Lecture Notes on Cardiovascular System

Prepared By: Mark Fredderick R Abejo R.N, MAN

MEDICAL AND SURGICAL NURSING

Cardiovascular System

Lecturer: Mark Fredderick R. Abejo RN, MAN

Anatomy and Physiology of the Heart

Cardiovascular system consists of the heart, arteries,  Pericardium – invaginated sac

veins & capillaries. The major function are circulation of blood,  Visceral – attached to the exterior of
delivery of O2 & other nutrients to the tissues of the body & myocardium
removal of CO2 & other cellular products metabolism  Parietal – attached to the great vessels and
diaphragm
Heart
 Papillary Muscle
 Muscular pumping organ that propel blood into the arerial Arise from the endocardial & myocardial surface of the
system & receive blood from the venous system of the body. ventricles & attach to the chordae tendinae
 Hollow muscular behind the sternum and between the lungs
 Located on the middle of mediastinum  Chordae Tendinae
 Resemble like a close fist Attach to the tricuspid & mitral valves & prevent eversion
 Weighs approximately 300 – 400 grams during systole
 Has heart wall has 3 layers
 Endocardium – lines the inner chambers of the  Separated into 2 pumps:
heart, valves, chordate tendinae and papillary  right heart – pumps blood through the lungs
muscles.  left heart – pumps blood through the peripheral
 Myocardium – muscular layer, middle layer, organs
responsible for the major pumping action of the
ventricles.  Chamber of the Heart
 Epicardium – thin covering(mesothelium), Atria
covers the outer surface of the heart  2 chambers, function as receiving chambers, lies
above the ventricles


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Lecture Notes on Cardiovascular System
Prepared By: Mark Fredderick R Abejo R.N, MAN

 Upper Chamber (connecting or receiving)  Coronary Veins

 Right Atrium: receives systemic venous blood
through the superior vena cava, inferior vena cava &
coronary sinus
 Left Atrium: receives oxygenated blood returning to
the heart from the lungs trough the pulmonary veins
Coronary sinus – main vein of the heart
Great Cardiac vein – main tributary of the coronary sinus
Oblique vein – remnant of SVC, small unsignificant
Heart Circulation

Ventricles
 2 thick-walled chambers; major responsibility for
forcing blood out of the heart; lie below the atria
 Lower Chamber (contracting or pumping)
 Right Ventricle: contracts & propels deoxygenated
blood into pulmonary circulation via the aorta
during ventricular systole; Right atrium has
decreased pressure which is 60 – 80 mmHg
 Left Ventricle: propels blood into the systemic
circulation via aortaduring ventricular systole; Left
ventricle has increased pressure which is 120 – 180
mmHg in order to propel blood to the systemic
circulation

 Heart Valves
 Tricuspid
 Pulmonic
 Mitral
 Aortic

Cardiac Conduction System

Properties of Heart Conduction System

• Automaticity
• Excitability
 Coronary artery – 1st branch of aorta • Conductivity
Right Coronary • Contractility
 SA nodal Branch – supplies SA node
 Right marginal Branch – supplies the right border
of the heart Structure of Heart Conduction System
 AV nodal branch – supplies the AV node
 Posterior interventricular artery – supplies both
ventricles
Left Coronary
 Circumflex branch – supplies SA node in 40 % of
people
 Left marginal – supplies the left ventricle
 Anterior interventricular branch aka Left anterior
descending(LAD)–supplies both ventricles and
interventricular septum
 Lateral branch – terminates in ant surface of the
heart

 Nodal tissues
SA Node( Sino-atrial, Keith and Flack)
 Primary Pacemaker
 Between SVC and RA
 Vagal and symphatetic innervation
 Sinus Rhythms

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Lecture Notes on Cardiovascular System
Prepared By: Mark Fredderick R Abejo R.N, MAN
AV Node( Atrioventricular , Kent and Tawara)
 At the right atrium
 3 zones
 AN Zone(atrionodal)
 N Zone (nodal)
 NH zone (nodal –HIS)
 Internodal and Interatrial Pathways
Connects SA and AV Node
Ant. Internodal(bachman) tract
Middle Internodal(wenkebach) tract
Posterior internodal(Thorel) tract
 Bundle of His/ Purkinje Fibers
Provides for ventricular conduction system
Fastest conduction among cardiac tissues
Right bundle
Left Bundle
Cardiac Action Potential
 Depolarization: electrical activation of a cell caused by
the influx of sodium into the cell while potassium exits
the cell
 Repolarization: return of the cell to the resting state
caused by re-entry of potassium into the cell while
sodium exits
 Refractory periods:
Effective refractory period: phase in which cells
are incapable of depolarizing
Relative refractory period: phase in which cells
require a stronger-than-normal stimulus to
depolarize
Anatomical Sequence of Excitation of the Heart
 (right atrium)
 sinoatrial node (SA)
 (right AV valve)
 atrioventricular node (AV)
 atrioventricular bundle (bundle of His)
 right & left bundle of His branches
 Purkinje fibers of ventricular walls
(from SA through complete heart contraction = 220 ms = 0.22 s)
a. Sinoatrial node (SA node) "the pacemaker" - has the
fastest autorhythmic rate (70-80 per minute), and sets the
pace for the entire heart; this rhythm is called the sinus
rhythm; located in right atrial wall, just inferior to the
superior vena cava
b. Atrioventricular node (AV node) - impulses pass from
SA via gap junctions in about 40 ms.; impulses are
delayed about 100 ms to allow completion of the
contraction of both atria; located just above tricuspid
valve (between right atrium & ventricle)
c. Atrioventricular bundle (bundle of His) - in the
interATRIAL septum (connects L and R atria)
d. L and R bundle of His branches - within the
interVENTRICULAR septum (between L and R
ventricles)
e. Purkinje fibers - within the lateral walls of both the L and
R ventricles; since left ventricle much larger, Purkinjes
more elaborate here; Purkinje fibers innervate “papillary
muscles” before ventricle walls so AV can valves prevent
backflow
Medical and Surgical Nursing
The Normal Cardiac Cycle
General Concepts
Systole - period of chamber contraction
Diastole - period of chamber relaxation
Cardiac cycle - all events of systole and diastole during one
heart flow cycle
Events of Cardiac Cycle
1. mid-to-late ventricular diastole: ventricles filled
 the AV valves are open
 pressure: LOW in chambers; HIGH in
aorta/pulmonary trunk
 aortic/pulmonary semilunar valves CLOSED
 blood flows from vena cavas/pulmonary vein INTO
atria
 blood flows through AV valves INTO ventricles
(70%)
2. ventricular systole: blood ejected from heart
 filled ventricles begin to contract, AV valves
CLOSE
 contraction of closed ventricles increases pressure
 ventricular ejection phase - blood forced out
 semilunar valves open, blood -> aorta & pulmonary
trunk
3. isovolumetric relaxation: early ventricular diastole
 ventricles relax, ventricular pressure becomes LOW
 semilunar valves close, aorta & pulmonary trunk
backflow
TOTAL CARDIAC CYCLE TIME = 0.8 second
(normal 70 beats/minute)
atrial systole (contraction) = 0.1 second
ventricular systole (contraction) = 0.3 second
quiescent period (relaxation) = 0.4 second
Cardiac Output - Blood Pumping of the Heart
General Concepts
• Stroke volume: the amount of blood ejected with each
heartbeat
• Cardiac output: amount of blood pumped by the
ventricle in liters per minute
• Preload: degree of stretch of the cardiac muscle fibers at
the end of diastole
• Contractility: ability of the cardiac muscle to shorten in
response to an electrical impulse
• Afterload: the resistance to ejection of blood from the
ventricle
• Ejection fraction: the percent of end-diastolic volume
ejected with each heartbeat
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Lecture Notes on Cardiovascular System
Prepared By: Mark Fredderick R Abejo R.N, MAN

