The power point of the CC Cardiology review from LNSC March 2013.

1. Cardiac Review
A&P, EKG, MI, Other Cardiac
Emergencies

2. What is ACS?
• ACS is coronary disease that is causing an
acute illness, inclusive of:
– Ischemia/unstable angina (UA or USA)
– Non-ST Elevation MI (NSTEMI)
– ST Elevation MI (STEMI)
• STEMI and NSTEMI are relatively new
terms; “NQMI” and similar terms are no
longer used
• The term “AMI” is still used and is usually
synonymous with STEMI

3. Epidemiology of ACS
• AMI most common 6am to noon due to
elevated bp, catacholamines and platelet
aggregability
• AMI more common in winter
• >1 million infarcts/500k US deaths per year
• Leading cause of mortality in US
• Annual cost >$120 billion per year

4. STEMI
• Acute phase is <6 hrs from onset
• Immediate transfer to interventional
cardiac cath lab is most effective
treatment!
• Fibrinolytics is also definitive treatment

5. Anatomy, PathoPhysiology

6. Cardiac A&P

7. Layers of the Heart
• 1. Endocardium-inner
• 2. Myocardium-
middle
• 3. Epicardium-outer
• 4. Pericardium-sac
around heart

8. Blood Flow through Heart
• Blood flows from VC
to the R atria.
• It crosses the
tricuspid valve into
the R ventricle.
• It goes past the
pulmonic valve into
the pulmonary artery
and the lungs.

9. Blood Flow cont.
• Blood comes from the
lungs via the pulm.
veins into the L atria.
• It crosses the mitral
valve into the L vent.
• It goes past the aortic
valve into the aorta
and the systemic and
coronary circulation.

10. Heart Valves
**Valve order T-P-M-A**
• Two types: atrioventricular and semilunar.
• AV: Open as the result of lower ventricular
pressure
– Tricuspid and Mitral valves
• Semilunar: Located between the ventricles
and great arteries
– Pulmonic and Aortic

11. Coronary Circulation
• Right and Left coronary arteries originating
at the coronary ostia at the base of the
aorta.
– Left Coronary Artery
• Left Anterior Descending
– Anterior, 2/3 of the septum, partial lateral
wall
• Left Circumflex
– Primary Lateral Wall circulation
– Right Coronary Artery
• Right atrium, right ventricle, inferior &
posterior wall of left ventricle.

12. Anterior Coronary Circulation

13. Posterior Coronary Circulation

14. Properties of Cardiac Cells
• Automaticity
• Excitability
• Conductivity
• Contractility

15. • Polarization: No electrical activity. Inside
of cell negative.
• Depolarization: Na+ rapidly rushes in and
causes inside to become positive.
• Repolarization: Na+ stops and K+ leaks
out as cell returns to resting levels.

16. Conduction System

17. Conduction System in Action

18. SA Node
• Initiates electrical
impulses at a rate of 60-
100 bpm.
• Reaches threshold and
depolarizes more rapidly
than other cardiac cell.
• Blood supply from SA
node artery (from RCA in
55% of hearts).

19. Internodal Pathways
• Anterior
• Middle
• Posterior

20. Atrioventricular Junction
• AV node and Bundle
of His
• Electrical link
between atria and
ventricle

21. AV Node
• Supplied by RCA in 90% of hearts and
LCx in 10%.
• Delays conduction to allow atria to empty

22. Bundle of His
• Dual blood supply from LAD and PDA
• Intrinsic pacemaker rate of 40-60 bpm
• Normally is the only electrical connection
between the atria and the ventricles.

23. Right and Left Bundle Branch
• RBB innervates RV
• LBB innervates the
septum and LV
• LBB has 3 divisions:
– Anterior fascicle
– Posterior fascicle
– Septal fascicle

24. Purkinje Fibers
• Spread from the septum into the papillary
muscles and downward into the apex of
the heart
• Penetrates 1/3 of the way into the ventricle
muscle mass
• Intrinsic rate of 20-40 bpm

25. Electrophysiology
• Depolarization
– Complete depolarization normally results in
muscle contraction
• Threshold
– minimal stimulus required to produce excitation of
myocardial cells

26. Electrophysiology
• Repolarization
– Process of returning to resting potential state
• Sodium influx stops and potassium leaves cell
• Sodium pumped to outside the cell
– Relative refractory period
• cell will respond to a second action potential but the
action potential must be stronger than usual
– Absolute refractory period
• cell will not respond to a repeated action potential
regardless of how strong it is

27. Electrophysiology
Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+
K+ K+ K+
K+ K+
Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+
Myocardial cells are POLARIZED. They have more positive charges
outside than inside.

