Cardiovascular system

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,
veins & capillaries. The major function are circulation of blood,
delivery of O2 & other nutrients to the tissues of the body &
removal of CO2 & other cellular products metabolism
Heart
 Muscular pumping organ that propel blood into the arerial
system & receive blood from the venous system of the body.
 Hollow muscular behind the sternum and between the lungs
 Located on the middle of mediastinum
 Resemble like a close fist
 Weighs approximately 300 – 400 grams
 Has heart wall has 3 layers
 Endocardium – lines the inner chambers of the
heart, valves, chordate tendinae and papillary
muscles.
 Myocardium – muscular layer, middle layer,
responsible for the major pumping action of the
ventricles.
 Epicardium – thin covering(mesothelium),
covers the outer surface of the heart
 Pericardium – invaginated sac
 Visceral – attached to the exterior of
myocardium
 Parietal – attached to the great vessels and
diaphragm
 Papillary Muscle
Arise from the endocardial & myocardial surface of the
ventricles & attach to the chordae tendinae
 Chordae Tendinae
Attach to the tricuspid & mitral valves & prevent eversion
during systole
 Separated into 2 pumps:
 right heart – pumps blood through the lungs
 left heart – pumps blood through the peripheral
organs
 Chamber of the Heart
Atria
 2 chambers, function as receiving chambers, lies
above the ventricles

Medical and Surgical Nursing 1 Abejo

 Upper Chamber (connecting or receiving)
 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
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
 Coronary artery – 1st branch of aorta
Right Coronary
 SA nodal Branch – supplies SA node
 Right marginal Branch – supplies the right border
of the heart
 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
 Coronary 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
Cardiac Conduction System
Properties of Heart Conduction System
• Automaticity
• Excitability
• Conductivity
• Contractility
Structure of Heart Conduction System
 Nodal tissues
SA Node( Sino-atrial, Keith and Flack)
 Primary Pacemaker
 Between SVC and RA
 Vagal and symphatetic innervation
 Sinus Rhythms

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
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

General Variables of Cardiac Output
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)
 End diastolic volume (EDV) - total blood collected in
ventricle at end of diastole; determined by length of
diastole and venous pressure (~ 120 ml)
 End systolic volume (ESV) - blood left over in ventricle
at end of contraction (not pumped out); determined by
force of ventricle contraction and arterial blood pressure
(~50 ml)
SV (ml/beat) = EDV (ml/beat) - ESV (ml/beat)
Normal SV = 120 ml/beat - 50 ml/beat = 70 ml/beat
Frank-Starling Law of the Heart - critical factor for stroke
volume is "degree of stretch of cardiac muscle cells";
more stretch = more contraction force
increased EDV = more contraction force
slow heart rate = more time to fill
exercise = more venous blood return
Regulation of Heart Rate (Autonomic, Chemical, Other)
1. Autonomic Regulation of Heart Rate (HR)
 Sympathetic - NOREPINEPHRINE (NE) increases heart
rate (maintains stroke volume which leads to increased
Cardiac Output)
 Parasympathetic - ACETYLCHOLINE (ACh) decreases
heart rate
 Vagal tone - parasympathetic inhibition of inherent rate
of SA node, allowing normal HR
 Baroreceptors, pressoreceptors - monitor changes in
blood pressure and allow reflex activity with the
autonomic nervous system
2. Hormonal and Chemical Regulation of Heart Rate (HR)
 epinephrine - hormone released by adrenal medulla
during stress; increases heart rate
 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
hypernatremia - HIGH Na+ concentration; can
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
with blood, remove wastes, & carry unoxygenated blood
back to the heart
Types of Blood Vessels
Arteries
Elastic-walled vessels that can stretch during systole &
recoil during diastole; they carry blood away from the
heart & distribute oxygenated blood throughout the body
Arterioles
Small arteries that distribute blood to the capillaries &
function in controlling systemic vascular resistance &
therefore arterial pressure
Capilliaries
The following exchanges occurs in the capilliaries
O2 & CO2
Solutes between the blood & tissue
Fluid volume transfer between the plasma &
interstitial space
Venules
Small veins that receive blood from capillaries &
function as collecting channels between the capillaries &
veins
Veins
Low-pressure vessels with thin small & less muscles than
arteries; most contains valves that prevent retrograde
blood flow; they carry deoxygenated blood back to the
heart. When the skeletal surrounding veins contract, the
veins are compressed, promoting movement of blood
back to the heart.

