Cardiovascular II Part 2

Report
Cardiovascular II Part 2
PVC
Premature Ventricular Contraction
2
PVC
Premature Ventricular Contraction
• Premature ventricular contracture
• With a PVC, diastolic volume is insufficient
for ejection of blood into arterial system.
– Therefore, no or weak pulse palpated.
• Few/day = OK, More/minute, the worse (>6).
• Common post MI, SNS activity,  K+,
hypoxia.
3
V-Fib
Ventricular Fibrillation
4
V-Fib
Ventricular Fibrillation
• Ventricle quivers but does NOT contract! 
– NO cardiac output and no pulses
• Cardiac Arrest!!
• Grossly disorganized pattern
5
V-Tach
Ventricular Tachycardia
6
V-Tach
Ventricular Tachycardia
• A bunch of PVC in a row
– Rhythm originates below Bundle of His, in ventricular
muscle.
• It is too fast, so ventricular filling is ineffective and CO is
ineffective
•
•
•
•
Wide, tall QRS complexes
Stops spontaneously or continues
Dangerous rhythm,  diastolic filling time   CO
Can cause Cardiac Arrest
7
Class I Antidysrhythmics
Diagram
8
Class I Antidysrhythmic
Myocardium
& His-Purkinje
System
SA Node &
AV Node
Lehne 5th ed
Figure 47-2
9
Class 1B: Lidocaine
Ventricular Dysrhthmias
10
Class 1B: Lidocaine
Ventricular Dysrhythmias
11
Class 1B: Lidocaine
Effects on the Heart and the ECG
12
Class 1B: Lidocaine
Effects on the Heart and the ECG
1. Blocks Na+ channels slow conduction thru
atria, ventricles, HIS-Purkinje
2. Reduces automaticity
-Slows the heart rate down
3. Accelerates repolarization (shortens action
potential)
•
•
No anticholinergic effect
No change in ECG
– See a restoration of sinus normal
13
Lidocaine
Precautions and Adverse Effects
14
Lidocaine
Precautions and Adverse Effects
• Metabolized by Liver
• Therapeutic range 1.5 – 5.0 microgm/ml
– Pretty narrow
• Adverse CNS Effects
– Drowsiness, confusion, paresthesia
• Toxicity
– Convulsions and respiratory arrest
15
Lidocaine
Administration
16
Lidocaine
Administration
• IV Push
– 50-100mg (1mg/kg)
– Comes in a preloaded syringe
• Infusion
– 1-4mg/min
– Diluted in D5W
• Special Considerations
– Use for as short a time as possible
– Reduce dosage in pts with liver disorders
17
Class III Antidysrhythmics
Potassium Channel Blockers
18
Class III Antidysrhythmic
• Potassium Channel Blockers: Amiodarone
• Approved for V-tach and V-fib.
• Delay repolarization of the ventricles
 Prolongs action potential and refractory period
 Increases PR and QT intervals
- as the QT interval lengthens, the person may develop
additional dysrhythmias
Initial  catecholamine release  brief exacerbation
of dysrhythmias
- Catecholamines speed up the heart and lead to stronger heart beats
block catecholamine release  vasodilation /
hypotension
19
Class III Antidysrhythmic
Myocardium
& His-Purkinje
System
SA Node &
AV Node
Lehne 5th ed
Figure 47-2
20
Non-Pharmacologic
Treatment of Dysrhythmias
21
Non-Pharmacologic
Treatment of Dysrhythmias
•
Cardioversion
– Synchronized,
coordinated shocking
of the heart
– Atrial fib
– V-tach
•
Defibrillation
– A shock that is
delivered as soon as
the buttons are
pushed
– V-fib
22
Automated External Defibrillator
23
Automated External Defibrillator
• Cardiac Arrest, AED “interrogates” rhythm.
– Waits to see what the rhythm is and then
delivers the shock as needed (timed for Vtach and not timed for V-fib.)
• Tells user what to do, eg. “Shock Now”
• Delivers shock for V-tach or V-fib.
