12/10/16
Cardiovascular
System
Disorders
DCLC, College of Nursing
GERALD VICTORIA, RN, MAN, US RN
DYSRHYTHMIAS
—  C. VENTRICULAR DYSRHYTHMIAS
—  1. PVC Premature Ventricular Complex
—  2. VT Ventricular Tachycardia
—  3. VF Ventricular Fibrillation
—  4. IVR Idioventricular Rhythm
—  5 VA Ventricular Asystole
—  D. CONDUCTION ABNORMALITIES
—  1. First Degree Atrio-Ventricular Block
—  2. Second Degree Atrioventricular Block
—  Type 1 & Type 2
—  3. Third Degree Atrioventricular Block
DYSRHYTHMIAS
—  Dysrhythmias are disorders of the formation
or conduction (both) of the electrical
impulse within the heart. These disorders
cause disturbances of:
—  1. The heart rate, the heart rhythm or both.
—  2. Changes in the hemodynamics (the
pumping action of the heart or blood
pressure).
DYSRHYTHMIAS
—  A. SINUS DYSRHYTHMIAS
—  1. Sinus Bradycardia <60
—  2. Sinus Tachycardia >100
—  3. Sinus Arrhythmia
—  B. ATRIAL DYSRHYTHMIAS
—  1 PAC Premature Atrial Complex
—  2. AF Atrial Flutter
—  3 AFib Atrial Fibrillation
DYSRHYTHMIAS
—  E. Adjunctive Modalities & Management
—  1 Pacemaker Therapy
—  2 Cardioversion & Defibrillation
—  Cardioversion
—  Defibrillation
—  3 Cardiac Conduction Surgery
—  Endocardial Isolation
—  Endocardial Resection
DYSRHYTHMIAS
— Dysrhythmias are diagnosed using ECG
or the electrocardiographic waveform.
They are named according to:
— 1 The site of origin of the impulse &
— 2 The mechanism of formation or
conduction involved.
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DYSRHYTHMIAS
— Sites of Origin
—  Sinus (SA) node
—  Atrial
—  Atrioventricular (AV) node
—  Ventricles
DYSRHYTHMIAS
— A. SINUS DYSRHYTHMIAS
— 1. Sinus Bradycardia <60
— 2. Sinus Tachycardia >100
— 3. Sinus Arrhythmia
DYSRHYTHMIAS
— B. ATRIAL DYSRHYTHMIAS
— 1 Premature Atrial Complex
— 2. Atrial Flutter
— 3 Atrial Fibrillation
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DYSRHYTHMIAS
—  Mechanism of Formation Conduction
—  Normal rhythm
—  Bradycardia
—  Tachycardia
—  Dysrhythmia
—  Flutter
—  Fibrillation
—  Premature Complex
—  Blocks
A. SINUS Dysrhythmias
—  1 Sinus Bradycardia <60
—  2 Sinus Tachycardia >100
—  3 Sinus Arrhythmia :
The A&V rhythm is irregular.
Increases at inspiration
Decreases at expiration
—  Causes: Heart Disease
—  Valvular Disease
—  Note: 1 No hemodynamic Effect: No Tx
B. Atrial Dysrhytmias
—  1 Premature Atrial Complex
—  Electrical impulse starts in the A before the next
normal impulse of the sinus node (SA node)
—  Causes:
—  Caffeine, Alcohol, Nicotine, Stretched Atrial
Myocardium (Hypervolemia)
—  Anxiety, Hypokalemia, Hypermetabolic Rates,
Atrial Ischemia, Injury or Infarction
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Atrial Dysrhytmias
—  1 Premature Atrial Complex Manifestations:
—  Sinus Tachycardia (>100)
—  Early: P Waves. Short PP Intervals, followed by
longer than normal PP waves (<2 PP, aka
Noncompensatory cause)
—  “My heart skipped a beat.” There is a difference
between the apical and radial pulse
—  Tx. 1. None if infrequent
—  2. >6/min = worsening, maybe the onset of A
fibrillation.
Atrial Dysrhytmias
—  2. Atrial Flutter
—  Causes: Same as A fibrillation
—  SSx: Saw toothed shape aka F Waves.
—  F waves make it difficult to determine the PR
—  interval.
—  PR interval: multiple.
—  Chest Pain
—  SOB
—  Decreased BP
Atrial Dysrhytmias
—  3 Atrial Fibrillation
—  Causes a rapid, disorganized & uncoordinated
twitching of atrial muscles. Ventricular and Atrial
Rate: 300-600. Ventricular Rate: usually 120-200
in untreated Atrial Fibrillation
—  Most common dysrhythmia that causes patients to
seek medical attention. Starts & stops suddenly.
May be:
—  1 Paroxysmal: occurs short time.
—  2. Chronic.
—  .
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Atrial Dysrhytmias
—  2. Atrial Flutter
—  Occurs in the Atrium. A rate 250-400. V rate
75-150.
—    Creates impulses at Atrial rate of 250-400/min.
The Atrial rate is faster than the AV node can
conduct. Not all Atrial impulses are conducted into
the AV causing a therapeutic block at the AV node.
(If all the A impulses were conducted to the V, the
V rate would also be 250-400 which may result in
Ventricular Fibrillation: A life threatening
dysrhythmia.
Atrial Dysrhytmias
—  2. Atrial Flutter
—   Tx:
—  1 Unstable: Electrical Cardioversion
—  2 Stable: IV Medications
—  Diltiazem (Cardizem)
—  Verapamil (Calan, Isoptin)
—  Betablockers
—  Digitalis
Atrial Dysrhytmias
—  3 Atrial Fibrillation
—  A rapid ventricular response reduces time
for ventricular filling resulting in a smaller
stroke volume. A & V contract at different
times. The atrial kick (the last part of
ventricular filling = 30% of CO) is also lost.
The shorter time in diastole reduces the time
available for coronary artery perfusion =
increasing risk for myocardial ischemia.
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Atrial Dysrhytmias
—  3 Atrial Fibrillation
—  Erratic atrial contraction promotes formation of a
thrombus within the atria:
—  = increased risk of embolism
—  = increased risk of stroke (brain attack)
—  Signs & Symptoms
—  Ventricular and Atrial Rate: 300-600
—  Ventricular Rate: usually 120-200 in untreated
Atrial Dysrhytmias
—  Causes
—  Associated with Advanced Age
—  Valvular heart disease, CAD, Cardiomyopathy
—  HTN
—  Hyperthyroidism, Pulmonary Disease
—  Acute to heavy Alcohol ingestion (Holiday heart
syndrome)
—  After Open Heart Surgery
—  Lone Atrial Fibrillation (without any underlying
pathophysiology)
Atrial Dysrhytmias
—  Treatment of Atrial Fibrillation
—  2B Stable: IV Medications [Diltiazem (Cardizem),
Verapamil (Calan, Isoptin), Betablockers
Digitalis].
—  Medications For Acute onset: Quinidine, Ibutilide,
Flecainide, Dofetilide, Propafenone, Procainamide
(Pronestyl), Disopyramide, or Amiodarone may be
given to achieve sinus rhythm.
—  IV: Adenosine (Adenocard, Adenosan) is also used
for conversion & assisting in diagnosis.
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Atrial Dysrhytmias
—  3 Atrial Fibrillation SS
—  V & A rhythm: Highly irregular
—  QRS Shape & Duration: Normal or Abnormal
—  P Wave: No discernible P Wave
—  PR Interval: Cannot be measured
—  P: QRS Ratio Many:1
—  Pulse deficits: numerical difference between apical
and radial pulse rates.
—  Leads to symptoms of irregular palpitations,
fatigue, malaise.
Atrial Dysrhytmias
—  Treatment of Atrial Fibrillation
—  1 Depends on cause and duration, patient
symptoms, age and comorbidities. Many patients
with AF converts to sinus rhythm within 24 hours
with no Tx.
—  2 Stable & Unstable AF: same as Atrial Flutter.
—  A. Unstable: Electrical Cardioversion (Note:
Cardioversion of AF that has lasted longer than 48
hours should be avoided unless pt received
anticoagulants due to high risk for embolization of
atrial thrombi.)
Atrial Dysrhytmias
—  Treatment of Atrial Fibrillation
—  Effective in controlling the ventricular rate
in Atrial Fibrillation:
—  1 Calcium Channel Blockers [Diltiazem
(Cardizem, Dilacor, Tiazac) and Verapamil
(Calan, Isoptin, Verelan).
—  2 Betablockers
—  3 Digoxin (used in pt with poor cardiac
function: ejection fraction < 40%)
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Atrial Dysrhytmias
—  Treatment of Atrial Fibrillation
—  Effective in controlling the ventricular rate
in Atrial Fibrillation:
—  4. Warfarin (for those with increased risk of
stroke: HTN Heart Failure, History of
Stroke)
—  5. Aspirin (substituted for warfarin – when
contraindicated.)
1. PVC Premature Ventricular Complex
—  PVC is an impulse that starts in a ventricle
and is conducted through the ventricles
before the next normal sinus impulse.
—  In pts without disease, PVC’s are not
serious.
—  In pts with acute MI, PVC’s may need more
aggressive therapy.
—  PVCs may possibly lead to or indicate VT
(ventricular tachycardia).
2. VT Ventricular Tachycardia
—  Three or more PVC’s in a row, at a rate
exceeding 100bpm-200bpm. May
precede Ventricular Fibrillation. VT is an
emergency because patients are usually
unresponsive and pulseless.
—  Causes
—  1. The same for PVC.
—  2. CAD (Coronary Artery Disease)
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DYSRHYTHMIAS
—  C. VENTRICULAR DYSRHYTHMIAS
—  1. PVC Premature Ventricular
Complex
—  2. VT Ventricular Tachycardia
—  3. VF Ventricular Fibrillation
—  4. IVR Idioventricular Rhythm
—  5 VA Ventricular Asystole
1. PVC Premature Ventricular Complex
—  Causes
—  1. Substances: PVC can occur in healthy
people (with the use of caffeine, nicotine, or
alcohol).
—  2. Cardiac Ischemia or Infarction
—  3. Increased Heart workload (exercise,
fever, hypervolemia, heart failure,
tachycardia, electrolyte imbalance –
especially hypokalemia).
2. VT Ventricular Tachycardia
—  Characteristics
—  1 V rate: 100-200bpm
—  2 A Rate: Sinus Rhythm. Maybe indeterminable
—  3. QRS: normal 0.12sec or >, abnormal shape
—  4. P Wave: Difficult to detect. PR interval are
irregular if P waves seen
—  5. P:QRS ratio – more QRS than P Waves
—  Treatment: Cardioversion / Defibrillation
(TOC).