Assessment of the Client with Cardiovascular
Disorders
Nursing History
Risk Factors
A. Non – Modifiable Risk Factor
 Age
 Gender
 Race
 Heredity
B. Modifiable Risk Factor
 Stress
 Diet
 Exercise
 Sedentary lifestyle
 Cigarette smoking
 Alcohol
 Hypertension
 Hyperlipidemia
 DM
 Obesity
 Type A personality
 Contraceptive Pills
Common Clinical Manifestations of Cardiovascular Disorders
a. Dyspnea
- Exertional
- Orthopnea
- Paroxysmal Noctural Dyspnea
- Cheyne-stokes
b. Chest Pain
c. Edema
- Ascites
- Hydrothorax
- Anasarca
d. Palpitation
e. Hemoptysis
f. Fatigue
g. Syncope and Fainting
h. Cyanosis
i. Abdominal Pain
j. Clubbing of fingers
k. Jaundice
Physical Assessment
Inspection:
– Skin color
– Neck vein distention
– Respirations
– Pulsations
– Clubbing
– Capillary refill
Palpation:
Heart Sounds: Stethoscope Listening
Overview of Heart Sounds (lub-du ; lub, dub )
lub - closure of AV valves, onset of ventricular systole
dub - closure of semilunar valves, onset of diastole
 Tricuspid valve (lub) - RT 5th intercostal, medial
 Mitral valve (lub) - LT 5th intercostal, lateral
 Aortic semilunar valve (dub) - RT 2nd intercostal
 Pulmonary semilunar valve (dub) - LT 2nd intercostals
S1 - due to closure of the AV(mitral/tricuspid) valves
- timing: beginning of systole
- loudest at the apex
S2 - due to the closure of the semi-lunar (pulmonic/aortic) valves
- timing: diastole
- loudest at the base
S3 – Ventricular Diastolic Gallop
Mechanism: vibration resulting from resistance to rapid
ventricular filling secondary to poor compliance
Timing: early diastole
Location: Apex (LV) or LLSB (RV)
Pitch: faint and low pitched
S4 - Atrial Diastolic Gallop
Mechanism: vibration resulting from resistance to late
ventricular filling during atrial systole
Timing: late diastole ( before S1)
Location: Apex ( LV) or LLSB (RV)
Pitch: low ( use bell)
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
Pericardial Friction Rub
 It is an extra heart sound originating from the pericardial sac
 Mechanism: Originates from the pericardial sac as it moves
 Timing: with each heartbeat

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

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
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
ECG Paper
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
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

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.
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.