28. Electrophysiology
Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+
K+ K+ K+ K+ K+
Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+
Stimulation of cell opens “fast” channels in cell membrane. Na+ rapidly
enters cell. Now there are more positive charges inside than outside.
The cell is DEPOLARIZED.

29. Electrophysiology
• Depolarization causes Ca2+ to be released
from storage sites in cell.
• Ca2+ release causes contraction.
Calcium couples the
electrical event of
depolarization to the
mechanical event of

30. Electrophysiology
Na+ Na+ Na+ Na+ K+ Na+ Na+ Na+ Na+
Na+
K+ K+
Na+ Na+
K+ Na+ Na+ Na+ Na+ Na+ K+ Na+ Na+
Cell then REPOLARIZES by pumping out K+ then Na+ to restore
normal charge balance.

31. Electrophysiology
Na+ Na+ Na+ Na+ K+ Na+ Na+ Na+ Na+
Na+
K+ K+
Na+ Na+
K+ Na+ Na+ Na+ Na+ Na+ K+ Na+ Na+
Finally, the Na+-K+ pump in the cell membrane restores the proper
balance of sodium and potassiuim.

32. Cardiac Conduction Cycle
Phase 0 = rapid Na influx
Phase 1 = stop Na influx, K efflux, Cl influx
Phase 2 = Ca influx, K influx Sarcomere:
Phase 3 = stop Ca influx, minimal K efflux, Na Fast Sodium
efflux Channels
Phase 4 = resting membrane potential state

33. EKG Basics

34. What is an electrocardiogram?
• Picture of the electrical activity of the heart
• Used to evaluate/monitor heart rate, effects of
disease, meds, or injury, pacemaker function,
electrolytes, conduction disturbances, mass of
muscle, orientation of heart in chest or presence
of ischemic damage.

35. Leads
• Record of electrical activity between two
electrodes.
• Averages the current flow at a specific
time in a portion of the heart.
• 3 types: standard limb leads, augmented
leads and precordial (chest) leads.
• Each has positive and negative pole.
• The positive electrode is like an “eye”.

36. Leads (cont.)
• If the impulse is moving toward the
positive electrode the waveform goes up.
• If away, the waveform goes down.
• If perpendicular, it will either be biphasic or
a straight line.
• No electrical activity is called the baseline
or isoelectric line.

37. Standard Limb Leads
• Leads I, II, III
• Einthoven’s triangle
• The voltage of I + III =
II

38. Lead I
• Shows lateral surface
of the left ventricle
• Normally is upright
because the impulse
is moving toward the
positive electrode.

39. Lead II
• Views inferior surface
of the left ventricle
• Normally positive
• Commonly used for
monitoring

40. Lead III
• Views inferior surface
of the left ventricle
• Usually the QRS is
positive but the P may
be +, - or biphasic

41. Augmented Limb Leads
• Letters stand for
“augmented voltage
___”
• Only consist of one
electrode on the body
surface
• Negative point is the
center

42. aVR
• Views heart from right
shoulder
• Does not view the
walls of the heart,
only the base and
great vessels
• Normally negative

43. aVL
• Views heart from the
left shoulder
• Views high lateral wall
of the left ventricle
• Usually biphasic
because
depolarization is
perpendicular to the
electrode

44. aVF
• Views the heart from
the left leg
• Views the inferior wall
of the left ventricle
• Should be positive

45. Precordial (Chest) Leads
• View the heart in the horizontal plane
• Each electrode is positive

46. V leads cont.
• V1: 4th ics to right of sternum, septum, negative
• V2: 4th ics to left of sternum, septum, biphasic
• V3: midway between V2 & V4, anterior, biphasic
• V4: 5th ics midclavicular line, anterior, biphasic
• V5: between V4 & V6 @ 5th ics, lateral, positive
• V6: midaxillary line in 5th ics, lateral, positive

47. Horizontal Plane (chest leads)

48. ECG Lead Placement

49. R wave progression
• From V1 to V6 the direction of the QRS complex
should change from negative to positive in a
gradual manner

