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Anatomy and Physiology

Cardiovascular system consists of the heart, arteries, veins &
capillaries. The major functions 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.
 Coronary artery – 1st branch of aorta
 Myocardium – muscular layer, middle layer,
responsible for the major pumping action of the  Right Coronary
 SA nodal Branch – supplies SA node
ventricles.
 Right marginal Branch – supplies the right border of
 Epicardium – thin covering(mesothelium), covers
the outer surface of the heart the heart
 AV nodal branch – supplies the AV node
 Pericardium – invaginated sac
 Posterior interventricular artery – supplies both
 Visceral – attached to the exterior of myocardium
 Parietal – attached to the great vessels and ventricles
diaphragm  Left Coronary
 Papillary Muscle  Circumflex branch – supplies SA node in 40 % of
Arise from the endocardial & myocardial surface of the people
ventricles & attach to the chordae tendinae  Left marginal – supplies the left ventricle
 Chordae Tendinae  Anterior interventricular branch aka Left anterior
Attach to the tricuspid & mitral valves & prevent eversion descending(LAD)–supplies both ventricles and
during systole interventricular septum
 Separated into 2 pumps:  Lateral branch – terminates in ant surface of the heart
 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
 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  Coronary Veins
blood out of the heart; lie below the atria  Coronary sinus – main vein of the heart
 Lower Chamber (contracting or pumping)  Great Cardiac vein – main tributary of the coronary sinus
 Right Ventricle: contracts & propels deoxygenated blood
 Oblique vein – remnant of SVC, small unsignificant
into pulmonary circulation via the aorta during
ventricular systole; Right atrium has decreased pressure
Heart Circulation
which is 60 – 80 mmHg
 Left Ventricle: propels blood into the systemic circulation
via aorta during 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
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Cardiac Conduction System a. Sinoatrial node (SA node) "the pacemaker" - has the fastest
autorhythmic rate (70-80 per minute), and sets the pace for
Properties of Heart Conduction System the entire heart; this rhythm is called the sinus rhythm;
• Automaticity located in right atrial wall, just inferior to the superior vena
• Excitability cava
• Conductivity b. Atrioventricular node (AV node) - impulses pass from SA via
• Contractility gap junctions in about 40 ms.; impulses are delayed about
100 ms to allow completion of the contraction of both atria;
Structure of Heart Conduction System 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

 Nodal tissues Events of Cardiac Cycle

 SA Node( Sino-atrial, Keith and Flack) 1. mid-to-late ventricular diastole: ventricles filled
 Primary Pacemaker  the AV valves are open
 Between SVC and RA  pressure: LOW in chambers; HIGH in aorta/pulmonary
 Vagal and symphatetic innervation trunk
 Sinus Rhythms  aortic/pulmonary semilunar valves CLOSED
 AV Node( Atrioventricular , Kent and Tawara)  blood flows from vena cavas/pulmonary vein INTO atria
 At the right atrium  blood flows through AV valves INTO ventricles (70%)
 3 zones 2. ventricular systole: blood ejected from heart
 AN Zone(atrionodal)  filled ventricles begin to contract, AV valves CLOSE
 N Zone (nodal)  contraction of closed ventricles increases pressure
 NH zone (nodal –HIS)  ventricular ejection phase - blood forced out
 Internodal and Interatrial Pathways  semilunar valves open, blood -> aorta & pulmonary
 Connects SA and AV Node trunk
 Ant. Internodal(bachman) tract 3. isovolumetric relaxation: early ventricular diastole
 Middle Internodal(wenkebach) tract  ventricles relax, ventricular pressure becomes LOW
 Posterior internodal(Thorel) tract  semilunar valves close, aorta & pulmonary trunk
 Bundle of His/ Purkinje Fibers backflow
 Provides for ventricular conduction system TOTAL CARDIAC CYCLE TIME = 0.8 second
 Fastest conduction among cardiac tissues (normal 70 beats/minute)
 Right bundle
atrial systole (contraction) = 0.1 second
 Left Bundle
ventricular systole (contraction) = 0.3 second
quiescent period (relaxation) = 0.4 second
Cardiac Action Potential
 Depolarization: electrical activation of a cell caused by the
Cardiac Output - Blood Pumping of the Heart
influx of sodium into the cell while potassium exits the cell
General Concepts
 Repolarization: return of the cell to the resting state caused
• Stroke volume: the amount of blood ejected with each
by re-entry of potassium into the cell while sodium exits
heartbeat
 Refractory periods:
• Cardiac output: amount of blood pumped by the ventricle in
 Effective refractory period: phase in which cells are
liters per minute
incapable of depolarizing
• Preload: degree of stretch of the cardiac muscle fibers at the
 Relative refractory period: phase in which cells end of diastole
require a stronger-than-normal stimulus to depolarize • Contractility: ability of the cardiac muscle to shorten in
response to an electrical impulse
Anatomical Sequence of Excitation of the Heart • Afterload: the resistance to ejection of blood from the
 (right atrium) ventricle
 sinoatrial node (SA) • Ejection fraction: the percent of end-diastolic volume
 (right AV valve) ejected with each heartbeat
 atrioventricular node (AV)
 atrioventricular bundle (bundle of His) General Variables of Cardiac Output
 right & left bundle of His branches 1. Cardiac Output (CO) - blood amount pumped per minute
 Purkinje fibers of ventricular walls  CO (ml/min) = HR (beats/min) X SV (ml/beat)
(from SA through complete heart contraction = 220 ms = 0.22 s)  Normal CO = 75 beats/min X 70 ml/beat
= 5.25 L/min
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2. Heart Rate (HR) - cardiac cycles per minute Vascular System

