4/6/2013

Cardiac Blood Flow

Beth Torres, PhD, RN, CCRN

CJW Medical Center

Events during Diastole

Events during Systole

Remember:
The cardiac muscle gets its perfusion during diastole.
Perfusion is determined by coronary perfusion pressure
Coronary Perfusion Pressure = Diastolic BP PCWP
3
Normal: 60 -80 mmHg

During systole the cardiac muscle has to overcome

the pressures ahead of each chamber:
The right ventricle meets low to no pressure in the lungs.
The left ventricle must overcome the diastolic pressure in the
4
aorta.

Compensation for Decreased Cardiac Output

Hemodynamics
Cardiac Output = HR x Stroke Volume (SV)

cardiac output heart rate.

Heart rate is controlled by stimulation of
both the sympathetic and
parasympathetic nervous system
Heart Rate

Normal Cardiac Output:

4-8liters / minute

Preload
Afterload

Cardiac Output
Stroke Volume

Contractility
Muscle Synchrony
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Stroke Volume (SV)

Preload
The force on the ventricle during relaxation (diastole)
Primary determinant is the volume of blood filling the
ventricle
Right Ventricle = RVEDP (Right heart preload):
Right Atrial Pressure (RAP); CVP
Normal values: 2-6mmHg

Stroke Volume- the amount of volume ejected

by the ventricle with each systolic contraction

OR, amount of blood ejected by the heart with
each beat
Normal: 60-130ml
SV = (CO/HR) x 1000

Left Ventricle = LVEDP (Left heart preload):

PCWP, PAWP, or PAOP
Pulmonary Artery Diastolic (PAD)
Left Atrial Pressure (LAP)
Normal values: 8-12mmHg

Contractility

Afterload

Defined as the squeezing force generated by the

ventricles.

Afterloadthe ventricular force or pressure

required to overcome impedance to ejection.
As impedance , ejection velocity and SV ,
while ventricular workload & O2 consumption

Refers to both the pressures of this ejection and the

amount of blood ejected.

Manipulate with inotropic drugs

Systemic vascular resistance (SVR): Left

Normal SVR: 900-1400 dynes /sec/cm-5

Best global measure is CO

Pulmonary vascular resistance (PVR): Right

Normal PVR: 50-250 dynes /sec/cm-5

Normal ejection fraction is 50 70 %

9

Cardiac Index

10

Supply

Cardiac Indexa more precise expression of CO,

which takes into account the patients size

Normal CI = 2.5-4.2 L/min

CI < 2.0 is considered cardiogenic shock

1.8-2.2 is low perfusion

Calculate:
CI =

&

Demand

Coronary artery patency

Diastolic filling time
Diastolic pressure
Hemoglobin
Arterial oxygen saturation
Oxygen extraction by the

tissue

Heart rate
Preload
Afterload
Contractility
Oxygen Demand

Oxygen Supply

CO

BSA
11

Heart

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Factors of SvO2 & ScvO2

SVO2
SVO2 amount of oxygen in the mixed

venous blood in the pulmonary artery

Normal SVO2: 70-75% (range 60-80%)
An estimate of the amount of oxygen
returning to the cardiopulmonary circulation
Reflects the patients ability to balance O2
supply and demand at the tissue level

SaO2

O2 Tissue
Consumption

CO

Hgb

13

Oxygen Delivery

Question

SvO2 = 75%

SaO2 = 100%

Venous
Return

Oxygen
Consumption

14

25%

Arterial
Oxygen
Delivery

Which of the following is a normal

compensatory response to a decrease in
cardiac output?
a. Increased oxygen delivery
b. Decreased oxygen consumption
c. Increased oxygen extraction
d. Decreased serum lactate

The Cell
15

Cardiac Assessment

16

Arterial Waveform

Hemodynamic Monitoring

Systolic Ejection (A)

Peak of waveform
Normal 90-140

ECG Interpretation

Diastole (C)
Lowest portion of waveform
Normal 60-90
Dicrotic Notch (B)
Closure of Aortic valve

Heart Sounds

17

A
B

C
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Review: Right Atrial Waveform

Peripheral Arterial Waveform

The PA catheter is threaded manually to the

right atrium. A continuous pressure reading
will demonstrate a CVP /RA waveform
Normal RA:
2-6 mmHG

19

Preload
What Decreases:
Hypovolemia
Position Change
Vasodilation
Right Heart Damage
Atrial Arrhythmias
Pericardial Effusion

20

CVP waveform
Pressure measurement is taken from

What Increases:

the a waveform (mean) at endexpiration

Normal RA/CVP: 2-6 mmHg

Vasoconstriction
fluid volume
ventricular filling

time
Bradycardia

PEEP
Tension

Pneumothorax
21

22

Pulmonary Artery Waveform

Right Ventricular Waveform

As the PA catheter floats through the pulmonic valve and

The RV is very irritable and ectopy is a potential

complication during PA catheter insertion
Watch the monitor closely for Ventricular
Tachycardia

into pulmonary circulation, the pulmonary systolic pressure

remains similar to RV systolic pressure
The catheter should stay here during continuous
monitoring.
Normal PA:
Sys: 20-30 mmHg
Dia: 5-10
Mean: 10-20

Normal RV:
Sys: 15-30
Dia: 2-6 mmHG

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Phlebostatic axis

Pulmonary Capillary Wedge Pressure

Advance until it becomes lodged in a
pulmonary artery slightly smaller at
than the inflated balloon.
No blood flows distal to the catheter
tip.
This pressure, the pulmonary artery
occlusion pressure (POAP), reflects
LV pressure when the mitral valve
is open.
Resembles CVP waveform. The a
wave falls later in the T-P cycle.

Head of the bed can range from flat to 60 degrees

PA pressures may be significantly different in patients

Normal PCWP:
4 12 mmHG

in a lateral position.
Allow 5 minutes for stabilization after changing the

patients position

The PCWP should be 1-4 mmHG

lower than the PAD.
IT SHOULD NEVER BE HIGHER!
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26

Technical Factor:
Mechanical Ventilation

Technical Factors:
Effect of Patient Respirations
If the patient is on a mechanical ventilator, the
positive pressure pushes up the PA tracing.
Ventilator Valleys
A PEEP > 10 will artificially elevate PA pressures
If patient is breathing spontaneously, the negative
pressure pulls down the PA tracing. Spontaneous
sky

The most accurate reading is obtained at respiratory

end expiration.
27

Technical Factor:
Spontaneous Respirations

28

Afterload

Normal SVR = 900-1400 dynes/sec/cm3

SVR = MAP-CVP x 80
CO
MAP = systolic BP + (2) diastolic BP
3
Example:

29

BP = 120/80 (93)
CVP = 5
CO = 5
SVR = [(93 5) / 5] x 80 = 1406
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ECG Monitoring

Pulmonary Vascular Resistance (PVR)

Pulmonary Vascular Resistance (PVR)

Treatment of Significant Arrhythmias

reflects blood flow through the pulmonary

circulation
The resistance is influenced by the
pulmonary capillaries & arteries
Normal PVR = 50-250 dynes/sec/cm
PVR = MPAP-PCWP x 80
CO
31

Conduction System

32

Refractory Period

33

Premature Ventricular Contractions

KEY CONCEPT: An electrical stimulus landing on

the T wave, may cause disorganized ventricular
contractions OR VENTRICULAR FIBRILLATION34

Question
The cardiac monitor shows the rhythm below
for your patient. Which of the following
medications might the physician order?

