Cardiovascular Nursing

CARDIOVASCULAR
NURSING
RALPH R. DELOS SANTOS
BACHELOR OF SCIENCE IN NURSING
Pamantasan ng Lungsod ng Maynila
4th Placer December 2012 NLE
DOCTOR OF MEDICINE (ongoing)
PLM College of Medicine
FORMER EMERGENCY AND TRAUMA STAFF NURSE
Emergency and Trauma Department
Gat Andres Bonifacio Memorial Medical Center
City Government of Manila
FUNCTIONAL ANATOMY OF THE HEART
ANATOMIC LAYERS OF THE HEART
EPICARDIUM
Outer most layer and
continuous with the
visceral pericardium
MYOCARDIUM
Muscular layer of the heart
which is responsible for
the contractility and
pumping action the heart.
ENDOCARDIUM
Lines the inner portion of
the heart and is continuous
with the lining of the valve
leaflets
BLOOD SUPPLY OF THE HEART
CLINICAL ANATOMY
PHYSIOLOGIC CONCEPTS
INOTROPY
Refers to the contractility of the heart regardless of
preload
Influenced by sympathetic stumulation
Agents which increase the contractility of the heart are
called POSITIVE INOTROPICS (e.g. Digoxin)
CHRONOTROPY
Refers to the heart rate (N: 60-100 bpm)
Agents which decrease the heart rate are called NEGATIVE
CHRONOTROPICS (e.g. Beta Andrenergic Blockers)
DROMOTROPY
Refers to the conduction velocity within the heart
PHYSIOLOGIC CONCEPTS: CARDIAC CYCLE
SYSTOLE: ATRIAL
Phase of contraction preceded by depolarization
of the SA Node
Depolarization of the Atrial Cells (P wave)
Contraction of the Atrium
The Atrial Kick
SYSTOLE: VENTRICULAR
Occurs after firing from the SA resulting to atrial
contraction
Impulse travels from SA to AV (with a delay or the
PR Interval)
Impulse from SA AV depolarizes the Ventricular
Cells (QRS Complex)
Contraction of the Ventricles
Effects: Closure of the AV Valves, Opening of the
Aortic and Pulmonic Valves
DIASTOLE: VENTRICULAR
Preceded by repolarization (T wave)
Ventricles relax (AV Valves open to fill
the ventricles as Atria contracts, as
explained earlier. Pulmonic and Aortic
Valves close to allow filling and
premature leaking)
The cycle repeats.
PRELOAD
Degree of stretch at the end of diastole
Determined by End-Diastolic Volume
Increases with increased Venous Return
AFTERLOAD
Resistance against the contracting
ventricles of the heart
Pressure required to open the AORTIC VALVE
STROKE VOLUME
Amount of blood ejected from the
ventricle per heart beat
CARDIAC OUTPUT
Amount of blood pumped from the
ventricle per unit of time (approx.
5L/min)
FRANK STARLING LAW OF THE HEART

States that the stroke volume of the
heart increases in response to an
increase in the volume of blood filling
the heart (the EDV) when all other
factors remain constant.
HEALTH HISTORY
Family history of Dyslipidemia and

Hypercholesterolemia, and Sudden
Death
Personal and Social History: Alcohol
intake, smoking, patient lifestyle.
Significant occupational factors and
stress level
ASSESMENT FINDINGS ASSOCIATED WITH
CARDIAC DISEASE
Chest pain and discomfort (complete description:
PQRST)
Dyspnea, Orthopnea, Paroxysmal Noctural Dyspnea
Edema and Weight Gain
Palpitations
Fatigue EARLIEST SYMPTOM ASSOCIATED WITH
CARDIOVASCULAR DISORDER!
Vital Signs
Murmurs
BASIC PRINCIPLES OF PHYSICAL EXAMINATION
VITAL SIGNS
BP: Observe for typical and special changes
associated with cardiac disease (e.g.
Orthostatic Hypotension, Pulsus Paradoxus)
HR: May indicate dysrhythmias
RR:May change due to pulmonary
complications or effect of pain
T:May change due to vasocontriction in
severe cardiac conditions
GENERAL APPEARANCE AND LEVEL OF

CONSCIOUSNESS
Is the patient calm or restless?
Does the facial expression reflect pain?
Is there apparent labored breathing?
SKIN
Clubbing of fingers
Edema
Pallor and Cyanosis
EVALUATION OF EDEMA
(for CHF by Guelph General Hospital)
SCORE DEPTH CHARACTER DISTORTION DISAPPEARANCE
1+ 2 mm or less SLIGHT PITTING NO RAPIDLY

DISTORTION
2+ 2-4 mm DEEPER PIT NO READILY 10-15 SECONDS
DETECTABLE
DISTORTION
3+ 4-6 mm NOTICEABLY SWOLLEN MAY LAST FOR 1

DEEP MINUTE
4+ 6-8 mm VERY DEEP DISTORTED MAY LAST FOR 2-5

MINUTES
HEAD AND NECK

Examine external eyes (Arcus Senilis, Xanthelasma
Palpebrarum)
Fundoscopy: Vascular Changes, Papilledema,
Roths Spots
Jugular Venous Distention
Carotid Palpation and Auscultation
Thyroid Enlargement
XANTHELASMA PALPEBRARUM
THORAX and PRECORDIUM

Inspection
Done in supine position
Record visible pulsation and confirm by palpation
Palpation
Palpate for the PMI and its localization
Observe for lifts and heaves of RVH
THORAX and PRECORDIUM

Auscultation of the Posterior Chest
Done to determine presence of crackles/rales
Auscultation of the Precordium
S1 and S2
Gallops: S3 and S4
Pericardial Friction Rub
DIAGNOSTICS IN CARDIOVASCULAR NURSING
ANCILLARY
Chest X-Ray (Non-Invasive)
CT / MRI (Non-Invasive)
Electrocardiographyand
Holter Monitoring (Non-
Invasive)
Echocardiography (Non-
Invasive)
ANCILLARY
Stress Testing (Non-Invasive):

(+)
ST-Segment Changes in EKG
Abnormal Heart Motion in
Echocardiography
INVASIVE ANCILLARY
Cardiac Catheterization
Introduction of a radiopaque
catheter guided by fluoroscopy to
assess coronary artery patency
and degree of obstruction
Administration of contrast agent
during a cardiac catheterization
procedure is called
ANGIOGRAPHY
Contrast dye can be an allergen
so implement necessary
precaution.
INVASIVE ANCILLARY
Done on OPD basis and requires non-
ambulation for 6 hours after the
procedure.
Right: (e.g. Swan-Ganz), for hemodynamic
monitoring. Femoral or Brachial Vein
Approach
Left: Angiographic Purposes. Femoral or
Radial Artery Approach
INVASIVE ANCILLARY
INVASIVE ANCILLARY
INVASIVE ANCILLARY
INVASIVE ANCILLARY
IMPORTANT NURSING POINTS!
Pre-procedure:
Fasting for 8-12 H before the procedure.
Explain that the procedure may last for at
least < 2 H on a hard table
Reassure that mild sedatives will be given IV
Prepare client to experience occasional
palpitations (due to stimulation of
myocardium): Encourage client to cough
and breathe deeply

Pre-procedure:
Tell client to expect a flushed
feeling and a sensation similar to
the need to void
Encourage client to express fears
and anxieties. Provide teaching.
Post-procedure:
Observe catheter site for bleeding and
hematoma and assess distal peripheral
pulses affected q 15 min for 1, and
every 1-2H until pulses are stable
Dorsalis pedis and posterior tibial
pulses in the lower extremity
Radial pulse in the upper extremity
Post-procedure:
Evaluate temperature and color,
complaints of pain, numbness, or
tingling sensation to determine s/sx of
arterial insufficiency. REPORT
IMMEDIATELY
Monitor for dysrhythmia

Post-procedure:
Patientwill remain on bedrest for 2 to
6 H after the procedure with the
affected leg straight and head
elevated to 30 degrees
Eh pano yun? Hindi ba magiging
prone yung patient sa DVT kasi
naka-bedrest siya?
Can we turn or ambulate the patient?
OPKORS!