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.
D. Hemodynamics Monitoring
1. CVP ( Central Venous Pressure )
 Reflects the pressure of the blood in the right atrium.
 Engorgement is estimated by the venous column that can
be observed as it rises from an imagined angle at th point
of manubrium ( angle of Louis).
 With normal physiologic condition, the jugular venous
column rises no higher than 2-3 cm above the clavicle
with the client in a sitting position at 45 degree angle.
 CVP is a measurement of:
- cardiac efficiency
- blood volume
- peripheral resistance
 Right ventricular pressure – a catheter is passed from a
cutdown in the antecubital, subclavian jugular or basilica
vein to the right atrium and attached to a prescribed
manometer or tranducer.
 NORMAL CVP is 2 -8 cm h20 or 2-6 mm Hg
 Decrease indicates dec. circulating volume, increase
indicates inc. blood volume or right heart beat failure.
 To Measure: patient should be flat with zero point of
manometer at the same level of the RA which
corresponds to the mid-axillary line of the patient or
approx. 5 cm below the sternum.
 Fluctuations follow patients respiratory function and will
fall on inspiration and rise on expiration due to changes
in intrapulmonary pressure. Reading should be obtained
at the highest point of fluctuation.
2. Pulmonary Artery Pressure ( PAP) Monitoring
 Appropriate for critically ill clients requiring more
accurate assessments of the left heart pressure
 Swan-Ganz Catheter / Pulmonary Artery Catheter is use
 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
CORONARY ARTERIAL DISEASE
ISCHEMIC HEART DISEASE
Results from the focal narrowing of the large and
medium-sized coronary arteries due to deposition of atheromatous
plaque in the vessel wall
Stages of Development of Coronary Artery Disease
1. Myocardial Injury: Atherosclerosis
2. Myocardial Ischemia: Angina Pectoris
3. Myocardial Necrosis: Myocardial Infarction
I. ATHEROSCLEROSIS
ATHEROSCLEROSIS ARTERIOSCLEROSIS
Narrowing of artery
Lipid or fat deposits
Tunica intima
Hardening of artery
Calcium and protein
deposits
Tunica media
A. PRESDISPOSING FACTORS
1. Sex: male
2. Race: black
3. Smoking
4. Obesity
5. Hyperlipidemia
6. Sedentary lifestyle
7. Diabetes Mellitus
8. Hypothyroidism
9. Diet: increased saturated fats
10. Type A personality
B. SIGNS AND SYMPTOMS
1. Chest pain
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.

 Prosthetic intravascular cylindric stent maintain
good luminal geometry after ballon deflation and
withdrawal.
 Intravascular stenting is done to prevent restenosis
after PTCA
Coronary Arterial Bypass Graft Surgery
Greater and lesser saphenous veins are commonly used for
bypass graft procedures
Objectives of CABG
1. Revascularize myocardium
2. To prevent angina
3. Increase survival rate
4. Done to single occluded vessels
5. If there is 2 or more occluded blood vessels CABG is
done
Nursing Management:
 Nitroglycerine is the drug of choice for relief of pain
from acute ischemic attacks
 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
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
8. Hypertension
9. CAD: Atherosclerosis
10. Thromboangiitis Obliterans
11. Severe Anemia
12. Aortic Insufficiency: heart valve that fails to open &
close efficiently
13. Hypothyroidism
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
located at sub sterna usually radiates from neck,
back, arms, shoulder and jaw muscles usually
relieved by rest or taking nitroglycerine(NTG)
3. Dyspnea
4. Tachycardia
5. Palpitations
6. Diaphoresis