General Variables of Cardiac Output hypernatremia - HIGH Na+ concentration; can

1. Cardiac Output (CO) - blood amount pumped per minute
 CO (ml/min) = HR (beats/min) X SV (ml/beat)
 Normal CO = 75 beats/min X 70 ml/beat
= 5.25 L/min
2. Heart Rate (HR) - cardiac cycles per minute
 Normal range is 60-100 beats per minute
 Tachycardia is greater than 100 bpm
 Bradycardia is less than 60 bpm
 Sympathetic system INCREASES HR
 Parasympathetic system (Vagus) DECREASES HR
3. Blood pressure - Cardiac output X peripheral resistance
 Control is neural (central and peripheral) and
hormonal
 Baroreceptors in the carotid and aorta
 Hormones- ADH, aldosterone, epinephrine can
increase BP; ANF can decrease BP
Regulation of Stroke Volume (SV)
block Na+ transport & muscle contraction
3. Other Factors Effecting Heart Rate (HR)
normal heart rate - fetus 140 - 160 beats/minute
female 72 - 80 beats/minute
male 64 - 72 beats/minute
1. exercise - lowers resting heart rate (40-60)
2. heat - increases heart rate significantly
3. cold - decreases heart rate significantly
4. tachycardia - HIGHER than normal resting heart rate
(over 100); may lead to fibrillation
5. bradycardia - LOWER than normal resting heart rate
(below 60); parasympathetic drug side effects; physical
conditioning; sign of pathology in non-healthy patient
Vascular System
Major function of the blood vessels isto supply the tissue

 End diastolic volume (EDV) - total blood collected in with blood, remove wastes, & carry unoxygenated blood
ventricle at end of diastole; determined by length of back to the heart
diastole and venous pressure (~ 120 ml)
 End systolic volume (ESV) - blood left over in ventricle
at end of contraction (not pumped out); determined by Types of Blood Vessels
force of ventricle contraction and arterial blood pressure
(~50 ml)
Arteries
SV (ml/beat) = EDV (ml/beat) - ESV (ml/beat)
Normal SV = 120 ml/beat - 50 ml/beat = 70 ml/beat Elastic-walled vessels that can stretch during systole &
recoil during diastole; they carry blood away from the

Frank-Starling Law of the Heart - critical factor for stroke heart & distribute oxygenated blood throughout the body
volume is "degree of stretch of cardiac muscle cells"; Arterioles
more stretch = more contraction force
Small arteries that distribute blood to the capillaries &
increased EDV = more contraction force function in controlling systemic vascular resistance &
slow heart rate = more time to fill
exercise = more venous blood return therefore arterial pressure
Capilliaries

Regulation of Heart Rate (Autonomic, Chemical, Other) The following exchanges occurs in the capilliaries
O2 & CO2
1. Autonomic Regulation of Heart Rate (HR)
Solutes between the blood & tissue
 Sympathetic - NOREPINEPHRINE (NE) increases heart Fluid volume transfer between the plasma &
rate (maintains stroke volume which leads to increased
Cardiac Output) interstitial space
Venules
 Parasympathetic - ACETYLCHOLINE (ACh) decreases
heart rate Small veins that receive blood from capillaries &
function as collecting channels between the capillaries &
 Vagal tone - parasympathetic inhibition of inherent rate
of SA node, allowing normal HR veins
Veins
 Baroreceptors, pressoreceptors - monitor changes in
blood pressure and allow reflex activity with the Low-pressure vessels with thin small & less muscles than
autonomic nervous system
arteries; most contains valves that prevent retrograde
blood flow; they carry deoxygenated blood back to the
2. Hormonal and Chemical Regulation of Heart Rate (HR)
heart. When the skeletal surrounding veins contract, the
 epinephrine - hormone released by adrenal medulla veins are compressed, promoting movement of blood
during stress; increases heart rate
back to the heart.
 thyroxine - hormone released by thyroid; increases heart
rate in large quantities; amplifies effect of epinephrine

 Ca++, K+, and Na+ levels very important;

hyperkalemia - increased K+ level; KCl used to
stop heart on lethal injection
hypokalemia - lower K+ levels; leads to
abnormal heart rate rhythms
hypocalcemia - depresses heart function
hypercalcemia - increases contraction phase

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Lecture Notes on Cardiovascular System
Prepared By: Mark Fredderick R Abejo R.N, MAN

Palpation:

Assessment of the Client with Cardiovascular

Disorders

Nursing History
Risk Factors

A. Non – Modifiable Risk Factor

 Age
 Gender
 Race
 Heredity Heart Sounds: Stethoscope Listening

B. Modifiable Risk Factor Overview of Heart Sounds (lub-du ; lub, dub )

 Stress
 Diet lub - closure of AV valves, onset of ventricular systole
 Exercise dub - closure of semilunar valves, onset of diastole
 Sedentary lifestyle
 Cigarette smoking  Tricuspid valve (lub) - RT 5th intercostal, medial
 Alcohol  Mitral valve (lub) - LT 5th intercostal, lateral
 Hypertension  Aortic semilunar valve (dub) - RT 2nd intercostal
 Hyperlipidemia  Pulmonary semilunar valve (dub) - LT 2nd intercostals
 DM
 Obesity S1 - due to closure of the AV(mitral/tricuspid) valves
 Type A personality - timing: beginning of systole
 Contraceptive Pills - loudest at the apex

Common Clinical Manifestations of Cardiovascular Disorders S2 - due to the closure of the semi-lunar (pulmonic/aortic) valves
- timing: diastole
a. Dyspnea - loudest at the base
- Exertional
- Orthopnea
- Paroxysmal Noctural Dyspnea
- Cheyne-stokes
b. Chest Pain
c. Edema
- Ascites
- Hydrothorax
- Anasarca
d. Palpitation S3 – Ventricular Diastolic Gallop
e. Hemoptysis Mechanism: vibration resulting from resistance to rapid
f. Fatigue ventricular filling secondary to poor compliance
g. Syncope and Fainting Timing: early diastole
h. Cyanosis Location: Apex (LV) or LLSB (RV)
i. Abdominal Pain Pitch: faint and low pitched
j. Clubbing of fingers
k. Jaundice S4 - Atrial Diastolic Gallop
Mechanism: vibration resulting from resistance to late
Physical Assessment ventricular filling during atrial systole
Timing: late diastole ( before S1)
Inspection: Location: Apex ( LV) or LLSB (RV)
– Skin color Pitch: low ( use bell)
– Neck vein distention
Heart Murmurs
Murmur - sounds other than the typical "lub-dub"; typically caused
by disruptions in flow

 Incompetent valve - swishing sound just AFTER the

normal "lub" or "dub"; valve does not completely close,
some regurgitation of blood

 Stenotic valve - high pitched swishing sound when blood

should be flowing through valve; narrowing of outlet in
the open state
– Respirations
– Pulsations Pericardial Friction Rub
– Clubbing
– Capillary refill  It is an extra heart sound originating from the pericardial sac
 Mechanism: Originates from the pericardial sac as it moves
 Timing: with each heartbeat

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Lecture Notes on Cardiovascular System
Prepared By: Mark Fredderick R Abejo R.N, MAN

 Location: over pericardium. Upright position, leaning 2. Coagulation Screening Test

forward
 Pitch: high pitched and scratchy. Sounds like sandpaper
being rubbed together
 Significance: inflammation, infection, infiltration
Classification of Clients with Diseases of the
Heart ( Functional Capacity )
 Class I. Patients with cardiac disease but without
resulting limitations of physical activity.
 Class II. Patients with cardiac disease resulting to slight
limitation of physical activity
 Class III. Patients with cardiac disease resulting in
marked limitation of physical activity. They are
comfortable at rest.
 Class IV. Patients with cardiac disease resulting in
inability to carry on any physical activity without
discomfort
a. Bleeding Time – measures the ability to stop bleeding after
small puncture wound
b. Partial Thromboplastin Time (PTT) – used to identify
deficiencies of coagulation factors, prothrombin and fibrinogen;
monitors heparin therapy.
c. Prothrombin Time (Pro-time) – determines activity and
interaction of the Prothrombin group: factors V (preacclerin), VII
(proconvertin), X (Stuart-Power factor), prothrombin and
fibrinogen; used to determine dosages of oral anti-coagulant.
Normal Values
Bleeding Time: 2.75-8 min
Partial Thromboplastin Time (PTT): 60 - 70 sec.
Prothrombin Time (PT): 12-14 sec.