Post-procedure:
For comfort, patient can be
turned from side to side.
PROVIDED, you keep the
affected extremity straight
Post-procedure:
Instruct patient to report chest
pain, bleeding, and discomfort
from the site
INCREASE FLUID INTAKE !!!
Assist patient when attempting to
get out of bed for the first time
(SAFETY)
LABORATORY
Complete Blood Count
Detection of infection
Hematocrit can be evaluated
for anemia
LABORATORY
Coagulation Studies
PT (11-14 s), PTT (25-35 s),
INR (0.8-1.2)
INR Target: 2.0-3.0
PT Target: 1.5-2.0 x control
LABORATORY
Serum Lipid
Cholesterol
Desirable: < 200 mg/dL
Borderline-high: 200 239
mg/dL
High: 240 mg/dL
LABORATORY
Serum Lipid
LDL-C
Optimal: < 100 mg/dL
Near
or Above Optimal: 100 129
mg/dL
Borderline-high: 130 -159 mg/dL
High LDL-C: 160 189 mg/dL
Very High: 190 mg/dL
LABORATORY
Serum Lipid
HDL-C
Low: < 40 mg/dL
High: 60 mg/dL
LABORATORY
Serum Electrolytes
Na+
K+
Mg 2+
Ca2+
PO43-
OUTLINE OF DISORDERS
DYSRHYTHMIA
CORONARY ARTERY DISEASES
VALVULAR HEART DISEASES
CARDIOMYOPATHY
HEART FAILURE
INFECTIOUS AND INFLAMMATORY HEART DISEASES
PERIPHERAL VASCULAR DISEASES
HYPERTENSION AND ITS MANAGEMENT
Ikaw ang nagpatibok sa
puso ko, ikaw din ang
nagturo dito na maguluhan
at tuluyang tumigil.
(Antidysrhythmic)
DIAGNOSE.
THE CARDIAC CIRCUIT
THE NORMAL EKG
P-R INTERVAL: 0.12 0.20 SECONDS

QRS COMPLEX: 0.04 0.10 SECONDS
Q-T INTERVAL: < 0.40 SECONDS
THE ELECTROCARDIOGRAM (EKG)
A diagnostic tool used to
record electrical activity
of the heart.
Reflects the electrical
aspect of cardiac cycle
and conduction
mechanism of the heart.
Physiologic alterations
can be detected by EKG
(e.g. Electrolyte
Imbalances, Coronary
Ischemia, and
Hypertrophy)
THE EKG LEADS
EINTHOVENS TRIANGLE
EH PANO KUNG STRIP NA MISMO?
BASICS OF INTERPRETATION
1. COMPUTE FOR THE HEART RATE
Method A:
Count the number of R in a 6-inch or 6-sec
strip
Multiply by 10
1. COMPUTE FOR THE HEART RATE

Method B:
Find an R wave crossing a large
box
Count the number of large boxes
until the next R wave
1: 300 BPM 6: 50
2: 150 7: 43
3: 100 8: 37
4: 75 9: 33
5: 60 10: 30
DETERMINE THE HEART RATE USING BOX METHOD

HALA! HINDI KO MEMORIZE YUNG
ILANG BEATS PER NUMBER OF BOX
50 BA? 100 BA?75 BA?

MAY TECHNIQUE BA?
OH SAPILITANG KAILANGANG
ISAPUSO?
TANDAAN.
HINDI DAPAT LAGING PUSO ANG

PINAPAIRAL.. KAILANGAN ISIP DIN.
#ganern
BALIK-ARAL
1: 300 bpm 6: 50 bpm

2: 150 bpm 7: 43 bpm
3: 100 bpm 8: 37 bpm
4: 75 bpm 9: 33 bpm
5: 60 bpm 10: 30 bpm
DYSRHYTHMIA
Disordersof the formation (AUTOMATICITY),

transfer of electrical impulse
(CONDUCTION), or multiple depolarization
(REENTRY) within the heart
Can result to failure in the pumping action
of the heart
REVIEW: THE CARDIAC CIRCUIT
SINOATRIAL NODE DISTURBANCES
SINUS BRADYCARDIA
SINUS TACHYCARDIA
SINUS BRADYCARDIA
HR < 60 bpm, slow SA firing
Usually benign in cases of athletics
Secondary to vagal stimulation, Increased ICP
SE of medications (Digitalis, Propranolol)
A drop in the HR can cause syncope
Mx: Atropine 0.5-1 mg IV push
Nx: Avoid vagal stimulation
SINUS TACHYCARDIA
HR > 100 bpm
Canbe caused by fever, hypermetabolism,
anxiety, and acute blood loss
SE of sympathomimetics
Decreased diastolic filling time
Mx: Beta Adrenergic Antagonists (Blockers)
ATRIAL DYSRHYTHMIAS
PREMATURE ATRIAL CONTRACTION

PAROXYSMAL ATRIAL TACHYCARDIA
ATRIAL FIBRILLATION
ATRIAL FLUTTER
PREMATURE ATRIAL CONTRACTIONS
An error of automaticity
Early beats arise from ectopic atrial foci
Usually
benign but if occurrence would
become more frequent, condition should
be evaluated
Sudden onset and termination of rapid

firing from an ectopic foci
Also known as SUPRAVENTRICULAR
P wave is lost in the preceding T wave
Occurs in various cardiac problems
Mx: ADENOSINE, Verapamil, Propranolol,
Sedatives, Cardioversion, Ablation
Nx: Vagal Maneuvers
ATRIAL FIBRILLATION
Most common supraventricular dysrhythmia
Disorganized and uncoordinated twitching of the
atrial musculature
Associated with Holiday Heart Syndrome
Usually occurs post-open heart surgery
AR: 300-600 / VR: 120-200
No discernible P wave and absent PR, F-waves
Theatrial kick is lost which reduces cardiac
output
ATRIAL FIBRILLATION
ATRIAL FIBRILLATION
Pooling of blood in the atria

facilitates thrombus formation
20-25% of CVAs are due to cardiogenic
emboli
GOALS: Prevention of
thromboembolism and correction of
dysrhythmia
ATRIAL FIBRILLATION
MEDICAL MANAGEMENT
Anticoagulationusing Heparin/Low-Molecular
Weight Heparin (Parenteral) or Warfarin (Oral)
INR target for Warfarin Therapy: 2.0 3.0
Ifpatient has contraindication to
anticoagulation (previous cerebral
hemorrhage, Hx of bleeding, GI bleeding, or
prone to falls), Aspirin can be a substitute
ATRIAL FIBRILLATION
MEDICAL MANAGEMENT
Restorationof sinus rhythm using medications
or cardioversion
Medications for dysrhythmia are usually given
after 4 to 6 weeks of anticoagulation
CARDIOVERSION
Anelective procedure for dysrhythmias caused
by reentry
Allows the SA to resume its pacemaker role
Synchronized with the QRS complex to avoid
discharge during repolarization
A QRS COMPLEX MUST BE PRESENT
Low voltage: 50 100 J
Done under analgesia or sedation
NURSING CARE IN CARDIOVERSION
BEFORE
Baseline EKG for dysrhythmia type
Full explanation of the procedure
Patient should fast, with normal electrolytes
For patients receiving Digitalis, obtain level
INR 2.0 3.0 after 4 -6 weeks of anticoagulation
Done at bedside, secure emergency equipment
Start IV for preoperative medications.
DURING
Setthe biphasic machine within a range of 50
200 J
Turn synchronizer to ON
Clear the patients area
Deliver the shock
Reassess rhythm, PR, BP, Oxygen Saturation and
airway
AFTER
Immediately assess EKG, Pulse, BP, Respiratory
Status
Address possibility of ventricular dysrhythmias
Monitor EKG and VS continuously for at least 2
hours
SUCCESSFUL: Back to Sinus Rhythm
Protect airway while patient is still sedated
ATRIAL FLUTTER
Conduction defect of the atria
AR: 250-400 bpm
VR: 75-150 bpm
Fires faster than what AV node can accommodate
and transmit to the ventricles
Can result to VFib
SAW-TOOTH PATTERN
Tx: Cardioversion, Diltiazem, Verapamil, Beta-
Blockers, Anticoagulation, IBUTILIDE
VENTRICULAR DYSRHYTHMIAS
PREMATURE VENTRICULAR CONTRACTION

VENTRICULAR TACHYCARDIA
TORSADES DE POINTES [torsad-de-pwant]
VENTRICULAR FIBRILLATION
Impulse that starts in the ventricle and is
conducted through the ventricles before the
next sinus impulse
Occurs earlier than the expected beat and is
not preceded by a P wave
Occurs in healthy individuals
Not serious unless in acute MI.
Characterized by wide, bizarre QRS
complex
WHEN IS A PREMATURE VENTRICULAR
CONTRACTION DANGEROUS?
Frequent (6 or more per minute)