The complexes have a QRS > .12 seconds.

Significance:
PVCs can occur in healthy persons with normal hearts and no
apparent cause.
Patients can be asymptomatic or feel racing heart / skipped
beats.
Frequent PVCs increase risk of fatal arrhythmias x 5.
Treat: More than 6/min, multi-focal, R on T configuration
35

a. Atropine
b. Adenocard
c. Cardizem
d. Amiodarone

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Amiodarone

A patient with which of the following is at

greatest risk for torsades de pointes?

Dosage:
Non-VT/V.fib: 150 mg IV over 10 min.
Pulseless VT/V.fib: 300mg IV bolus

a. Depressed ST segment
b. Tall, tented T waves

Adverse effects:
Hypotension and bradycardia are common
during initial bolus.
May be prevented by slowing the rate of
infusion.

c.

Prolonged QT interval

d. u-wave

37

Second Line Drug: Lidocaine

38

Too Fast

Administration:
Bolus: 1.0-1.5 mg/kg IVP; may repeat in 5-10

minutes to max of 3mg/kg

Infusion: 1-4 mg/min

Does not prolong QT

Adverse effects:
Confusion (most common), seizures,

tremors.

39

Sinus Tachycardia

40

Supraventricular Tachycardia

Rate: 100-150 bpm

Significance:
If very fast, the heart cannot refill & results

in CO

This tachycardia originates above the ventricles, but

below the SA node.
Characteristics:
Rate: Rapid! Usually 160-250. May start / stop abruptly.
QRS is normal looking.
No bizarre, early, or late beats.

TREAT THE CAUSE!

Too fast to see a P wave.

Significance:
Must treat if prolonged
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Atrial Flutter

SVT Treatment

Significance:
Consider this a hazardous rhythm because it can
suddenly change to a rapid ventricular response.

Try VAGAL maneuvers.

If not effective, administer:
ADENOSINE
Indicated for stable SVT
unresponsive to vagal maneuvers.
Dose: 6 mg IV PUSH
12 mg IV PUSH
12 mg IV PUSH

If patient is stable, no initial treatment.

If ventricular rate is rapid, treatment is required.

Adenosine depresses sinus & AV node activity.

HALF LIFE: 10 seconds

Not effective in ventricular rhythms.

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44

Atrial Fibrillation

Question

R-R interval is always irregular

Significance:
If stable or chronic may be tolerated.
If patient has symptoms, treatment will be
required.
Consider hazardous because ventricular rate
can suddenly .
Also lose atrial kick, which is 20% of the CO

A 69-year-old patient presents to the ED with

complaints of palpitations and irregular heart
beats for the last three of days. The cardiac
monitor shows atrial fibrillation, a heart rate of
136 beats/min. His blood pressure is 124/76 mm
Hg. Which of the following medications would
the physician likely order?
a.
b.
c.
d.

Lidocaine
Cardizem
Corvert
Adenocard

45

46

To Control Rate,
Use Selective - Blockers

Irregular Narrow Complex

Tachycardia: Control of Rate

Non-Selective:
Propranolol (Inderal)
Nadolol (Corgard)

Rate can be controlled by:

Selective agents:

Beta Blockers
Calcium Channel Blockers
Amiodarone *

Atenolol (Tenormin)
Betaxolol (Zebeta)
Metoprolol (Lopressor)

Vasodilatory, Non-selective
Labetalol (Normodyne)

*Not considered a first line

agent for narrow complex
tachycardias

Carvedilol (Coreg)

Shortest half-life:
Esmolol
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Ventricular Tachycardia

To Control Rate:
Use Calcium Channel Blockers

Wide & bizarre QRS (> .12 sec)

Significance:

Slows AV node conduction & prolongs AV

nodal refractoriness

Treatment is REQUIRED
Pulse or NO Pulse?
Pulse & STABLE? Use AMIODARONE
Pulse & UNSTABLE
ELECTRICAL CARDIOVERSION

Example: Diltiazem
Do not use in:
Drug-induced tachycardia
Heart blocks
Concurrent use of Beta blockers.
49

Question

50

Electrical Cardioversion

The nurse should perform which of the

following interventions for a patient
with chest pain, hypotension, and
tachycardia at a rate of 180 beats/min?
a. Administer amiodarone 150mg IV over 10
min
b. Administer adenosine 6 mg rapid IVP
c. Perform synchronized cardioversion
d. Defibrillate with 300 joules

Immediate electrical cardioversion is indicated

for a patient with serious signs & symptoms
related to tachycardia.

51

Synchronized Cardioversion:
Energy Selection

52

Synchronized Cardioversion:
Energy Selection
If the rhythm does not change, recharge to 200 joules
& repeat

Start with 100 joules.

Repeat with 300 joules & 360 joules, if needed.

Complications include:
Deterioration into ventricular fibrillation
Embolization of a thrombus

Push the Synch button!

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Synchronized Cardioversion:
Pre-Medication

Too Slow

For awake, alert patients who are hemodynamically

stable, pre-medicate with both a sedative and a
analgesic
Sedatives

Diazepam
Midazolam
Etomidate

Analgesics

Fentanyl
Morphine
Merperidine

Watch for apnea &

hypoventilation after
sedation.
Frequent vital signs are
required before
& after cardioversion
55

3Heart Block

Sinus Bradycardia
Characteristics:
HR > 60
All intervals within

normal limits
except rate

56

Significance:

PREPARE TO PACE!

May be normal in

New guidelines:
chronotropic drips

healthy, young
patient.
Treat symptomatic
bradycardias!

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58

Temporary Pacemakers

Symptomatic Bradycardia
Treat Bradycardia with BRADE

Use an external generator. 3 types:

Atropine: 0.5 mg IV push

Transcutaneous

Repeat every 3 5 min to total of 0.04 mg/kg (3 mg)

Dopamine: 2 to 10 mcg/kg/min

Transvenous

Epinephrine gtt: Start at 1 mcg/ min and titrate

to patient response.

Epicardial

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60

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Transcutaneous Pacemaker

Transvenous Pacemaker
Epicardial Pacemaker

Temporary
Generator

Epicardial Pacemaker
Lead Placement

Transvenous Pacemaker
Lead Placement
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62

The NASPE/BPEG Generic (NBG) Code

External Pacing
Position

Category Chamber(s)
Paced

Pacing producers an electrical artifact on

the strip called a spike.