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3. Ventricular Fibrillation
—  Rapid & organized ventricular rhythm that
causes ineffective quivering of the ventricles.
There is no atrial activity on ECG.
—   Characteristics:
—  1 Vrate: >300bpm. V Rhythm: irregular, no
pattern.
—  2 QRS Complex: Irregular, unrecognizable.
—  3 Absence of audible heartbeat, palpable
pulse, & respirations. Cardiac arrest &
death are imminent if VF is not corrected.
4. Idioventricular Rhythm
—  Aka Ventricular Escape Rhythm occurs
when the impulse starts in the conduction
system below the AV node. When the
sinus fails to create an impulse (eg. From
increased vagal tone) or when an impulse is
created but cannot be conducted through the
AV node (due to AV block), the Purkinje
Fibers automatically discharge an
impulse.
4. Idioventricular Rhythm
— Intervention
— 1. Identify underlying cause
— 2. Administer IV atropine & vasopressor
medications and initiate emergency
transcutaneous pacing.
— 3. Bed rest is prescribed so as not to
increase the cardiac workload.
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3. VF Ventricular Fibrillation
—  Treatment
—  1 Immediate Defibrillation is treatment of choice.
—  2 Activation of Emergency Services. * 1&2 Placing a
call for emergency assistance and defibrillator takes
precedence over CPR. Application of an AED
(Automatic External Defibrillator) is included in
BLS classes.
—  3. After defibrillation: eradicate the cause &
administer vasoactive & antiarrhythmic
medications alternating with defibrillation to
convert VF to normal sinus rhythm.
4. Idioventricular Rhythm
—  Characteristics (when not caused by AV block)
—  1. V Rate: ranges from 20-40, If the rate
exceeds 40, the rhythm is known as
accelerated idioventricular rhythm (AIVR)
—  2. V rhythm: regular
—  3. QRS shape & duration: Bizarre abnormal
shape. Duration is 0.12 seconds or more.
5 VA Ventricular Asystole
— Commonly called flatline.
—  C h a r a c t e r i z e d
by absent QRS
complexes although P Waves may be
apparent for a short duration in two
different leads.
— There is no heartbeat, no palpable
pulse, no respiration. Without
immediate intervention, VA is fatal.
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5 VA Ventricular Asystole
—  Treatment
—  1. CPR and Emergency services are necessary to
keep the patient alive.
—  2. Identify causes: Hypoxia, acidosis, severe
electrolyte imbalance, drug overdose, hypothermia.
—  3. Intubation and IV access.
—  4. Transcutaneous pacing
—  5. Bolus of epinephrine should be administered
and repeated at 3-5minute intervals followed by
1mg boluses of atropine at 3-5minute intervals.
D. CONDUCTION ABNORMALITIES
—  AV Blocks occur when the conduction of the
Atrial impulse to the Ventricle through the
AV nodal area is decreased or stopped.
—  To Assess Conduction abnormalities
—  1. Identify the rhythm (sinus rhythm, sinus
arrhythmia)
—  2. Identify the PR interval for possible AV
Block.
D. CONDUCTION ABNORMALITIES
—  Clinical Signs & Symptoms
—  1 1 st degree AV block rarely causes
hemodynamic effect.
—  2 Other blocks may result in decreased HR,
CO, perfusion to vital organs (brain, heart,
kidneys, lungs, and skin).
—  3 3rd degree blocks (from Digitalis) toxicity
may be stable or (from MI) unstable.
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DYSRHYTHMIAS
—  D. CONDUCTION ABNORMALITIES
—  1. 1st D AV Block
—  First Degree Atrio-Ventricular Block
—  2. 2nd D AV Block
—  Second Degree Atrioventricular Block
—  Type 1 & Type 2
—  3. 3rd D AV Block
—  Third Degree Atrioventricular Block
D. CONDUCTION ABNORMALITIES
—  Causes of blocks
—  1. Medications (digitalis, calcium channel
blockers, beta-blockers)
—  2. Myocardial ischemia & infarction
—  3. Myocarditis
—  4. Valvular disorder
—  5. Increased Vagal tone (from suctioning,
anal stimulation) with sinus bradycardia.
D. CONDUCTION ABNORMALITIES
—  Treatment
—  1. Always treat the patient, not the rhythm
—  2. Treatment is based on the hemodynamic effect of
the rhythm.
—  3. Transcutaneous pacing: temporary means of
pacing a patient’s heart using a defibrillator to
deliver electric current through the patient’s chest.
Current is increased until there is Electrical or
Mechanical capture [QRS complex with tall, broad T
wave]. SpO2 is used to confirm mechanical
capture.).
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1st D AV Block
First Degree Atrio-Ventricular Block
—  Occurs when all the atrial impulses are
conducted through the AV node into the
ventricles at a rate slower than normal.
—  Characteristics
—  A. V & A rate & rhythm: depends on underlying
rhythm. B. QRS shape & duration: Normal or
abnormal. C. P Wave: Shows sinus rhythm
—  D. PR Interval: Greater than 0.20 seconds
(normal is 0.12)
—  E. P:QRS Ratio = 1:1
2nd D AV Block
Second Degree Atrio-Ventricular Block
— Type 1 Characteristics
—  The RR starts off with long
interval & gradually shortens until
there is another long RR.
— PR interval becomes longer with each
succeeding ECG complex until there is
a P Wave not followed by a QRS.
3rd D AV Block
Third Degree Atrio-Ventricular Block
—  AKA AV dissociation or Complete block.
Occurs when no atrial impulse is
conducted thru AV node into the ventricles.
—  In 3rd degree AV Block, 2 impulses stimulate
the heart: 1 stimulate the atria (P Wave) while
another 1 stimulates the ventricles (junctional
or ventricular escape rhythm = QRS). P waves
may be seen but the atrial electrical activity is
not conducted down into the ventricles to cause
QRS complex.
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2nd D AV Block
Second Degree Atrio-Ventricular Block
— Type 1
— Occurs when all but one of the
atrial impulses are conducted
through the AV node into the
ventricles. Each atrial impulse
takes a longer time for conduction
than the one before until one
impulse is fully blocked.
2nd D AV Block
Second Degree Atrio-Ventricular Block
— Type 2
— Occurs when only some of the atrial
impulses are conducted through
the AV node into the ventricles.
— Type 2 Characteristics
— P:QRS ratio = 2:1, 3:1, 4:1, 5:1
3rd D AV Block
Third Degree Atrio-Ventricular Block
—  3rd D AV Block Characteristics
—  PP & RR interval both regular.
—  PP and RR intervals are not equal.
—  PR interval is very irregular
—  P: QRS ratio = more P waves than QRS
complex.
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3rd D AV Block
Third Degree Atrio-Ventricular Block
—  Treatment
—  1. Increase the HR to produce a normal CO.
—  2. Pt is stable with no symptoms: decrease the
cause (withholding medication or treatment).
—  3. For SOB, chest pains or lightheadedness, or low
BP, an IV bolus of atropine is initial TOC.
—  4. If pt does not respond to Atropine or has
Acute MI, transcutaneous pacing is started.
—  5. Permanent pacemaker may be necessary if
block persists.
DYSRHYTHMIAS
1 Pacemaker Therapy
— A pacemaker is an electronic device
that provides electrical stimuli to
the heart muscle. Pacemakers are used
in a pt with a slower than normal
impulse formation or a conduction
disturbance that causes symptoms.
They may also be used to control some
tachydysrhythmias that do not
respond to medication therapy.
DYSRHYTHMIAS
2 Cardioversion & Defibrillation
—  Treatments for tachydysrhythmias. They are
used to deliver an electrical current to
depolarize a critical mass of myocardial cells.
When the cells repolarize, the sinus node is
usually able to recapture its role as the
pacemaker.
—  The difference between cardioversion and
defibrillation is the timing of electrical current
delivery. Defibrillation is usually performed as
an emergency procedure. Cardioversion is
usually a planned procedure.
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DYSRHYTHMIAS
—  E. Adjunctive Modalities & Management
—  1 Pacemaker Therapy
—  2 Cardioversion & Defibrillation
—  Cardioversion
—  Defibrillation
—  3 Cardiac Conduction Surgery
—  Endocardial Isolation
—  Endocardial Resection
DYSRHYTHMIAS
1 Pacemaker Therapy
—  1 Biventricular (both ventricles) pacing
may be used to treat advanced heart failure.
—  2 Permanent pacemakers are used most
commonly for irreversible complete
heart block.
—  3 Temporary pacemakers are used (eg.
After MI, after open heart surgery) to
support patients until they improve or
receive a permanent pacemaker.
DYSRHYTHMIAS
— Cardioversion involves the delivery of a
timed electrical current to terminate a
tachydysrhythmia. In cardioversion, the
defibrillator is set to synchronize with
the ECG on a cardiac monitor so that the
electrical impulse discharges during
ventricular depolarization (QRS
complex). (If done on T wave = VT)
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DYSRHYTHMIAS
—  Defibrillation is used in emergency situations
as the treatment of choice for VF and pulseless
VT.
—  Defibrillation depolarizes a critical mass of
myocardial cells at once. When they repolarize, the
sinus node usually recaptures its role as the
pacemaker.
—  The voltage required is usually higher than
cardioversion. If 3 defibrillations of increasing