24
Implantable
Cardioverter/Defibrillator
25
Implantable Cardioverter/Defibrillator
• Like a pacemaker
• Monitors and analyzes rhythm
• Delivers shock to terminate V-tach, V-fib
26
Radiofrequency Catheter
Ablation
27
Radiofrequency Catheter
Ablation
• Cardiac cath and electrophysiologic (EP) test
• Identify cardiac tissue site which causes
dysrhythmia while in the cath lab
– Map the myocardium
• RF energy delivered to destroy the tissue so
that that focus/area does not fire anymore
– Remember, you can’t pace meatloaf
• Dead myocardium or heart tissue will not
respond to pacing
28
Antidysrhythmic Drugs
Summary
29
Antidysrhythmic Drugs
Summary
• Class I
–Depress phase 0 in depolarization
–Block sodium channels
• Class II (Beta-blockers)
–Depress phase 4 in depolarization
–Block beta 1 & 2 adrenergic receptors
HR
Contractility
30
Antidysrhythmic Drugs: Summary
• Class III (Potassium Channel Blockers)
–Prolong phase 3 (repolarization)
• Class IV (Calcium Channel Blockers)
–Depresses phase 4 depolarization
–Prolongs phases 1 & 2 repolarization
31
Management of
Cardiac Dysrhythmias
32
Management of
Cardiac Dysrhythmias
REMEMBER:
Many drugs used to treat dysrhythmias
also may worsen them
or cause new ones!
33
CORONARY HEART DISEASE
AND
ACUTE MYOCARDIAL INFARCTION
(MI OR AMI)
34
Coronary Circulation
35
Coronary Circulation
• Two main coronary arteries
arise from coronary sinus
(above aortic valve)
– The orifices are above
the aorta
• The heart perfuses during
diastole because it is when
the coronary arteries are
open
• Primary factor responsible
for perfusion of coronary
arteries is BP in aorta
• s aortic pressure ->
s coronary blood flow
36
Coronary Circulation
Diagram
37
Coronary Circulation
Diagram
LV
LV
38
Coronary Arteries
39
Coronary Arteries
• Right coronary artery
– Nourishes right side, SA node, AV node – may lead to
heart block
• Left coronary artery
– A block in the left coronary artery leads to death
because it sends blood to the left side of the heart
and then to the body
– Left anterior descending
– Left circumflex
40
41
ISCHEMIC HEART DISEASE
A.K.A CORONARY HEART DISEASE
A.K.A CORONARY ARTERY DISEASE
ANGINA
42
Coronary Heart Disease
43
Coronary Heart Disease
• Heart disease caused by impaired coronary blood
flow (atherosclerosis)
• Cause angina, dysrhythmias, conduction defects,
heart failure, sudden death, myocardial infarction
(“heart attack”)
• If blood flow is temporarily inadequate (due to
increased oxygen demand), ischemia produces pain
(angina).
• Myocardial Infarction is myocardial cell/tissue death
due to oxygen starvation
44
Assessment of Coronary
Blood Flow
45
Assessment of Coronary
Blood Flow
• ECG
• Exercise Stress Testing
• Pharmacologic Stress Testing
– May give catecholamines, such as
epinephrine, norepinephrine
• Nuclear Imaging
• Cardiac Catheterization /Coronary
angiography
46
Collateral Circulation
47
Collateral Circulation
• With gradual occlusion of large coronary
vessels, the smaller collateral vessels  in size
and provide alternative channels for blood
flow
– Allow perfusion to the myocardium that is below
and is distal to the blood flow
• One of the reasons CHD does not produce
symptoms until it is far advanced is that the
collateral channels develop at the same time
the atherosclerotic changes are occurring.
48
Collateral Circulation
Diagram
49
Collateral
Circulation
Diagram
50
50
Pathogenesis of CAD
Atherosclerosis
51
Pathogenesis of CAD
Atherosclerosis
• Most common cause of CAD
• Plaque disruption is most the frequent
cause of MI, sudden death
• Can affect one or all three major
coronary arteries/branches
52
Plaque
53
Plaque
• Plaques typically do not occlude the whole
coronary artery but produce a narrowing that
restricts blood flow.
– In times of increased oxygen demand, such as with
exercise, the restricted blood flow may produce
ischemia in cells supplied by that artery.
– This produces the pain of angina.
54
Plaque Rupture
55
Plaque Rupture
• A plaque may become unstable and rupture,
causing a clot to form which may completely
occlude the artery.
