cardiac diseases.
– Coronary artery disease
– Myocardial infraction

• Occurs as a result of impaired pumping capability
of the heart
– Ventricular contraction or increased afterload
– Blood in ventricle exceeds the amount able to pump
out.
– Blood backs up behind affected ventricle.
– Causing increased hydrostatic pressure
– Fluid leaks out of capillaries to interstitial spaces.
Heart Failure—Pathophysiology

• Pathophysiology of heart failure
– Left-sided heart failure causes pulmonary edema.
– Right-sided heart failure causes peripheral edema.
– Most common cause of right-sided heart failure is
left-sided heart failure.
– Cor pulmonale: right-sided heart failure occurs from
increased resistance in lungs.

• Pathophysiology of heart failure (continued)
– Kidneys become hypoperfused.
 Water retention and increased blood pressure
– Frank–Starling’s law of the heart
 The greater the stretch on myocardial contractile fibers,
the greater the force with which they will contract.

• Pathophysiology of heart failure (continued)
– Mechanisms of compensation
 Chronic vasoconstriction and tachycardia
– Edema
 Increased pressure in vascular system forces fluid out of
capillaries into interstitial spaces.
– Right-sided heart failure
 Jugular venous distention (JVD), congestion of peripheral
veins, and fluid in abdominal cavity (ascites)

• Assessment and management of heart failure
– Worsening of existing failure or acute onset of heart
failure
– May present with hypoperfusion, respiratory distress,
pulmonary edema, and myocardial ischemia

Table 21-3
Findings Associated with Respiratory Distress Help
Increase or Decrease Your Suspicion of Heart Failure
Finding Likelihood of Heart Failure
Sudden onset or increased severity of dyspnea ↑
Onset while reclining or lying down ↑
Edema of ankles and feet ↑
Abdominal distension ↑
Crackling breath sounds ↑
Clear breath sounds ↓
Unilaterally absent, decreased, or abnormal breath
sounds
↓
Cough May ↑ or ↓ depending on characteristics
Pink, frothy sputum ↑
Yellow, green, or brown sputum ↓
Fever, chills ↓
Very high blood pressure ↑
Hypotension ↑
History of heart failure ↑
Recent rapid weight gain ↑

(continued)
– General impression
 Sitting up and struggling to breathe; crackling sounds with
breathing
– Chief complaint
– Additional resources
– Primary assessment
 Risk of compromise to ABCs; altered mental status
 Airway adjuncts, suction, oxygen, CPAP, ventilation by BVM

(continued)
– Need for airway interventions
 Jeopardized by pink frothy sputum
 Best managed by endotracheal intubation and positive
pressure ventilation
 Responsive patients may feel suffocated and only able to
tolerate a nasal cannula.
– CPAP
 Can reduce fluid crossing into alveoli

(continued)
– Secondary assessment
 Responsive
– OPQRST
– Paroxysmal nocturnal dyspnea
– History
• Hypertension, atrial fibrillation
– Vitals
– Focused exam
• Auscultate for crackles; look for edema

(continued)
– Position of comfort
– Oxygen administration, CPAP, and assisted ventilations
 Maintain SpO2 at 95% or higher.
– If patient has chest pain/discomfort, consider ACS.
 Aspirin, nitroglycerin, IV
 Nitroglycerin may be useful even with ACS (follow protocol).
– IV—caution with fluids
– Consult medical control.

• Reassessment
– Continuously reevaluate the components of the primary
assessment.
– Altered mental status
 Confusion, agitation, and decreased level of
responsiveness—indications of progressively poor perfusion
and cerebral hypoxia
– Respiratory effort
 Quickly progress to failure and arrest.
– Circulatory status
 Anticipate possibility of cardiac arrest.

Cardiogenic Shock (1 of 2)
• Left ventricular dysfunction decreases cardiac
output, causing hypotension and poor tissue
perfusion.
– AMI, heart failure, other cardiac problems
• Compensation attempts
– Tachycardia, pallor, cool skin, and diaphoresis
– Inability to compensate causes hypoperfusion of
brain, leading to altered mental status, anxiety, or
unresponsiveness

Cardiogenic Shock (2 of 2)
• Obtain large-bore IV access.
– IV bolus may help increase preload and cardiac output.
Follow protocol.
• Hypotension critical
– Do not delay transport.
– Consider paramedic support to facility with surgical and
cardiac capabilities.

Hypertension (1 of 2)
• Systolic pressure greater than or equal to
140 mmHg; diastolic pressure greater than
or equal to 90 mmHg
• Complications include left ventricular hypertrophy,
heart failure, myocardial ischemia, stroke, aortic
aneurysm or dissection, and renal failure.
• Hypertensive emergency with rapid, symptomatic
increase in blood pressure
– Systolic greater than 160 mmHg, diastolic greater
than 94 mmHg

Hypertension (2 of 2)
• Symptoms
– Hematuria, chest pain, blurred vision, headache,
neurologic changes, pulmonary edema, bounding
pulse, nausea, vomiting, seizures, oliguria, and
epistaxis
• Prehospital care
– Maintain airway, ventilation, oxygenation, and
circulation.
– Nitroglycerin is not used to reduce blood pressure.