50. R Wave Progression

51. ECG paper

52. Waveforms

53. Waveforms and Intervals

54. 12 Lead Layout

55. 12 Lead EKG Technique
• Effective contact between electrode and
skin is essential
• Try to exclude artifact
– Internal (larger patients)
– External (60hz noise)
• Precise placement of precordial
electrodes
• Correct patient position

56. Technically Accurate EKG Tracing
• Remember Einthoven’s triangle
• Lead I + Lead III = Lead II
• P waves positive in lead II and negative in aVR
• R waves in V1-V6 should gradually progress
from negative to upright
• Check standardization box before interpreting
the EKG tracing

57. Interpretation of the 12-Lead ECG
• In the limb leads
– P wave is typically upright in leads I, II, aVL
and aVF
– P wave is often biphasic in lead III and is
negatively deflected in lead aVR
• In precordial leads
– P wave is typically upright in leads V5 and V6
– Lead V1 is biphasic, and leads V2 and V4 are
variable

58. Interpretation of the 12-Lead ECG
• Septal depolarization is not always seen
on the ECG. When it is, there will be a
small Q wave in leads I, aVL, V5, and V6.
• The T wave will usually be recorded in a
positive deflection in the same leads that
record a positive deflection in the R wave.

59. Systematic Approaches
• Use the same method of analysis each
time to ensure consistent interpretation.
• Questions to consider when looking for
arrhythmias
– Is the rhythm fast or slow?
– Is the rhythm regular or irregular?
– Are there any P waves?
– Are all P waves the same?

60. Systematic Approaches
• Questions to consider (continued)
– Does each QRS complex have a P wave?
– Is the PR interval constant?
– Are the P waves and QRS complexes
associated with each other?
– Are the QRS complexes narrow or wide?
– Are the QRS complexes grouped or not?
– Are there any dropped beats?

61. Blocks and Axis Deviation

62. Hemiblock
• Block of one of
the two fascicles
of the left bundle
branch system
• Marked axis
deviation often
indicates
hemiblock

63. Trifascicular System
• Part of the electrical conduction system
– Right bundle branch
– Left bundle branch
• Branches into two separate fascicles
• Left anterior hemifascicle (fascicle)
• Left posterior hemifascicle (fascicle)

64. Remember This?

65. Trifascicular System
• Electrical impulse can travel to the
ventricles in three ways:
– Right bundle branch
– Left anterior hemifascicle
• Blood supply from LAD
– Left posterior hemifascicle
– Blood supply from RCA and circumflex

66. Left Anterior Hemiblock
• Anterior hemifascicle of left bundle branch
blocked
– Ischemia, necrosis
• ECG finds:
– Pathological left-axis deviation
– Small Q wave in LI
– Small R wave in LIII
– Narrow QRS possible

67. Left Anterior Hemiblock
Bledsoe/Benner, Critical Care
Paramedic

68. Left Posterior Hemiblock
• Posterior fascicle of left bundle branch
blocked
• ECG finds:
– Pathological right-axis deviation
– Small R waves in LI
– Small Q waves in LIII
– Right ventricular hypertrophy
• Clinically more significant than left anterior
block

69. Left Posterior Hemiblock

70. Clinical Significance of
Hemiblock
• Mortality rate for patients with AMIs with
hemiblocks four times greater than those
without
• Risk factor for complete heart block
– Patient considered high risk if AV block
presents with hemiblock
• In AMI setting, can indicate proximal artery
occlusion

71. Axis
• Definition: axis is the average vector
(direction) of the cardiac electrical impulse
in the vertical plane.
• We are concerned with the QRS axis,
which is the direction of the ventricular
depolarization impulse.

72. Axis
• What does this mean?
– The electrical impulse that depolarizes the
heart travels a certain route thru the heart
– The vertical plane is the one that runs head to
toe when the patient is facing forward
– The average direction the impulse travels in
this plane is the axis
– Simple, right?!