voltage have been unsuccessful, CPR is initiated
and ALS treatments are begun.
DYSRHYTHMIAS
—  (ICD) Implantable Cardioverter
Defibrillator is a device that detects &
terminates life-threatening episodes of
VT or VF in high risk patients. An ICD
consists of a generator and at least one
lead that can sense intrinsic electrical
activity and deliver an electrical impulse.
The device is implanted much like a
pacemaker.
D. CONDUCTION ABNORMALITIES
—  Collaborative Problems (Potential complications)
—  1. Heart Failure may develop.
—  2. Thromboembolism (potential complication of AF).
—  3. Medication Adverse Effects
—  Nursing Interventions
—  1. Monitor & manage dysrhythmias. Evaluate the VS
and hemodynamics.
—  2. Monitor pt: lightheaded, dizzy, or fainting.
—  3. Monitor dysrhythmia (Obtain 12 Lead ECG, analyze
rhythm strips).
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DYSRHYTHMIAS
—  The use of epinephrine or vasopressin may
make it easier to convert dysrhythmia to a normal
rhythm with defibrillation. These drugs also
increase cerebral and coronary artery blood flow.
After the meds is given, 1 minute of CPR is
performed, defib is again administered.
Antiarrhythmic meds such as amiodarone
(Cordarone, Pacerone), Lidocaine (xylocaine), Mg
or Procainamide are given if V dysrhythmia
persists. Treatment continues until stable rhythm
resumes or it is determined pt cannot be revived.
D. CONDUCTION ABNORMALITIES
—  NURSING DIAGNOSIS
—  1 Decreased CO
—  2 Anxiety RT fear of the unknown
—  3 Deficient knowledge about the dysrhythmia & Tx
Planning and Goals
—  1. Maintain CO
—  2. Minimize Anxiety
—  3. Acquiring knowledge
—  4. Eradicate or decrease incidence of dysrhythmias
(by decreasing contributory factors)
D. CONDUCTION ABNORMALITIES
—  Nursing Interventions
—  4. Manage meds, dysrhythmia (caffeine, stress, meds
non-compliance). Assist lifestyle changes.
—  5. Minimize anxiety: calm & reassuring attitude.
—  Home & Community Based Care
—  6. Teach self-care. Explain dysrhythmia & CO.
Emphasize importance of medications timing:
maintain a therapeutic serum level.
—  7. For lethal dysrhythmias, establish a family plan of
action in case of emergency.
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Evaluation: Abnormal Conduction
(Expected Patient Outcomes)
—  1. Maintains normal CO by demonstrating
—  A. Normal VS, LOC.
—  B. Decreased episodes of dysrhythmias.
—  2. Reduced anxiety & ability to act in emergency.
—  3. Understanding of dysrhythmias & treatment.
—  A. Dysrhythmias & effects.
—  B. Meds & rationale. Therapeutic serum level.
—  C. Describes a plan to decrease dysrhythmia.
—  D. Actions in case of emergency.
CARDIAC CONDUCTION SURGERY
—  1. Endocardial Isolation:
—  An incision separates the area where the
dysrhythmias originates from the endocardium.
The incision, stitch & resulting scar tissues
prevent dysrhythmia from affecting the whole
heart.
—  2. Endocardial Resection
—  The origin of the dysrhythmia is identified &
peeled away from the endocardium. No
reconstruction or repair is necessary.
(CAD) CORONARY ARTERY DISEASE
— A. Coronary Atherosclerosis
— Hardening & Blockage
— B. Angina Pectoris
— Acute Ischemia: Decreased blood flow
— C. Myocardial Infarction
— Chronic Ischemia, Necrosis
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Abnormal Conduction
Electrophysiologic Studies (EP)
—  An EP is a type of cardiac catheterization with
multiple electrodes inserted through the femoral
vein, threaded into the IVC, advanced into the heart.
The electrodes allow the introduction of a pacing
stimulus at a precise time interval (programmed
stimulation).
—  An EP is used to:
—  1. Assess function or dysfunction of SA & AV nodes.
—  2. Assess antiarrhythmic meds & devices.
—  3. Treat dysrhythmias by destroying causative cells
(ablation therapy).
CARDIAC CONDUCTION SURGERY
—  3. Catheter Ablation Therapy (CAT)
—  Specific cells that cause tachydysrhythmias
are destroyed during or after EP. Indications
for CAT are: AF & unresponsive VT.
—  3 Ablation methods
—  a. Radiofrequency ablation.
—  b. Cryoablation
—  c. Electrical Ablation
(CAD) CORONARY ARTERY DISEASE
— I CORONARY ARTERY DISEASE
(CAD):
— Studies indicate that CAD is a repeated
inflammatory response to artery wall
injury leading to changes in the arterial
wall. Most prevalent Cardiovascular disease.
—  High levels of CRP (or C-reactive proteins = a
marker of vascular endothelium.) are
associated with calcification and risk of CAD.
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A. CORONARY Atherosclerosis
—  The abnormal accumulation of
lipid, or fat substances & fibrous
tissue in the coronary blood vessel
wall. The lipids, fat substances or
fibrous tissues create blockages or
narrow the vessels and reduces
blood flow to the myocardium.
A. CORONARY Atherosclerosis
—  Manifestations (SS)
—  Progressive blood flow blocks: Ischemia
—  Chest pain due to ischemia: AP
—  ECG changes
—  High level of Cardiac Enzymes
—  Dysrhythmias
—  Sudden Death (Sudden Cardiac Death)
A. CORONARY Atherosclerosis
—  HDL (Normal HDL 40-60mg/dL)
—  Promotes use of total cholesterol by transporting
LDL to the liver where it is biograded & excreted.
—  LDL (160mg/dL. <100 for those with CAD)
—  Has a harmful effect on the arterial wall &
accelerates atherosclerosis.   Healthy Diet: Serving size, fat serving,
—  Desired: Low LDL and High HDL. LDL &
Cholesterol: controlled through diet and activity
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A. CORONARY Atherosclerosis
—  Pathophysiology:
—  Fat & lipids are deposited in arterial intima wall
—  Inflammatory response (T Lymphocytes &
monocytes that become macrophages) infiltrate
the area to ingest the lipids & then die
—  Smooth muscle cells within vessels form a
fibrous cap over fatty core called atheromas or
plaques that protrude into the lumen
—  Narrowing & obstructing blood flow.
—  (Thrombus into emboli: ischemia, AP, AMI)
A. CORONARY Atherosclerosis
—  Modifiable Risk Factors (Precipitating)
—  1 Increased Lipid (LDL), Cholesterol Levels
—  2 Cigarette-Tobacco
—  3 HTN
—  4 DM
—  5 Lack of Estrogen (Women, Menopause)
—  6 Physical Inactivity
—  7 Obesity (BMI > 28)
—  Non-Modifiable: Age, Heredity, African
A. CORONARY Atherosclerosis
NURSING INTERVENTIONS
—  1 Promote Lifestyle Changes.
—  Prevention of CAD through the 4 Modifiable
Risks factors:
—  A . D i e t a r y m e a s u r e s t o r e d u c e
Cholesterol. Consult a dietician (Heart
saturated fat, cholesterol, fiber). Low salt low
fat. Grill.
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A. CORONARY Atherosclerosis
NURSING INTERVENTIONS
—  1 Promote Lifestyle Changes.
—  B. Stop Smoking (Reduces CAD risk 50%)
—  B.1. Smoking increases blood Carbon
Monoxide level.
—  B.2. Smoking increases Nicotinic Acid: a
catecholamine that cause coronary arteries to
constrict, & increases HR & BP.
—  B.3. Smoking increases platelet adhesion =
higher probability of thrombus formation.
A. CORONARY Atherosclerosis
NURSING INTERVENTIONS
—  D. Control DM (Blood sugar >140, or HbA1C >7)
—  2. Other Measures:
—  E. HRT: Estrogen
—  F. Physical Activity: Regular exercise (30mins x
3-4x a week. Walk & swim: does not stop ability to
talk. Stop: chest pain, SOB, dizziness, lightheaded).
—  G. Weight Loss Program (Obesity is BMI >
28). Consult Dietitian
—  H. Folic Acid (reduces homocysteine)
A. CORONARY Atherosclerosis
NURSING INTERVENTIONS
—  D. Nicotinic Acids or Niacin (Nicor, Niaspan)
decrease lipoprotein synthesis, lowers triglycerides,
& increases HDL.
—   E. Folic Acid or Fibrates (Clofibrate [Atromid-S]
decreases the synthesis of cholesterol, reduces
triglycerides, increases HDL.
—  F . B i l e A c i d s e q u e s t r a n t s o r r e s i n s
(Cholestyramine [LoCholest, Questran, Prevalite])
bind and breakdown cholesterol in the intestine,
lowers LDL.
12/10/16
A. CORONARY Atherosclerosis
NURSING INTERVENTIONS
—  C. Decrease HTN (140/90mmHg)
—  C.1. HTN leads to stiffening/hardening of
blood vessels which leads to injury &
inflammatory response.
—  C.2. HTN increases the work of the LV
(pumps harder to eject blood) which causes
the heart to enlarge & thicken
(hypertrophy). This may eventually lead to
Heart Failure.
—   
A. CORONARY Atherosclerosis
NURSING INTERVENTIONS
—  3. Medications as Rx
—  A. Thrombolytic Therapy
—  B. HRT: Hormone Replacement Therapy
—  C. Lipid lowering agents
—  1. HMG-CoA (statins) blocks cholesterol
synthesis, lowers LDL & triglycerides, inc HDL.
—  Levostatin (Mevacor, 20-80mg)
—  Prevastatin (Pravachol, 20-40mg)
—  Simvastatin, Fluvastatin (Zocor, Lescol 20-80mg)
—  Atorvastatin (Lipitor, 10-80mg)
B. Angina Pectoris
—  Episodes of paroxysmal pain or pressure in
the anterior chest. The cause is insufficient
coronary blood flow (ischemia) which leads
to a decreased oxygen supply not enough to
meet the increased myocardial oxygen demand.
—   Pathophysiology
—  Atherosclerosis or Atherosclerotic Disease
obstructs a significant portion of the major
coronary artery.
13
 12/10/16