Coupled with normal beats (bigeminy)
Multiform
In pairs after every third beat
(trigeminy)
After an Acute Myocardial Infarction
On the T wave
PVC: MULTIFORM
PVC: BIGEMINY
PVC: TRIGEMINY
PVC: QUADRIGEMINY
MANAGEMENT
Isolated PVCs are benign and not treated
Ifsymptomatic (due to reduction in CO),
patient may receive LIDOCAINE or
AMIODARONE
Monitor HR, rhythm, and VS continuously
Provide quiet, restful environment
From an irritable ventricular focus
which takes over as pacemaker
Life-threatening dysrhythmia, 3 or
more PVCs in a row
No P waves, No P-R Interval (bakit
kaya?)
VR: 100-200
Characterized
by extremely rapid, erratic
impulse conduction and formation
Leads to inadequate myocardial contractions
Over-alleffect is loss of cardiac output and
tissue hypoperfusion
No P, QRS, T waves
Death occurs within minutes without
intervention (CPR, Defibrillation, Medications)
MANAGEMENT
START CPR! immediately until defibrillator is
engaged
Defibrillate up to THREE TIMES IF NEEDED.
200 J then 300 J then 360 J
VENTRICULAR ASYSTOLE
Absent QRS
CPR as immediate management
Epinephrine 1 mg IV bolus q 3-5 min for 3 doses
(no routine Atropine)
Identification and correction of etiology
Inability to respond terminates the code.
AHA 2015 BASIC LIFE SUPPORT
HIGHLIGHTS
KEY POINTS:
Activation of emergency response can be
through mobile telephone, so you dont need
to leave the victims side
Still C-A-B
30 chest compressions : 2 breaths is lone
rescuer
Chest compression from at least 100/min
(2010) to 100 120/min
AHA 2015 BASIC LIFE SUPPORT
HIGHLIGHTS
KEY POINTS:
Depth of compression: at least 2 in (5 cm) but
not greater that 2.4 in (6 cm)
Allow full chest recoil after each compression
Minimize pauses (interruption should be < 10
seconds)
Bystanders may administer NALOXONE.
Ventilation
Rate: 1 breath (delivered in 1
second, observe for chest rise) every 6 seconds
(10 breaths per minute)
AHA 2015 ADVANCED CARDIOVASCULAR
LIFE SUPPORT HIGHLIGHTS
KEY POINTS:
Back to EPINEPHRINE
Lidocaine after ROSC in pVT/VF
Useof Beta-Blockers is associated with better
outcomes
ETCO2 > 10 mm Hg after 20 minutes of
resuscitation as component of prediction of
success
TargetTemperature: 32 36 centigrade for at
least 24 Hours
AHA 2015 ADVANCED CARDIOVASCULAR
LIFE SUPPORT HIGHLIGHTS
KEY POINTS:
Whento prognosticate: 72 HOURS AFTER
RETURN TO NORMOTHERMIA
Organ Donation (Liver and Kidney)
DEFIBRILLATOR
Deliversbiphasic current thorough paddles to
completely depolarize the heart producing a
transient asystole
CARE OF CLIENTS UNDERGOING
BEFORE DEFIBRILLATION
Determine responsiveness, activate emergency
response
Call for defibrillator and E-cart
ASSESSMENT: A-B-C
CPR until defibrillator is in place
Verify EKG in 2 leads
Remove NTG patch (if present)
DURING DEFIBRILLATION
Lubricate paddle with electrode gel
Do not over-apply the gel
Paddle Placement:
Paddle 1 (held by left hand): 2nd ICS Right of
Sternum
Paddle 2 (held by right hand): Apex
Call for clearance!
DEFIBRILLATION
AFTER
Immediately assess the EKG and pulse
May be repeated if unsuccessful
(Refer TO AHA 2015 Recommendations)
THE ATRIOVENTRICULAR BLOCKS
FIRSTDEGREE
SECOND DEGREE
MOBITZ I (WENCKEBACH
PHENOMENON)
MOBITZ II
THIRD DEGREE
FIRST DEGREE
Slowed SA AV transmission
Seen as prolonged P-R Interval
Relatively
benign and requires no
management
Ifcaused by Digitalis, medication should be
discontinued
SECOND DEGREE AV BLOCK: MOBITZ I
(WENCKEBACH PHENOMENON)
Seriesof P-QRS with increasing PR

intervals
Followed
by an unconducted P resulting to
absent QRS (dropped)
Usually
benign but requires management if
symptomatic
SECOND DEGREE AV BLOCK: MOBITZ I
(WENCKEBACH PHENOMENON)
SECOND DEGREE AV BLOCK: MOBITZ II
Onlysome of SA impulses are conducted via
AV into the ventricles
Regular PP and PR intervals
May progress to higher forms of blocks
THIRD DEGREE AV BLOCK
No atrial impulse is conducted to the
ventricles
The atria and ventricles work independently
from one another. COMPLETELY BLOCKED
2 impulses stimulate the heart
If symptomatic, Tx: Atropine Sulfate
Severe cases: Pacing
THIRD DEGREE AV BLOCK
NURSING CONSIDERATIONS FOR PATIENTS
WITH DYSRHYTHMIA
Identification of possible source of dysrhythmia
Monitor patients hemodynamics and perfusion status
Verifyhistory of previous occurrences of fatigue,
syncope, light-headedness, chest discomfort
Cardiac examination for possible murmurs
Monitor EKG, Serum Electrolytes
Lifestyle
Modification: Stress Reduction, Anxiety
Management, Avoidance of Intake of Known Stimulants
NURSING DIAGNOSIS: DECREASED CARDIAC OUTPUT
PACEMAKER THERAPY
Electronic device that provides
electrical stimuli to the heart
muscle (ARTIFICIAL SA)
Used in slower-than-normal
impulse formation
Permanent Pacemaker is used
for irreversible complete heart
blocks
Temporary Pacemaker is used
to support patients until they
improve (post-MI, Open Heart
Surgery)
PACEMAKER THERAPY
THREE IMPORTANT TERMS
PACE: Ability to produce impulse

CAPTURE: Ability of impulse to initiate
contraction
SENSE: Ability to detect intrinsic electrical
activity
PACEMAKER DESIGN AND TYPES
SINGLECHAMBER: PACES ATRIA OR

VENTRICLE
DUAL CHAMBER: PACES BOTH CHAMBER
PACEMAKER DESIGN AND TYPES
Endocardial (Transvenous): MOST
COMMON in emergency
Issues: Thrombophlebitis, Sepsis
Epicardial (Transthoracic): Done
usually during surgery
Issues: Tamponade, Infection
External (Transcutaneous): Pads
applied on the chest wall, no
punctures.
MODES
FIXED-RATE
Non-demand/asynchronous
Paces, doesnt sense
Fires constantly, appropriate in no
electrical activity
Dangerous if heart has electrical
activity (REVIEW: BAKIT KAYA?)
MODES
DEMAND
Fires only if HR goes below the
predetermined rate
Paces and senses
POWER SOURCES
Mercury-Zinc Battery (3-4 years)

Lithium Cell (up to 10 years)
Plutonium-238 (20 years)
COMPLICATIONS RELATED TO
PACEMAKER PLACEMENT
Infection
Bleeding and Hematoma
Hemothorax
Myocardial Perforation
Phrenic Nerve Stimulation
SAANG TYPE PWEDE MAG-APPLY ANG EXCEPT ?

CONCERNS ASSOCIATED PACEMAKER
Malfunction(manifested by decreasing
cardiac output) Dizziness
Inhibited by strong electromagnetic fields
Recent designs are now safe even in the
presence of household appliances
(microwave oven) as long as these are not
held close to pacemaker generator and
appliances are properly grounded
Avoid magnets
CONCERNS ASSOCIATED PACEMAKER
Inform radiologic technician before MRI
Stayaway from High-voltage transmission
lines and substations
Avoidthe said factors especially if patient
would by symptomatic (dizziness and
palpitations)
Refrain from using chainsaw and welding
device
Donot lift more than 5 -10 lbs for the first
6 weeks. Normal activity can be resumed
after 6 weeks
DISORDERS OF THE CORONARY
VESSELS
CORONARY ARTERY DISEASE
Most prevalent CV disorder
Majorcontributor to the
development of CAD is
ATHEROSCLEROSIS
Characterized by abnormal
deposition of fatty substances
and fibrous tissue within the
vessel wall (ATHEROMA).
DISORDERS OF THE CORONARY VESSELS
CORONARY ARTERY DISEASE
Ultimatelyresults to narrowing of the vessel
lumen leading to obstruction or detachment
of thrombus causing embolism of the
coronary arteries.
Obstructionleads to reduction in blood flow
causing ischemia and other CAD
manifestations.
Presents as ANGINA PECTORIS
ANGINA PECTORIS
Episodes
or paroxysms of PAIN and
PRESSURE in the anterior chest.
Associatedwith impairment of blood flow
to the heart.
COMMON TRIGGERS:
Physical exertion
Exposure to cold
Heavy meals
Stress-provoking situations
ANGINA
Mechanism of pathogenesis is related to

ischemia
Maypresent as feeling of indigestion or
choking to chest heaviness
Retrosternal (deep behind the sternum)
ANGINA
P Provoked usually by activity /
Palliated by rest and Nitroglycerin
Q Vague, knife-like, squeezing
R 90% is restrosternal to left arm,
elbow, jaw, right shoulder, epigastric
S Described as discomfort to feeling of
impending doom
T Usually less than 5 minutes
TYPES OF ANGINA
STABLE ANGINA
Onset is usually predictable and
consistent pain that occurs on exertion
and is relieved by rest.
UNSTABLE ANGINA
AKA Pre-infarction Angina / Crescendo
Angina
Occurs longer and pain in usually
increasing in character
Persists at rest
VARIANT ANGINA
Prinzmetals Angina / Vasospastic Angina
DIAGNOSTICS
EKG
Stress Test until reaching the 85% maximal
heart rate
Coronary Angiography
CXR
MEDICAL MANAGEMENT
THE OVER-ALL GOAL IS