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 )
 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. Hypothyroidism
1. Chest pain
Excruciating visceral, viselike pain with sudden
onset located at substernal& rarely in
precordial
Usually radiates from neck, back, shoulder,
arms, jaw & abdominal muscles (abdominal
ischemia): severe crushing
Not usually relieved by rest or by
nitroglycerine
2. N/V
3. Dyspnea
4. Increase in blood pressure & pulse, with gradual
drop in blood pressure (initial sign)
5. Hyperthermia: elevated temp
6. Skin: cool, clammy, ashen
7. Mild restlessness & apprehension
8. Occasional findings:
Pericardial friction rub
Split S1& S2
Rales or Crackles upon auscultation
S4 or atrial gallop
C. DIAGNOSTIC PROCEDURED
1. Cardiac Enzymes
CPK-MB: elevated
Creatinine phosphokinase(CPK):elevated
Heart only, 12 – 24 hours
Lactic acid dehydrogenase(LDH): is increased
Serum glutamic pyruvate transaminase(SGPT):
is increased
Serum glutamic oxal-acetic
transaminase(SGOT): is increased
2. Troponin Test: is increased
3. ECG tracing reveals
ST segment elevation
T wave inversion
Widening of QRS complexes: indicates that
there is arrhythmia in MI
4. Serum Cholesterol & uric acid: are both increased
5. CBC: increased WBC
D. NURSING INTERVENTIONS
Goal: Decrease myocardial oxygen demand
1. Decrease myocardial workload (rest heart)
Establish a patent IV line
Administer narcotic analgesic as ordered: Morphine
Sulfate IV: provide pain relief(given IV because
after an infarction there is poor peripheral perfusion
& because serum enzyme would be affected by IM
injection as ordered)
Side Effects: Respiratory Depression
Antidote: Naloxone (Narcan)
Side Effects of Naloxone Toxicity: is tremors
2. Administer oxygen low flow 2-3 L / min: to prevent
respiratory arrest or dyspnea & prevent arrhythmias
3. Enforce CBR in semi-fowlers position without bathroom
privileges(use bedside commode): to decrease cardiac
workload
4. Instruct client to avoid forms of valsalva maneuver
5. Place client on semi fowlers position
6. Monitor strictly V/S, I&O, ECG tracing & hemodynamic
procedures
7. Perform complete lung / cardiovascular assessment
8. Monitor urinary output & report output of less than 30 ml
/ hr: indicates decrease cardiac output
9. Provide a full liquid diet with gradual increase to soft diet:
low in saturated fats, Na & caffeine
10. Maintain quiet environment
11. Administer stool softeners as ordered:to facilitate bowel
evacuation & prevent straining
12. Relieve anxiety associated with coronary care
unit(CCU)environment
13. Administer medication as ordered:
a. Vasodilators:Nitroglycirine (NTG), Isosorbide
Dinitrate, Isodil (ISD): sublingual
b. Anti Arrythmic Agents: Lidocaine (Xylocane),
Brithylium
Side Effects: confusion and dizziness
c. Beta-blockers: Propanolol (Inderal)
d. ACE Inhibitors: Captopril (Enalapril)
e. Calcium Antagonist: Nefedipine
f. Thrombolytics / Fibrinolytic Agents: Streptokinase,
Urokinase, Tissue Plasminogen Activating Factor
(TIPAF)
Side Effects:allergic reaction, urticaria, pruritus
Nursing Intervention: Monitor for bleeding
time
g. Anti Coagulant
Heparin
Antidote: Protamine Sulfate
Nursing Intervention: Check for Partial
Thrombin Time (PTT)
Caumadin(Warfarin)
Antidote:Vitamin K
Nursing Intervention: Check for
Prothrombin Time (PT)
h. Anti Platelet: PASA (Aspirin): Anti thrombotic
effect
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
Arrhythmia: caused by premature ventricular
contraction
Cardiogenic shock: late sign is oliguria
Left Congestive Heart Failure
Thrombophlebitis: homan’s sign
Stroke / CVA
Dressler’s Syndrome(Post MI Syndrome):client
is resistant to pharmacological agents:
administer 150,000-450,000 units of
streptokinase as ordered
g. Importance of participation in a progressive activity
program
h. Resumption of ADL particularly sexual intercourse:
is 4-6 weeks post cardiac rehab, post CABG &
instruct to:

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

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

9. provide a dietary intake which is low in saturated
fats and caffeine
10. Institute bloodless phlebotomy
 ROTATING TOURNIQUET
 Rotated clockwise every 15 minutes to
promote a decrease in venous return
11. Health teaching and discharge planning
 Prevent complications : Arrhythmia, Shock,
Thrombophlebitis, MI, Cor pulmonale – RV
hypertrophy
 Regular adherence to medications
 Diet modifications
 Importance of ffup care
HYPERTENSION
Is an abnormal elevation of Bp, systolic pressure above
140 mmHg and or diastolic pressure above 90mmHg at
least two readings
WHO: BP >160/95 mmHg
AHA: BP >140/90 mmHg
In hypertension, vasoconstriction – vasospasm –
increases PVR – decrease blood flow to the organ.
Target Organs:
 Heart : MI, CHF, Dysrhythmias
 Eyes: blurred / impaired vision, retinopathy,
cataract.
 Brain: CVA, encephalopathy
 Kidneys : renal insufficiency, RF
 Peripheral Bloods Vessels – aneurysm,
gangrene
CLASSIFICATION OF BP FOR ADULTS 18 YRS AND
OLDER (PHIL. SOCIETY OF HPN)
Optimal
o <120 mmHg / <80 mmHg
Recheck in 2 years.
Normal
o 120-129 mmHg / 80-84 mmHg
Recheck in 2 years.
High normal
o 130-139 mmHg / 85-89 mmHg
Recheck in 1 year.
Stage 1 (mild) HPN
o 140-159 mmHg / 90-99 mmHg
Confirm in 2 months.
Stage 2 (moderate) HPN
o 160-179 mmHg / 100-109 mmHg
Evaluate within a month.
Stage 3 (severe) HPN
o 180-209 mmHg / 110-119mmHg
Evaluate within a week.
Stage 4 (very severe) HPN
o 210 mmHg / >/=120 mmHg Evaluate
A. CLASSIFICATION
 Essential / Idiophatic / Primary HPN, accounts
for 90 – 95% of all cases of HPN, cause is
unknown
 Secondary HPN, due to known causes ( Renal
failure, Hypertension )
 Malignant Hypertension, is severe, rapidly
progressive elevation in BP that causes rapid onset
of end organ complication
 Labile HPN, intermittently elevated BP
 Resistant HPN, does not respond to usual
treatment
 White Coat HPN, elevation of B only during
clinic or hospital visits
 Hypertensive Crisis, situation that requires
immediate blood pressure lowering 240mmHg /
120 mmHg
B. RISK FACTORS
1. Family history
2. Age
3. High salt intake
4. Low potassium intake
5. Obesity
6. Excess alcohol consumption
7. Smoking
8. Stress
1. Headache
2. Epistaxis
3. Dizziness
4. Tinnitus
5. Unsteadiness
6. Blurred vision
7. Depression
8. Nocturia
9. Retinopathy
D. TREATMENT STRATEGIES
Non-pharmacologic therapy
1. Low salt diet.
2. Weight reduction.
3. Exercise.
4. Cessation of smoking.
5. Decreased alcohol consumption.
6. Psychological methods: Relaxation / meditation.
7. Dietary decrease in saturated fat.
Drug therapy
Stepped Care
o Progressive addition of drugs to a regimen,
starting with one, usually a diuretic, and adding,
in a stepwise fashion, a sympatholytic,
vasodilator, and sometimes an ACE inhibitor.
Monotherapy
o Advantageous because of its simplicity, better
patient compliance, and relatively low
incidence of toxicity.
CATEGORIES OF
ANTI-HYPERTENSIVE DRUGS
Drugs that alter sodium and water balance  Diuretics.
Loop diuretics
Thiazides
Spironolactone and Triamterene
Drugs that alter sympathetic nervous system function 
Sympatholytic drugs.
Centrally-acting sympatholytics
 Clonidine
 Guanabenz
 Guanfacine
 Methyldopa
Peripherally-acting sympatholytics
 Guanadrel
 Guanethidine
 Reserpine
a-blockers
 Doxazosin
 Prazosin
b-blockers
 Acebutolol - Labetalol
 Atenolol - Metoprolol
 Betaxolol - Nadolol
 Bisoprolol - Penbutolol
 Carteolol - Pindolol
 Carvedilol - Propranolol
 Esmolol - Timolol

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.