Diagnostic Assessment 3. Erythrocyte sedimentation rate ( ESR)

It is a measurement of the rate at which RBC’s settle out
Purposes: of anticoagulated blood in an hour
It is elevated in infectious heart disorder or myocardial
1. To assist in diagnosing MI infarction
2. To identify abnormalities
3. To assess inflammation Normal Values
4. To determine baseline value Male: 15-20 mm/hr
5. To monitor serum level of medications Female: 20-30 mm/hr
6. To assess the effects of medications
4. CARDIAC Proteins and enzymes
A. Blood Studies
a. CK- MB ( creatine kinase)
1. Complete Blood Count  Most cardiac specific enzymes
 Accurate indicator of myocardial dammage
a. RBC count- # of RBCs/ mm3 of blood, to diagnose anemia and  Elevates in MI within 4 hours, peaks in 18 hours and
ploycythemia then declines till 3 days
 Normal value is 0-7 U/L or males 50-325 mu/ml
b. Hemoglobin- # of grams of hgb/ 100ml of blood; to measure the Female 50-250 mu/ml
oxygen-carrying capacity of the blood
b. Lactic Dehydrogenase (LDH)
c. Hematocrit – expressed in %; measures the volume of RBCs in  Most sensitive indicator of myocardial damage
proportion to plasma; used also to diagnose anemia and  Elevates in MI in 24 hours, peaks in 48-72 hours
polycythemia and abnormal hydration states Return to normal in 10-14 days
 Normally LDH1 is greater than LDH2
d. RBC indices- measure RBC size and hemoglobin content  Lactic Dehydrogenase (LDH)
a. MCV (mean corpuscular volume)  MI- LDH2 greater than LDH1 (flipped LDH pattern)
b. MCH (mean corpuscular hemoglobin)  Normal value is 70-200 IU/L (100 – 225 mu/ml)
c. MCHC (mean corpuscular hemoglobin concentrarion)
c. Myoglobin
e. Platelet count- # of Platelet/ mm3; to diagnose  Rises within 1-3 hours
thrombocytopenia and subsequent bleeding tendencies  Peaks in 4-12 hours
 Returns to normal in a day
f. WBC count- of WBCs/ mm3 of blood; to detect infection or  Not used alone
inflammation  Muscular and RENAL disease can have elevated
myoglobin
g. WBC Differential count- determines proportion of each WBC
in a sample of 100 WBCs; used to classify leukemias d. Troponin I and T
 Troponin I is usually utilized for MI
Normal Values  Elevates within 3-4 hours, peaks in 4-24 hours and
persists for 7 days to 3 weeks!
RBC: Women – 4.2-5.4 million/mm3  Normal value for Troponin I is less than 0.6 ng/mL
Men – 4.7-6.1 million/mm3  REMEMBER to AVOID IM injections before
Hgb: Women – 12-16 g/dl obtaining blood sample!
Men – 13-18 g/dl  Early and late diagnosis can be made!
Hct : Women – 36-42%
Men – 42-48% e. SERUM LIPIDS
WBC: 5000-10,000/mm3  Lipid profile measures the serum cholesterol,
Granulocytes triglycerides and lipoprotein levels
Neutrophils: 55-70%  Cholesterol= 200 mg/dL
Eosinophils: 1-4%  Triglycerides- 40- 150 mg/dL
Basophils: 0.5-1.0%  LDH- 130 mg/dL
Agranulocytes  HDL- 30-70- mg/dL
Lymphocytes: 20-40%  NPO post midnight (usually 12 hours)
Monocytes: 2-8%
Platelets: 150,000-450,000/mm3

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Lecture Notes on Cardiovascular System
Prepared By: Mark Fredderick R Abejo R.N, MAN

B. Non-Invasive Procedure

1. Cardiac Monitoring / Electrocardiography (ECG)

A non-invasive procedure that evaluates the electrical
activity of the heart

a. Limb Leads

b. Precordial Leads

Deflection Waves of ECG

1. P wave - initial wave, demonstrates the depolarization from SA

Node through both ATRIA; the ATRIA contract about 0.1 s after
start of P Wave.

2. QRS complex - next series of deflections, demonstrates the

depolarization of AV node through both ventricles; the ventricles
contract throughout the period of the QRS complex, with a short
delay after the end of atrial contraction; repolarization of atria also
obscured

The precordial leads VI –V6 are part of the 12 lead EKG.
They are not monitored with the standard limb leads
c. 12 lead ECG
3. T Wave - repolarization of the ventricles (0.16 s)
4. PR (PQ) Interval - time period from beginning of atrial
contraction to beginning of ventricular contraction (0.16 s)
5. QT Interval - the time of ventricular contraction (about 0.36 s);
from beginning of ventricular depolarization to end of
repolarization.

2. Holter Monitoring
 A non-invasive test in which the client wears a Holter
monitor and an ECG tracing recorded continuously over
a period of 24 hours
 Instruct the client to resume normal activities and
maintain a diary of activities and any symptoms that may
develop

ECG Paper

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Lecture Notes on Cardiovascular System
Prepared By: Mark Fredderick R Abejo R.N, MAN
3. Stress Test
 A non-invasive test that studies the heart during
activity and detects and evaluates CAD
 Exercise test, pharmacologic test and emotional test
 Treadmill testing is the most commonly used stress
test
 Used to determine CAD, Chest pain causes, drug
effects and dysrhythmias in exercise
 Pre-test: consent may be required, adequate rest , eat
a light meal or fast for 4 hours and avoid smoking,
alcohol and caffeine
 During the test: secure electrodes to appropriate
location on chest, obtain baseline BP and ECG
tracing, instruct client to exercise as instructed and
report any pain, weakness and SOB, monitor BP and
ECG continuously, record at frequent interval
 Post-test: instruct client to notify the physician if
any chest pain, dizziness or shortness of breath .
Instruct client to avoid taking a hot shower for 10-12
hours after the test
4. Pharmacological stress test
 Use of dipyridamole
 Maximally dilates coronary artery
 Side-effect: flushing of face
 Pre-test: 4 hours fasting, avoid alcohol, caffeine
 Post test: report symptoms of chest pain
5. ECHOCARDIOGRAM
 Non-invasive test that studies the structural and
functional changes of the heart with the use of ultrasound
 Client Preparation: instruct client to remain still during
the test, secure electrodes for simultaneous ECG tracing,
explain that there will be no pain or electrical shock,
lubricant placed on the skin will be cool.
6. Phonocardiography
 Is a graphic recording of heart sound with simultaneous
ECG.
Medical and Surgical Nursing
C. Invasive Procedure
1. Cardiac Catheterization ( Coronary Angiography /
Arteriography )
 Insertion of a catheter into the heart and surrounding
vessels
 Is an invasive procedure during which physician
injects dye into coronary arteries and immediately
takes a series of x-ray films to assess the structures
of the arteries
 Determines the structure and performance of the
heart valves and surrounding vessels
 Used to diagnose CAD, assess coronary atery
patency and determine extent of atherosclerosis
 Pretest: Ensure Consent, assess for allergy to
seafood and iodine, NPO, document weight and
height, baseline VS, blood tests and document the
peripheral pulses
 Pretest: Fasting for 8-12 hours, teachings,
medications to allay anxiety
 Intra-test: inform patient of a fluttery feeling as the
catheter passes through the heart; inform the patient
that a feeling of warmth and metallic taste may
occur when dye is administered
 Post-test: Monitor VS and cardiac rhythm
 Monitor peripheral pulses, color and warmth and
sensation of the extremity distal to insertion site
 Maintain sandbag to the insertion site if required to
maintain pressure
 Monitor for bleeding and hematoma formation
2. Nuclear Cardiology
 Are safe methods of evaluating left ventricular muscle
function and coronary artery blood distribution.
 Client Preparation: obtain written consent, explain
procedure, instruct client that fasting may be required for
a short period before the exam, assess for iodine allergy.
 Post Procedure: encourage client to drink fluids to
facilitate the excretion of contrast material, assess
venipuncture site for bleeding or hematoma.
 Types of Nuclear Cardiology
o Multigated acquisition (MUGA) or cardiac
blood pool scan
 Provides information on wall motion
during systole and diastole, cardiac
valves, and EF.
o Single-photon emission computed
tomography (SPECT)
 Used to evaluate the myocardium at
risk of infarction and to determine
infarction size.
o Positron emission tomography (PET)
scanning
 Uses two isotopes to distinguish
viable and nonviable myocardial
tissue.
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Lecture Notes on Cardiovascular System
Prepared By: Mark Fredderick R Abejo R.N, MAN

o Perfusion imaging with exercise testing

 Determines whether the coronary
blood flow changes with increased
activity.
 Used to diagnose CAD, determine
the prognosis in already diagnosed
CAD, assess the physiologic
significance of a known coronary
lesion, and assess the effectiveness of
various therapeutic modalities such
as coronary artery bypass surgery,
percutaneous coronary intervention,
or thrombolytic therapy.
 Client Preparation: obtain consent, insertion is under
strict sterile technique, usually at the bedside, explain to
client the sterile drapes may cover the face, assists to
position client flat or slight T-postion as tolerated and
instruct to remain still during the procedure
 Nursing Care During Insertion: Monitor and document
HR,BP and ECG during the procedure
CARDIAC DISORDER