QRS appears wide & bizarre (like a PVC)

II

III

IV

Chamber(s)
Sensed

Response to
Sensing

Programmability
Rate Modulation

Antitachyarrhythmia
Function(s)

O = None

O = None

O = None

O = None

O = None

A = Atrium

A = Atrium

T = Triggered

P = Simple Programmable

P = Pacing

V = Ventricle

V = Ventricle

I = Inhibited

M = Multiprogrammable

S = Shock

D = Dual (A+V)

D = Dual (A+V)

D = Dual (T+I)

C = Communicating

D = Dual (P+S)

R = Rate Modulation
Manufacturers
Designation
Only

63

S = Single
(A or V)

S = Single
(A or V)

Note: Positions I through III are used

exclusively for antibradyarrhythmia
function

64

Sensitivity

Pacing Codes
VVI

the number,
sensitivity(more sensitive)

Pacing in Ventricle only

Sensing in Ventricle only
Response will be inhibited if it senses activity
in the Ventricle

65

5.0v

2.8v

1.4v

66

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Loss of Capture

Troubleshooting

Electrical stimuli delivered by

the pacemaker does not initiate depolarization of
the atria or ventricle

Failure to capture
Improper Sensing
Loss of Output

Atrial

No capture

Ventricular

No capture

Fusion

67

68

Undersensing

Failure to Capture

Failure of the pacemaker to sense

intrinsic R-waves or intrinsic P-waves
Leads to OVER PACING
69

Undersensing: Causes

70

Undersensing

Battery depletion
Decreased QRS voltage
Fusion beat
Dislodged/fractured lead
Inappropriate sensitivity setting
What to do:
Increase the sensitivity by
lowering the number
(lower the fence)
71

72

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Oversensing

Oversensing

Inhibition of the pacemaker by events the

pacemaker should ignore

What to do:
Eliminate interference
Adjust sensitivity: Make less sensitive by
increasing the number (raise the fence)

Leads to UNDER PACING

73

No Output

74

OH, NO!

Pacemaker fails to emit stimuli at the

programmed intervals

Battery depletion/pacemaker off

Faulty cable connection

Oversensing

Dislodged/fractured lead
75

Ventricular Fibrillation

76

Defibrillation
Energy Requirements for adults:
If using a biphasic defibrillator:
150- 200 joules initially
For second and subsequent shocks, use
the same energy or higher
If using a monophasic defibrilators:
Select a dose of 360 joules for all shocks

Significance:
Requires immediate defibrillation & CPR!
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Epinephrine:

Epinephrine

Special considerations / Cautions

Administer 1 mg (10 ml of 1:10,000)

every 3 5 minutes

May be given via ETT

Instill 2 to 2.5 mg into ETT

Stimulation of alpha adrenergic receptors:

peripheral vasoconstriction & coronary

& cerebral blood flow

If given IV, be sure to flush with 20 ml of

fluid or elevated arm

High doses have not been shown to

improve survival

Makes ventricular fibrillation more

responsive to defibrillation

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80

Pulseless Electrical Activity

Vasopressin

Any organized rhythm that DOES NOT PRODUCE

Can be substituted for the first or second dose of

epinephrine

A PULSE.
Characteristics: Variable

Give 40 units IV bolus.

Significance:

Immediate CPR is required.

Look for possible reversible causes.

Effects:

Coronary perfusion pressure

Vital organ blood flow
Cerebral oxygen delivery

81

Asystole

82

PULSELESS ARREST / ASYSOLE

Treat PEA with P-E-A:
Possible Causes
Epinephrine
Atropine (old)

Continue CPR and administer:

Epinephrine 1 mg IV, every 3 5 minutes
Atropine 1 mg IV, every 3 5 minutes
83

(up to 3 doses) (OLD guideline)

84

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PULSELESS ARREST / ASYSOLE

Therapeutic Hypothermia

No electrical therapy is indicated.

Move quickly to identify reversible causes:
Hs:
Hypothermia,
Hypoxemia,
Hypoglycemia,
Hypovolemia,
Hydrogen ions
(acidosis),
Hypo-hyperkalemia

Recommended for
witnessed pulseless VT &
VF arrests

Ts:
Toxins,
Tamponade,
Tension pneumothorax,
Thrombosis (cardiac and
pulmonary),
Trauma
Tablet (overdose)

May be beneficial in
PEA/Asystole arrests

Potential complications
Infection
Bradycardia
Electrolyte imbalances

Cool to 32-34C for 12-24

hours
Prevent shivering

Potassium
Calcium
Phosphorus
Magnesium

Hyperglycemia

85

Heart Sounds
S3: ventricular gallop
Normal in children
Adults: LVEDP
(preload); LV failure
Summation gallop
S4, S1,S2, S3
CHF, anemia,
ischemic hearts

86

Systolic murmurs
Aortic stenosis
Pulmonic stenosis
Mitral insufficiency
Tricuspid
insufficiency
Diastolic murmurs
Aortic insufficiency
Pulmonic
insufficiency
Mitral stenosis
Tricuspid stenosis
87

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Risk Factors

Acute Coronary Syndromes (ACS)

The common
pathophysiology is ruptured
or eroded plaque.

Cigarette smoking
Hypertension

Obesity
Diabetes Mellitus

SBP > 160 mm Hg

Gender/Age

DBP > 95 mm Hg

Sedentary lifestyle

Hyperlipidemia
Total chol >240
mg/dL

Family history

HDL <35 mg/dL

89

90

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Classification of Infarct

Coronary Arteries

Right coronary (RCA)

Left coronary (LCA)

STEMI- ST segment elevation

Non-STEMI- Non-ST segment elevation infarct

The goal is to open the artery to restore blood

flow.

TIME IS MUSCLE

Want to treat within 12 hours

Late restoration of patent artery still increases

survival

Left anterior

descending (LAD)
Circumflex (CF)

91

Supplies blood to:

SA node-55% hearts
AV node-90% hearts

Right Coronary
Artery

RA & RV muscle

92

Left Anterior Descending

Coronary Artery
Supplies blood to:
Anterior/lateral surface LV

Bundle of His

Anterior 2/3

Inferiorposterior wall of LV

intraventricular septum

1/3 septum, posterior

R bundle branch

fascicle of left bundle

branch
Inferior surface RV

Anterior L bundle branch

LV papillary muscle
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Ischemia: T wave Changes

Left Circumflex

The normal T wave has the following

characteristics:

Supplies blood to:

AV node 10% hearts
SA node in 45% hearts
Lateral posterior surface of LV
Portion of posterior wall

Asymmetry
The T wave is normally positive in leads I, II, V3 to V6
The T wave is less than 2/3 the height of the preceding

R wave.

95

96

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Abnormal T Waves: Ischemia

Abnormal T Waves: Potassium

If a T wave is flipped and symmetrical, it suggests ischemia

T waves that are tall and peaked suggest elevated potassium levels

97

The ST segment

Abnormal ST Segments: Ischemia

The key thing to identify with the ST segment is

its relationship to the baseline.