73. Axis
• Measured in degrees
– 0° is at 3 o’clock
– 180° is at 9 o’clock
– Degrees are positive
from 3 o’clock to
9 o’clock in clockwise
direction
– Degrees are negative
from 3 o’clock to
9 o’clock in
counterclockwise
direction

74. Axis Quadrants
• The axis circle is divided into four
quadrants
– Normal= 0° to +90°
– RAD= +90° to ±180°
– LAD= 0° to -90°
– Indeterminate axis= -90° to ±180°
• This makes sense as the normal impulse travels
from SA node to ventricles in a SW direction!
• All quadrants besides normal are “deviated”

75. Rapid Axis and
Hemiblock Determination
• See “Rapid Axis and Hemiblock Chart” on the
next slide.
– Designed to help clinicians quickly determine
presence of axis deviation and hemiblock
• Two ways to use chart
– When cardiac monitor does not provide axis angle:
• Assess LI, II, and III on ECG
• Determine if QRS complex is deflected more positively or
negatively in each lead
• Compare finds to “Rapid Axis and Hemiblock Chart”
– When cardiac monistor provides axis angle:
• Compare monitor readout (don’t trust machine)

76. Rapid Axis and
Hemiblock Determination

77. Thumbs Up/Down Hemiblock
• Useful for quick determination
• Lead I and III – visualize as thumbs of
someone facing you

78. Normal Axis

79. Left Deviation

80. Right Deviation
Bledsoe/Benner, Critical Care
Paramedic

81. Extreme Right Deviation

82. Significance of Axis Deviation
• Shifts away from infarcted tissue
• Left Deviation – Left Hypertrophy, WPW,
Septal defects, Hyperkalemia
• Right Deviation – Right Hypertrophy, Left
Posterior Hemiblock, PE, Atrial defects,
Chronic lung disease
• Extreme Right – V-Tach, Paced,
Anterolateral Infarct

83. Bundle Branch Blocks
• Definition
– Block to the left or right bundle branch system
• Left bundle branch block more clinically significant
– Higher mortality
– Results in wide QRS
∀ >120 ms
• Etiology
– Myocardial ischemia, infarction
– Congenital defects

84. Bundle Branch Blocks

85. Bundle Branch Blocks

86. Bundle Branch Blocks
“Turn Signal Criteria”
• MCL-1, any of the precordial leads can be
used
• QRS must be >120 ms

87. Bundle Branch Blocks
“Turn Signal Criteria”
• Technique
• View the QRS of V1 (or MCL-1)
• Lies immediately over the right ventricle and provides the best
view of the superior aspect of the interventricular septum
• Identify the J point of the QRS
• Draw a horizontal line from the J point either to an
intersecting line of the QRS or to the beginning of the
QRS
• Will produce a triangle pointing upward or downward
• When pointing upward, triangle indicates a right bundle branch block
• When you push a vehicle’s turn signal upward, the signal lights
indicate a right turn
• When pointing downward, triangle indicates left bundle branch block
• When you pull a vehicle’s turn signal downward, the signal lights
indicate a left turn

88. Bundle Branch Blocks
“Turn Signal Criteria”

89. Rate-Dependent Bundle
Branch Blocks
• Bundle blocks appreciated with
tachycardic rhythms
– A-fib
– A-flutter
• Tachycardia results in:
– Increased myocardial oxygen demand
– Decreased preload
• Decreased preload = decreased cardiac output
– Decreased cardiac output can lead to ischemia

90. Rate-Dependent Bundle
Branch Blocks
• Easy to misidentify as VT
– VT therapy could result in rapid hemodynamic
compromise
• MCL-1 useful for differentiating
tachycardia with BBB from VT
– RSR’ complex >120 ms = RBBB, not VT
– QRS >120 ms = LBBB, not VT

91. Chest Pain and MI

92. Coronary Plaques
• Have the consistency
of toothpaste
• Cells within plaque
synthesize and
secrete proteins that
promote clot
formation
• Prone to rupture if
they are large and
have a soft lipid core

93. Coronary Artery Obstruction
• If the clot partially occludes the artery:
– Acute coronary syndrome or unstable angina
• If the clot fully occludes the artery:
– Myocardial infarction

94. Angina
• Stable
– Onset with physical exertion or stress. Lasts 1 – 5
minutes and is relieved by stress.
• Unstable
– Change in Stable angina frequency, quality, duration, or
intensity. Lasts >10 minutes despite rest and/or NTG.
• Variable
– Spontaneous noted at rest (sleeping); relieved by NTG
• Silent
– Asymptomatic with evidence of ischemia
• Mixed
– Combination of the above

95. Types of Infarctions
• Divided into Transmural and non-transmural
MIs.
• Transmural: Extends through full thickness of
the myocardium and includes the endocardium
and epicardium.
• Subendocardial: Damage is limited to the
subendocardial surface.