D. Hemodynamics Monitoring CORONARY ARTERIAL DISEASE

ISCHEMIC HEART DISEASE
1. CVP ( Central Venous Pressure )
 Reflects the pressure of the blood in the right atrium.
 Engorgement is estimated by the venous column that can Results from the focal narrowing of the large and
be observed as it rises from an imagined angle at th point medium-sized coronary arteries due to deposition of atheromatous
of manubrium ( angle of Louis). plaque in the vessel wall
 With normal physiologic condition, the jugular venous
column rises no higher than 2-3 cm above the clavicle
Stages of Development of Coronary Artery Disease
with the client in a sitting position at 45 degree angle.
1. Myocardial Injury: Atherosclerosis
2. Myocardial Ischemia: Angina Pectoris
3. Myocardial Necrosis: Myocardial Infarction

 CVP is a measurement of:

- cardiac efficiency I. ATHEROSCLEROSIS
- blood volume
- peripheral resistance ATHEROSCLEROSIS ARTERIOSCLEROSIS
 Right ventricular pressure – a catheter is passed from a
cutdown in the antecubital, subclavian jugular or basilica Narrowing of artery Hardening of artery
vein to the right atrium and attached to a prescribed Lipid or fat deposits Calcium and protein
manometer or tranducer. deposits
Tunica intima
 NORMAL CVP is 2 -8 cm h20 or 2-6 mm Hg Tunica media
 Decrease indicates dec. circulating volume, increase
indicates inc. blood volume or right heart beat failure.
A. PRESDISPOSING FACTORS
 To Measure: patient should be flat with zero point of
1. Sex: male
manometer at the same level of the RA which
2. Race: black
corresponds to the mid-axillary line of the patient or
3. Smoking
approx. 5 cm below the sternum.
4. Obesity
 Fluctuations follow patients respiratory function and will
5. Hyperlipidemia
fall on inspiration and rise on expiration due to changes
6. Sedentary lifestyle
in intrapulmonary pressure. Reading should be obtained
7. Diabetes Mellitus
at the highest point of fluctuation.
8. Hypothyroidism
9. Diet: increased saturated fats
10. Type A personality
2. Pulmonary Artery Pressure ( PAP) Monitoring
 Appropriate for critically ill clients requiring more
B. SIGNS AND SYMPTOMS
accurate assessments of the left heart pressure
1. Chest pain
 Swan-Ganz Catheter / Pulmonary Artery Catheter is use
2. Dyspnea
3. Tachycardia
4. Palpitations
5. Diaphoresis

C. TREATMENT

Percutaneous Transluminal Coronary Angioplasty and

Intravascular Stenting
 Mechanical dilation of the coronary vessel wall by
compresing the atheromatous plaque.
 It is recommended for clients with single-vessel
coronary artery disease.

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Lecture Notes on Cardiovascular System
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 Prosthetic intravascular cylindric stent maintain Nursing Management:

good luminal geometry after ballon deflation and
withdrawal.  Nitroglycerine is the drug of choice for relief of pain
 Intravascular stenting is done to prevent restenosis from acute ischemic attacks
after PTCA  Instruct to avoid over fatigue
 Plan regular activity program
For Saphenous Vein Site:
 Wear support stocking 4-6 week postop
 Apply pressure dressing or sand bag on the site
 Keep leg elevated when sitting

3 Complications of CABG
1. Pneumonia: encourage to perform deep breathing,
coughing exercise and use of incentive spirometer
2. Shock
3. Thrombophlebitis

II. ANGINA PECTORIS

Transient paroxysmal chest pain produced by insufficient

blood flow to the myocardium resulting to myocardial
ischemia
Clinical syndrome characterized by paroxysmal chest
pain that is usually relieved by rest or nitroglycerine due
to temporary myocardial ischemia

Types of Angina Pectoris

 Stable Angina: pain less than 15 minutes, recurrence is less

frequent.
 Unstable Angina : pain is more than 15 mins.,but not less
than 30 minutes, recurrence is more frequent and the
Coronary Arterial Bypass Graft Surgery
intensity of pain increases.
 Variant Angina ( Prinzmetal’s Angina ): Chest pain is on
longer duration and may occur at rest. Result from coronary
vasospasm.
 Angina Decubitus: paroxysmal chest pain that occur when
the client sits or stand.

A. PRESDISPOSING FACTORS
1. Sex: male
2. Race: black
3. Smoking
4. Obesity
5. Hyperlipidemia
6. Sedentary lifestyle
Greater and lesser saphenous veins are commonly used for 7. Diabetes Mellitus
bypass graft procedures 8. Hypertension
9. CAD: Atherosclerosis
10. Thromboangiitis Obliterans
11. Severe Anemia
12. Aortic Insufficiency: heart valve that fails to open &
close efficiently
13. Hypothyroidism
14. Diet: increased saturated fats
15. Type A personality

B. PRESIPITATING FACTORS
4 E’s of Angina Pectoris
1. Excessive physical exertion: heavy exercises, sexual
activity
2. Exposure to cold environment: vasoconstriction
3. Extreme emotional response: fear, anxiety,
excitement, strong emotions
4. Excessive intake of foods or heavy meal

C. SIGNS AND SYMPTOMS

1. Levine’s Sign: initial sign that shows the hand
clutching the chest
2. Chest pain: characterized by sharp stabbing pain
Objectives of CABG located at sub sterna usually radiates from neck,
1. Revascularize myocardium back, arms, shoulder and jaw muscles usually
2. To prevent angina relieved by rest or taking nitroglycerine(NTG)
3. Increase survival rate 3. Dyspnea
4. Done to single occluded vessels 4. Tachycardia
5. If there is 2 or more occluded blood vessels CABG is 5. Palpitations
done 6. Diaphoresis