– Results in no bloodflow
– Occlusion of the artery causes death of the cardiac
cells downstream that are supplied by that artery.
– When the cells die, that is an infarction – hence the
name myocardial infarction.
– Have about 90 minutes to restore the blood flow to
prevent permanent damage
56
Atherosclerosis in Coronary
Artery
57
Atherosclerosis in Coronary Artery
Plaque rupture and disruption of atheroma 
 lipid core/contents exposed to blood
 platelet aggregationcoagulation cascade
 fibrin clot
Give aspirin quickly to prevent or reduce the
clotting
 thrombosis, vasospasm
 myocardial ischemia
 Coronary arteries unable to supply blood to
meet metabolic demands of the heart
58
Angina
59
Angina
• Angina: symptomatic paroxysmal chest
pain or pressure sensation associated with
transient myocardial ischemia
60
Stable Angina
61
Stable Angina
• Occurs with exertion or stress
• Predictable
• If plaque becomes unstable and ruptures, it
leads to platelet aggregation and unstable
angina
62
63
Variant or Vasospastic Angina
64
Variant or Vasospastic Angina
• Occurs during rest or with minimal activity
(nocturnal, Prinzmetal’s)
65
Silent Myocardial Ischemia
66
Silent Myocardial Inschemia
• Occurs in the absence of anginal pain
– Tend to be endocardial, in the inner layer of the
myocardium
67
Unstable Angina
68
Unstable Angina
• Symptoms at rest lasting >20 minutes
• Marked limitations of ordinary activity
(walking 1–2 blocks, climbing a flight of
stairs)
• Recent acceleration in anginal signs, not
responsive to nitroglycerine
69
70
Acute Myocardial Infarction
71
Acute Myocardial Infarction
• Acute myocardial infarction (STEMI or NSTEMI)
– ST segment elevation myocardium infarction
• STEMI - complete occlusion of bloodflow
– Significant change on the EKG
• NSTEMI – partial occlusion of a blood vessel by a
thrombus
72
73
74
Characteristics of Plaque Rupture
75
Characteristics of Plaque Rupture
• Spontaneous
– SNS activation BP,  HR,  contraction
– Triggering event (stress: emotional, physical)
• Diurnal
– Plaque rupture is more common in the first hour of
arising
– SNS “surge” on arising
• SNS major player
– Beta-adrenergic blockers
• Block the adrenergic response so the patients will not
have the same response to a SNS surge
76
“Severe” Coronary Stenosis and
Vulnerable Plaques Co-exist
77
“Severe” Coronary Stenosis and Vulnerable
Plaques Co-exist
Califf, Atlas of Heart Diseases 2001
78
Ischemia, Injury, and Infarction
79
Ischemia, Injury, and Infarction
Three Zones of Damage
• Infarction = Necrosis
– MI, dead cells
– Beyond hope of recovery but can
stop in from increasing
• Injury
– Some recovery possible
• Can still perfuse it and restore it to
become viable
– Not dead yet
• Ischemia
– Full recovery possible
• Do not want the patient to extend
the size of the infarct
– Increase oxygen
– Decrease the demand on the
heart
80
Zones of Tissue Damage
81
Zones of Tissue Damage
Goal is to limit the area of
necrosis (infarction) !
• Necrotic myocardial cells
are gradually replaced with
scar tissue
• Scar tissue cannot contract
or conduct action potentials,
cannot respond to drugs or
pacing
82
An Acute MI (AMI) Leaves Behind
an Area of Yellow Necrosis
83
An Acute MI (AMI) Leaves Behind an
Area of Yellow Necrosis
84
Pathologic Changes in Zones of
Injury
85
Pathologic Changes in Zones of
Injury
• Ischemic areas cease to function within
minutes
• Irreversible damage/death to myocardial
cells occurs within 20-40 minutes
• Early reperfusion (20min) after onset of
ischemia can prevent necrosis, prevent
further ischemia and necrosis
86
Extent of the Infarct
87
Extent of the Infarct
Extent of infarct depends on :
• Location
• Extent of occlusion
• Amount of heart tissue supplied by vessel,
duration of occlusion
• Metabolic needs of the affected tissue
• Extent of collateral circulation
– A couch potato will probably have a lot
more collateral circulation
88
Types of Infarct
89
Types of
Infarct
• Transmural infarct
– Full thickness of ventricular
wall,
– Occurs with obstruction of a
single artery;
– May involve RV, LV and/or IV
septum
• Subendocardial infarct
– Involve inner 1/3 to 1/2
ventricular wall,
– May occur with severely
narrowed arteries or with
occlusion of a very small
artery
Porth, 2007, Essential of Pathophysiology, 2nd ed.,
Lippincott, p. 328.