B. Angina Pectoris B. Angina Pectoris

—  Typical AP pain factors: —  Types & Characteristics of AP
—  1 Physical exertion (increases O2 demand)
—  2 Exposure to Cold (causes vasoconstriction —  1. According to Severity
& increase BP, increases O2 demand) —  Type Activity evoking AP Limits to
—  3 Heavy Meals: increase blood flow to
mesenteric area for digestion, reducing blood Activity
available to heart. —  I Prolonged Exertion None
—  4. Stress or Emotions: Causes release of —  II Walking >2Blocks Slight
Adrenaline, increases BP, increases myocardial —  III Walking<2Blocks Marked
workload. —  IV Minimal or at Rest Severe

B. Angina Pectoris B. Angina Pectoris

—  2. Types of AP
—  1 Stable Angina: predictable & consistent pain on
exertion relieved by rest.
—  2 Unstable Angina (aka Preinfarction or
Crescendo Angina) frequent & longer than stable)
—  3 Intractable Angina (Refractory angina) severe
incapacitating chest pain
—  4 Variant Angina (aka Prinzmetal Angina) is pain
at rest with reversible ST segment elevation.
—  5 Silent Ischemia: ECG changes during a stress
test but patient reports no pain symptoms.
—  Manifestations or SS
—  Anxiety. Angina subsides with rest & nitroglycerin.
—  Heavy Sensation in upper chest. Mild to severe
retrosternal chest pain (behind upper middle 3rd
sternum)
—  Poorly localized pain or radiating to neck, jaw,
shoulders, inner aspects of upper (left) arms.
—  Choking, strangling, Indigestion
—  Weak or numb arms, wrists, hands with pain
—  SOB, Diaphoresis, Dizziness, Lightheadedness, N&V

B. Angina Pectoris B. Angina Pectoris

—  Assessment & Diagnosis —  Management is aimed at decreasing O2 demand
—  Based on SS manifestations of ischemia history of the myocardium & increasing the O2 supply.
—  12 Lead ECG —  1. Medical management: Nitroglycerin & rest.

—  Blood Values —  2. Surgical Revascularization procedures (to

—  Exercise or Pharmacologic Stress Test (ECG)
—  Recommended: Cardiac Catheterization &
Coronary Artery Angiography)
restore blood supply)
—  A. PCI Percutaneous Coronary Interventional
Procedures
—  B. CABG (Coronary Arterial Bypass Graft)
—  C. PTMR (Percutaneous Transluminal Myocardial
Revascularization)

14

B. Angina Pectoris
—  A . PCI Percutaneous Coronary
Interventional Procedures
—  A.1. PTCA Percutaneous Transluminal
Coronary Angioplasty
—  A.2. Intracoronary stents
—  A.3 Atherectomy
B. Angina Pectoris
—  1 Medications & Therapy for Angina:
—  A. Nitroglycerin
—  B. Betablocking Agents
—  C. Calcium Channel Blockers
—  D. Antiplatelet & Anticoagulant Medications
—  E. Oxygen Administration
—  F. Alternative Therapies.
B. Angina Pectoris
—  A. Nitroglycerin Tablet Health Teaching:
—  2. Nitroglycerin is volatile & inactivated by heat,
moisture, air, light, and time. Carry medication
at all times in its original capped dark bottle
(unstable). Do not store in metal or plastic
pillboxes. Renew supply every 6 months.
—  3. Nitroglycerin may be taken in anticipation of
activities that may produce pain (before
exercise, stair climbing, sexual intercourse and
stress).
12/10/16
B. Angina Pectoris
—  1 Medications & Therapy for Angina:
—  A. Nitroglycerin
—  B. Betablocking Agents
—  C. Calcium Channel Blockers
—  D. Antiplatelet & Anticoagulant Medications
—  E. Oxygen Administration
—  F. Alternative Therapies.
B. Angina Pectoris
—  A. Nitroglycerin Health Teaching:
—  Self-administered prn, sublingual in tablet
& spray.
—  Nitroglycerin Tablet:
—  1. Make sure the mouth is moist, saliva is not
swallowed until the nitroglycerin tablet
dissolve. If pain is severe, crush tablet with
teeth for faster sublingual absorption.
B. Angina Pectoris
—  A. Nitroglycerin Tablet Health Teaching:
—  4. Pt should note how long it takes for
nitroglycerin to relieve discomfort.
—  5. If pain persists after taking 3 SL tablets at 5
minute intervals, emergency medical services
should be called (possible MI).
—  6. Possible SE of Nitroglycerin: flushing,
throbbing headache, Hypotension, Tachycardia.
15