ST depression suggests ischemia in the

The normal ST segment is isoelectric or level with the

area viewed by that lead

ST depression is considered significant if:

baseline
Normal ST
Segment

Elevated ST
Segment

98

Depressed
ST Segment

Depression >1 mm below the baseline

Depression is seen in 2 or more leads

facing the same area of the heart

ST depression occurs in < 20 minutes of ischemia.
99

ST Depression

100

ST Segment Elevation: Injury

ST elevation is considered
significant if:
Elevation is > 1 mm in the

limb leads or > 2 mm in the

precordial leads
Elevation occurs in two or
more leads facing the same
area of the heart
101

ST elevation occurs within

20-40 minutes after injury
occurs.
102

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ST Elevation

Q Waves: Infarction
Pathological Q wave represents an area of dead
tissue or infarction.
The Q wave is > 0.04 seconds wide
The Q wave is >1/4 of the height of the R wave
that follows.
Q waves usually take up 24 hours to develop.
They do not reveal when the infarction
occurred.
Early development of Q waves predicts a
large infarction.
103

Pathologic Q Waves

104

Cardiac Markers
CPK 3 isoenzymes
CPK-MB is more specific to myocardium. Normal values:
CK (Total) - Males < 180, Females <130
CK MB Mass - < 8.0
CK Relative Index - < 4.0
Can be falsely elevated in renal failure, skeletal muscle injury,
marathon runners
Elevations do not occur for up to 6 hours after injury.
Troponin I
Elevations start within 3 hours after ischemic event.
Normal value: < 0.6
Remains elevated longer than CPK -MB
Highly sensitive markers for cardiac injury
105

Case Study

106

Risk Stratification

45 y.o. Male w/ history of CRD, HTN, and

pancreatitis. Onset of abd pain in am. Felt like
severe gas. Not like previous pancreatitis pain.

Initial Interventions
(within 10 minutes)
Targeted history

Biomarker

1230

1900

0445

<0.04

245.4

258.35

3792

3487

493.8

330.5

Oxygen, Monitor, IV (Oh, MY!)

12 lead ECG

Troponin I
CK
CK-MB

2.8

Vital signs
Serum Markers

Goal:

Door to Drug: 30 minutes

Door to Balloon: 90 minutes

MONA
107

108

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The 12 Lead ECG:

Four Column Layout
12 Lead ECG machines layout the various
leads in 4 standard columns:

109

110

12 Lead ECG Layout

Using the 12 Lead ECG:

Localization of Problems

High Lateral
High Lateral
Inferior

Lateral

AVR None

V1 Septal

V4 Anterior

II Inferior

AVL Lateral

V2 Septal

V5 Lateral

III Inferior

AVF Inferior

V3 Anterior

V6 Lateral

Septal
Anterior

Low Lateral

Note: This one has 2 leads of rhythm strips

111

Localizing Injury
Affected
Part

Vessel(s)
Involved

Leads

Anterior

LAD

V3, V4

Inferior

RCA

II, III, avF

Lateral
Septal

Circumflex
LAD

V5, V6, I, avL

V1, V2

Posterior

Circumflex; Reciprocal
RCA
changes, V1, V2

Right
RCA
Ventricular

112

TREATMENT

Electrical Complications
PVC, SVT, 2 AV Mobitz II,
CHB, BBB, Hemiblocks
PVC, SB, ST, JR, PAC, Atrial
Fib, 2 AV Mobitz II
(Wenckeback)
PVC, SB, ST, PAC, A. Fib
Same as Anterior
Same as Inferior

V4R
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MONA Greets Them at the Door

Treatment
STEMI

Non-STEMI
NO

Time from onset <12 hr ?

Admit to monitored bed

YES

Reperfusion:
Door to needle: < 30 min
Door to balloon: < 90 min
NTG
Beta Blockers
ACE Inhibitors
Statin Therapy
Heparin
Clopidogrel

Non-Diagnostic

NTG
Beta Blockers
ACE Inhibitors
Statin Therapy
Heparin
Glycoprotein
IIB/IIIA Inhibitor
Clopidogrel

Follow serial markers

Repeat ECG
Consider stress test

Early Invasive Therapy within 48 hr of AMI

Oxygen:
Continue for at least
initial 6 hours, then
DC if oxygen
saturation is >90%.

Nitroglycerin: Dilates

Aspirin: Inhibits
platelet aggregation.
Give 162- 325 mg as
soon as patient
arrives in ED.
CHEW.

If NTG does not relieve pain:

coronary arteries to increase

blood flow to heart.
preload by venous
dilation. Give:

Give Morphine 2-4 mg IV

every 5- 15 minutes until

pain free.
Morphine relieves anxiety /
pain & acts as vasodilator.

115

Question

Re-Perfusion Strategy: Fibrinolytics

Breaks up the fibrin network that binds clots
together
Indications:
ST elevation in 2 or more leads
Onset of symptoms < 12 hours
MAY CAUSE DEATH FROM BRAIN
HEMORRHAGE
Agents available : alteplase (tPA, Activase),
retaplase (Retavase), streptokinase (Streptase),
tenecteplase (TNKase)

116

Which of the following lab results should be

reported to the cardiologist for a patient
with ACS who is scheduled to go for cardiac
catherization & possible PCI?
a. aPTT 65 sec
b. Troponin 0.2ng/ml
c. Serum K+ 4.9 mEq/L
d. Serum creatinine 2.3 mg/dL

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118

Adjunctive Medications

If a Blockage is found:
Multiple options are available
Balloon angioplasty
Coronary atherectomy
Stent placement
Laser

receptor blocking agents

Clopidogrel (Plavix);

Prasugrel (Effient)
Heparin, Lovenox
ACE Inhibitors & ARBs
Statins
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Blockers

Blockers

Mechanism of action:
Blocks catecholamines

from binding to adrenergic receptors.

heart rate, blood
pressure, and myocardial
contractility
AV nodal conduction
incidence of primary
ventricular fibrillation

Absolute
Contraindications
Severe CHF
SBP < 100 mm HG
Acute asthma
2nd or 3rd degree heart block

Cautions
Mild / moderate CHF
Heart rate <60
History of asthma
Insulin dependent
diabetes
Severe Peripheral
Vascular Disease

121

Heparin vs. Enoxaparin (Lovenox)

Unfractionated heparin
Given as a continuous infusion
Keep PTT within target range of 50 to 70 (1.5 to 2x
baseline)
Reversal agent: Protamine sulfate
Low molecular weight- Enoxaparin
Given as an injection every 12 hours

122

Medications to Prevent Platelet Aggregation

CAUTION: Use of these agents have resulted in bleeding
complications such as retroperitoneal bleeds at PCI site &
intracranial hemorrhage.

Glycoprotein IIB/IIIC

Clopidogrel (Plavix):

Inhibitors

Irreversible inhibition of

(Reopro, Aggrastat, Integrelin)

platelet aggregates

Inhibit platelet aggregation

Start 300 mg dose at the

Shown to decrease mortality &

time of reperfusion,
continue 75 mg daily
dose for 8 days.
May need to withhold
for 5 7 days prior to
CABG
124

should be used in all patients

with non-STEMI as soon as
possible in conjunction with
aspirin, heparin, clopidogrel,
and early PCI

DO NOT administer either within 6 hours of nonspecific fibrinolytic

123

ACE Inhibitors

RAS & ACE Inhibitors

Decreased renal
blood flow

Mechanism of action

JG cells
stimulated

Renin
released

Reaction with
angiotensinogen

Reduces BP by inhibiting angiotensin-

converting enzyme
Alters left ventricular remodeling that occurs

Increased
blood vol.

post MI by inhibiting tissue ACE

Lowers peripheral vascular resistance by
vasodilation
Reduces mortality and CHF after an acute MI

Improved renal
blood flow

125

Na+, H2O
retention

Aldosterone
secretion

Increased arterial
blood pressure

Angiotensin I then
II production

Vasoconstriction

126

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MI Complications

Statins
complications such as reinfarction, recurrent
angina, and arrhythmias

Dysrhythmias most

occurs with inferior /

common complication
of the deaths occur within

both total cholesterol and LDL.