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Lecture Notes on Cardiovascular System
Prepared By: Mark Fredderick R Abejo R.N, MAN
D. DIAGNOSTIC PROCEDURE
1. History taking and physical exam
2. ECG: may reveals ST segment depression & T wave
inversion during chest pain
3. Stress test / treadmill test: reveal abnormal ECG
during exercise
4. Increase serum lipid levels
5. Serum cholesterol & uric acid is increased
E. MEDICAL MANAGEMENT
1. Drug Therapy: if cholesterol is elevated
Nitrates: Nitroglycerine (NTG)
Beta-adrenergic blocking agent: Propanolol
Calcium-blocking agent: nefedipine
Ace Inhibitor: Enapril
2. Modification of diet & other risk factors
3. Surgery: Coronary artery bypass surgery
4. Percutaneuos Transluminal Coronary Angioplasty
(PTCA)
F. NURSING INTERVENTIONS
1. Enforce complete bed rest
2. Give prompt pain relievers with nitrates or narcotic
analgesic as ordered
3. Administer medications as ordered:
A. Nitroglycerine(NTG): when given in small
doses will act as venodilator, but in large doses
will act as vasodilator
 Give 1st dose of NTG: sublingual 3-5
minutes
 Give 2nd dose of NTG: if pain persist after
giving 1st dose with interval of 3-5
minutes
 Give 3rd& last dose of NTG: if pain still
persist at 3-5 minutes interval
NTG Tablets(sublingual)
 Keep the drug in a dry place, avoid
moisture and exposure to sunlight as it
may inactivate the drug
 Change stock every 6 months
 Offer sips of water before giving
sublingual nitrates, dryness of mouth may
inhibit drug absoprtion
 Relax for 15 minutes after taking a tablet:
to prevent dizziness
 Monitor side effects: orthostatic
hypotension, flushed face. Transient
headache & dizziness: frequent side effect
 Instruct the client to rise slowly from
sitting position
 Assist or supervise in ambulation
NTG Nitrol or Transdermal patch
 Nitropatch is applied once a day, usually
in the morning.
 Avoid placing near hairy areas as it may
decrease drug absorption
 Avoid rotating transdermal patches as it
may decrease drug absorption
 Avoid placing near microwave ovens or
during defibrillation as it may lead to
burns (most important thing to remember)
B. Beta-blockers: decreases myocardial oxygen
demand by decreasing heart rate, cardiac output
and BP
Propanolol
Metropolol
Pindolol
Atenolol
 Assess PR, withhold if dec.PR
 Administer with food ( prevent GI upset )
Medical and Surgical Nursing
 Propanolol: not given to COPD cases: it causes
bronchospasm and DM cases: it cause
hypoglycemia
 Side Effects: Nausea and vomiting, mental
depression and fatigue
C. Calcium – Channel Blockers: relaxes smooth
cardiac muscle, reduces coronary vasospasm
Amlodipine ( norvasc )
Nifedipine ( calcibloc )
Diltiazem ( cardizem )
 Assess HR and BP
 Adminester 1 hour before meal and 2 hours
after meal ( foods delay absorption )
4. Administer oxygen inhalation
5. Place client on semi-to high fowlers position
6. Monitor strictly V/S, I&O, status of
cardiopulmonary fuction & ECG tracing
7. Provide decrease saturated fats sodium and caffeine
8. Provide client health teachings and discharge
planning
 Avoidance of 4 E’s
 Prevent complication (myocardial infarction)
 Instruct client to take medication before
indulging into physical exertion to achieve the
maximum therapeutic effect of drug
 Reduce stress & anxiety: relaxation techniques
& guided imagery
 Avoid overexertion & smoking
 Avoid extremes of temperature
 Dress warmly in cold weather
 Participate in regular exercise program
 Space exercise periods & allow for rest periods
 The importance of follow up care
9. Instruct the client to notify the physician
immediately if pain occurs & persists despite rest &
medication administration
III. MYOCARDIAL INFARCTION
Death of myocardial cells from inadequate oxygenation,
often caused by sudden complete blockage of a coronary
artery
Characterized by localized formation of necrosis (tissue
destruction) with subsequent healing by scar formation &
fibrosis
Heart attack
Terminal stage of coronary artery disease characterized
by malocclusion, necrosis & scarring.
Types of M.I
 Transmural Myocardial Infarction: most dangerous type
characterized by occlusion of both right and left coronary
artery
 Subendocardial Myocardial Infarction: characterized by
occlusion of either right or left coronary artery
The Most Critical Period Following Diagnosis of
Myocardial Infarction
6-8 hours because majority of death occurs due to
arrhythmia leading to premature ventricular contractions
(PVC)
A. PREDISPOSING FACTORS
1. Sex: male
2. Race: black
3. Smoking
4. Obesity
5. CAD: Atherosclerotic
6. Thrombus Formation
7. Genetic Predisposition
8. Hyperlipidemia
11 Abejo
Lecture Notes on Cardiovascular System
Prepared By: Mark Fredderick R Abejo R.N, MAN

9. Sedentary lifestyle 2. Administer oxygen low flow 2-3 L / min: to prevent

10. Diabetes Mellitus respiratory arrest or dyspnea & prevent arrhythmias
11. Hypothyroidism 3. Enforce CBR in semi-fowlers position without bathroom
12. Diet: increased saturated fats privileges(use bedside commode): to decrease cardiac
13. Type A personality workload
4. Instruct client to avoid forms of valsalva maneuver
B. SIGNS AND SYMPTOMS 5. Place client on semi fowlers position
1. Chest pain 6. Monitor strictly V/S, I&O, ECG tracing & hemodynamic
Excruciating visceral, viselike pain with sudden procedures
onset located at substernal& rarely in 7. Perform complete lung / cardiovascular assessment
precordial 8. Monitor urinary output & report output of less than 30 ml
Usually radiates from neck, back, shoulder, / hr: indicates decrease cardiac output
arms, jaw & abdominal muscles (abdominal 9. Provide a full liquid diet with gradual increase to soft diet:
ischemia): severe crushing low in saturated fats, Na & caffeine
Not usually relieved by rest or by 10. Maintain quiet environment
nitroglycerine 11. Administer stool softeners as ordered:to facilitate bowel
2. N/V evacuation & prevent straining
3. Dyspnea 12. Relieve anxiety associated with coronary care
4. Increase in blood pressure & pulse, with gradual unit(CCU)environment
drop in blood pressure (initial sign) 13. Administer medication as ordered:
5. Hyperthermia: elevated temp a. Vasodilators:Nitroglycirine (NTG), Isosorbide
6. Skin: cool, clammy, ashen Dinitrate, Isodil (ISD): sublingual
7. Mild restlessness & apprehension b. Anti Arrythmic Agents: Lidocaine (Xylocane),
8. Occasional findings: Brithylium
Pericardial friction rub Side Effects: confusion and dizziness
Split S1& S2 c. Beta-blockers: Propanolol (Inderal)
Rales or Crackles upon auscultation d. ACE Inhibitors: Captopril (Enalapril)
S4 or atrial gallop e. Calcium Antagonist: Nefedipine
f. Thrombolytics / Fibrinolytic Agents: Streptokinase,
C. DIAGNOSTIC PROCEDURED Urokinase, Tissue Plasminogen Activating Factor
1. Cardiac Enzymes (TIPAF)
CPK-MB: elevated Side Effects:allergic reaction, urticaria, pruritus
Creatinine phosphokinase(CPK):elevated Nursing Intervention: Monitor for bleeding
time
Heart only, 12 – 24 hours
g. Anti Coagulant
Lactic acid dehydrogenase(LDH): is increased
Heparin
Serum glutamic pyruvate transaminase(SGPT):
Antidote: Protamine Sulfate
is increased
Nursing Intervention: Check for Partial
Serum glutamic oxal-acetic
transaminase(SGOT): is increased Thrombin Time (PTT)
2. Troponin Test: is increased Caumadin(Warfarin)
3. ECG tracing reveals Antidote:Vitamin K
ST segment elevation Nursing Intervention: Check for
T wave inversion Prothrombin Time (PT)
Widening of QRS complexes: indicates that h. Anti Platelet: PASA (Aspirin): Anti thrombotic
effect
there is arrhythmia in MI
Side Effects:Tinnitus, Heartburn, Indigestion /
Dyspepsia
Contraindication:Dengue, Peptic Ulcer Disease,
Unknown cause of headache

14. Provide client health teaching & discharge planning

concerning:
a. Effects of MI healing process & treatment regimen
b. Medication regimen including time name purpose,
schedule, dosage, side effects
c. Dietary restrictions: low Na, low cholesterol,
avoidance of caffeine
d. Encourage client to take 20 – 30 cc/week of wine,
whisky and brandy:to induce vasodilation
e. Avoidance of modifiable risk factors
f. Prevent Complication
4. Serum Cholesterol & uric acid: are both increased
5. CBC: increased WBC Arrhythmia: caused by premature ventricular
contraction
D. NURSING INTERVENTIONS Cardiogenic shock: late sign is oliguria
Left Congestive Heart Failure
Goal: Decrease myocardial oxygen demand Thrombophlebitis: homan’s sign
Stroke / CVA
1. Decrease myocardial workload (rest heart) Dressler’s Syndrome(Post MI Syndrome):client
Establish a patent IV line is resistant to pharmacological agents:
Administer narcotic analgesic as ordered: Morphine administer 150,000-450,000 units of
Sulfate IV: provide pain relief(given IV because streptokinase as ordered
after an infarction there is poor peripheral perfusion g. Importance of participation in a progressive activity
& because serum enzyme would be affected by IM program
injection as ordered) h. Resumption of ADL particularly sexual intercourse:
Side Effects: Respiratory Depression is 4-6 weeks post cardiac rehab, post CABG &
Antidote: Naloxone (Narcan) instruct to:
Side Effects of Naloxone Toxicity: is tremors