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
Wine
Chocolate
Pickles
Sausages
Soy sauce
3. Preventing Non-compliance
 Inform the client that absence of symptoms
does not indicate control of BP
 Advise the client against abrupt withdrawal of
medication, rebound hypertension may occur.
 Device ways to facilitate remembering of
taking medications
PERIPHERAL VASCULAR DISORDERS
ANEURYSM
It is the localized, irreversible dilatation of an artery
secondary to an alteration in the integrity of its wall.
Most common type is AAA ( abdominal aortic aneurysm )
The most common cause is hypertension
A. CLASSIFICATIONS
 Fusiform Aneurysm , involves outpouching of the
both side of the artery
 Saccular Aneurysm , outpouching of only one side
of the artery.
 Dissecting Aneurysm, involves separation or tear in
the tunica intima and tunica media
B. RISK FACTOR
1. Age
2. Tobacco use
3. HPN
4. Atherosclerosis
5. Race
6. Gender
7. Family history
1. Pulsating mass over abdomen (AAA)
2. Presence of the bruit sound
3. Low back pain
4. Lower abdominal pain
5. Flank pain
6. Shock
D. MEDICAL / SURGICAL MANAGEMENT
1. Hypertensive Medication
2. Surgery if aneurysm is greater than 4 cm
 Teflon graft
 Dacron graft
 Gortex graft
E. NURSING INTERVENTIONS
1. Monitor the following
 VS
 Hemodynamic measurements
 Urine output
 BUN and creatinine
 Bowel sounds
 Passage of flatus
 Peripheral pulses
2. Promoting Fluid Volume
 Check dressing for excessive drainage
 Assess for abdominal pain or backpain
 Assess Hgb and Hct values
ARTERIAL ULCERS
I. THROMBOANGITIS OBLITERANS ( Buerger’s Dse. )
– acute inflammatory condition affecting the smaller and
medium sized arteries and veins of the lower extremities.
IDIOPATHIC
1. High risk group  men 30 years old above
2. Chronic smoking
B. SIGNS AND SYMPTOMS  Consistent to all arterial
diseases
1. Intermittent claudication – leg pain upon strenuous
walking r/t temporary ischemia
2. Cold sensitivity and skin color changes
 White/pallor  bluish/cyanosis  red/rubor
 (+) especially post smoking
3. Decreased peripheral pulses’ volume particularly in
dorsalis pedis and posterior tibial
4. Trophic changes
5. Ulceration
6. Gangrene formation
C. DIAGNOSTICS
1. Oscillometry – reveals a decrease in peripheral
pulse volume
2. Doppler UTZ – decrease in blood flow to affected
extremity
3. Angiography – site and extent of malocclusion

1. Encourage slow progressive physical activity
 Walking 3-4x/day
 Out of bed 3-4x/day
2. Medications as ordered
 Analgesics
 Vasodilators
 Anticoagulants
3. Instruct patient to avoid smoking and exposure to
cold environment
4. Institute foot care management
 Avoid barefoot walking
 Straight nails
 Lanolin cream for feet
 (-) constricting clothes
5. Assist in surgery: BKA
II. REYNAULD’S DISEASE – characterized by acute episodes
of arterial spasms involving the digits of hands and fingers
1. High risk group  women 40 years old up
2. Smoking
3. Collagen diseases
 SLE
 RA
4. Direct hand trauma
 Piano playing
 Excessive typing (tsk tsk! Lagot!)
 Carpal tunnel syndrome
 Operating chainsaw (nyek!)
 Writing (tsk tsk, kaya dapat may module eh!
Grr!)
1. Intermittent claudication
2. Cold sensitivity and skin color changes
 White/pallor  bluish/cyanosis  red/rubor
 (+) especially post smoking
3. Trophic changes
4. Ulceration
5. Gangrene formation
C. DIAGNOSTICS
1. Oscillometry – reveals a decrease in peripheral
pulse volume
2. Angiography – site and extent of malocclusion
 Analgesics
 Vasodilators
2. Encourage pt to wear gloves
3. Instruct: avoid smoking and exposure to cold
environment
VENOUS ULCERS
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
1. Hereditary
2. Congenital weakness of veins
3. Thrombophlebitis
4. Cardiac diseases
5. Pregnancy
6. Obesity
7. Prolonged immobility  prolonged standing and
sitting
1. Pain after prolonged standing
2. Dilated tortuous skin veins which are warm to touch
3. Heaviness in the legs
C. DIAGNOSTICS
1. Venography
2. Trendelenburg’s test – reveals that veins distend
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)
1. Smoking
2. Obesity
3. Prolonged use of OCPs
4. Chronic anemia
5. Diet high in saturated fats
6. DM
7. CHF
8. MI
9. Post-cannulation (insertion of various catheters)
10. Post-surgical operation
1. Pain at the affected extremity
2. Presence of cyanosis
3. Dilated tortuous veins
4. (+) HOMAN’S  pain on calf on dorsiflexion
C. DIAGNOSTICS
1. Venography
2. Doppler UTZ
3. Angiography
1. Elevate the legs above heart level
2. Apply warm moist pack to relieve lymphatic
congestion
3. Measure circumference of leg muscles to determine
if it is swollen
4. Anti-embolic stockings
 Analgesics
 Anticoagulants – heparin
6. Prevent complications
 Pulmonary embolism

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