TO DECREASE THE
OXYGEN DEMAND
CLINICAL PHARMACOLOGY
PHARMACOTHERAPEUTICS
NITRATES (Nitroglycerin, Isosorbide Dinitrate)
BETA-ADRENERGIC ANTAGONISTS (Metoprolol,
Atenolol)
CALCIUM-CHANNEL BLOCKERS (Diltiazem)
ANTIPLATELET AGENTS (ASPIRIN, Clopidogrel)
ANTICOAGULANTS (Enoxaparin, Fondaparinux)
SPECIAL NOTES ON NITROGLYCERIN
SUBLINGUAL NITROGLYCERIN
Given q 5 mins for 3 doses
Instruct patient to make sure the mouth is moist,
and saliva is not swallowed.
For severe pain, may crush the tablet to hasten
absorption
Keep medication at all times, keep inside original
container
Explain sensitivity of medication, should be
replaced every 6 months
Discuss side effects
SPECIAL NOTES ON NITROGLYCERIN
TOPICAL NITROGLYCERIN (PASTE/PATCH)
Rotate site to prevent irritation
Select a well perfused area
NTG Paste is applied 3-4x daily or every 6 hours,
except night time.
NTG Patch is applied every morning and removed
at 10 PM
This is to provide 6-8 H nitrate-free period during
night time to prevent tolerance
TOPICAL NITROGLYCERIN (PASTE/PATCH/SPRAY)
NURSING INTERVENTIONS
During angina attack, stop patient activities and

facilitate bed rest in a semi-fowlers position
Assess angina (is it really angina?)
Facilitate EKG within 10 minutes
Obtain
baseline VS prior to administration of
medications
Oxygen support at 2 L/min by nasal cannula

Reduceanxiety and give appropriate comfort
measures for pain
Promote lifestyle modification, quit smoking, low
salt / low fat diet
MYOCARDIAL INFARCTION
Life-threateningcondition characterized by
formation of localized necrotic areas within
the myocardium
Due to sudden occlusion of a coronary artery
Triggered
by strenuous physical activity,
severe emotional stress, exposure to cold
Can also be caused by coronary vasospasm
MOST COMMONLY AFFECTED: ANTERIOR WALL
STEMI vs NSTEMI
TEACHING MOMENT
ASSESSMENT AND DIAGNOSTICS
The diagnosis of MI is based on

presenting symptoms, EKG,
and laboratory results.
THE ELECTROCARDIOGRAPHY OF ACUTE
MYOCARDIAL INFARCTION
Assists in the diagnosis of MI

Should be done within 10 minutes from the time
the patient reports pain or arrives in the ED
Used in monitoring the progression or resolution
of MI
QUESTION
Two patients, Buddy/29 and Rafael/30
arrived in the Emergency Department,
both with chief complaint of chest
tightness after binge drinking in a
wedding event. As a routine
procedure, you facilitated the EKG of
these patients. You received the
results.
WHICH PATIENT HAS AMI?
SURE KA NA?
YOU STILL CANNOT SAY.
THE SERUM MARKERS
CREATINE KINASE (CK-MM, CK-MB, CK-BB)
CK-MBis cardiac-specific, hence rises
remarkably in cardiac cell damage (AMI)
Most specific index for the diagnosis of MI
TROPONIN (T, I, C)
Usedmore frequently and routinely to
identify myocardial infarction
The GOLD STANDARD
THE SERUM MARKERS
OTHER MARKERS
LDH
AST
MYOGLOBIN
SO SUDDENLY I HAVE THIS
PATIENT COMPLAINING OF
CHEST PAIN AND THIS IS VERY
TYPICAL OF MYOCARDIAL
INFARCTION
WHAT SHOULD I DO?
AS A GENERAL RULE!
A PATIENT WITH MANIFESTATION OF
MYOCARDIAL INFARCTION SHOULD:
Assume the DOOR-TO-NEEDLE approach
in LESS THAN 30 MINUTES. Contact EMS!
Fromthe onset of chest pain, patient
should be brought within 30 MINUTES for
THROMBOLYTIC THERAPY
ORwithin 1 HOUR for INTERVENTIONAL
CARDIOLOGY
SO WHEN IS AN INDICATED
MANAGEMENT INDICATED?
DETERMINE THE TYPE OF AMI
If there is the persistence of ST-
Segment Elevation, we
immediately reperfuse.
Thrombolysis
Percutaneous Intervention
If NSTEMI vs Unstable Angina,
usually receives anti-ischemic
management.
MEDICAL MANAGEMENT
Analgesics (Morphine Sulfate)
Intravenous Nitrates (ISDN Drip)
Beta Blockers (Metoprolol)
ACE Inhibitors (Captopril/Enalapril)
MEDICAL MANAGEMENT
Antiplatelet (ASPIRIN, Clopidogrel,
Ticlopidine)
Anticoagulant (Heparin, Enoxaparin,
Fondaparinux)
Other Cardio-supportive Medications to
Combat Shock (Dobutamine, Dopamine)
Antidysrhythmics
NOTES ON THROMBOLYSIS
Used to dissolve existing clots
-ASE (Streptokinase, Urokinase, Alteplase [t-PA])
CONTRAINDICATIONS:
Cranial Pathology or Trauma within past 3 mo.
Previous allergic reaction to the medications
Recent Streptococcal infection or received
Streptokinase in the past 6-12 months
COMPLICATIONS OF MYOCARDIAL INFARCTION
DYSRHYTHMIA
Cause of 40-50% of deaths post-AMI (MOST
COMMON CAUSE OF DEATH AFTER AMI)
Monitor for fatal PVCs, SVT, Heart Blocks
CARDIOGENIC SHOCK
Cause of 9% of deaths post-AMI
Decreased myocardial contraction leading to
decline in Cardiac Output and BP
HEART FAILURE AND PULMONARY EDEMA

MOST COMMON CAUSE OF DEATH OF ADMITTED
PATIENTS WITH CARDIAC DISORDER
Cause of 1/3 of deaths due to AMI (33%)
MYOCARDIAL NECROSIS
Causes Rupture of Heart Muscle and VSD
PERICARDITIS
Due to inflammatory mechanism
Usually 2-4 days after AMI
DRESSLERS SYNDROME:
Late appearing pericarditis (6 weeks to months)
Autoimmune cause is suggested
Avoid anticoagulants which may precipitate
Cardiac Tamponade
CORONARY ARTERY BYPASS GRAFTING
Done if vessel occlusion is 70% (60% if left main
coronary artery)
The patient is first put on CARDIOPULMONARY
BYPASS:
An Extracorporeal Machine takes over the
function of the heart and lungs
Hemodilution: Blood is diluted using crystalloid
Hypothermia: 28-36 degrees centigrade
Heparinized (Anticoagulated)
Done if vessel occlusion is 70% (60% if left main
coronary artery)
The patient is first put on CARDIOPULMONARY BYPASS
after Cardioplegia.
An Extracorporeal Machine takes over the function of
the heart and lungs
Hemodilution: Blood is diluted using isotonic crystalloid
Hypothermia: 28-36 degrees centigrade
Heparinized (Anticoagulated)
Great Saphenous Vein

Internal Mammary Artery
Right Gastroepiploic Artery
CARDIAC REHABILITATION
PHASE 1 (INPATIENT)
Begins with admission to the CCU, Tertiary
Preventive Measures
Bed rest for 24 H, commode will be used for
bowel movement
2-gram salt diet
After first day, may ambulate to a bedside
chair for 15-20 minutes if asymptomatic
PHASE 1 (INPATIENT)
When transferred from CCU to regular room,
bathroom privileges and self-care activities
are resumed. Brief hallway walks are
allowed with supervision
In every activity monitor HR and BP: RULE
OF 25. HR should not increase by 25%, BP
should not increase more than 25 mm Hg
PHASE 2 (IMMEDIATE OUTPATIENT)

Rule: If asymptomatic, then early discharge
Alas siete ng umaga, basa-
basa pa buhok mo.
Dumating yung pasyente
mo noong isang linggo na
inatake sa puso.
Nakangiti siya sayo. Ikaw
pala ang sinadya niya upang
pasalamatan ka niya.
Nahihiya ka pa na abutin
iyong bigay niya. Sabi mo
pa, Naku! Nag-abala ka
pa. Wag na.. Wag na
Pero aminin mo gusto mo
talaga.
Dahil binigyan ka siyempre
extra accommodating ka,
tinanong mo siya kung ano
maipaglilingkod mo sa
kaniya.
Tinanong ka niya.
Nurse, kapag gumaling ba ko
sa atake, pwede pa rin kami
magtalik ni Misis?
Sexual activity esumes usually after 4-8
weeks post-AMI
Must be able to climb two flights of strairs
Must be able to walk 3-4 mi/hr
No eating nor drinking of alcoholic
beverages immediately before sexual
activity.