B. Angina Pectoris
—  Topical Nitroglycerin (applied to skin as
patch or paste)
—  1. Read instructions.
—  2. Rotate site to avoid skin irritation.
—  3. Apply in well perfused area for absorption.
Not to hairy parts or scarred tissues.
—  4. Protect clothing from the oil base in the
paste.
B. Angina Pectoris
—  B. Betablocking Agents
—  Reduces O2 consumption by blocking Beta
Adrenergic Sympathetic Stimulation. The
result is a slow & decreased HR, decreased
BP, decreased contractility (force) which
balances demand & supply of O2. Helps
control chest pain. Examples
—  Propranolol (Inderal), Atenolol (Tenormin)
—  Metoprolol (Lopressor, Toprol)
B. Angina Pectoris
— B. Betablocker SE
— Nursing Intervention:
— 1. Monitor VS (HR, BP, RR) & ECG
closely.
— 2.Caution against abruptly stopping
Betablockers (withdrawal syndromes
occur). R: Angina may worsen, MI
develops.
12/10/16
B. Angina Pectoris
—  Topical Nitroglycerin (patch or paste)
—  5. Prevent tolerance: Avoid long-term
equally spaced dosing schedule or application
of topical nitroglycerin. Rx: paste is applied
3-4x a day or q6 hours (exclude a
midnight dose). Patch is applied every
morning & removed at 10pm.
—  Allow a 6-8hours nitrate free period to
prevent tolerance.
B. Angina Pectoris
—  B. Betablocker SE & Possible CI:
(Parasympathetic)
—  Hypotension, Bradycardia
—  AV Block
—  Decompensated Heart Failure
—  Bronchoconstrictions
—  Others: Hyperlipidemia, Fatigue,
Depression, Decreased Libido, Masking
of Hypoglycemia.
B. Angina Pectoris
—  C. Calcium Channel Blockers decrease
SA & AV node conductivity. Result is slower
HR & decreased contraction (decreased
inotropic effect), decreased heart workload.
Examples (*DOC):
—  Amlodipine (Norvasc)* Felodipine (Plendil) *
—  Verapamil (Calan, Isoptin, Verelan)
—  Diltiazem (Cardizem, Dilacor, Tiazac)
—  [Nifedipine (Procardia) note poor tolerance &
increases MI risk.]
16

B. Angina Pectoris
—  D. Antiplatelet & Anticoagulant Medications
—  1. Aspirin
—  2. Clopidogrel and Ticlopidine
—  3. Heparin
—   E. Oxygen Administration
—  Administered at onset of chest pain to increase
O2 & decrease angina.
—  The therapeutic effect of O2 is determined by
observing rate & rhythm of respiration, SpO2.
B. Angina Pectoris
—  Nursing Diagnoses
—  1 Ineffective Myocardial Tissue Perfusion
secondary to CAD as evidenced by chest pain or
equivalent.
—  2 Anxiety RT fear of Death
—  3 Deficient knowledge about the underlying
disease and methods for avoiding complications
—  4 Non-compliance, ineffective management of
therapeutic regimen RT failure to accept
necessary lifestyle changes
B. Angina Pectoris
—  Plan and Goals
—  Immediate & appropriate treatment of Angina
—  Prevent Angina
—  Reduce of Anxiety
—  Awareness of Disease process & understanding
Rx care
—  Adherence to Self-Care Program
—  Absence of Complications
12/10/16
B. Angina Pectoris
—  F. Alternative Therapies. As researched:
—  1. Acupuncture
—  2. IV ginseng (Panax Quinquefolium)
—  3. Astralagus (Astralagus Membranaceus)
—  4. Angelica (Angelica Sinensis)
—  5. CoQ10 or Coenzyme Q10 prevents heart
failure progression.
—  (6. Meditation: decreases HR, BP, O2
demand, Anxiety, Stress)
B. Angina Pectoris
—  Collaborative Problems &
—  Potential Complications
—  Acute Pulmonary Edema
—  Congestive Heart Failure
—  Cardiogenic Shock
—  Dysrhythmias & Cardiac Arrest
—  MI
—  Myocardial Rupture
—  Pericardial Effusion & Cardiac Tamponade
B. Angina Pectoris
—  Nursing Interventions
—  1. Manage pain immediately. Stop all activities.
Bed rest. Semifowlers. R: to reduce O2 reqmt.
—  2. Assess type of Angina - same or different?
Different angina = worsening. Pain assessment:
—  P = Position, location, provocation
—  Q = Quality
—  R = Radiation, Relief
—  S = Severity (0-10), other Symptoms
—  T = Timing (how long ago did pain start)
17

B. Angina Pectoris
—  3. Assess VS, SS of respiratory distress. If in
hospital, assess for ECG changes in ST segment
& T wave. (Note: ECG is non-diagnostic in MI.
Abnormal Q Wave: develop within 1-3 days)
—  4. Nitroglycerin
—  5. Reduce Anxiety. Assess & address fears.
Therapies: Music & Movies etc.
—  6. Prevent Pain: Balance activities with rest
periods.
—  7. Teach Home Care.
B. Angina Pectoris
—  Expected Outcomes
—  3. Understands ways to avoid complications.
—  a. Describes the process of angina, how to prevent
complications
—  b. Exhibits normal ECG & Cardiac enzyme levels
—  d. No SS of Acute MI
—  4. Adheres to self care programs
—  a. Takes meds as Rx
—  b. Keeps health appointments
—  c. Implements plan for reducing risk factors
C. Myocardial Infarction
— “Time is muscle.”
— The area of infarction takes time to
develop. As the cells are deprived of
O2, ischemia develops. Cellular
(muscle) injury occurs. Over time,
lack of O2 results in infarction or
death of (muscle) cells.
12/10/16
B. Angina Pectoris
—  Expected Outcomes
—  1. Pt reports pain is relieved promptly
—  a. Recognizes symptoms & acts immediately
—  b. Seeks medical assistance if pain persists or
changes in quality
—  2. Reports decreased anxiety
—  a. Accepts diagnosis
—  b. Diet regimen, lifestyle change
—  c. Does not exhibit SS of anxiety.
C. Myocardial Infarction
—  AKA Heart Attack, Coronary Occlusion, MI.
The myocardial cells are permanently
destroyed (die, necrosis). Acute Coronary
Syndrome: AP & MI are considered
different points along the same continuum.
—  Like unstable angina, MI is caused by
ischemia to coronary artery due to
atherosclerosis & blockage caused by
embolus or thrombus.
C. Myocardial Infarction
—  Pathophysiology: Occlusion (Atherosclerosis) –
Decreased blood & O2 - Ischemia – cellular injury -
necrosis - MI
—  Causes (Imbalance: decreased O2 supply &
increased O2 demand)
—  1 Atherosclerosis
—  2 Vasospasm (constriction or narrowing)
—  3. Decreased O2 (Blood loss, anemia, or low BP)
—  4 . I n c r e a s e d d e m a n d f o r O 2 ( r a p i d H R ,
thyrotoxicosis, cocaine)
18

C. Myocardial Infarction
—  Manifestations
—  1. Sudden chest pain that continues despite
rest & medication.
—  2. Asymptomatic : 50-63%.
—  3. Same as AP. Sympathetic or SNS SS: HR &
RR may be increased. Anxious or restless.
Cool, pale, moist skin. (Atypical symptoms:
SOB, female, younger than 55yo, normal
ECG.)
C. Myocardial Infarction
—  Diagnosis
—  B. Laboratory tests diagnose MI (CK or
creatinine Kinase & LDH levels or Lactic
Dehydrogenase)
—  1 CK MM = skeletal Muscle
—  2 CK BB = Brain Tissues
—  3 CK MB = Heart Muscles. Assesses
Acute MI. Value increases a few hours to 24
hours of MI.
C. Myocardial Infarction
—  Medical management goal is:
—  1. Minimize myocardial damage, prevent Cx.
—  2. Preserve myocardial function
—  Goals are achieved by
—  1.Reperfusing area: Thrombolytics or Sx (PTCA)
—  2. Reducing O2 demand
—  3. Increasing O2 supply with meds, O2, bed rest.
—  Resolution of pain & ECG changes are indicators
that O2 demand & supply are balanced.
12/10/16
C. Myocardial Infarction
—  Diagnosis Prognosis depends on obstruction.
—  A. ECG helps diagnose acute MI if taken within
10minutes of pain or arrival at hospital. Usual MI
locations: LV. ECG changes:
—  T wave inversion (repolarization is delayed)
—  ST segment elevation (injured cells repolarize more
rapidly than normal cells)
—  ST segment depression (injury on endocardium)
—  Abnormal Q wave infarction: develop in 1-3days =
no depolarization current from necrotic tissue.
C. Myocardial Infarction
—  Diagnosis
—  C. Myoglobin: Heme protein that helps
transport O2. Myoglobin starts to increase
within 1-3 hours & peaks in 12 hours of heart
muscle injury. Negative results R/O MI.
—  E. Troponin (C, I, T). Troponin I & T levels
increase in a few hours and remains elevated
for weeks & helps identify a Unstable Angina
or Acute MI.
C. Myocardial Infarction
Pharmacology & Therapies
—  1. Thrombolytics. Dissolves clots & thrombus in
coronary artery (thrombolysis) allowing blood to
flow thru (reperfusion) minimizing infarction size,
preserving ventricular function. Administered asap
(30mins) after MI SS. Example:
—  A. Streptokinase (Kabikinase, Streptase). CI if
recently infected with Streptococcus.
—  B. Alteplase (Activase)
—  C. Reteplase (r-PA, TNKase)
—  D. Anistreplase (Eminase)
19