1st hour of symptoms -usually due to v. fib

Stabilize platelets, improve endothelial

function, & inhibit inflammatory response.

Heart failure Can range

Should be started within 24 hours

from mild dysfunction to CHF

to cardiogenic shock.

127

Question
Your MI patient suddenly develops LOC, a weak, thready
pulse, and bilateral posterior crackles in the lower lung fields.
VS: 78/46; HR 139; RR 25
u/o < 30 ml for the last hour
O2 sat 89% on 4L NC
You suspect

RV infarction:
posterior MI. Incidence
around 40%
Patients with RV infarct
need VOLUME & are
very sensitive to NTG

Emboli:
Thrombi form on inner

wall at site of MI. Most

common with large
anterior MI.

Papillary muscle
rupture

128

Assistance to the Failing Ventricle:

Intra Aortic Balloon Counterpulsation

a. Stroke
b. ARDS
c.

Pulmonary embolus

d. Cardiogenic shock
129

IABP Placement

130

IABP- How does it work?

Inflation during diastole

When the IABP balloon is properly

placed, it is just distal to the left

subclavian artery.
If the IABP balloon is displaced

proximally, it can occlude the takeoff of the left subclavian artery

If the IABP balloon is displaced

Aortic root pressure

Aortic diastolic pressure
Coronary perfusion pressure

CPP = Aortic diastolic pressure

myocardial wall tension
Oxygen supply
Stroke volume = Heart rate

distally, it can occlude the take-off

of the renal arteries
131

132

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Primary Effect of IABP Therapy

IABP- How does it work?

Supply
Deflation immediately
prior to systole
Aortic end-diastolic

Demand

pressure
Impedance to ejection
Afterload
Oxygen demand

Supply Balloon Inflation

Demand Balloon Deflation
133

Indications
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.

134

Contraindications

Cardiogenic shock
Refractory ventricular failure
Unstable refractory angina / impending infarction
Mechanical complications due to acute myocardial
infarction
Ischemia related to intractable ventricular
arrhythmias
Cardiac support for high risk general surgical and
coronary angiography / angioplasty patients
Septic shock
Weaning from cardiopulmonary bypass
Intra-operative pulsatile flow generation
Support for failed angioplasty and valvuloplasty

Severe aortic insufficiency

Abdominal or aortic aneurysm
Severe calcific aorta-iliac disease or

peripheral vascular disease

135

Congestive Heart Failure: Definition

Question

Systolic failure: cardiac contractility

An IABP is used to manage cardiogenic shock in

order to increase
a.

Diastolic failure: impaired cardiac relaxation

and abnormal ventricular filling.

Coronary perfusion during systole

The heart is unable to generate a cardiac output

sufficient to meet the demands of the body.
Manifested by:
Poor tissue perfusion and congestion of the
vascular beds
Symptoms of inadequate tissue perfusion

b. Myocardial oxygen supply

c.

136

LV filling volume

d. LV systolic pressure

137

138

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Pathophysiology:
Systolic Dysfunction
Impaired LV contractility results in

reduced ejection fraction (EF < 40%)

Ventricle is dilated, thin walled

Dilated Heart
(Systolic Failure)

Etiology:
Acute Myocardial Infarction
Coronary Artery Disease,
Hypertension
Valvular Heart Disease
Toxins
Endocrine
Congenital

Chronic Heart Failure:

Pathophysiology

Myocardial Toxicity

Morbidity
Mortality

Hypertrophic Heart
(Diastolic Failure)

Sarcoidosis
Amyloidosis

140

Forward Failure

BNP
ANP

Peripheral vasoconstriction
Hemodynamic alterations

Remodeling and
progressive
worsening LV function

Left Ventricular Failure

Fall in LV Performance

Activation of RAAS, SNS

Normal systolic function with the impaired

ability of the ventricle to relax (lusitropy) and
fill with blood
filling pressures result due to stiff ventricles
Ventricle is thickened and concentrically
hypertrophied
Etiology
Hypertension, coronary artery disease
Cardiomyopathy
Aortic Stenosis
Infiltrative diseases

139

Myocardial
Injury

Pathophysiology:
Diastolic Dysfunction

Heart Failure Symptoms

Signs of Decreased CO
Fatigue, poor exercise
tolerance
Tachycardia
Narrow pulse pressure
Cool, pale, diaphoretic
Altered mental status
Decreased urine output

Backward Failure

Signs of Elevated
Pulmonary Pressure
Dyspnea, tachypnea
Orthopnea
Cough, wheeze
Hypoxia
Respiratory Alkalosis
Crackles, rhonchi
S3,S4

141

142

Right Ventricular Failure

Dependent edema

What kind of
heart failure
does this man
have
Right or Left ?

RAP/CVP
Fluid vol. Backs into portal system
GI s/s
Ascites
Nocturia
Weakness, fatigue
Murmur of TR
143

144

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Classification of Heart Disease

ACC/AHA Heart Failure Stage

A
B

Structural heart disease,

but no symptoms of heart
failure

With cardiac disease, but

asymptomatic and without
limitations of physical activity

Structural heart disease

with prior or current
symptoms of heart failure

II

Symptoms with moderate

exertion resulting in slight
limitation of physical activity

III

Symptomatic with minimal

exertion resulting in marked
limitations of physical activity

IV

Symptomatic at rest. Inability

to carry on any physical
activity without discomfort

Refractory heart failure

requiring specialized
interventions

Compensatory Mechanisms

NYHA Functional Class

At high risk for heart failure,

but no symptoms or
structural heart disease

None

In the short term, compensatory mechanisms

maintain cardiac output.
In the long term, all of these factors trigger a
process of pathologic growth and remodeling.
Include:
Stimulation of SNS
Activation of Renin-Angiotensin-Aldosterone System
Hypertrophy
145

146

VENTRICULAR REMODELING

Myocardial Hypertrophy
Decrease contractilitydecreased stroke
volumeActivation of SNS & RAAS
Increased ventricular volumes

Late compensatory mechanism

Larger cells less contractile & require more oxygen

Increased ventricular pressures

Ischemia leads to fibrosis and necrosis

Increased ventricular wall tension

Thinning of ventricle wall & chamber dilation
Decrease contractility

Fibrous tissue deposits

HEART FAILURE

147

148

Pharmacologic

Pillars of Treatment:

Systolic Treatment

Drug Therapy using the A-B-C-Ds

Loop diuretics
Spironolactone

Diastolic Treatment

ACE inhibitors: Block RAAS

Beta Blockers

Diuretics

Beta blockers: Block SNS

ACE inhibitors

Beta Blockers

Contractility: Digitalis

Digoxin

ACE inhibitors
Calcium Channel

Diuretics, VasoDILATORS:

Blockers

Preload & Afterload

149

150

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4/6/2013

Angiotensin II Receptor Antagonists: ARBs

Beta Blocker Selection

Beta blockers recommended for heart failure include:

Indicated for patients who cannot

tolerate ACE Inhibitors.
Act directly on angiotensin receptors.
Increased selectivity & specificity by
directly blocking angiotensin
receptors
Example: Losartan
both preload and afterload
Fewer side effects