Caution against use of Viagra
May return to work after 8-9 weeks if
asymptomatic, coincides with full physical
examination and diagnostics
PHASE 3 (INTERMEDIATE OUTPATIENT)
Continuation for 4-6 months
Emphasis of exercise, activity, and
endurance
PHASE 4 (MAINTENANCE OUTPATIENT)

Final and unsupervised
NURSING DIAGNOSES
Possible Nursing Diagnosis

Ineffective Cardiopulmonary Tissue
Perfusion r/t reduced Coronary
Blood Flow
Potential Altered Tissue Perfusion
r/t Left Ventricular Dysfunction
Relief of pain and other signs of
ischemia
Monitor VS and hemodynamics
Identify and report respiratory
complications
Promote adequate tissue perfusion
Reduce Anxiety
Lifestyle Modification
ACQUIRED VALVULAR DISORDERS
PROLAPSE
REGURGITATION
STENOSIS
MITRAL VALVE PROLAPSE
Pathophysiology
Ballooning of the leaflet to the
atrium during systole
Blood backflows from the left
ventricle to the left atrium
Manifestations
SOB
Light-headedness
Syncope
Palpitation
Diagnostic Findings
Murmur: Systolic Click
Crackles
Confirmed by Echocardiography
Medical-Surgical Management
Symptomatic approach
Calcium-channel blockers, Beta-blockers
Mitral Valve Repair / Replacement
Nursing Management
Instruct patient to avoid stimulants
Educatepatient regarding need for
prophylactic antibiotics during invasive
procedures
MITRAL REGURGITATION
Pathophysiology
MOST COMMON
Associated with MI, papillary
muscle failure, heart
enlargement.
Left Ventricular to Atrial
Backflow
Clinical Manifestations
Dyspnea
Fatigue
Pulmonary Congestion
MITRAL REGURGITATION
Diagnostic Findings
Systolic high-pitched blowing murmur at apex
Same as that of CHF
MV Replacement of Valvuloplasty
MITRAL STENOSIS
Pathophysiology
Narrowing of the opening of
the mitral valve
Inability of blood to flow
from LA LV
Backflow effects
DOB FIRST SYMPTOM!
Fatigue
Left-sided Heart Failure-
like
MITRAL STENOSIS
Diagnostic Findings
Low-pitched rumbling diastolic murmur
Antibiotic prophylaxis
Anticoagulant Therapy
Valvuloplasty / Valve Replacement Surgery
AORTIC REGURGITATION
Pathophysiology
Blood from the aorta backflows
to the LV during diastole
Diastolic Overload: Blood
entering the LV from LA, plus,
blood flowing backwards from
aorta to LV.
Aortic insufficiency: Fatigue
Forceful heartbeats
LV Failure
AORTIC REGURGITATION
Assessment and Diagnostic Findings
High-pitched diastolic murmur
Widened pulse pressure
Water-Hammer Pulse
Prophylactic Antibiotics for invasive
procedures
Valvuloplasty
/ Valve Replacement
TREATMENT OF CHOICE
AORTIC STENOSIS
Pathophysiology
Progressive narrowing of the valve
orifice
Inability of blood to flow through the
aortic valve
LV overload and hypertrophy
Usually asymptomatic
Fatigue
Dyspnea
Ischemic effects to the myocardium
Possible MI
AORTIC STENOSIS
Assessment and Diagnostic Findings

Loud, rough systolic murmur
Crescendo-Decrescendo Murmur
Prophylactic Antibiotics
Definitive treatment is Valve Replacement
Surgery
NURSING MANAGEMENT OF
Assess
understanding of the progressive
nature of the diseases.
Encourage client to report new symptoms
or change in the previously experienced
symptoms
Emphasize the importance of prophylactic
antibiotics before any invasive procedures
Educate patient regarding predilection of
bacteria to diseased heart valves
NURSING MANAGEMENT OF
MonitorVS, obtain baseline. Include
assessment for the presence of murmur and
adventitious breath sounds
Patient may feel clicks due to prosthesis
Emphasize need to comply to medications
and dietary modification
Weigh daily and report a gain of 2 pounds
/ day or 5 pounds / week.
CARDIOMYOPATHY
Heart muscle disease associated

with cardiac dysfunction
Classified according to structural
and functional abnormalities of the
heart muscle
TYPES OF CARDIOMYOPATHY
HYPERTROPHIC CARDIOMYOPATHY
DILATED CARDIOMYOPATHY
RESTRICTIVE CARDIOMYOPATHY
GENERAL PATHOPHYSIOLOGY OF
CARDIOMYOPATHIES
All end-up in or culminate in impaired
cardiac output
Decreased stroke volume leads to
sympathetic and RAAS activation.
Lead to increased systemic vascular
resistance and sodium retention
MOST COMMON
Characterized by significant dilation of the
ventricles without increase in wall thickness
Decreased muscular elements
Poorsystolic function and more blood is left
in the heart after contraction
Results in valve regurgitation
Associated
with PREGNANCY (Peripartum
Cardiomyopathy)
COMPLICATIONS
Usually to ineffective pumping of the
heart with SNS activation
Development of dysrhythmia
Blood pooling and thrombosis
HYPERTROPHIC CARDIOMYOPATHY
The heart increases in size and mass, especially
the septal portion
Increased mass reduces cavity or space (caliber)
inside the heart
Septal hypertrophy blocks flow from Left Atrium
as well as outflow from Left Ventricle
Diastolic (filling) function of the heart is
impaired.
Most common manifestation is DYSPNEA (90%)
This has genetic predisposition
RESTRICTIVE CARDIOMYOPATHY
Diastolic dysfunction caused by rigid

ventricular walls
Impairs ventricular stretch and
diastolic filling
Least common type
Secondary to infiltrative diseases
(Amyloidosis)
HISTOPATHOLOGY: CARDIAC AMYLOIDOSIS
CONGO RED STAIN UNDER

LIGHT MICROSCOPY
CLINICAL MANIFESTATIONS
Patient usually remains stable

Dilated and restrictive cardiomyopathy
are first diagnosed when patients
exhibit signs and symptoms of heart
failure
May experience dyspnea, paroxysmal
nocturnal dyspnea, bipedal edema
ASSESSMENT AND DIAGNOSTIC FINDINGS
COMMON FINDINGS DIAGNOSTICS

Tachycardia Echocardiography
Murmur CXR
Crackles EKG
Jugular Venous
Distention
Pitting edema
Hepatomegaly
MEDICAL AND SURGICAL MANAGEMENT
MEDICAL MANAGEMENT
Identify and manage the underlying or
precipitating causes.
Address HF with medications, low-sodium diet,
exercise-rest regimen
Control possible complications (e.g. dysrhythmias)
Limit fluid to 2 L / day
SURGICAL MANAGEMENT
HF can be addressed by Cardiac Transplantation
PRINCIPLES OF
CARDIAC TRANSPLANTATION
Standard and effective treatment for

clients with end-stage heart disease
Cadaveric method of finding donor
Mortality due to procedure usually
occurs within 30 days post-operative
PRINCIPLES OF
WHO IS A TYPICAL CANDIDATE?
Severe symptoms uncontrolled by medical therapy
No other surgical option
Age < 65 y/o
Prognosis <12 months to live
Ejection Fraction < 25%
PRINCIPLES OF
WHO IS NOT A CANDIDATE?