C. Myocardial Infarction
Pharmacology & Therapies
—  2. Analgesics: Morphine Sulfate (Duramorph,
Astramorhph) reduces heart workload.
—  3. Angiotensin Converting Enzyme
Inhibitors (ACE-I).
—  4 . P C I P e r c u t a n e o u s C o r o n a r y
Intervention Used to treat Atherosclerosis: it
opens the occluded coronary artery in Acute MI,
& promotes reperfusion of heart. PCI is
performed immediately in 60 minutes (Time is
muscle).
C. Myocardial Infarction
—  Nursing Diagnoses
—  1. Ineffective Cardiopulmonary tissue perfusion RT
reduced coronary blood flow from coronary
thrombus & atherosclerotic plaque.
—  2. Potential impaired gas exchange RT fluid overload
from left ventricular dysfunction.
—  3. Potential altered peripheral tissue perfusion RT
decreased CO from left ventricular dysfunction.
—  4. Anxiety RT fear of death.
—  5. Deficient knowledge about post MI self-care.
C. Myocardial Infarction
—  Planning and Goals
—  The main goal is balance O2 supply with O2
demand as manifested by:
—  1 Relieve pain or ischemic SS. Prevent next
MI.
—  2 Absence of respiratory dysfunction
—  3 Attain & maintain adequate tissue perfusion
by decreasing the heart’s workload, reduced
anxiety.
12/10/16
C. Myocardial Infarction
Pharmacology & Therapies
—  5. Cardiac Rehabilitation
—  An after-MI education program to extend &
improve the quality of life, limit effects of
atherosclerosis, return the pt to work & a pre-
illness lifestyle, enhance psychosocial &
vocational status & prevent another MI.
—  Physical activity & conditioning is gradual.
Pt’s are instructed to stop exercise if these
symptoms develop: chest pain, dyspnea,
weakness, fatigue, palpitations.
C. Myocardial Infarction
—  Potential Complications
—  1. Acute pulmonary Edema
—  2. Heart Failure
—  3. Cardiogenic Shock
—  4. Dysrhythmias and Cardiac Arrest
—  5. Pericardial effusion & cardiac
tamponade
—  6. Myocardial rupture
C. Myocardial Infarction
—  Revascularization with
—  1 Thrombolytic therapy
—  2 Emergent PCI
—  3 Aspirin, Betablocker, Nitroglycerin,
Heparin. Morphine (for relief of pain,
anxiety, reduction of preload)
—  4 Oxygen (Flow rate of 2-4L/min to maintain
O2Sat @96-100%)
20

C. Myocardial Infarction
—  1 Cardiac Catheterization & invasive
procedure to resolve atherosclerotic lesions.
—  A. IV or into the Coronary Artery in cardiac
catheterization laboratory.
—  B. Antiplatelet & Anticoagulant Meds
—  1. Aspirin
—  2. Clopidogrel and Ticlopidine
—  3. Heparin
C. Myocardial Infarction
—  2. Surgical Revascularization
—  A. PCI Percutaneous Coronary Intervention
—  A.1. PTCA or Percutaneous Transluminal
Coronary Angioplasty. PTCA improves blood
flow within a coronary artery by “cracking“ the
atheroma. After verifying the location of the
atheroma, a balloon tipped dilation catheter is
inflated & then deflated. Complications: closure,
bleeding, pseudoaneurysm, fistula, arterial
thrombosis and distal embolization.
C. Myocardial Infarction
— A.3 Atherectomy
— Invasive procedure removing the
atheroma or plaque from a
coronary artery using a catheter
with diamond chips that rotates like
a drill, pulverizing the lesion.
12/10/16
Invasive Coronary Artery Procedures
—  1 Percutaneous Transluminal Coronary Angioplasty(PTCA)
—  2 Transmyocardial Revascularization
—  3 Coronary Artery Revascularization
—  Traditional Coronary Artery Bypass Graft (CABG)
—  Cardiopulmonary Bypass (CPB)
—  Minimally Invasive Direct CABG (MIDCAB)
—  Combination Percutaneous Transluminal
Coronary Angioplasty & Coronary Angioplasty &
CABG
C. Myocardial Infarction
—  A.2. Intracoronary Stents or Coronary
Artery Stent
—  A stent (woven structural support for a vessel
at risk of acute closure) is placed over the
angioplasty balloon. When the balloon is
inflated, the mesh expands and presses
against the vessel wall, holding the artery
open. Prevents coronary artery recoil
(constriction) and stenosis.
C. Myocardial Infarction
—  B. CABG (Coronary Arterial Bypass
Graft)
—  Under GA, surgeon makes a sternal incision,
connects patient to CPB machine. A blood
vessel from another part of the patient’s
body (saphenous vein, left internal
mammary artery) is grafted distal to the
coronary lesion, bypassing the
obstruction. CPB machine is discontinued
and incision is closed. Pt is admitted to a
CCU.
21

C. Myocardial Infarction
—  CPB Cardiopulmonary Bypass
—  E x t r a c o r p o r e a l
circulation. CPB
machine uses a heart lung machine to
maintain perfusion to other body organs and
tissues while the surgeon works in a
bloodless surgical field. This procedure
mechanically circulates & oxygenates
blood for the body while bypassing the heart
and lungs.
C. Myocardial Infarction
—  Nursing Process:
—  Cardiac Surgery Patient Assessment
—  Neurologic Status
—  Cardiac Status
—  Respiratory Status
—  Peripheral Vascular Status
—  Renal Function
—  Fluid & Electrolyte Status
—  Pain
C. Myocardial Infarction
COMPLICATIONS after Cardiac Surgery
—  A. Decreased CO Causes:
— 3. HR Alterations:
—  Too fast or too slow or dysrhythmias.
— 4. Conctractility Alterations:
—  Cardiac failure, MI, Electrolyte
imbalance, hypoxia.
— 5. Decreased UO. (<25mL/hr)
12/10/16
C. Myocardial Infarction
—  MIDCAB Minimally Invasive Direct
CABG
—  Under GA, surgery prepares incisions on the
chest wall for a left or right anterior
thoracotomy or for a midsternal or midline
upper laparotomy. The graft is prepared for
the bypass.
—  C. PTMR (Percutaneous Transluminal
Myocardial Revascularization)
C. Myocardial Infarction
COMPLICATIONS after Cardiac Surgery
—  A. Decreased CO: Causes:
—  1. Preload Alterations: Too little or too much
blood volume returning to the heart because
of hypovolemia, persistent bleeding, cardiac
tamponade, or fluid overload.
—  2. Afterload Alterations: Hypertension and
arterioles are too constricted or too dilated
because of alterations in body temperature or
use of vascoconstrictors and vasodilators.
C. Myocardial Infarction
COMPLICATIONS after Cardiac Surgery
—  B. F&E Imbalance. NI:
—  1. Monitor Electrolytes specially Potassium,
Magnesium, Sodium, & Calcium.
—  2. Monitor I&O, Weight.
—  3. Monitor VS (BP, HR) CVP, Atrial pressure,
Left Atrial or Pulmonary Pressure.
—  4. Monitor Hct levels, neck vein distention,
edema, liver size, & breath sounds (crackles,
wheezing).
22