 Normal range is 60-100 beats per minute  Major function of the blood vessels isto supply the tissue with
 Tachycardia is greater than 100 bpm blood, remove wastes, & carry unoxygenated blood back to
 Bradycardia is less than 60 bpm the heart
 Sympathetic system INCREASES HR
 Parasympathetic system (Vagus) DECREASES HR Types of Blood Vessels
3. Blood pressure - Cardiac output X peripheral resistance Arteries
 Control is neural (central and peripheral) and hormonal  Elastic-walled vessels that can stretch during systole & recoil
 Baroreceptors in the carotid and aorta during diastole; they carry blood away from the heart &
 Hormones- ADH, aldosterone, epinephrine can increase distribute oxygenated blood throughout the body
BP; ANF can decrease BP Arterioles
 Small arteries that distribute blood to the capillaries &
Regulation of Stroke Volume (SV) function in controlling systemic vascular resistance &
 End diastolic volume (EDV) - total blood collected in ventricle therefore arterial pressure
at end of diastole; determined by length of diastole and Capilliaries
venous pressure (~ 120 ml)  The following exchanges occurs in the capilliaries
 End systolic volume (ESV) - blood left over in ventricle at end  O2 & CO2
of contraction (not pumped out); determined by force of  Solutes between the blood & tissue
ventricle contraction and arterial blood pressure (~50ml)
 Fluid volume transfer between the plasma & interstitial
space
SV (ml/beat) = EDV (ml/beat) - ESV (ml/beat)
Venules
Normal SV = 120 ml/beat- 50 ml/beat = 70 ml/beat
 Small veins that receive blood from capillaries & function as
collecting channels between the capillaries & veins
Frank-Starling Law of the Heart - critical factor for stroke volume is
Veins
"degree of stretch of cardiac muscle cells";
more stretch = more contraction force  Low-pressure vessels with thin small & less muscles than
increased EDV = more contraction force arteries; most contains valves that prevent retrograde blood
flow; they carry deoxygenated blood back to the heart. When
 slow heart rate = more time to fill
the skeletal surrounding veins contract, the veins are
 exercise = more venous blood return
compressed, promoting movement of blood back to the
heart.
Regulation of Heart Rate (Autonomic, Chemical, Other)
1. Autonomic Regulation of Heart Rate (HR)
ASSESSMENT
 Sympathetic - NOREPINEPHRINE (NE) increases heart rate
(maintains stroke volume which leads to increased Cardiac
Nursing History
Output)
Risk Factors
 Parasympathetic - ACETYLCHOLINE (ACh) decreases heart
A. Non – Modifiable Risk Factor
rate
 Age
 Vagal tone - parasympathetic inhibition of inherent rate of SA
 Gender
node, allowing normal HR
 Race
 Baroreceptors, pressoreceptors - monitor changes in blood
 Heredity
pressure and allow reflex activity with the autonomic nervous
B. Modifiable Risk Factor
system
 Stress
2. Hormonal and Chemical Regulation of Heart Rate (HR)
 Diet
 epinephrine - hormone released by adrenal medulla during
 Exercise
stress; increases heart rate
 Sedentary lifestyle
 thyroxine - hormone released by thyroid; increases heart rate
 Cigarette smoking
in large quantities; amplifies effect of epinephrine
 Alcohol
 Ca++, K+, and Na+ levels very important;
 Hypertension
 hyperkalemia - increased K+ level; KCl used to stop
 Hyperlipidemia
heart on lethal injection
 DM
 hypokalemia - lower K+ levels; leads to abnormal  Obesity
heart rate rhythms  Type A personality
 hypocalcemia - depresses heart function  Contraceptive Pills
 hypercalcemia - increases contraction phase
 hypernatremia - HIGH Na+ concentration; can block Common Clinical Manifestations of Cardiovascular Disorders
Na+ transport & muscle contraction a. Dyspnea
3. Other Factors Effecting Heart Rate (HR) - Exertional
normal heart rate - fetus 140 - 160 beats/minute - Orthopnea
female 72 - 80 beats/minute - Paroxysmal Noctural Dyspnea
male 64 - 72 beats/minute - Cheyne-stokes
1. exercise - lowers resting heart rate (40-60) b. Chest Pain
2. heat - increases heart rate significantly c. Edema
3. cold - decreases heart rate significantly - Ascites
4. tachycardia - HIGHER than normal resting heart rate (over - Hydrothorax
100); may lead to fibrillation - Anasarca
5. bradycardia - LOWER than normal resting heart rate (below d. Palpitation
60); parasympathetic drug side effects; physical conditioning; e. Hemoptysis
sign of pathology in non-healthy patient f. Fatigue
g. Syncope and Fainting
h. Cyanosis
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i. Abdominal Pain Timing: late diastole ( before S1)