Carvedilol (a non-selective agent)

Metoprolol: Long acting
Bisoprolol

Doses may need to be titrated gradually over a period of

several weeks.
Selective agents incidence
of:
Bronchospasm
Cold extremities
Other peripheral side effects
151

Preload: Diuretics
GOAL: To restore fluid balance
Beneficial effects
Excrete sodium and water
Decrease CVP
Symptom relief
Decrease shortness of
breath & edema

152

Preload / Afterload: Vasodilators

Vasodilators that target
Preload:
Nitroglycerin
Morphine

Detrimental effects
Electrolyte imbalances
Decrease renal
function
Activates RAAS
Hypotension

Vasodilators that target

Afterload:
Nipride
NTG at > 50mcg/min

Use Daily Weight

For diuresis monitoring
153

Contractility

Nitrates not as
Effective as ACE
Inhibitors

154

BNP: Brain Natriuretic Peptide

Natriuretic peptides are a family of naturally

Digoxin: Used for inotropic support

occurring molecules.
Actions:

Dobutamine: Used short term

cardiac preload by causing vasodilatation &

vascular capacitance.
sympathetic tone.
Induce natriuesis (sodium excretion) by actions
on renal vasculature and tubules.

Milrinone: Used for patients who develop

tolerance to dobutamine

155

156

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BNP Measurement

Natrecor (Nesiritide)

Measurement of BNP can differentiate patients with

heart failure from patients without heart failure.
BNP level >100 is indicative of HF
May also be elevated in right sided failure due to
pulmonary disease and end stage renal disease.
May see false negative in patients with flash
pulmonary edema and heart failure due to mitral
regurgitation.

Synthetic natriuretic peptide (BNP)

Approved for IV use in acute decompensated heart
failure
pulmonary pressures
Improves dyspnea
Contraindicated with systolic BP < 90
Monitor closely for hypotension and
arrhythmias

157

158

Adjunct Therapies

Left Ventricular Assist Device

All AT RISK patients should be on:

Beta blockers
ACE
Statins Believed to decrease inflammatory response

May also require:

Anticoagulants If patient develops atrial fibrillation
Antiarrhythmics

Physical conditioning
Consider:

Biventricular Pacing / Cardiac Re-synchronization

IABP
Assist Devices
Transplant
159

160

Question

Heart Transplant

A patient status-post heart transplant develops

second degree heart block, Type II. VS: 86/40; HR
44; RR 24. The patient c/o chest pain. Skin is
warm and dry. Breath sounds clear. You should
a. Prepare for transcutaneously pacing
b. Draw labs to determine if patient is rejecting the heart
c. Administer 0.5 mg atropine
d. Reassure the patient that what he is experiencing is

normal after a heart transplant

161

162

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4/6/2013

Acute Inflammatory Diseases

Question

Myocarditis

Acute rejection in cardiac transplantation is

diagnosed by:
a. ECG
b. Chest x-ray
c. Echocardiography
d. Endomycardial biopsy

Endocarditis
Pericarditis

163

Myocarditis

164

Question

Inflammation of the myocardium

Etiology: viral, bacterial, parasitic, fungal,
radiation to chest
Acute or chronic
S/S: chest soreness, burning: with inspiration;
syncope; fever; S3, S4;
Dx: WBC; CK-MB; Cardiomegaly; diffuse ST
& T wave abnormalities; SVT or ventricular
dysrhythmias

Which of the following medication

regimens would be most appropriate to
relieve chest pain in a patient with
diagnosis of myocarditis?
a.

NTG 1/150 grains sublingual

b. Furosemide 40 mg IV
c.

Ibuprofen 800 mg PO

d. Morphine sulphate 2 mg IV

165

Infective Endocarditis

166

Question

Definition: Inflammation of the

endocardium, usually occurring in the
membranous lining of the heart valves

The valve most often effected by infective

endocarditis is:
a. Mitral
b. Aortic
c. Tricuspid
d. Pulmonary

Etiology:
Congenital or acquired heart disease
Invasive monitoring (PA catheters,

temporary pacing wires, etc)

Cardiac surgery
IV catheters / dialysis access devices
GI / GU tubes (Foley cath)
Dental procedures / poor oral hygeineg use

167

168

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Infective Endocarditis:
Presentation

Janeway
lesions

Infectious symptoms (fever, chills, malaise)

Fatigue, night sweats, anorexia, weight loss
Symptoms of heart failure

Infectious Endocarditis
Diagnosis: Blood cultures; TEE
Management
Prevention:
Patients with valve disease should receive antibiotics prior to any
invasive procedure
Good hygiene
No street drugs
Decrease myocardial oxygen demand
Control and treat infection
Antibiotics for 6 8 weeks
Monitor for complications
Systemic emboli
Valve surgery may be required

New murmur (aortic insufficiency most common)

Vascular signs:
Splinter hemorrhages
Petechiae on chest, oral mucosa, abdomen
Janeway lesions: Flat, erythematous lesion on

palm, soles of feet

Roths spots: Round white lesions on retina
Oslers nodes: Painful nodules on fingers,

toes

Oslers
Nodes
169

Pericarditis

Pericarditis

Etiology:

Presentation:
Sharp, stabbing pain that radiates to the left
shoulder
Aggravated by inspiration, supine position
Relieved by sitting up or leaning forward
Dyspnea, tachypnea
Tachycardia
Murmur / rub
Fever
Diagnostic:

Idiopathic
Post MI May be acute

170

(within 7 days) or
Dresslers syndrome
(occurs 2 wks or more
later)
Trauma
Infection
Radiation
Drugs

Troponin elevated, WBC

Definition:
Inflammatory process involving the
visceral or parietal pericardium

Diffuse ST elevation in all leads

171

Pericarditis - Management

Cardiac Tamponade

Management
Non-steroidal anti-inflammatory drugs
Treat cause
Monitor for complications:

172

If fluid accumulates in the pericardial sac, there is

potential for development of cardiac tamponade.
Tamponade has a constrictive effect on the heart.
Must be treated urgently!

TAMPONADE
Dysrhythmias

Anticipate pericardiocentesis or pericardial

window

173

174

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4/6/2013

Hypertension Definitions

Question

Hypertension: Elevation in BP above 140 /90 on at least 3 separate

occasions
Hypertensive Urgency: Develops over days to weeks. Characterized
by diastolic BP, but are usually not associated with end organ
damage.
Hypertensive Crisis: Elevation severe enough to cause the threat of
immediate vascular necrosis and end organ damage. Usually > 180 / 120
or MAP over 150.

The classic triad (Becks triad) of symptoms of

cardiac tamponade are:
a. Rales, muffled heart sounds, bradycardia
b. Widened pulse pressure, atrial dysrhythmias
c. Tachycardia, hypotension, narrow pulse
pressure
d. Hypertension, flushing, pulse paradoxus

Accelerated: DBP >120

Malignant: DBP > 140

Hypertensive Emergency: Develops over hours to days. BP must be

lowered within minutes to an hour to reduce potential complications or
new / progressive end organ damage.
Hypertensive Encephalopathy: BP > 250/ 150
175

176

Hypertensive Crisis

Principles of Treatment

Goal: Reduce cardiac & renal mortality and morbidity

BP = CO x PVR

Usually require ICU admission

BP= Cardiac Output x Peripheral Vascular Resistance

Reduce BP gradually to maintain cerebral perfusion.