90
Types of Coronary Heart Disease
91
92
Chest Pain Assessment
93
Chest Pain Assessment
• P – Provocation
• Q – Quality
– Tell me about it...
– Describe the pain
• R – Region/Radiation
• S – Severity
• T – Timing
– Does it occur at night or during the day
– Predictability
94
Categories (PQRST)
95
Categories (PQRST)
 risk
for
MI
• Angina that occurs with stress
(physical/emotional)
– Relieved within minutes by rest
or NTG (nitroglycerine)
• Angina that occurs with rest
• Is of new onset
• Increasing intensity
96
Chronic Ischemic Heart Disease
97
98
Stable Angina
99
Stable Angina
• Fixed coronary obstruction
• 02 Demand   02 supply pain
– Physical/emotional stress, cold
• Provoked by stressor
– Relieved with rest/NTG (nitroglycerine)
• Not everyone with CHD has angina
– Sedentary lifestyle (couch potatoes), development
of collateral circulation, altered perception pain
100
Locations of Angina
101
Angina
Usual distribution
of pain
Less common sites of pain distribution
Typically precordial, substernal
102
Variant or Vasospastic Angina
103
Variant or Vasospastic Angina
• “Prinzmetal’s angina”
– Comes and goes without any predictability
• Due to coronary artery spasms
• Occurs during rest or with minimal exertion,
frequently nocturnal
• Mechanism is uncertain
– Possibilities may include SNS activation, VSM
Ca++ channel dysfunction, imbalance of
endothelial cell vasodilating/constricting
substances
• Dysrhythmias can occur
104
– Person usually aware; High risk sudden death
Variant or Vasospastic Angina
Diagram
105
Variant or Vasospastic Angina
Diagram
A 38-year-old man was scheduled to undergo invasive coronary angiography after cardiac
scintigraphy revealed silent ischemia of the anterior myocardial wall
Hamon M and Hamon M. N Engl J Med 2006;355:2236
106
Acute Coronary Syndrome (ACS)
107
Acute Coronary Syndrome (ACS)
Unstable or
ruptured plaque
NSTEMI
STEMI
108
Acute Coronary Syndrome
(ACS)
Unstable Angina
109
Acute Coronary Syndrome (ACS)
Unstable Angina
110
Unstable Angina
•
Severe
•
Clinical syndrome of myocardial ischemia
ranging between stable angina and MI
•
Usually due to atherosclerotic plaque
disruption, platelet aggregation
111
Presentations of Unstable Angina
112
Presentations of Unstable Angina
1. Symptoms at rest (> 20 minutes)
2. Severe, frank pain, new onset (< 1month)
- Pain crescendos
3. More severe, prolonged, or frequent
113
Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 392.
114
Acute Coronary Syndrome (ACS)
ST-segment Elevation
115
Acute Coronary Syndrome (ACS)
ST-segment Elevation
116
ST Segment Elevation
117
ST Segment Elevation
• ST segment elevations are
indicative of myocardial
damage or ischemia.
• It may take some time
(minutes to hours) for the
changes to show up, and
they may not be present in
all EKG leads.
– The placement of the
leads and the
occurrence of ST
elevation indicates
where the MI is
occurring
Porth, 2007, Essentials of Pathophysiology, 2nd ed.,
Lippincott, p. 394.
118
ECG
STEMI vs. NSTEMI
119
ECG
STEMI vs. NSTEMI
120
Non ST Segment Elevation
Myocardial Infarction (NSTEMI)
121
Non ST Segment Elevation Myocardial Infarction
(NSTEMI)
• How is this different from unstable angina or STEMI?
• Unstable angina, plaque disruption but no thrombus or
occlusion of the coronary artery, therefore no myocardial cell
death (no MI).