Table 21-4 (1 of 2)
Drugs Commonly Prescribed for Patients with
Cardiovascular Disease
Drug Classification Use
doxazosin (Cardura), prazosin
(Minipress)
Alpha-receptor blockers, which block
alpha effects of sympathetic nervous
system
Hypertension
atenolol (Tenormin), metoprolol
(Lopressor), propranolol (Inderal)
Beta-receptor blockers, which block
the beta effects of the sympathetic
nervous system
Angina, tachycardia, hypertension
labetalol (Normodyne, Trandate) Combined alpha- and beta-blocker,
which blocks both alpha and beta
sympathetic nervous system effects
Hypertension
lisinopril (Zestril), enalapril (Vasotec),
captopril (Capoten)
Angiotensin-converting enzyme
(ACE) inhibitors, which prevent
production of angiotensin II, a
hormone that causes vasoconstriction
Hypertension, heart failure
amiodarone (Cordarone), digoxin
(Lanoxin), procainamide (Pronestyl)
Antidysrhythmics Cardiac dysrhythmia suppression;
digoxin also used in heart failure

Table 21-4 (2 of 2)
Drugs Commonly Prescribed for Patients with
Cardiovascular Disease
Drug Classification Use
aspirin, dipyridamole (Permole),
clopidogrel (Plavix)
Antiplatelet drugs Platelet aggregation prevention,
AMI and stroke risk reduction
warfarin (Coumadin) Anticoagulant Blood clotting prevention
diltiazem (Cardizem), nifedipine
(Procardia), verapamil (Covera)
Calcium channel blocker, which
reduces muscle contraction to cause
vasodilation
Angina, hypertension, and
Dysrhythmia
atorvastatin (Lipitor), lovastatin
(Mevacor), simvastatin (Zocor)
Statins, which reduce cholesterol High blood lipid levels for AMI risk
Reduction
hydrochlorothiazide (HydroDiuril),
bemetanide (Bumex), furosemide
(Lasix)
Diuretics, which reduce excess fluid
volume
Hypertension and heart failure
nitroglycerin Vasodilator Angina

Aortic Aneurysm and Dissection
• Aorta
– Responsible for large amount of mechanical stress that
occurs with cardiac contraction
– Elastin is replaced with collagen.
– Aorta becomes narrow and less elastic; systolic blood
pressure increases.
– Sets stage for aortic aneurysm and aortic dissection

Figure 21-26
Aortic aneurysm and aortic rupture.

Aortic Aneurysm (1 of 8)
• Diameter of aorta increases 50% or more from
original size.
• Aneurysm
– Widening greater than 3 to 4 cm
• Abdominal aortic aneurysm (AAA)
– Wall becomes thinner, with risk of rupture.
– Once ruptures, survival unlikely
– Death from uncontrollable hemorrhage

• Risk factors for aortic aneurysm
– Genetic disposition
– Male gender
– Old age
– Bacterial infection
– Atherosclerosis and its risk factors: smoking,
hypertension, inflammation, lipid disease

• Patient may complain of
– Abdominal “fullness”
– Abdominal pain
– Back pain
– Vague gastrointestinal symptoms
• Pulsating mass
• Rapid transport; administer oxygen; initiate IV with
large-bore catheter and blood tubing

Figure 21-27
Aortic dissection. A tear in the tunica intima allows blood to be forced between the
layers of the aorta.

• Aortic dissection
– Tear in tunica intima of arterial wall
– Occurs in ascending thoracic aorta, descending
thoracic aorta, aortic arch, abdominal aorta
– Complications often fatal; diagnosed rapidly
– Obstruction of arteries branching from aorta,
myocardial infarction, renal failure, pulseless
extremities

• Aortic dissection (continued)
– Massive hemorrhage: tunica externa ruptures
– Aortic valve may rupture, leading to heart failure.
– Blood may leak into pericardial sac: cardiac
tamponade.
– Tremendous pain in chest, with “tearing” or “ripping”
sensation

• Aortic dissection (continued)
– Ensure patent airway with adequate ventilation;
administer high-flow oxygen.
– Start large-bore IV at TKO rate.
– Unless hypotension present, do not administer fluids.
– If hypotension present, rupture of adventitia has likely
occurred.

• Heart rate disturbances
– Normal adult heart rate: 60 to 100 beats per minute
– Bradycardia: abnormal stimulation of vagus nerve;
abnormalities in cardiac conduction system (heart
blocks)
– Bradycardia: symptomatic or asymptomatic
– If hypotensive, consult medical direction about
administering fluid bolus.

• Heart rate disturbances (continued)
– Tachycardia: variety of conditions can lead to increase
in heart rate.
– Paroxysmal supraventricular tachycardia (PSVT)
dysrhythmia: palpitations, chest pain, shortness
of breath
– High-flow oxygen; IV in place
– Treated with medications and synchronized
cardioversion

Chapter Summary (1 of 3)
• Ability to survive depends on heart pumping
blood to cells with oxygen and nutrients, removing
wastes.
• Cardiovascular system prone to disease; heart
less effective as pump, damaged blood vessels,
can cause sudden death.
• Acute coronary syndromes from atherosclerosis;
limits or stops flow of oxygenated blood to
myocardium; ischemia and infarction of
myocardium ensue.

• Advanced EMTs can play critical role in improving
survival from cardiovascular emergencies.
• Advanced EMTs have ability to administer
therapeutic medications in initial treatment of ACS.
• When heart damaged by AMI, high blood
pressure, or other mechanisms, it can fail as
pump.

• Two presentations: heart failure, cardiogenic
shock
• Advanced EMTs must recognize these
emergencies, provide initial treatment, and
transport.
• Other cardiovascular emergencies:
– Aortic aneurysm and dissection
– Hypertensive emergencies
– Sudden cardiac death

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