C. Myocardial Infarction
COMPLICATIONS after Cardiac Surgery
—  C. Impaired Gas Exchange: An ET tube &
ventilator assistance may be used for 24 hours.
Stable patients are extubated 2-4hours after
surgery (reduces anxiety RT inability to
communicate).
—  SS of IGE:
—  1. Restlessness, Anxiety, Fighting the ventilator
—  2. Cool Skin & Cyanosis (buccal mucosa, lips,
nailbeds, lips, earlobes)
C. Myocardial Infarction
COMPLICATIONS after Cardiac Surgery
—  NI to Restore CO
—  1. Report asap to Physician who may Rx:
—  A. BT, Fluids
—  B. Digitalis, Antidysrhythmics, diuretics,
vasodilators, vasopressors.
—  2. Ensure adequate Gas Exchange
—  A. Maintain patency of ET: suction.
—  B. Manual resuscitation with Ambu-bag to
minimize hypoxia <> suctioning.
C. Myocardial Infarction
COMPLICATIONS after Cardiac Surgery
—  NI to Restore CO
—  4. Promote Comfort
—  A. Assess verbal & non-verbal cues of Pain
—  B. Pain Activates SNS = Adrenaline = (VS) HR
increase & increased afterload & decreased CO.
—  C. PCA. Opiods & toxicity (observe for Respiratory
Depression) Note: Naloxone is opiod antagonist.
—  D. Support incision during deep breathing &
coughing
—  E. Respiratory exercises
12/10/16
C. Myocardial Infarction
COMPLICATIONS after Cardiac Surgery
—  C. Impaired Gas Exchange:
—  3. Tachycardia
—  4. Breath sounds (detect fluid in lungs & lung
expansion)
—  5. Arterial blood gasses: (SpO2, SaO2, CO2)
—  D. Impaired Cerebral Circulation:
—  Brain function
C. Myocardial Infarction
COMPLICATIONS after Cardiac Surgery
—  NI to Restore CO
—  3. Monitor F&E through I&O
—  A. Intake: IV, NGT, OFI
—  B. Output: UO, NGT drainage, Chest
Drainage
—  C. Report any dehydration, fluid overload,
electrolyte imbalance.
C. Myocardial Infarction
COMPLICATIONS after Cardiac Surgery
—  NI to Restore CO
—  5. Assess & maintain body temperature
—  A. Usually Hypothermic: warm cotton
blankets, heat lamps.
—  B. After surgery, infection can cause
hyperthermia, increasing metabolism and
cardiac workload. (Hypothermia decreases
tissue oxygenation & heart workload).
23

C. Myocardial Infarction
—  Expected Patient Outcomes
—  1. Maintain adequate CO, Gas Exchange, F&E
—  2. Pt experiences decreased symptoms of
sensory perception disturbance
—  3. Experiences relief of pain
—  4. Maintains adequate tissue perfusion
—  5. Maintains normal body temperature
—  6. Performs self care activities.
Classification of
VALVULAR DISORDERS
—  When valves do not open or close properly,
blood flow is affected.
—  1 Regurgitation: Valves do not close
completely. Blood flows backward.
—  2 Prolapse: Valve leaflet stretches back into
the atrium during systole. Blood regurgitates.
—  3 S t e n o s i s : V a l v e s d o n o t o p e n
completely. Blood flow through the valve is
reduced.
1 Mitral Valve Prolapse (MVP)
—  MVP Medical Management
—  (aimed at controlling symptoms)
—  1. Dysrhythmias:
—  A. Diet. Advise patient to eliminate caffeine,
alcohol, & smoking.
—  B. Anti-Arrhythmics medications.
—  2. Chestpain: a. Nitrates b. Calcium
channel blockers & Beta Blockers.
—  3. Heart Failure
12/10/16
VALVULAR DISORDERS
— 4 Valves
—  1 Tricuspid: RA & RV
—  2 Mitral: LA & LV
—  3 Pulmonic Valve:
—  RV & Pulmonary Artery
—  4 Aortic Valve: LV & Aorta
VALVULAR DISORDERS
1 Mitral Valve Prolapse (MVP)
—  1 Portion of the mitral valve leaflet stretches
& balloons back into the atrium during
systole (the valve does not remain closed
during V contraction).
—  2 Sometimes hereditary with no symptoms
but can progress to sudden death.
—  SS: 1. Mitral click: Extra heart sound
—  2. Arrhythmia
—  3. Pain
Valvular Disorders
1 Mitral Valve Prolapse (MVP)
—  MVP Nursing Management
—  1. Explain the need to inform Dr. of SS.
—  2. Explain need for prophylactic antibiotic
therapy during invasive procedures & possible
infections (Dental, GU or GI procedures) that
may spread systemically.
—  3. Explain diet. Read product labels of OTC
meds which may produce dysrhythmias.
—  4. Explore diet, activity, sleep & other lifestyle
factors.
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VALVULAR DISORDERS
2 Mitral Regurgitation (MR)
—  2.A. Valve do not close properly, resulting in
backflows or blood regurgitating from LV back
into the LA during systole.
—  2.B. As backward flowing blood is added to the
blood flowing in from the lungs, the LA stretches.
Eventually, LA hypertrophies & dilates.
—  2.C. Blood flow from the lungs is diminished &
the lungs become congested, adding strain to
the RV.
VALVULAR DISORDERS
2 Mitral Regurgitation (MR)
 MR Medical Management:
— 1. Same as for CHF.
— 2. Surgical intervention consists of
mitral valve replacement or
valvuloplasty (surgical repair of the
heart valves.)
VALVULAR DISORDERS
3 Mitral Stenosis (MS)
—  4. LA has great difficulty moving blood into
the ventricle because of the increased
resistance of narrowed valves.
—  5. LA dilates (stretches) and hypertrophies
(thickens) because of increased blood volume.
—  6. Pulmonary circulation becomes congested.
—  7. RV strains to contract against high
pulmonary arterial pressure. RV fails.
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VALVULAR DISORDERS
2 Mitral Regurgitation (MR)
—  2.D. Chronic MR is often asymptomatic. Acute MR
often manifests as CHF (Dyspnea, fatigue, weakness,
palpitations, SOB on exertion, cough from
pulmonary congestion)
—  MR Assessment:
—  1. Systolic Murmur – a high pitched, blowing
sound at the apex.
—  2. AF.
—  3. Diagnosis by Echocardiography
—   
VALVULAR DISORDERS
3 Mitral Stenosis (MS)
—  1. Narrowed opening of valves causes
obstruction of blood flowing from the LA into
the LV.
—  2. Usually caused by RHF or Rheumatic
Endocarditis which thickens valve leaflets &
chordae tendinae. The leaflets fuse together.
—  3 . E v e n t u a l l y , M V o r i f i c e n a r r o w s
progressively & obstructs blood flow into the
LV. A. Normal MV opening = 3 fingers
diameter. B. MS = pencil diameter.
VALVULAR DISORDERS
3 Mitral Stenosis (MS)
—  Manifestations (1-3) & Assessment (4-5)
& Diagnosis (6)
—  1. Dyspnea on exertion or DOB (as a result of
pulmonary venous hypertension).
—  2. Progressive fatigue as a result of low CO.
—  3. Hemoptysis (may expectorate blood).
Cough & experience repeated respiratory
infections.
—  4. Weak pulse and Atrial dysrhythmias: AF.
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VALVULAR DISORDERS VALVULAR DISORDERS

3 Mitral Stenosis (MS) 3 Mitral Stenosis (MS)
—  Manifestations (1-3) & Assessment (4-5) —  Medical Management
& Diagnosis (6) —  1. Antibiotic prophylaxis to prevent infection
recurrence.
—  4. Weak pulse and Atrial dysrhythmias: AF.
—  2. CHF treatment.
—  5. A low pitched, rumbling diastolic murmur is
—  3. Anticoagulants (to decrease risk of Atrial
heard at the apex.
thrombus).
—  6. Echocardiography, Electrocardiography, & —  4. Treatment for Anemia.
Cardiac Catheterization with Angiography. —  5. Surgical Treatment:
—  A. (Percutaneous Transluminal) Valvuloplasty (open
or rupture the fused mitral valves).
—  B. Mitral Valve Replacement.

Valvular Disorders Valvular Disorders

AORTIC REGURGITATION
—  1 The backflow of blood from the Aorta into the LV
during diastole.
—  2 Maybe caused by:
—  A. Inflammatory lesions that deform the leaflets of
the aortic valve, preventing them from completely
closing.
—  B. Endocarditis, congenital abnormalities, syphilis,
dissecting aneurysm (that causes dilation or tearing
of the ascending aorta) or deterioration of aortic
valve replacement.
AORTIC REGURGITATION
—  3. Pathophysiology:
—  A. Blood from aorta returns to LV during diastole
in addition to blood normally delivered by LA.
—  B. The LV dilates to accommodate increased
volume of blood. It hypertrophies to increase
muscle strength to expel more blood with above
normal force – raising BP.
—  C. Arteries attempt to compensate for higher
pressures by reflex vasodilation.
—  D. The peripheral arterioles relax, reducing
peripheral resistance & Diastolic BP.