98. Ischemia, Injury and Infarction –
12 Leads
• Changes usually begin early and progress
• May take more than an hour for changes
to show
• 20-30% of infarcts do not change the
12-lead EKG
-must base diagnosis on labs and
clinical presentation

99. Hyperacute T Waves
• The T wave can become tall and narrow
because of ischemia.
• The first change that might appear is an
upward slanting of the ST segment and a
subtle enlargement of the T wave.
• The hyperacute T waves are localized to
the area of ischemia and infarction.

100. ST-Segment Elevation
• Caused by changes that affect ventricular
depolarization and repolarization
• Non-MI changes can also cause this
condition
– Left BBB
– Ventricular rhythms
– LVH
– Pericarditis
– Early repolarization

101. ST-Segment Elevation
• A persistent ST-segment elevation may
indicate a ventricular aneurysm.
• In benign J-point elevation, the T wave is
clearly distinguished as a separate wave.
• With myocardial disease, the elevated J
point bows upward and merges with the T
wave.

102. J-Point
Point where QRS ends and ST segment begins

103. Sharp and Diffuse J Points

104. Ischemia
• Lack of blood may be due to a decreased
supply or an increased demand
– Causes a delay in repolarization
• ST segment is depressed if it is more than
1 mm below the isoelectric line at .04 sec
past the J-point
• Inverted T waves are always normal in
aVR and may be normal in III and V1

105. Injury
• Injured tissue does not depolarize
completely and remains more positive
than other tissue
• ST segment is elevated more than 1mm
above the baseline at 0.04 sec after the
J-point in 2 or more related leads

106. Infarction
• Q waves must be wider the 0.04 sec &/or
greater than 25% of the height of the R
wave
• Q waves may be normal in III and aVR
• Small Q waves in I, aVL, V5 and V6 are not
infarction but are septal depolarization
• Q waves in the V leads is also known as
poor R wave progression

107. Reciprocal Changes
• Mirror image that occurs when two
electrodes view the AMI from opposite
angles
– Tall, upright T waves
– ST seg depression
– Taller R waves
• May or may not be present and may
indicate more severe damage

108. Evolution of MI

109. Reciprocal Leads and Their
Corresponding Locations

110. Inferior Wall MI
• May involve RV and/or LV
• Usually RCA and sometimes LCx
• Indicative changes: II, III, aVF
• Reciprocal changes: I, aVL
– Sometimes anterior precordial leads

111. Inferior Wall MI

113. Right Ventricular(inferior)
Infarction

114. Inferior MI
• Bradycardia
• Atrial fib
• AV Blocks:
– 1st degree, 2nd degree type I, 3rd degree with junctional
escape mechanism
• Hypotension (treat with fluids)
• Possible NTG, Morphine intolerance
• Hiccoughs, Vomiting, JVD
• Will Have clear lungs
• Possible RV failure (RCA involved)

115. Anterior MI
• Left ventricle
• Involves the LAD
• Indicative changes: V1-4

116. Anterior MI

118. Anterior MI
• Sinus tachycardia
• AV blocks
– 2nd degree II, 3rd degree with ventricular escape
mechanism
• Bundle Branch Blocks
– Beware if RBBB b/c septal arteries are high in LAD
and a lot of muscle has probable been damaged
• LV failure
• Pulmonary edema
• Hypotension is bad sign

119. Lateral Wall MI
• Left Ventricle
• Involves the LCx
• Indicative changes: I, aVL, V5-6
• Reciprocal changes: II, III, aVF

120. Lateral Wall

121. Lateral Wall
• Bradycardia
• Possible junctional rhythms
• Possibly AV Blocks
– 1st degree
– 2nd degree, type I
– 3rd degree, junctional escape mechanism

122. Posterior Wall
• Back of LV
• Generally involves the
LCx but may be PDA
coming off RCA
• Indicative changes: V7-9 (if
you do posterior leads)
• Reciprocal changes: (look
for these as your best
clues)
– Tall R waves in V1-2
– ST depression in V1-2
• Frequently paired with
inferior MI

123. Posterior MI

124. Non-Q wave MI
• Subendocardial MI
• 30% of all MI’s
• Non-specific ST-T wave changes without
Q wave formation
• Usually hemodynamically stable
• Risk of “extension” is significant