j. Clubbing of fingers Location: Apex ( LV) or LLSB (RV)
k. Jaundice Pitch: low ( use bell)

Physical Assessment Heart Murmurs

Inspection: Murmur - sounds other than the typical "lub-dub"; typically caused by
– Skin color disruptions in flow
– Neck vein distention  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
– Respirations  Location: over pericardium. Upright position, leaning forward
– Pulsations  Pitch: high pitched and scratchy. Sounds like sandpaper being
– Clubbing rubbed together
– Capillary refill  Significance: inflammation, infection, infiltration
Palpation: 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
Heart Sounds: Stethoscope Listening 3. To assess inflammation
4. To determine baseline value
Overview of Heart Sounds (lub-du ; lub, dub ) 5. To monitor serum level of medications
 lub - closure of AV valves, onset of ventricular systole 6. To assess the effects of medications
 dub - closure of semilunar valves, onset of diastole
 Tricuspid valve (lub) - RT 5th intercostal, medial A. Blood Studies
 Mitral valve (lub) - LT 5th intercostal, lateral
 Aortic semilunar valve (dub) - RT 2nd intercostal 1. Complete Blood Count
 Pulmonary semilunar valve (dub) - LT 2nd intercostals a. RBC count- # of RBCs/ mm3 of blood, to diagnose anemia and
S1 - due to closure of the AV(mitral/tricuspid) valves ploycythemia
- timing: beginning of systole b. Hemoglobin- # of grams of hgb/ 100ml of blood; to measure the
- loudest at the apex oxygen-carrying capacity of the blood
S2 - due to the closure of the semi-lunar (pulmonic/aortic) valves c. Hematocrit – expressed in %; measures the volume of RBCs in
- timing: diastole proportion to plasma; used also to diagnose anemia and polycythemia
- loudest at the base 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
S3 – Ventricular Diastolic Gallop g. WBC Differential count- determines proportion of each WBC in a
Mechanism: vibration resulting from resistance to rapid sample of 100 WBCs; used to classify leukemias
ventricular filling secondary to poor compliance
Timing: early diastole Normal Values
Location: Apex (LV) or LLSB (RV) RBC: Women – 4.2-5.4 million/mm3
Pitch: faint and low pitched Men – 4.7-6.1 million/mm3
S4 - Atrial Diastolic Gallop Hgb: Women – 12-16 g/dl
Mechanism: vibration resulting from resistance to late Men – 13-18 g/dl
ventricular filling during atrial systole Hct : Women – 36-42%
Men – 42-48%
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WBC: 5000-10,000/mm3  LDH- 130 mg/dL