In hypertensive emergency:

All antihypertensives must act by:

cardiac output
peripheral vascular resistance.

Decrease MAP 25% within first hour

Decrease to 160/ 100 within next 2- 6 hours, then gradual reduction over

next 24 hours

Agents:
Sodium nitroprusside, fenoldopam, hydralazine
Hydralazine good in eclampsia
177

Question

178

Cardiomyopathy

When admitting a patient with hypertensive

crisis, the nurses immediate concern is
to prevent which of the following
complications?
a. Stroke
b. End organ failure
c. Seizures
d. Left ventricular hypertrophy

Dilated
Hypertrophic (Idiopahtic

hypertrophic subaortic stenosis

[IHSS])
Restrictive

179

180

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Cardiomyopathy: Dilated

Cardiomyopathy: Hypertrophic
mass & thickening of myocardium

Myocardial fibers degenerate & fibrotic changes

occur

Fibrosis occurs

Systolic and diastolic dysfunction

Mitral Insufficiency

LV chamber in size

Ventricles rigid & stiff

LA dilates
May develop outflow obstruction

Ventricular rhythms common cause of death

181

182

Your patient, admitted with cardiomyopathy, c/o

dyspnea, & palpitations. CM: SR, no ectopy.
You anticipate management to include

Cardiomyopathy: Restrictive
Restricted filling of ventricles
Etiology: Idiopathic; Amyloidosis

a.Insertion of a left ventricular assist device

compliance; LV stiff & can not dilate or

contract well in systole

b.Preparing the patient for a cadiomyoplasty

c. Administration of enalopril (Captopril)

LVEDP ; contractility ; CO HF
Death

d.Loading the patient with digoxin

183

Cardiomyopathy: Rx
ACE inhibitors
B-blockers
Antidysrhythmic
agents
Antibiotics (at risk for
infectious
endocarditis)

184

Coronary Artery Bypass Grafting

The internal mammary artery
is frequently used because of its
long-term patency.
Other conduits include:

DCM: + inotropes;
diuretics
HOCM: Avoid agents
that preload; avoid +
inotropes (can worsen
obstruction)

Saphenous veins
Radial artery
Gastroepiploic artery
Inferior epigastric artery

185

CABG remains the treatment of choice for patients with three

vessel coronary artery disease, complex lesions, or more than
75% occlusion of the left main.

186

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4/6/2013

Question

Question

Upon arrival to the ICU

post-CABG, the patient
has the following:
BP 180/110;
HR 70, 100% paced;
RAP 6; PAD 10
CO 3.5
U/O 60 ml

Upon turning the postoperative CABG

patient, the nurse observes 200 ml of
bloody drainage in the CT drainage
system. The nurse should perform which
of the following?
a.

Autotransfuse the patient

b. Aggressively strip the CT tubing

What should the nurse do

first?

Obtain lab for coagulation studies

d. Continue to monitor the patients CT drainage
c.

a. Bolus with 250ml to

RAP & PAD
b. NTG gtt by 6.6
mcg/min to BP
c. pacer to 75 to
improve CO
d. Administer
propranolol 1 mg IV
to BP

187

After a mitral valve replacement, the patient

is most likely to have which of the following as
part of the patients plan of care?

188

Valve Surgery
The primary cause for valve disease is

rheumatic fever.
Most commonly affected the aortic and

a. Ace-inhibitor
b. Beta-blocker

mitral valves
If allowed to persist, congestive heart

failure can occur.

Positive inotropic agent

d. Anticoagulant
c.

Surgical repair can include replacement

of the defective valve with either a

mechanical or tissue valve.
Patients with mechanical valves will
require lifetime anticoagulation
189

Cardiac Trauma

190

Question

Cardiac contusion is the most common blunt

injury to the heart.

Following a motor-vehicle accident, pericardial

tamponade is suspected. Which of the
following findings is consistent with traumatic
tamponade?
a. Muffled heart sounds
b. Pericardiocentesis of 50ml of blood
c. ST-segment depression in the limb leads
d. Rales on auscultation

Rarely fatal, but should be suspected if the patient

has anterior chest wall trauma and fractures of the

sternum and ribs.
Signs are similar to MI with ST changes and elevation
of enzymes
ECG changes: RBBB; ST; ventricular dysrhythmias
Right ventricle is most often affected

Aortic rupture is the result of a blunt trauma

deceleration injury
191

192

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Aortic Aneurysms

Which of the following findings is most

indicative of a leaking abdominal aortic
aneurysm?

Thoracic or Abdominal.
Abdominal are more common (65%)
Two patterns:

a. Back pain

b. Bounding peripheral pulses

Weakness and bulging of the entire vessel

wall
Weakness and bulging within the vessel
wall

Patients with an aneurysm may be

c. Intermittent claudication

asymptomatic
Rupture of the aneurysm causes acute
pain that radiates to the back,
unrelieved by changes in position.
Mortality from rupture is 90%. The
only chance for survival is emergent
repair.

d. Nausea and vomiting

193

Aortic Dissection

194

Question

Tear in the intimal layer of the aorta

allows blood to flow into the medial layer,

creating a false channel.
It is usually accompanied by
hypertension that is not well
controlled.
Most common is ascending aorta
dissection, with many occurring only
centimeters from the aortic valve.
High risk of death from acute aortic
regurgitation and pericardial
tamponade.
Symptoms: Severe tearing or
ripping chest pain, moves to the back
as dissection progresses

Post-endovascular AAA repair, a patient has the

following findings: BP 124/76; HR 92; RR 18. Distal
pulses 2+, cap refill 2 sec. Groin without s/s of
hematoma. U/O is 20ml/hr for 2 hours. The most
likely cause of the decreased u/o is:
a. Renal toxic effects of contrast agents
b. Occlusion of the renal artery by the endograft
c. Hypovolemia due to operative blood loss
d. Hypovolemia due to retroperitoneal bleeding

195

196

Your patient has a history of hypertension and CAD.

Assessment reveals skin temperature of legs &
feet, pulses & pallor when the legs are elevated &
reddish-blue discoloration of the legs. Patient c/o
leg pain. You suspect
a. Peripheral arterial disease
b. Chronic venous insufficiency
c. Acute arterial occlusion
d. Deep vein thrombosis

Question
On PO day 2 after an AAA, your patient develops
hypotension, tachycardia, abdominal
distention, and WBC. These findings
indicate
a. Post-op graft infection
b. Ischemic colitis
c. Aortic-enteric fistula
d. Abdominal compartment syndrome

197

198

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4/6/2013

Acute Peripheral Vascular Insufficiency

Acute Arterial Occlusion
Peripheral Stents
Medications: Antiplatelet; Thrombolytics
Carotid Stenosis
Endartarectomy

Question
After aorto-femoral
bypass surgery for
acute arterial
occlusion, your
patient has
CPK, K+ 5.9 mE/L
PaO2 90
PaCO2 24
HCO3 19

This patient is at risk for

developing
a.
b.
c.
d.