Medical and Surgical Nursing 12 Abejo

Lecture Notes on Cardiovascular System
Prepared By: Mark Fredderick R Abejo R.N, MAN

Make sex as an appetizer rather than dessert Aminophylline to reduce

Instruct client to assume a non weight bearing bronchospasm caused by severe
position congestion.
Client can resume sexual intercourse: if can Vasodilators to reduce venous return
climb or use the staircase Diuretics to decrease circulating
i. Need to report the ff s/sx: volume
Increased persistent chest pain
Dyspnea V. PERICARDITIS / DRESSLER’S SYNDROME
Weakness
Fatigue Is the inflammation of the pericardium which occurs
Persistent palpitation approximately 1 – 6 weeks after AMI.
Light headedness Results as an antigen – antibody response. The necrotic
j. Enrollment of client in a cardiac rehabilitation tissues play the role of an antigen, which trigger antibody
program formation. Inflammatory process follows.
k. Strict compliance to mediation & importance of Constrictive Pericarditis is a condition in which a chronic
follow up care inflammatory thickening of the pericardium compresses
the heart so that it is unable to fill normally during
diastole.
IV. CARDIOGENIC SHOCK ( POWER/PUMP FAILURE )
A. SIGNS AND SYMPTOMS
Is a shock state which result from profound left 1. Pain in the anterior chest, aggravated by coughing,
ventricular failure usually from massive MI. yawning, swallowing, twisting and turning the torso,
It result to low cardiac output, thereby systemic relieved by upright, leaning forward position.
hypoperfusion. 2. Pericardial friction rub – scratchy, grating or
cracking sound
A. SIGNS AND SYMPTOMS 3. Dyspnea
1. Decrease systolic BP 4. Fever, sweating, chills
2. Oliguria 5. Joints pains
3. Cold, clammy skin 6. Arrhythmias
4. Weak pulse
5. Cyanosis B. NURSING INTERVENTIONS
6. Mental lethargy
7. Confusion 1. Elevate head of bed, place pillow on the overbed
table so that the patient can lean on it.
B. MEDICAL MANAGEMENT 2. Bed rest
1. Counterpulsation ( mechanical cardiac assistance / 3. Administer prescribed pharmacotherapy.
diastolic augmentation ) a. ASA to suppress inflammatory process
Involves introduction of the intra – aortic b. Corticosteriods for more severe symptoms
balloon catheter via the femoral artery 4. Assist in pericardiocentesis if cardiac tamponade is
Intra Aortic Balloon Pump augments present.
5. Pericardiocentesis is aspiration of blood or fluid
diastole, resulting in increased perfusion
from pericardial sac.
of the coronary arteries and the
myocardium and a decrease in left
ventricular workload.
VI. CARDIAC TAMPONADE
The balloon is inflated during diastole, it
is deflated during sytole.
Also known as pericardial tamponade, is an emergency
Indications:
condition in which fluid accumulates in the pericardium
 Cardiogenic shock
(the sac in which the heart is enclosed).
 AMI
If the fluid significantly elevates the pressure on the heart
 Unstable Angina
it will prevent the heart's ventricles from filling properly.
 Open heart surgery
This in turn leads to a low stroke volume.
C. NURSING INTERVENTIONS The end result is ineffective pumping of blood, shock,
and often death.
1. Perform hemodynamic monitoring
2. Administer oxygen therapy A. PREDISPOSING FACTORS
3. Correct hypovolemia. Administer IV fluids as 1. Chest trauma ( blunt or penetrating )
ordered 2. Myocardial ruptured
4. Pharmacology: 3. Cancer
a. Vasodilators: Nitroglycerine 4. Pericarditis
b. Inotropic agents:Digitalis, Dopamine 5. Cardiac surgery ( first 24 – 48 hours )
c. Diuretics : Furosemide 6. Thrombolytic therapy
d. Sodium Bicarbonate, Relieve lactic acidosis
5. Monitor hourly urine output, LOC and arrhythmias B. SIGNS AND SYMPTOMS
6. Provide psychosocial support 1. Beck’s Triad
7. Decrease pulmonary edema  Hypotension
a. Auscultate lung fields for crackles and wheezes  Jugular venous distension
b. Note for dyspnea, cough , hemoptysis and  Muffled heart sound
orthopnea 2. Pulsus paradoxus ( drop of at least 10 mmHg in
c. Monitor ABG for hypoxia and metabolic arterial BP on inspiration )
acidosis 3. Tachycardia
d. Place in fowler’s position to reduce venous 4. Breathlessness
return 5. Decrease in LOC
e. Administer during therapy as ordered:
Morphine sulfate to reduce venous
return.

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Lecture Notes on Cardiovascular System
Prepared By: Mark Fredderick R Abejo R.N, MAN

C. NURSING INTERVENTIONS 3. Pulmonary embolism (char by chest pain and

dyspnea)
1. Administer oxygen 4. Pulmonic stenosis
2. Elevate head of bed, place pillow on the overbed 5. Left sided heart failure
table so that the patient can lean on it.
3. Bed rest B. SIGNS AND SYMPTOMS (Venous congestion)
4. Administer prescribed pharmacotherapy. 1. Jugular vein distention
c. ASA to suppress inflammatory process 2. Pitting edema
d. Corticosteriods for more severe symptoms 3. Ascites
5. Assist in pericardiocentesis and thoracotomy 4. Weight gain
6. Pericardiocentesis is aspiration of blood or fluid 5. Hepatosplenomegaly
from pericardial sac. 6. Jaundice
7. Pruritus/ urticaria
8. Esophageal varices
CONGESTIVE HEART FAILURE 9. Anorexia
10. Generalized body malaise

Inability of the heart to pump blood towards systemic C. DIAGNOSTICS

circulation 1. CXR – cardiomegaly
2. CVP – measures pressure in right atrium; N = 4-
I. LEFT-SIDED HEART FAILURE 10cc H2O
 During CVP: trendelenburg  to prevent
A. PREDISPOSING FACTORS pulmo embolism and to promote ventricular
1. 90% - Mitral valve stenosis filling
 RHD  Flat on bed post CVP, check CVP readings
 Inflammation of mitral valve  Hypovolemia – fluid challenge
 Anti-streptolysin O titer (ASO) – 300 todd  Hypervolemia – diuretics (loop)
units 3. Echocardiography – reveals enlarged heart chamber
 Penicillin, PASA, steroids  Muffled heart sounds  cardiomyopathy
 Aging  Cyanotic heart diseases
2. MI  TOF  “tet” spells  cyanosis with
3. IHD hypoxemia
4. HPN  Tricuspid valve stenosis
5. Aortic valve stenosis  Transposition of aorta
 Acyanotic
B. SIGNS AND SYMPTOMS  PDA – machine-like murmur
1. Pulmonary edema/congestion  DOC: indomethacin SE: corneal
 Dyspnea, PND (awakening at night d/t cloudiness
difficulty in breathing), 2-3 pillow orthopnea 4. Liver enzymes
 Productive cough (blood tinged)  SGPT up
 Rales/crackles  SGOT up
 Bronchial wheezing
 Frothy salivation D. NURSING MANAGEMENT
2. Pulsus alternans (A unique pattern during which the
amplitude of the pulse changes or alternates in size Goal: increase myocardial contraction  increase CO;
with a stable heart rhythm.)This is common in Normal CO is 3-6L/min; N stroke volume is 60-70ml/h2o
severe left ventricular dysfunction.)
3. Anorexia and general body malaise 1. Administer medications as ordered
4. PMI displaced laterally, cardiomegaly  Cardiac glycosides
5. S3 (ventricular gallop)  Digoxin (N=.5-1.5, tox=2)
 Tox: Anorexia, N&V; A: Digibind
C. DIAGNOSTICS  Digitoxin – given if (+) ARF; metabolized
1. CXR – cardiomegaly in liver and not in kidneys
2. PAP – pulmonary arterial pressure  Loop diuretics
 Measures pressure in right ventricle  Lasix – IV push, mornings
 Reveals cardiac status  Bronchodilators
3. PCWP – pulmonary capillary wedge pressure  Aminophylline (theophylline)
 Measures end-systolic and end-diastolic  Tachycardia, palpitations
pressure (elevated)
 CNS hyperactivity, agitation
 Done through cardiac catheterization (Swan-
 Narcotic analgesics
Ganz)
 Morphine sulfate – induces vasodilation
4. Echocardiograph – reveals enlarged heart chamber
 Vasodilators
5. ABG analysis reveals elevated PCO2 and decreased
 NTG and ISDN
PO2 (respiratory acidosis)  hypoxemia and
 Anti-arrhythmic agents
cyanosis
 Lidocaine (SE: dizziness and
Tracheostomy  for severe respiratory distress and laryngospasm  confusion)
performed at bedside within 10-15 minutes  Bretyllium
 YOU DON’T GIVE BETA-BLOCKERS TO
CVP  reveals fluid status; Normal = 4-10cm H2o; right atrium THESE PATIENTS
PAP – cardiac status; left atrium 2. Administer O2 inhalation at 3-4 L/minute via NC as
ALLEN’S test – collateral circulation ordered  high flow
Cardiac Tamponade: pulsus paradoxus, muffled heart sounds, HPN
3. High fowler’s, 2-3 Pillows
4. Restrict Na and fluids
II. RIGHT SIDED HEART FAILURE
5. Monitor strictly VS and IO and Breath Sounds
6. Weigh pt daily and assess for pitting edema
A. PREDISPOSING FACTORS
7. abdominal girth daily and notify MD
1. Tricuspid valve stenosis
8. provide meticulous skin care
2. COPD