Valvular Disorders Valvular Disorders

AORTIC REGURGITATION AORTIC REGURGITATION
—  AR Manifestations (1-5) Assessment (6-8) & —  6. Diastolic Murmur heard as high pitched
Diagnostics: blowing sound at 3-4th ICS at L sternal border.
—  1. Maybe asymptomatic —  7. Widened Pulse Pressure (S-D BP)
—  2. Forceful heartbeat felt in the neck or head. —  8. Water Hammer Pulse: the pulse strikes the
Palpable arterial pulsations at the carotid & palpating finger with a quick sharp stroke and then
temporal arteries. (Increased force & volume of suddenly collapses.
blood ejected from the hypertrophied LV) —  9. Diagnosis by:
—  3. Exertional dyspnea & fatigue. —  A. Echocardiogram B. Radionuclide imaging
—  4. Progressive SS of LV failure (breathing —  C. ECG D. MRI
difficulties at night: orthopnea, paroxysmal —  E. Cardiac Catheterization.
nocturnal dyspnea)

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Valvular Disorders
AORTIC REGURGITATION
—  AR Medical Management
—  1. Antibiotic Prophylaxis before invasive
procedure.
—  2. HF and Dysrhythmias treated
—  3 . A o r t i c V a l v u l o p l a s t y o r v a l v e
replacement is the TOC performed before
LV failure. Recommended for pt with LV
hypertrophy.
Valvular Disorders
AORTIC STENOSIS
—  AS Manifestations
—  1 Asymptomatic
—  2. Exertional dyspnea (LV failure)
—  3. Dizziness & syncope (decreased blood flow to
the brain)
—  4. Angina Pectoris (increased O2 demand in LV,
decreased perfusion in coronary arteries).
—  5. BP: low or normal. Low pulse pressure
(30mmHg or < because of decreased blood flow)
Valvular Disorders
AORTIC STENOSIS
—  AS Nursing Management
—  1 Teach patient about AS diagnosis, progression &
treatment plan.
—  2 Teach pt to report change or new symptoms.
Emphasize prophylactics before invasive procedures
(susceptibility to endocarditis). Schedule meds,
activities. Weigh daily: report gains of >2 in 1 day,
5Lbs in 1 wk.
—  3. Monitor VS, Lung sounds, peripheral pulses,
fatigue, L sided failure: exertional or nocturnal
dyspnea, coughing, hemoptysis, respi infections.
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Valvular Disorders
AORTIC STENOSIS
—  AORTIC STENOSIS
—  Narrowing of the aortic valve: the orifice between
the LV and the aorta.
—  Pathophysiology: Progressive narrowing of the
aortic valve may be congenital or from rheumatic
endocarditis. The LV overcomes the obstruction
by contracting more slowly but with more force
than normal. The obstruction increases pressure
on the LV which results in hypertrophy. The heart
begins to fail and manifest SS.
Valvular Disorders
AORTIC STENOSIS
— AS Management
—  1 Antibiotic prophylaxis to prevent
endocarditis (for any stenosis).
— 2. Medications are Rx after LV failure or
dysrhythmias.
— 3. Surgical replacement of aortic valve.
Valvular Procedures
Repair & Replacement
—  1. Valvuloplasty
—  A. Commisurotomy: The valves have
leaflets. The sites where the leaflets meet is the
commissure. A commisurotomy is the
separation of fused leaflets.
—  B. Annuloplasty: Repair of the valve
annulus (junction of the valve leaflets and the
muscular heart wall) under GA (General
Anesthesia) & CPB (Cardiopulmonary Bypass)
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Valvular Procedures Valvular Procedures

Repair & Replacement
— 1. Valvuloplasty
— C. Leaflet Repair: Removal of extra
leaflet tissue in the case of stretching,
ballooning, or other excess tissue leaflets,
shortening or tearing.
—  D. Chordoplasty: Repair of the
chordae tendinae in the mitral valve.
Repair & Replacement
—  2. (Prosthetic) Valve Replacement
—  When leaflets or annulus are immobilized by
calcification, the valve is removed & replaced under
GA & CPB. Types of Valves:
—  A. Mechanical Valves
—  B. Biologic Valves
—  The SS of backward heart failure resolves in a few
hours or days. Postop complications: bleeding,
thromboembolism, infection, CHF, HTN,
dysrhythmias, hemolysis, and mechanical
obstruction of the valve.

Valvular Procedures
Repair & Replacement Congenital Heart Defects
—  B. Biologic Valves
—  1 Patent Ductus Arteriosus Connection
—  Xenograft (Heterograft): from pigs (porcine) or
between the aorta and pulmonary artery.
cows (bovine). Viable for 7-10 years. Do not generate
thrombi – no need for anticoagulants. —  2 Atrial Septal Defects Connection
—  Homograft: portions of the aortic valve, pulmonic
between the two atrias.
valve, pulmonary artery are harvested from cadavers —  3 Ventricular Septal Defects
& stored cryogenically. Expensive. Lasts 10-15 years —  Connection between the ventricles.
& resistant to thrombi & subacute endocarditis.
—  4 Pulmonary Stenosis Narrowing at
—  Autograft: from the patients own pulmonic valve &
pulmonary artery. Viable for 20 years. No need for
the entrance of the pulmonary artery
anticoagulants.

Congenital Heart Defects Inflammatory Heart Diseases

—  5 Tetralogy of Fallot
—  VSD, ASD, Pulmonic stenosis, overriding of the
aorta
—  6 Transposition of the Great Vessels
—  Exchange between the aorta and pulmonary artery
—  7 Coarctation of the Aorta
—  Narrowing of the aorta near the ductus arteriosus
—  8 Kawasaki Disease
—  Inflammation of the arterioles lead to aneurysms

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INFLAMMATORY Heart Diseases ENDOCARDITIS

ENDOCARDITIS B. Medical management:
A. Gen Info:
1. Drug therapy:
1. Inflammation of the endocardium; platelets &
fibrin deposit on the mitral & aortic valves causes a. Antibiotics specific to sensitivity of
deformity, insufficiency, or stenosis. organism cultured
2. Caused by bacterial infection (common): S. b. PenG & Streptomycin if organism
Aureus. S. Viridans, B Hemolytic Streptococcus, not known
Gonococcus
c. Antipyretics
3. Precipitating factors: RHD, open heart surgery,
GU/OB Gyn Surgery, dental extractions 2. Cardiac surgery to replace valve

ENDOCARDITIS
C. Assessment findings: D. Interventions:
1. Fever, malaise, fatigue, dyspnea & cough
acute upper quadrant pain, joint pain
2. Petechiae, murmurs, edema, splenomegaly,
hemiplegia & confusion, hematuria
3. Elevated WBC & ESR. Decreased Hgb & Hct.
4. Diagnostic tests: positive blood culture for
causative organism
ENDOCARDITIS
1. Antibiotics as Rx
2. Control temperature
3. Assess for vascular complications & pulmonary
embolism
4. Provide ct teaching & discharge planning
- types of procedures, antibiotic therapy
- S/S to report: persistent fever, fatigue, chills,
anorexia, joint pains
- avoidance of individuals with known infections

MYOCARDITIS
A. General Info:
An acute or chronic inflammation of the
myocardium as a result of pericarditis, systemic
infection or allergic response.
B. Assessment:
- fever, pericardial friction rub, gallop rhythm
- murmur, signs of heart failure, fatigue, dyspnea
- tachycardia, chest pain
MYOCARDITIS
C. Implementation:
1. Assist client to assume a position of comfort
2. Administer analgesics, salicylates, NSAIDS
3. Administer O2, provide adequate rest periods
4. Limit activities: decrease workload of heart
5. Treat underlying cause
6. Administer meds. as Rx:
- antibiotics, diuretics, ACE inhibitors, digitalis
7. Monitor complications: thrombus, heart failure,
cardiomyopathy

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PERICARDITIS
A. General Info:
1. Inflammation of the visceral & parietal
pericardium
2. Caused by bacterial, viral, or fungal
infection; collagen diseases; trauma; acute
MI, neoplasms, uremia, radiation, drugs
(procainamide, hydralazine, Doxorubicin
HCL)

PERICARDITIS PERICARDITIS
B. Medical management: C. Assessment findings:
1. Determination & elimination/control of 1. Chest pain with deep inspiration (relieved by
underlying cause. sitting up), cough, hemoptysis, malaise.
2. Drug therapy 2. Tachycardia, fever, pericardial friction rub,
cyanosis or pallor, jugular vein distension
a. Pain relief 3. Elevated WBC & ESR, Increase SGOT
b. Anti-inflammatory: Corticosteroids, 4. Diagnostic test:
*salicylates (aspirin), indomethacin. a. chest x-ray shows increased heart size
3. Antibiotics specific to corganism. b. ECG: ST elevation, T wave inversion

PERICARDITIS
D. Interventions:
1. Ensure comfort, bed rest with semi- or high
Fowler’s position
2. Monitor hemodynamics
3. Administer meds as Rx & monitor effects
4. Provide ct. teaching & discharge planning:
- S/S of pericarditis indicative of recurrence (chest
pain intensified by lying down and relieved when
sitting up; medication regimen

30