Dysrhythmias
Graft occlusion
Pulmonary embolus
Heart Failure

199

Question

Question
A patient is receiving thrombolytics via
continuous infusion for acute limb
ischemia suddenly complains of pain in
the affected extremity. The most
appropriate nursing action includes:

After femoral-popliteal bypass surgery, patient

c/o pain unrelieved by narcotics. Dressing D
& I. Skin warm, pale, & dry. Cap refill 2 sec.
Distal pulses 2+. Motor strength slightly .
Gastrocnemius muscle slightly swollen & is
doughy to palpation. These findings are
consistent with
a.
b.
c.
d.

200

a. Administer narcotic pain medication to relieve the

pain

b. Elevate the affected extremity above the level of

the heart

Compartment syndrome
Graft occlusion
Development of false aneurysm
Heparin induced thrombocytopenia (HIT)

c. Notify the MD that the patient may have

compartment syndrome

d. Discontinue the thrombolytic infusion and notify

the MD

201

202

Structural Heart Defects:

Atrial septal defects

Structural Heart Defects

Left-to-right shunt
resulting in right
chamber overload

Atrial septal defects

Ventricular septal defects

RA, RV dilate

Valvular disease

Leads to pulmonary
hypertension
Dysrhythmias: Afib,
A.Flutter, PR
prolongation,
Incomplete RBBB. LAD
203

Treatment:
Antibiotics to prevent
endocarditis
Manage heart failure s/s
Surgical repair

204

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Structural Heart Defects:

Ventricular Septal Defects

Valvular Disease

Left-to-right shunt

Mitral Regurgitation

Pulmonary HTN
S/S
Tachypnea
Sweating
Hemoptysis
Heart Failure
Holosystolic murmur

Mitral Stenosis

Treatment
Antibiotics
Manage HF s/s
Surgical repair

Aortic Regurgitation
Aortic Stenosis
205

206

Other Structural Defects

Coarctation of Aorta

Patent Ductus Artiosus

workload LA & LV
Left-sided HF

Narrowing of lumen &

flow

Tx

Tx

Ab

Ab

Tx HF

Antihypertensives

Surgical Closure

Surgery (1-5 yo)

Lets Test Ourselves Some More!

207

Which of the following vasopressors is

indicated for low CO syndrome when the
desired effect is vasoconstriction without
tachycardia?
a. Norepinephrine (Levophed)
b. Phenylephrine (Neosynephrine)
c. Dopamine
d. Epinephrine

208

Your patient c/o chest pain. The ECG shows ST

elevation in Leads II, III, & aVF. You
administer NTG 1/150 grains SL. The
patients BP drops from 136/84 to 82/50
mmHg. The most likely cause of the
decrease in BP is:
a. Right ventricular MI
b. Papillary muscle rupture
c. Hypersensitivity to NTG
d. Rupture of a ventricular free wall
209

210

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4/6/2013

Two hrs post-CABG, patient

has these findings:
BP 80/62 (68)
CVP 15
These findings are
consistent with:
PAD 14
a. Normal post-op
CO 3
course
CT output 50ml/hr
b. Myocardial stunning
for 2 hrs.
c. Cardiac tamponade
d. Perioperative MI

Your post-op patient has a HR 132, BP

80/66, PCWP 5, Hgb 8.
Which medication would help?
a.
b.
c.
d.

Vasopressin 20 unit IVP

Administer 1 unit of PRBC
Administer 250ml NS bolus
Start dopamine at 10mcg/kg/min

211

Which of the following medications will

worsen the symptoms of hypertropic
cardiomyopathy?
a. Calcium channel blockers
b. Amiodarone
c. Beta Blockers
d. Nitrates

212

Patient admitted to the ICU status postcardiac arrest. Immediate

management of this patient includes:
a. Monitoring for hyperkalemia
b. Maintaining a blood glucose 120-

150mg/dL

c. Initiating clinically induced hypothermia

d. Monitoring labs for WBC & Plt counts

213

Chest pain that is NOT relieved by rest

& NTG is called:

Coronary artery perfusion is

dependent upon:
a.
b.
c.
d.

214

Diastolic pressure
Systolic pressure
Afterload
SVR

a.
b.
c.
d.

215

Variant angina
Stable angina
Unstable angina
Prinzmetals angina

216

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A patient admitted with CHF has the

following: BP 94/60, HR 125, RR 24,
u/o 50 ml for 2 hours. Cool clammy &
LOC. Which of the following would
be included in the patients plan of
care?

The primary function of drug

therapy with beta-blockers in
heart failure is to:
a. Increase blood pressure
b. Block compensatory mechanisms
c. Increase urine output
d. Decrease dysrhythmias

Positive inotropes, diuretics, vasodilators

a.

b. ACE-inhibitors, adenosine, beta-blockers

Beta-blockers, diuretics, calcium-channel blockers

c.

d. Negative inotropes, digoxin, antidysrhythmics

217

218

A direct effect of sodium nitroprusside

(Nipride) is to:

Which of the following medications best

improves LV function?

a. Decrease stroke volume

a. Dopamine (Intropin)

b. Increase venous return

b. Captopril (Capoten)

c. Decrease afterload

c. Digoxin (Lanoxin)

d. Increase pulmonary vascular resistance

d. Procainamide (Pronestyl)

219

Which of the following pulmonary artery

catheter findings would be anticipated
in a patient with chronic emphysema?

Which of the following findings is most

consistent with high left ventricular
filling pressure?
a.
b.
c.
d.

220

a.

Sinus bradycardia
Diastolic murmur
Peripheral edema
Bibasilar crackles

b.
c.
d.

221

Increased RAP
Decreased RAP
Increased PCWP
Decreased PCWP
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4/6/2013

Two hours after a permanent DDD pacemaker is

inserted for SSS, the patient goes into atrial
fibrillation. Which of the following pacing
modes is indicated for this patient?

Which of the following is a

contraindication to the use of an
IABP?

a.

a. Aortic valve insufficiency

b.

b. Mitral valve insufficiency

c.
d.

c. Ventricular aneurysm

DVI
DDD
VAT
VVI

d. Ventricular septal defect

223

In patients with angina, CCB are effective

because they:

224

Your patient c/o chest pain that is sharp,

constant, & worse when lying down. The
pain lessens when sitting up & leaning
forward. These symptoms are consistent
with
a. Pulmonary embolism
b. Abdominal aortic aneurysm
c. Pericarditis
d. Myocardial infarction

a. Inhibit vasodilation
b. Increase myocardial contractility
c. Increase venous return
d. Reduce myocardial oxygen consumption

225

*New PCCN Cardiac Content

226

Thanks

Starting 06-26-2013, content includes:

Genetic Cardiac Disease
Long QT syndrome,

Special thanks to
Carol Boswell, RN, MSN, CCRN
for the use of many of her slides in this
presentation.

Brugada syndrome

Minimally-invasive cardiac surgery (i.e., nonsternal

approach)
Vascular disease: minimally-invasive interventions
(e.g., stents, endografts)
Cardiomyopathies: stress-induced (e.g., Takotsubo)
227

228

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Questions?
Beth Torres, PhD, RN, CCRN
CJW Medical Center,
Chippenham Campus
[email protected]
804-327-4186

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