Medical and Surgical Nursing 14 Abejo

Lecture Notes on Cardiovascular System
Prepared By: Mark Fredderick R Abejo R.N, MAN

9. provide a dietary intake which is low in saturated  Hypertensive Crisis, situation that requires
fats and caffeine immediate blood pressure lowering 240mmHg /
10. Institute bloodless phlebotomy 120 mmHg
 ROTATING TOURNIQUET
 Rotated clockwise every 15 minutes to B. RISK FACTORS
promote a decrease in venous return 1. Family history
11. Health teaching and discharge planning 2. Age
 Prevent complications : Arrhythmia, Shock, 3. High salt intake
Thrombophlebitis, MI, Cor pulmonale – RV 4. Low potassium intake
hypertrophy 5. Obesity
 Regular adherence to medications 6. Excess alcohol consumption
 Diet modifications 7. Smoking
 Importance of ffup care 8. Stress

C. SIGNS AND SYMPTOMS

1. Headache
2. Epistaxis
HYPERTENSION 3. Dizziness
4. Tinnitus
5. Unsteadiness
6. Blurred vision
Is an abnormal elevation of Bp, systolic pressure above 7. Depression
140 mmHg and or diastolic pressure above 90mmHg at 8. Nocturia
least two readings 9. Retinopathy
WHO: BP >160/95 mmHg
D. TREATMENT STRATEGIES
AHA: BP >140/90 mmHg
In hypertension, vasoconstriction – vasospasm –
Non-pharmacologic therapy
increases PVR – decrease blood flow to the organ.
1. Low salt diet.
Target Organs: 2. Weight reduction.
 Heart : MI, CHF, Dysrhythmias 3. Exercise.
 Eyes: blurred / impaired vision, retinopathy, 4. Cessation of smoking.
cataract. 5. Decreased alcohol consumption.
 Brain: CVA, encephalopathy 6. Psychological methods: Relaxation / meditation.
 Kidneys : renal insufficiency, RF 7. Dietary decrease in saturated fat.
 Peripheral Bloods Vessels – aneurysm,
gangrene Drug therapy
Stepped Care
CLASSIFICATION OF BP FOR ADULTS 18 YRS AND o Progressive addition of drugs to a regimen,
OLDER (PHIL. SOCIETY OF HPN) starting with one, usually a diuretic, and adding,
in a stepwise fashion, a sympatholytic,
Optimal vasodilator, and sometimes an ACE inhibitor.
o <120 mmHg / <80 mmHg Monotherapy
Recheck in 2 years. o Advantageous because of its simplicity, better
Normal patient compliance, and relatively low
o 120-129 mmHg / 80-84 mmHg incidence of toxicity.
Recheck in 2 years.
High normal CATEGORIES OF
o 130-139 mmHg / 85-89 mmHg ANTI-HYPERTENSIVE DRUGS
Recheck in 1 year.
Drugs that alter sodium and water balance  Diuretics.
Stage 1 (mild) HPN Loop diuretics
o 140-159 mmHg / 90-99 mmHg Thiazides
Confirm in 2 months. Spironolactone and Triamterene
Stage 2 (moderate) HPN
o 160-179 mmHg / 100-109 mmHg
Evaluate within a month. Drugs that alter sympathetic nervous system function 
Stage 3 (severe) HPN Sympatholytic drugs.
o 180-209 mmHg / 110-119mmHg Centrally-acting sympatholytics
Evaluate within a week.  Clonidine
Stage 4 (very severe) HPN  Guanabenz
o 210 mmHg / >/=120 mmHg Evaluate  Guanfacine
 Methyldopa
Peripherally-acting sympatholytics
A. CLASSIFICATION
 Guanadrel
 Essential / Idiophatic / Primary HPN, accounts
 Guanethidine
for 90 – 95% of all cases of HPN, cause is
 Reserpine
unknown
a-blockers
 Secondary HPN, due to known causes ( Renal
 Doxazosin
failure, Hypertension )
 Prazosin
 Malignant Hypertension, is severe, rapidly
progressive elevation in BP that causes rapid onset b-blockers
of end organ complication  Acebutolol - Labetalol
 Labile HPN, intermittently elevated BP  Atenolol - Metoprolol
 Resistant HPN, does not respond to usual  Betaxolol - Nadolol
treatment  Bisoprolol - Penbutolol
 White Coat HPN, elevation of B only during  Carteolol - Pindolol
clinic or hospital visits  Carvedilol - Propranolol
 Esmolol - Timolol

Medical and Surgical Nursing 15 Abejo

Lecture Notes on Cardiovascular System
Prepared By: Mark Fredderick R Abejo R.N, MAN

Vasodilators
Direct vasodilators
 Diazoxide - Hydralazine
 Minoxidil - Nitroprusside
 Fenoldopam
Calcium channel blockers
 Amlodipine - Nifedipine
 Diltiazem - Nimodipine
 Felodipine - Nisoldipine
 Isradipine - Nitrendipine
 Manidipine - Nicardipine
 Lacidipine - Verapamil
 Lercanidipine - Gallopamil

AGENTS THAT BLOCK THE PRODUCTION OR

ACTION OF ANGIOTENSIN
 ACE inhibitors
 Benazepril - Moexipril
 Captopril - Quinapril
 Enalapril - Perindopril
 Fosinopril - Ramipril
 Lisinopril - Trandolapril
AT1-receptor blockers
 Irbesartan - Losartan
 Telmisartan - Valsartan
 Candesartan - Eprosartan
 Olmesartan

DRUGS FOR HYPERTENSIVE EMERGENCIES OR

CRISES

Trimethaphan
o 1 mg/ml IV infusion; titrate;
instantaneous onset
Sodium nitroprusside
o 5-10 mg/L IV infusion; titrate;
instantaneous onset
Diazoxide
o 300-600 mg Rapid IV push;
instantaneous onset
Nifedipine
o 10-20 mg Sublingual or chewed;
onset within 5-30 min.
Labetalol
o 20-80 mg IV at 10-minute intervals (max.dose:
300mg); immediate onset

MECHANISMS OF DRUG ACTION

PRINCIPLES OF DRUG THERAPY

Monotherapy is generally reserved for mild to moderate

HPN; it has gained popularity because of its simplicity,
fewer side effects, and improved patient compliance.
More severe HPN may require treatment with several
drugs that are selected to minimize adverse effects of
combined regimen.
Treatment is initiated with any of 4 drugs depending on
individual patient: Diuretic, b-blocker, ACEI, and a Ca-
channel blocker; if BP is inadequately controlled, a 2nd-
drug is then added.
HPN may co-exist with other disease that may be
aggravated by some of the anti-HPN agents.
Lack of patient compliance is the most common reason
for failure of anti-HPN therapy; it is important to enhance
compliance by carefully selecting a drug regimen that
minimizes adverse effects.
Therapy is directed at preventing disease that may occur
in the future, rather than in relieving present discomfort
of the patient.