Systemic Diseases
Infection
Cancer
Ketamine (Substance) Abuser
PRINCIPLES OF
IMPORTANT POINTS
To be transplanted within 6H
Newly transplanted heart has no autonomic
control
Orthotopic vs Heterotopic Transplantation
Transplant Immunosuppression (e.g. Cyclosporine
A, Tacrolimus, Prednisone)
MOST RELIABLE TO DETERMINE REJECTION:
ENDOMYOCARDIAL BIOPSY
Strict hemodynamic monitoring
ORTHOTOPIC TRANSPLANTATION
HETEROTOPIC TRANSPLANTATION
HEART FAILURE
Inability of the heart to pump sufficient

blood to meet oxygen and nutritional needs
of the body
A clinical syndrome of fluid overload and
inadequate tissue perfusion
Systolic (Forward) vs Diastolic (Backward)
Dysfunction
THE NEW YORK ASSOCIATION
CLASSIFICATION
CLASS I CLASS II
Ordinary physical activity Slight limitation in ADL
does not cause fatigue, CLASS III
dyspnea, palpitations,
Marked limitation in ADL
and chest pains
Comfortable at rest
Asymptomatic, no ADL
limitation CLASS IV
Symptomatic at rest.
PATHOPHYSIOLOGY
TEACHING MOMENT.
ASSESSMENT AND DIAGNOSTIC FINDINGS
ASSESSMENT DIAGNOSTICS
Patientsusually become Ancillary
aware when they are CXR, 12-Lead EKG,
already symptomatic Echocardiography
Mayco-exist with other Laboratory
diseases
Routine Chemistry
PE:Signs and Symptoms
Electrolytes, BNP
of Congestive Heart
Failure
Angiotensin-Converting Enzyme Inhibitor

Angiotensin Receptor Blockers
Beta Blockers
Vasodilators (e.g. Hydralazine, Isosorbide Dinitrate
Diuretics
Digitalis
IMPORTANT NOTES ON DIGITALIS
It is a cardiac glycoside TOXIC EFFECTS
Improvescontractility, Fatigue, Depression,
hence improves cardiac Malaise, Anorexia, Nausea,
output Vomiting (early effects)
Therapeutic Level: 0.5 Arrhythmia (SA/AV Block)
2.0 ng/mL, level is
analyzed 6-10 H after the
ANTIDOTE
last dose
Digitalis Immune Fab
(Digibind)
NURSING CONSIDERATIONS
Assess clinical response, signs of
improvement from digitalis
therapy
Assess presence of hypokalemia
and other electrolyte disturbances
Before administration, check for
VS with emphasis in APICAL PULSE
RATE (HEART RATE)
IF< 60 bpm AND WITH ATRIAL FIBRILLATION,OR
THE RHYTHM BECOMES REGULAR WITHHOLD!
(HERALDS AND IMPENDING AV BLOCK)
Itis a common practice to withhold if HR < 60
bpm in sinus rhythm, but withholding is usually
not needed since digitalis does not affect SA
automaticity
PR interval is more important than AHR in
determining when to withhold.
Observe for visual changes: YELLOW-
GREEN DISTORTION, snowy vision,
yellow halos.
Weigh patient daily.
NURSING MANAGEMENT
NURSING DIAGNOSES
Activity
intolerance r/t to imbalance
between oxygen supply and demand
Excess fluid volume r/t sodium intake
Anxiety r/t breathlessness
NURSING MANAGEMENT
INTERVENTIONS
Promote adequate rest and light activity,
stop if necessary
3-5 min, 1-4x a day of activity
Monitor fluid volume, weight gain.
Low-sodium diet, be aware of other sources
of sodium
During rest, head elevation 20-30 cm or 8-
10 in blocks, reduces preload.
CARDIOGENIC SHOCK
Occurs when the heart cannot pump

enough blood to supply the needs of
the body
Seen in conditions with 40% myocardial
necrosis, valvular dysfunction,
cardiomyopathy
PATHOPHYSIOLOGY
Degree of shock is proportional to the
extent of ventricular dysfunction
Secondary to loss of cardiac
contractile power
Marked reduction in SV and CO
Reduced systemic perfusion
Proceeds to progressive pulmonary
edema
A vicious cycle of dysfunction
MEDICAL MANAGEMENT
Correct the underlying problem to

reduce further damage to the heart
Correction of dysrhythmia
Address pulmonary signs and symptoms
Correction of reduced CO (IV
resuscitation)
Oxygen support
VASOPRESSOR THERAPY
Norepinephrine Bitartrate (Levophed)
High-dose Dopamine (10 mcg/ kg /min )
The purpose is the preserve perfusion to the heart
and the brain, but can compromise other organs
(e.g. Kidney) Not used early in CHF.
INOTROPIC THERAPY
Dopamine ( 2 - 8 mcg / kg / min )
Dobutamine
These increase cardiac contractility
INTRAAORTIC BALLOON PUMP
NURSING MANAGEMENT
Critical care monitoring (ICU Set-Up)
Frequent cardiac rhythm,
hemodynamic monitoring
Strict I & O monitoring
Rapid identification and correction of
arising complications
Provide rest
INFECTIOUS AND INFLAMMATORY
DISEASES OF THE HEART
INFECTIOUS DISEASES
Rheumatic Fever
Infective Endocarditis
INFLAMMATORY DISEASE
Pericarditis
Myocarditis
RHEUMATIC FEVER
Associated with Group A Beta Hemolytic
Streptococcal Infection
Immunologic mechanism
Clinical Manifestations originate from immune
reaction to underlying infectious pathology
Results to valvular impairment
May present as valvular heart disease.
MOST COMMON AGE: Between 6 15 years old
Prevented by prompt treatment of
tonsillopharyngeal infections using antibiotics and
elective tonsillectomy
RHEUMATIC FEVER
Associated with Group A Beta Hemolytic
Streptococcal Infection. Appears 1-6 weeks after.
Immunologic mechanism
Clinical Manifestations originate from immune
reaction to underlying infectious pathology
Results to valvular impairment
May present as valvular heart disease.
MOST COMMON AGE: Between 6 15 years old
Prevented by prompt treatment of
tonsillopharyngeal infections using antibiotics and
elective tonsillectomy
PATHOGENESIS
Diffuse, proliferative, and exudative
inflammatory process
Involves the heart, joints,
subcutaneous tissues, CNS, and skin
Has underlying immune mechanism
Affects valves causing a button-hole
like deformity.
Results to possible pulmonary
complication
SALIENT CLINICAL FEATURES
CARDITIS/PANCARDITIS
MOST DESTRUCTIVE consequence
Causes Heart Blocks, Valve Diseases
MIGRATORY POLYARTHRITIS
MOST COMMON FINDING
Affects large joints
Responds to salicylates
CARDITIS/PANCARDITIS
MOST DESTRUCTIVE consequence
Causes Heart Blocks, Valve Diseases
Presence of ASCHOFF BODIES
MIGRATORY POLYARTHRITIS
MOST COMMON FINDING
Affects large joints
Responds to salicylates
ASCHOFF BODY
ANITSCHKOW CELL (CATERPILLAR CELL)
SYNDENHAMS CHOREA (Dance of St. Vitus)
Disorder of basal ganglia
Aimless involuntary movements
ERYTHEMA MARGINATUM
Rash seen on the trunk
Application of heat intensifies the rash
SUBCUTANEOUS NODULES
Painless, free nodules of the knees, knuckles,
and elbow seen usually only in children
JONES CRITERIA
MAJOR MINOR (CLINICAL)
Carditis Previous RF/RHD
Migratory Polyarthritis Arthralgia
Sydenhams Chorea Fever
Erythema Marginatum MINOR (LABORATORY)
Subcutaneous Nodules Increased ESR, CRP, WBC
Prolonged PR Interval
Plus: (+) Culture, ASO

MANAGEMENT
Eradicate Infection
Prompt treatment with Penicillin
Maximize Cardiac Output

Prevention of Heart Failure via Cortcicosteroids
Provide Comfort
Administer salicylates as ordered
Emphasize Hygiene
INFECTIVE ENDOCARDITIS
Infectious and inflammatory process of the
endocardium, especially the valves
Can be SUBACUTE which develops over
several weeks or months caused by
Streptococcus viridans
Can be ACUTE which appears over days or
weeks caused by Staphylococcus aureus
Can affect normal, damaged, and replaced
valves (Prosthesis)
Increased incidence among:

IV drug users
Immunosuppressed patients
Hemodialysis patients
Surgical patients
Intubated and catheterized patients
Patients with oral diseases
Diagnosed using the DUKES CRITERIA