125. Serum Cardiac Markers
• CK-MB subfomes for Dx within 6 hrs of MI onset
• cTnI and cTnT efficient for late Dx of MI
• CK-MB subform plus cardiac-specific Troponin
best combination
• Do not rely solely on Troponins because they
remain elevated for 7-14 days and compromise
ability to diagnose recurrent infarction

126. MI Management and Treatment
• Nitrates to improve coronary blood flow;
venous pooling reduces cardiac output, O2
use, and decreased preload.
• Morphine vasodilates and decreases
preload and afterload. Decreases
sympathetic tone causing a decreased HR
and O2 consumption.
• Beta-blockers decrease HR and contractility
and increase diastolic filling time.
• Calcium Channel Blockers produce dilation
of the coronary arteries and collateral
vessels, decreasing contractility and
conduction.

127. Clot Prevention and Destruction
• ASA & G2B3A
– Inhibit platelet aggregation
– Integrilin, aggrastat, repro, plavix, ticlin
• Heparin / LMWH
– Deactivates thrombin and factors IX, X, XI, XII.
– Lovenox
• Fibrinolytics
– Activate plasminogen to plasmin
– TPA, Retavase

128. Thrombolytics
• Indications
– New onset ST segment elevation MI
• Contraindications
– Relative: HTN, recent trauma, pregnancy
– Absolute: Active internal bleeding,
suspected aortic dissection, intracranial
neoplasm, prior hemorrhagic CVA or any
CVA <1 yr old.

129. Angioplasty
• Best outcome if <90 minutes from onset
• Treat chest pain
• Inhibit clotting
• Watch for bleeding and reocclusion post
procedure.
– Leg kept straight
– Head of bed < 30 degrees elevation

130. Other Emergencies

131. Pericarditis
• Inflammation of the pericardium, the
membrane that surrounds the heart
– May cause ST-segment elevation and T-wave
flattening or inversion
– ST-segment and T-wave changes tend to be
throughout all leads of the ECG.
– The T wave usually does not invert until the
ST segment has returned to baseline.

132. Pericarditis
• Diagnostics
– Help determine etiology of pericarditis
– White blood cells
• Elevated in infection
– ESR
• Elevated in infection
– EKG
• Diffuse ST segment changes
• PR segment depression
• Inverted T waves

133. Pericarditis
• Management
– NSAIDs
– Antibiotic therapy

134. Pericardial Effusion
• Pathophysiology
– Abnormal buildup of fluid in the pericardial sac
– Secondary to:
• Pericarditis
• Trauma
– Places pressure on heart, decreases diastolic
filling pressures

135. Cardiomyopathies
• Cardiac disorders whose dominant feature is
pathologic change to the myocardium
• Include:
– Primary cardiomyopathies
• No underlying cause identified
– Secondary cardiomyopathies
• Have demonstrable underlying cause
• Three major categories
– Dilated cardiomyopathies
– Hypertrophic cardiomyopathies
– Restrictive cardiomyopathies

136. Dilated Cardiomyopathy
• Pathophysiology
– Myocardium enlarged, dilated
– All four chambers can be involved
– Often idiopathic
– Toxic, metabolic, infectious factors may be
involved
– Decreased SV, EF = Increased end systolic
volume
– Increased end systolic volume = Increased end
systolic pressure = Dilated chambers

137. Dilated Cardiomyopathy
• Clinical manifestations
– Fatigue, weakness
– Progressive signs and symptoms of CHF
– Right and left side
– S3, S4 summation gallop
– Mitral/tricuspid regurgitation murmurs

138. Dilated Cardiomyopathy
• Diagnostics
– Imaging studies
• Radiograph
– Cardiomegaly
– Pulmonary edema
– Pleural effusion
• Echocardiogram
– Dilated ventricle
– EF <45 percent
– ECG
• Often nonspecific
• BBB, intraventricular conduction delay

139. Dilated Cardiomyopathy
• Management
– Treat heart failure
– Anticoagulants

140. Hypertrophic Cardiomyopathy
(HCM)
• Pathophysiology
– Nondilated, hypertropic left ventricle
– Unknown etiology
– Thought to be genetic
– Asymmetric thickening of septum, ventricular wall
– Asymmetric tension on papillary muscles results in
valvular regurgitation
– Results in:
• Decreased ventricular compliance
• Decreased ventricular end diastolic volume
• Increased pressure gradient