Medical and Surgical Nursing 16 Abejo

Lecture Notes on Cardiovascular System
Prepared By: Mark Fredderick R Abejo R.N, MAN

E. NURSING INTERVNTIONS
1. Patient Teaching and Counselling
 Teaching about HPN and its risk factors
 Stress therapy
 Low NA and low saturated fat
 Avoid stimulants ( caffeine, alcohol, smoking )
 Regular pattern of exercise
 Weight reduction if obese
2. Teaching about medication
 The most common side effects of diuretics are
potassium depletion and orthostatic
hypotension.
 The most common side effect of the different
antihypertensive drugs is orthostatic
hypotension.
 Take anti – hypertensive medications at regular
basis
 Assume sitting or lying position for few
minutes
 Avoid very warm bath
 Avoid prolonged sitting and standing
 Avoid alcoholic beverages
 Avoid tyramine – rich foods ( proteins ) as
follows: ( this may cause hypertensive crisis )
Aged cheese
Liver
Beer D. MEDICAL / SURGICAL MANAGEMENT
1. Hypertensive Medication
Wine
2. Surgery if aneurysm is greater than 4 cm
Chocolate
 Teflon graft
Pickles  Dacron graft
Sausages  Gortex graft
Soy sauce
3. Preventing Non-compliance E. NURSING INTERVENTIONS
 Inform the client that absence of symptoms 1. Monitor the following
does not indicate control of BP  VS
 Advise the client against abrupt withdrawal of  Hemodynamic measurements
medication, rebound hypertension may occur.  Urine output
 Device ways to facilitate remembering of  BUN and creatinine
taking medications  Bowel sounds
 Passage of flatus
 Peripheral pulses
2. Promoting Fluid Volume
 Check dressing for excessive drainage
PERIPHERAL VASCULAR DISORDERS  Assess for abdominal pain or backpain
 Assess Hgb and Hct values

ANEURYSM
ARTERIAL ULCERS
It is the localized, irreversible dilatation of an artery
secondary to an alteration in the integrity of its wall. I. THROMBOANGITIS OBLITERANS ( Buerger’s Dse. )
Most common type is AAA ( abdominal aortic aneurysm ) – acute inflammatory condition affecting the smaller and
The most common cause is hypertension medium sized arteries and veins of the lower extremities.
IDIOPATHIC
A. CLASSIFICATIONS
 Fusiform Aneurysm , involves outpouching of the A. PREDISPOSING FACTORS
both side of the artery 1. High risk group  men 30 years old above
 Saccular Aneurysm , outpouching of only one side 2. Chronic smoking
of the artery. B. SIGNS AND SYMPTOMS  Consistent to all arterial
 Dissecting Aneurysm, involves separation or tear in diseases
the tunica intima and tunica media 1. Intermittent claudication – leg pain upon strenuous
walking r/t temporary ischemia
B. RISK FACTOR 2. Cold sensitivity and skin color changes
1. Age  White/pallor  bluish/cyanosis  red/rubor
2. Tobacco use  (+) especially post smoking
3. HPN 3. Decreased peripheral pulses’ volume particularly in
4. Atherosclerosis dorsalis pedis and posterior tibial
5. Race 4. Trophic changes
6. Gender 5. Ulceration
7. Family history 6. Gangrene formation

C. SIGNS AND SYMPTOMS C. DIAGNOSTICS

1. Oscillometry – reveals a decrease in peripheral
1. Pulsating mass over abdomen (AAA) pulse volume
2. Presence of the bruit sound 2. Doppler UTZ – decrease in blood flow to affected
3. Low back pain extremity
4. Lower abdominal pain 3. Angiography – site and extent of malocclusion
5. Flank pain
6. Shock
Medical and Surgical Nursing 17 Abejo
Lecture Notes on Cardiovascular System
Prepared By: Mark Fredderick R Abejo R.N, MAN

D. NURSING MANAGEMENT
1. Encourage slow progressive physical activity A. PREDISPOSING FACTORS
 Walking 3-4x/day 1. Hereditary
 Out of bed 3-4x/day 2. Congenital weakness of veins
2. Medications as ordered 3. Thrombophlebitis
 Analgesics 4. Cardiac diseases
 Vasodilators 5. Pregnancy
 Anticoagulants 6. Obesity
3. Instruct patient to avoid smoking and exposure to 7. Prolonged immobility  prolonged standing and
cold environment sitting
4. Institute foot care management
 Avoid barefoot walking B. SIGNS AND SYMPTOMS
 Straight nails 1. Pain after prolonged standing
 Lanolin cream for feet 2. Dilated tortuous skin veins which are warm to touch
 (-) constricting clothes 3. Heaviness in the legs
5. Assist in surgery: BKA
C. DIAGNOSTICS
1. Venography
II. REYNAULD’S DISEASE – characterized by acute episodes 2. Trendelenburg’s test – reveals that veins distend
of arterial spasms involving the digits of hands and fingers quickly < 35 seconds  incompetent valves

D. NURSING MANAGEMENT (consistent to all venous

ulcers)
1. Elevate legs above heart level  increased venous
return (2-3 pillow elevation)
2. Measure circumference of leg to determine swelling
3. Anti-embolic stocking, full support panty hose
4. Medications as ordered  analgesics
5. Assist in surgery
 Vein stripping and ligation (more effective, no
recurrence)
 Sclerotherapy
 For spider-web varicosities
 Cold solution injection
 SE: thrombosis

II. THROMBOPHLEBITIS / DEEP VEIN THROMBOSIS

(DVT)
A. PREDISPOSING FACTORS
1. High risk group  women 40 years old up A. PREDISPOSING FACTORS
2. Smoking 1. Smoking
3. Collagen diseases 2. Obesity
 SLE 3. Prolonged use of OCPs
 RA 4. Chronic anemia
4. Direct hand trauma 5. Diet high in saturated fats
 Piano playing 6. DM
 Excessive typing (tsk tsk! Lagot!) 7. CHF
 Carpal tunnel syndrome 8. MI
 Operating chainsaw (nyek!) 9. Post-cannulation (insertion of various catheters)
 Writing (tsk tsk, kaya dapat may module eh! 10. Post-surgical operation
Grr!) 11. Sedentary lifestyle
B. SIGNS AND SYMPTOMS
1. Intermittent claudication B. SIGNS AND SYMPTOMS
2. Cold sensitivity and skin color changes 1. Pain at the affected extremity
 White/pallor  bluish/cyanosis  red/rubor 2. Presence of cyanosis
 (+) especially post smoking 3. Dilated tortuous veins
3. Trophic changes 4. (+) HOMAN’S  pain on calf on dorsiflexion
4. Ulceration
5. Gangrene formation C. DIAGNOSTICS
C. DIAGNOSTICS 1. Venography
1. Oscillometry – reveals a decrease in peripheral 2. Doppler UTZ
pulse volume 3. Angiography
2. Angiography – site and extent of malocclusion
D. NURSING MANAGEMENT
D. NURSING MANAGEMENT 1. Elevate the legs above heart level
1. Administer medications as ordered 2. Apply warm moist pack to relieve lymphatic
 Analgesics congestion
 Vasodilators 3. Measure circumference of leg muscles to determine
2. Encourage pt to wear gloves if it is swollen
3. Instruct: avoid smoking and exposure to cold 4. Anti-embolic stockings
environment 5. Administer medications as ordered
 Analgesics
 Anticoagulants – heparin
VENOUS ULCERS 6. Prevent complications
 Pulmonary embolism
I. VARICOSE VEINS – abnormal dilation of the veins of the
lower extremities d/t incompetent valves leading to increased
venous pooling and venostasis  decreased venous return

Medical and Surgical Nursing 18 Abejo