(combination of clinical and microbiologic
methods)
Valve affectation presents as acquired
valvular heart disease depending on the
type of valvular malfunction
MANIFESTATIONS
Stroke or TIA, AMI, Pulmonary Embolism
Petechiae on the neck
Roths Spots: Yellow/White center surrounded by
bright red halo seen using ophthalmoscope
Splinter Hemorrhages: Under the nails
Oslers Node: Painful nodules on tipoff digits
Janeways Lesion: Flat non-tender red spots on
the palm of hand and soles of feet
ROTHS SPOT
SPLINTER HEMORRHAGES
OSLERS NODES
JANEWAYS LESION
DIAGNOSIS
Blood culture
Complete Blood Count
Cardiac Examination (e.g. presence of murmur)
EKG and Echocardiography
MANAGEMENT
Administration of appropriate antibiotic/s

depending on culture and sensitivity
Monitor for cardiac and neurologic complications
Treat fever (pano kung elderly??)
Provide adequate nutrition
Provide adequate rest
MYOCARDITIS
Inflammation of the myocardial wall
Associated with and occurs as a sequela of viral
infections: MOST COMMON is COXSACKIE
Results in impaired myocardial contraction
leading to heart failure
Patient may develop ANGINA or AMI-like
manifestations
PERICARDITIS
Inflammation of the visceral and parietal

pericardium
Fibrinous (dry, usual in chronic) vs Exudative
Normal Amount (50 mL) is exceeded causing
tamponade (when massive effusion develops)
Presents as pain in the chest, friction rub, fever
CARDIAC TAMPONADE
Life-threatening accumulation of fluid in the

pericardial sac
Restricts flow of the blood back to the heart
(diastolic malfunction) which results to drop in
cardiac output)
CARDIAC TAMPONADE
BECKS TRIAD
Hypotension
Jugular Venous Distention
Muffled, Distant Heart Sound
CARDIAC TAMPONADE
OTHER SALIENT MANIFESTATION
Elevated Venous Pressures
Right and Left Heart Failure Signs and Symptoms
Pulsus Paradoxus
MANAGEMENT
Periocardiocentesis
PERICARDIOCENTESIS
Diseasesinvolving blood vessels (arteries,
veins, and their branches)
Arterial
diseases result to loss of oxygen
and nutrient supply to distal areas
Venousdiseases result to inability to
reabsorb fluid (together with the
lymphatics) and stasis of blood in the distal
areas contributing to a possible
thromboembolic formation
ASSESSMENT FINDINGS
Intermittent Claudication
Most important subjective manifestation of
chronic arterial occlusive disease
Crampy pain in the extremities consistently
reproduced by some degree of activity or exercise
Result of oxygen lack
Seen if 50-75% of arterial lumen is obstructed
Pain occurs one joint level below the disease
process
ASSESSMENT FINDINGS
Rest Pain
Limb-threatening condition
Worse at night
Extremity should be lowered
Decreased Pulses
PULSE GRADING
3+ BOUNDING
2+ NORMAL
1+ WEAK
0 - ABSENT
Changes in Skin Color

Pallor Results from inadequacy of blood
flow, further pallor on elevation.
Rubor
Cyanosis
ARTERIAL vs VENOUS INSUFFICIENCY
CHARACTERISTIC ARTERIAL VENOUS
PAIN Intermittent claudication to Aching, cramping
sharp, unrelenting,
constant
PULSES Diminished or absent Present but

palpation is
hindered by edema
SKIN CHARACTERISTICS Dependent rubor Pigmented

elevation pallor
Dry and shiny, cool-to-cold,
loss of hair
CHARACTERISTIC ARTERIAL VENOUS
ARTERIAL vs VENOUS INSUFFICIENCY
ULCER CHARACTERISTICS
LOCATION Tip of toe, Malleoli
pressure areas
PAIN Very painful Minimal pain

DEPTH OF ULCER Deep Superficial
ULCER BASE Circular Irregular
LEG EDEMA Minimal Moderate to
severe
DIAGNOSTICS
CT Angiography
MRI
Doppler UTZ
Interventional Cardiology: Angiography
Ankle-Brachial Index
DIAGNOSTICS
CT Angiography
MRI
Doppler UTZ
Interventional Cardiology: Angiography
Ankle-Brachial Index
ANKLE BRACHIAL INDEX
ANKLE BRACHIAL INDEX
INTERPRETATION
0.9 (0.9 to 1.3) NORMAL
<0.89 to >0.60 MILD PAD
<0.59 to >0.40 MODERATE PAD
<0.39 SEVERE PAD
NURSING MANAGEMENT: THE PATIENT
WITH ARTERIAL INSUFFICIENCY
ASSESSMENT
Complete health history, identify risk factors
Identify specific manifestations, color, pulse
changes, and ulcers
NURSING DIAGNOSES
Ineffective peripheral tissue perfusion r/t
compromised circulation
Risk for impaired skin integrity r/t compromised
circulation
Deficient knowledge regarding self-care activities
INTERVENTIONS
Positioning below the level of the heart
Head elevation of about 15 cm, reclining
chair, sit with feet resting on the floor
Isometric exercises to promote circulation
Monitor for pain attacks
Apply warmth to promote flow
INTERVENTIONS
Avoid excessive exposure to cold adequate
clothing
If patient chills, warm bath or drink is helpful
In providing warmth, temperature of heat
source should not exceed body temperature
INTERVENTIONS
Instruct
patient to test bath water, use
thermometer (32.2 to 35 centigrade)AVOID HOT-
WATER BOTTLES and HEATING PADS
Applyheating pads on the abdomen to trigger
reflex vasodilation and this is safer than direct
application.
INTERVENTIONS
Avoid nicotine
Avoid trauma to ischemic sites
Never go barefoot
Avoid high heels and pointed shoes
Wear sturdy, well-fitting shoes or slippers
to prevent foot injury and blisters
Useneutral soaps to prevent
drying/cracking of skin, may apply lotion
but not between toes
INTERVENTIONS
Fingernails and toenails should be
carefully trimmed straight across and
sharp edges are filed to follow contour
Thick/brittle nails cannot be trimmed
safely consult a podiatrist!
Corn/calluses should be removed by
professionals
THROMBOANGIITIS OBLITERANS
(BUERGERS DISEASE)
Recurring
inflammation of
intermediate and
small arteries and
veins of the
extremities
Highly-associated
with smoking
Believed to be a form
of vasculitis
Symptoms
Major symptom: PAIN
Foot cramps, instep claudication
Relieved by rest
Signs
Intense rubor (reddish-blue
discoloration)
Absent pedal pulses but normal
proximal pulses
May progress to ulceration
Management
Vasodilators
Treatment and debridement of ulcers
Prevention of spread of infection
AVOID SMOKING.
AMPUTATION
Ifamputated, elevate for the first 24H

Monitor for hematoma
Elastic bandage fitting two fingers
Bandage is removed and reapplied as
prescribed (q6H using figure of 8)
RAYNAUDS DISEASE
Episodic digital Hyper responsiveness
ischemia manifesting to cold
as sequential: Vasospastic
blanching cyanosis mechanism affecting
after cold exposure more women than
then a period of rubor men
(reactive)
Rarely gangrenous
Triggered by
emotional stress,
cause in unknown but
is often associated
with autoimmune
disorders
TREATMENT
Dress
warmly and avoid cold exposure (hats
and mittens should be worn all the time
when exposed to environment)
Smoking is contraindicated
CCB as treatment
Alpha-1 Antagonist (Prazosin)
AORTIC ANEURYSM
Localized sac or dilation formed at a weak area of
the aorta
Classified according to form:
TRUE ANEURYSMS All three layers are affected
SACCULAR: One side of vessel only
FUSIFORM: Entire circumference becomes dilated,
spindle-shaped
DISSECTING: Actually not a true aneurysm but a
hematoma due to separation of layers
PSEUDO (FALSE) ANEURYSMS Clot forms but
does not communicate
AORTIC ANEURYSM
Atherosclerosisis a suspect to the

development of aneurysms
Leads ultimately to hemorrhage and
death
TYPES OF ANEURYSMS
(THIS WAS ASKED VERBATIM IN THE NLE)
LIFTED FROM BRUNNER AND SUDDARTHS TEXTBOOK OF MEDICAL-SURGICAL NURSING 12TH EDITION
ETIOLOGIC CLASSES
CONGENITAL INFLAMMATORY (Non-
Marfans, Ehlers-Danlos infectious)
MECHANICAL (Hemodynamic) SLE, Takayasus Arteritis
AVFistula, Amputation- INFECTIOUS (Mycotic)
related Bacterial,
Fungal,
TRAUMATIC (Pseudoaneurysm) Spirochetal
Penetrating injuries
THORACIC AORTIC ANEURYSM
Caused by atherosclerosis
Thoracic area is the most common site for
dissecting aneurysm
Variable presentation
Pulsating mass surrounding the intrathoracic
structures
Pain is the most prominent symptom
If the aneurysm lies near the trachea, patient
may experience voice changes, dyspnea,
dysphagia
CXR
Transesophageal Echocardiography
CT Scan
MEDICAL-SURGICAL MANAGEMENT
Treated by surgical repair
Aggressive BP control
Systolic BP maintained at 100-120 mm Hg
THERAPEUTICS
Hydralazine
Esmolol
Atenolol
SURGICAL
Repair the aneurysm, vascular grafting
#nursinggoals
Prevent rupture
BP monitoring
Strict UO monitoring
Do not palpate the pulsating mass!
Provide rest and comfort
ABDOMINAL AORTIC ANEURYSM
Still,
atherosclerosis is the most common
cause
PATHOPHYSIOLOGY
All aneurysms involve the tunica media
Prone to weakness
Hypertension is a risk
MANIFESTATIONS
Time-Bomb
Apparent pulsating mass
ASSESSMENT
Systolic bruit may be heard over the mass