• NSTEMI, a thrombus partially occludes a coronary artery.
Depending on the degree of occlusion and oxygen demand of
downstream heart cells, there may be myocardial cell death
(an MI) but insufficient to produce ST segment elevations.
• The patient may not have unstable angina
• The amount of the infarction depends on how much blood flow is
getting through
122
Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 392.
123
ST Segment Elevation MI
124
ST Segment Elevation MI
• Characterized by ischemia of cardiac tissue
• Area of infarction is determined by the
coronary artery that is affected and by its
distribution of blood flow
– 40-50% of time – LAD
• Influences CO, BP, and likelihood of
survival or death
– 30-40% of time – RCA
• Will see blocks on the EKG due to SA
node or AV node dysfunction
– 15-20% of time - LCA
125
Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 392.
126
Diagnosis of CHD and MI
127
Diagnosis of CHD and MI
• Good history and identification of risk
factors
• R/O Other causes of CP, such as GERD
• ECG
• Serum myocardial markers
• Stress testing
–May be exercise or pharmacological
• Cardiac catheterization
128
“Classic” Manifestations of MI
129
“Classic” Manifestations of MI
• Abrupt onset or progression of unstable,
non-ST elevation, which then moves to
become ST elevation
• Pain is severe, crushing, “someone sitting
on my chest”
• Radiates to left arm, jaw, neck
• MI pain is prolonged, not relieved by rest
and/or NTG (unlike angina)
• N/V, SNS activation   HR,  RR,
diaphoresis, cool/clammy skin
130
ECG Changes
131
ECG Changes
• T wave inversion
• ST segment elevation
• Abnormal Q wave
(may not appear immediately)
– Wider and bigger where the MI
is present
• Once a QI develops, it does
not ever go away
• Changes can occur over
time, depending on duration
of ischemia (extent and
location)
• Changes may not be present
in all leads – take 12-lead
EKG
– Will only be present over
the area that is infarcted
132
ST Segments
133
ST Segments
• 1st to change during
ischemia or MI
because myocardial
repolarization is
altered.
• Ischemia reduces
membrane potential
and shorten duration
of AP in ischemic
area.
134
Abnormal Q Waves
135
Abnormal Q Waves
• Develop because
there is no
depolarizing current
conduction from
necrotic tissue
• May not appear
immediately
• Diagnostic of MI
• Q waves are
permanent after MI
136
Serum Markers for Ischemia and
MI
137
Serum Markers for Ischemia and MI
• Necrotic cells release intracellular enzymes into
blood stream
• Measure these in blood
– The larger the number, the larger the amount of
necrotic tissue
– CK-MB (Creatine-kinase-myocardial bands)
– Troponin
– C-reactive Protein
• An inflammatory marker
138
CK-MB
139
CK-MB
• CK is normal in all muscle cells
–Has three isoenzymes BB, MM, MB
• CK-MB Creatine kinase -myocardial bands
is cardiac specific
• Elevated within 8 hours after MI
• Returns to normal in 2-3 days
• Nl ~ 24-195 IU/L
140
Troponin (TnC, TnI, TnT)
141
Troponin (TnC, TnI, TnT)
• Very cardiac specific
– Most sensitive marker
• Part of the actin-myosin filament
• Elevate more quickly than the CK-MB
– Rises within 3 hours after MI
– Remains elevated 3-4 days and up to 10 days
• Diagnostic of MI; No change with ischemia
• Nl ~ 0.4 ng/ml
142
C-Reactive Protein (CRP)
143
C-Reactive Protein (CRP)
• Marker of chronic inflammation
• May be a marker of risk
• Identifies people before they are
symptomatic
• May guide preventative therapy in the
future
• Non-specific because it increases with
any inflammatory response
144
Timeline of Cardiac Markers
145
Timeline of Cardiac Markers
Troponin
CK-MB
Hr 1 2 3 4 5 6 7 8 9 10 11 12 Day 2 3 4 5
146
Acute Coronary Syndrome
Concept Map
147
ACS
No ST Elevation
Unstable Angina
Pain is severe
No ECG s
No change in markers
because they are not
having an MI
STEMI
NSTEMI
Unstable angina
No ECG s
Elevation of serum markers,
including troponin and CKMB
148
Infarction
Diagram
149
150

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