141. Hypertrophic Cardiomyopathy
(HCM)
• Clinical manifestations
– Patients often asymptomatic
– Systolic murmur
– Dyspnea
– Chest pain, angina, palpitations
– Fatigue, weakness, vertigo, syncope

142. Hypertrophic Cardiomyopathy
(HCM)
• Diagnostics
– Imaging
• Radiograph
• Left ventricular hypertrophy
– ECG
• Nonspecific intraventricular conduction
• Bundle branch block
– Echocardiogram
• Decreased left ventricular ejection fraction

143. Hypertrophic Cardiomyopathy
(HCM)
• Management
– Pharmacology
– Beta-blockers
– Calcium channel blockers

144. Restrictive Cardiomyopathy
• Pathophysiology
– Ventricular stiffness leads to diastolic dysfunction
– Resembles constrictive pericarditis
– Progressive limitation of ventricular filling
secondary to endocardial and myocardial lesions
• Scarring
– Reduced cardiac output

145. Restrictive Cardiomyopathy
• Clinical manifestations
– Chest pain
– Dyspnea with exertion
– Exercise intolerance
– Evidence of right ventricular failure
– JVD
– Hepatomegaly
– Ascities
– Anasarca
– Mitral/tricuspid murmurs, S3 and S4 sounds

146. Restrictive Cardiomyopathy
• Diagnostics
– Radiograph
• Pulmonary congestion
– ECG
• Sinus tachycardia
• Atrial fibrillation
• Biventricular hypertrophy

147. Restrictive Cardiomyopathy
• Management
– Fluid restriction
– Diuretic therapy
– Antidysrhythmic therapy

148. Aortic Stenosis
• Pathophysiology
– Opening of aortic valve is narrowed and obstructs
forward blood flow into aorta
– Left ventricle attempts to increase SV and CO
– Results in left ventricular hypertrophy
• Clinical manifestations
– Typically presents with triad of:
• Angina, Exertional syncope, Dyspnea on exertion
– Left Axis Deviation, Left Hypertrophy
• Treatment includes nitrates, diuretics, digitalis,
IABP as bridge to surgery

149. Aortic Regurgitation /
Insufficiency
• Pathophysiology
– Leaking aortic valve
– Rising left ventricular pressures result in:
• Left ventricular dilation, Left ventricular
hypertrophy, Left heart failure
• Presentation
– CHF, Hypotension, Angina, Wide Pulse
Pressure, Corrigan’s Pulse
• Treatment – surgical repair

150. Mitral Stenosis
• Stenotic valve obstructs forward blood
flow from the left atrium into the left
ventricle
• Results in elevated left atrial pressure
• Pulmonary hypertension
– Right ventricle can fail
• Rheumatic fever most common cause
• Clinical presentation
– Exertional dyspnea, orthopnea, fatigue,
malaise, palpable diastolic thrill

151. Mitral Stenosis
• Management
– Treat symptoms of congestive heart failure
– Use diuretics
– Give nitrates
– Treat atrial fibrillation
– Conduct digitalis
– Complete anticoagulation for new-onset atrial
fibrillation
– Intervene surgically

152. Hyperkalemia
• Elevated potassium level (normal 3.5 – 5 mEq/L)
• Diagnostic criteria
– T-wave abnormalities (tall and peaked)
– Intraventricular conduction delays
– P-wave abnormalities (missing or decreased
amplitude)
– ST-segment changes simulating an injury pattern
– Cardiac arrhythmias (predominantly bradycardias)
– Sinusoidal ECG pattern

153. Hypokalemia
• Decreased level of potassium
• Diagnostic criteria
– ST-segment depression
– Slightly decreased amplitude of the T waves
– Minimal prolongation of the QRS interval
– U wave is usually small and follows the T
wave.

154. Hypercalcemia
• Elevated levels of calcium
(normal 8.5 – 10.5 mg/dl)
• Diagnostic criteria
– Shortening of the ST-segment,
which, in turn, shortens the QT
interval
– PR interval may be prolonged
– QRS may lengthen
– T waves may become flat or invert

155. Hypocalcemia
• Reduced levels of calcium
• Diagnostic criteria
– A prolongation of the ST segment that
produces a lengthening of the QT interval

156. Coronary Artery Spasm
• Variant or Prinzmetal’s
angina
• May occur spontaneously
or:
– Exposure to cold
– Emotional stress
– Vasoconstricting meds
– Cocaine
– Smoking
• Mimics MI

157. QUESTIONS?