Duplex UTZ
CT Scan
Ruptureis likely to occur as sizes wider
than 6 cm
NURSING MANAGEMENT
Anticipate possible rupture

Monitor BP Sudden decrease may
suggest rupture intraperitoneally
Monitor adherence to medical
therapeutics
Signs of impending rupture: Severe
back pain or abdominal pain
DISSECTING ANEURYSM
Associated with poorly controlled HPN
Usual in MEN/50 to 70 years of age
Due to rupture of the intimal layer dissection
of layers
Tearing quality of pain in the anterior chest
radiating to the back
Severe hypotension may follow Death
STANFORD CLASSIFICATION
TYPE A: Involves the ASCENDING AORTA
TYPE B: Does not involve the ASCENDING AORTA
IMPORTANT NURSING POINTS
Post-endovascular repair: LIE SUPINE for 6H

Headof bed may be elevated up to 45
degrees after 2 H
Bedpan should be used while on bedrest,
FC to UB may be used as well.
VSand Doppler assessment: q15 min x 4
times, q30 min x 4 times, q1H x 4 times,
then as directed
IF ANGIOGRAM WAS DONE:
Catheterization site should be observed
frequently for swelling hematoma
Report immediately BP elevation
Resume pre-procedure diet and fluids are
encouraged
IV until able to drink
Promotes excretion of contrast, prevents contrast
nephropathy
6H post procedure, patient may logroll to side and
may ambulate with assistance to bathroom
VENOUS DISORDERS
Venous Thrombosis
Deep Vein Thrombosis
Thrombophlebitis
Phlebothrombosis
VENOUS DISORDERS
Can also be classified as:

ACUTE
CHRONIC
ACUTE: THROMBOPHLEBITIS
Can be easily diagnosed and is usually

iatrogenic
Deep Vein Thrombosis (DVT) is the
thrombophlebitis of deep veins
Seen in 40% of patients who underwent
major surgery
Triggered by VIRCHOWS TRIAD

Venous stasis is usually caused by
immobilization, surgery, prolonged travel,
CVD, paralysis,
Hypercoagulability can be caused by
malignancy (ovarian or visceral) or blood
dyscrasias
Vessel injury can be due to trauma
MANAGEMENT:
Preventive through exercise
Sequential Compression Device (e.g.
Kendall) Not used in known DVT
Pharmacologic Methods
MANAGEMENT:
Preventive through exercise
Sequential Compression Device (e.g.
Kendall) Not used in known DVT
Used for longer than 24H
Removed BID to inspect skin and to
allow perspiration to evaporate
Pharmacologic Methods
Review history of the patient,

inheritable coagulation disorders,
neoplastic diseases, recent major
surgery
Assess and compare bilateral thigh to
ankle circumferences
Check for presence of varicosities
MOST COMMON: UNILATERAL LEG SWELLING

Pain, redness, or warmth
Homans Sign
Venous Duplex Scan
D-Dimer
MOST COMMON: UNILATERAL LEG SWELLING

Pain, redness, or warmth
Homans Sign
Venous Duplex Scan
D-Dimer
PREVENTION AND THERAPEUTICS
Elevate
foot of bed 6 inches with slight
knee bending
MEDICAL
Anticoagulation
Thrombolytics
SURGICAL
Doneif anticoagulation or thrombolysis is
contraindicated
IVC Filter to prevent PE (major AIM!)
NURSING MANAGEMENT
COMPRESSION STOCKINGS
Sustains evenly distributed pressure over the
calves
Improves blood flow
May be knee-high, thigh-high, panty hose
Prevent rolling down can cause further stasis
Removed at night and reapplied before legs are
lowered from bed to the floor
When removed, check for skin irritation
Contraindicated in pitting edema
CHRONIC VENOUS INSUFFICIENCY
Venous valve impairment with reflux
Surficial vein / Deep vein
MANIFESTATIONS
Edema
Pigmentation
Pain
Symptoms are more apparent in the evening
Ulcers
MANAGEMENT
Elevate the legs, 15-30 mins x 2 H
When sleeping elevate the foot about 15
cm
Walking should be encouraged
Avoid leg crossing, tight garments
Compression stocking: Apply after leg
raising when the level of pooled blood is
reduced
Manage Leg Ulcers Antibiotics
HYPERTENSION
TYPES
Primary 95% (approx.)
Secondary 5% (approx.)
HYPERTENSIVE CRISES
Hypertensive
Emergency Necessitates
IMMEDIATE lowering
Hypertensive Urgency Lowered within a
few hours
HYPERTENSION
NON-MODIFIABLE RISK FACTORS

Family History
Age (30 to 50 y/o)
Gender: Male preponderance
Ethnicity: African-Americans
HYPERTENSION
MODIFIABLE RISK FACTORS

Diabetes
Stress Level
Obesity
Nutrient consumption (e.g. Sodium)
Substance Abuse
HYPERTENSION
DISEASE MECHANISM
Primary: Fluid volume disturbances, RAAS
Dysfunction
Secondary:
MOST COMMON CAUSES are Chronic
Glomerulomephritis and Renal Artery
Stenosis
Increased Adrenal Cortical Function
Excessive production of catecholamines
HYPERTENSION
VESSEL CHANGES
Vascularchanges lead to
reduced flow to important
organs (e.g. heart, brain,
kidneys, and retina)
JNC 7
MODIFIABLE RISK FACTORS
Diabetes
Stress Level
Obesity
Nutrient consumption (e.g. Sodium)
Substance Abuse
FIN.

Cardiovascular Nursing

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CARDIOVASCULAR

FRANK STARLING LAW OF THE HEART

Family history of Dyslipidemia and

GENERAL APPEARANCE AND LEVEL OF

1+ 2 mm or less SLIGHT PITTING NO RAPIDLY

3+ 4-6 mm NOTICEABLY SWOLLEN MAY LAST FOR 1

4+ 6-8 mm VERY DEEP DISTORTED MAY LAST FOR 2-5

HEAD AND NECK

THORAX and PRECORDIUM

THORAX and PRECORDIUM

Stress Testing (Non-Invasive):

IMPORTANT NURSING POINTS!

IMPORTANT NURSING POINTS!

IMPORTANT NURSING POINTS!

P-R INTERVAL: 0.12 0.20 SECONDS

1. COMPUTE FOR THE HEART RATE

DETERMINE THE HEART RATE USING BOX METHOD

50 BA? 100 BA?75 BA?

HINDI DAPAT LAGING PUSO ANG

1: 300 bpm 6: 50 bpm

Disordersof the formation (AUTOMATICITY),

PREMATURE ATRIAL CONTRACTION

Sudden onset and termination of rapid

Pooling of blood in the atria

PREMATURE VENTRICULAR CONTRACTION

Frequent (6 or more per minute)

Seriesof P-QRS with increasing PR

PACE: Ability to produce impulse

SINGLECHAMBER: PACES ATRIA OR

Mercury-Zinc Battery (3-4 years)

SAANG TYPE PWEDE MAG-APPLY ANG EXCEPT ?

Mechanism of pathogenesis is related to

THE OVER-ALL GOAL IS

During angina attack, stop patient activities and

Oxygen support at 2 L/min by nasal cannula

The diagnosis of MI is based on

Assists in the diagnosis of MI

HEART FAILURE AND PULMONARY EDEMA

Great Saphenous Vein

PHASE 2 (IMMEDIATE OUTPATIENT)

PHASE 2 (IMMEDIATE OUTPATIENT)

PHASE 4 (MAINTENANCE OUTPATIENT)

Possible Nursing Diagnosis

Assessment and Diagnostic Findings

Heart muscle disease associated

Diastolic dysfunction caused by rigid

CONGO RED STAIN UNDER

Patient usually remains stable

COMMON FINDINGS DIAGNOSTICS

Standard and effective treatment for

WHO IS NOT A CANDIDATE?

Inability of the heart to pump sufficient

Angiotensin-Converting Enzyme Inhibitor

Occurs when the heart cannot pump

Correct the underlying problem to

Plus: (+) Culture, ASO

Maximize Cardiac Output

Increased incidence among:

Diagnosed using the DUKES CRITERIA

Administration of appropriate antibiotic/s

Inflammation of the visceral and parietal

Life-threatening accumulation of fluid in the

Changes in Skin Color

PULSES Diminished or absent Present but