Granulocytes  HDL- 30-70- mg/dL
Neutrophils: 55-70%  NPO post midnight (usually 12 hours)
Eosinophils: 1-4%
Basophils: 0.5-1.0% B. Non-Invasive Procedure
Agranulocytes
Lymphocytes: 20-40% 1. Cardiac Monitoring / Electrocardiography (ECG)
Monocytes: 2-8% A non-invasive procedure that evaluates the electrical activity
Platelets: 150,000-450,000/mm3 of the heart

2. Coagulation Screening Test a. Limb Leads

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. b. Precordial Leads

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) The precordial leads VI –V6 are part of the 12 lead EKG.
 Most cardiac specific enzymes They are not monitored with the standard limb leads
 Accurate indicator of myocardial dammage
 Elevates in MI within 4 hours, peaks in 18 hours and c. 12 lead ECG
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 ECG Paper
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
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 Pre-test: 4 hours fasting, avoid alcohol, caffeine

 Post test: report symptoms of chest pain

5. ECHOCARDIOGRAM

Deflection Waves of ECG

1. P wave - initial wave, demonstrates the depolarization from SA
 Non-invasive test that studies the structural and functional
Node through both ATRIA; the ATRIA contract about 0.1 s after start of
changes of the heart with the use of ultrasound
P Wave.
 Client Preparation: instruct client to remain still during the
2. QRS complex - next series of deflections, demonstrates the
test, secure electrodes for simultaneous ECG tracing, explain
depolarization of AV node through both ventricles; the ventricles
that there will be no pain or electrical shock, lubricant placed
contract throughout the period of the QRS complex, with a short delay
on the skin will be cool.
after the end of atrial contraction; repolarization of atria also obscured
3. T Wave - repolarization of the ventricles (0.16 s)
6. Phonocardiography
4. PR (PQ) Interval - time period from beginning of atrial contraction
 Is a graphic recording of heart sound with simultaneous
to beginning of ventricular contraction (0.16 s)
ECG.
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

C. Invasive Procedure

1. Cardiac Catheterization ( Coronary Angiography /

Arteriography )
3. Stress Test
 Insertion of a catheter into the heart and surrounding
 A non-invasive test that studies the heart during activity
vessels
and detects and evaluates CAD
 Is an invasive procedure during which physician injects
 Exercise test, pharmacologic test and emotional test
dye into coronary arteries and immediately takes a
 Treadmill testing is the most commonly used stress test
series of x-ray films to assess the structures of the
 Used to determine CAD, Chest pain causes, drug
arteries
effects and dysrhythmias in exercise
 Determines the structure and performance of the heart
 Pre-test: consent may be required, adequate rest , eat a
valves and surrounding vessels
light meal or fast for 4 hours and avoid smoking, alcohol
 Used to diagnose CAD, assess coronary atery patency
and caffeine
and determine extent of atherosclerosis
 During the test: secure electrodes to appropriate
 Pretest: Ensure Consent, assess for allergy to seafood
location on chest, obtain baseline BP and ECG tracing,
and iodine, NPO, document weight and height, baseline
instruct client to exercise as instructed and report any
VS, blood tests and document the peripheral pulses
pain, weakness and SOB, monitor BP and ECG
 Pretest: Fasting for 8-12 hours, teachings, medications
continuously, record at frequent interval
to allay anxiety
 Post-test: instruct client to notify the physician if any
 Intra-test: inform patient of a fluttery feeling as the
chest pain, dizziness or shortness of breath . Instruct
catheter passes through the heart; inform the patient
client to avoid taking a hot shower for 10-12 hours after
that a feeling of warmth and metallic taste may occur
the test
when dye is administered
 Post-test: Monitor VS and cardiac rhythm
4. Pharmacological stress test
 Monitor peripheral pulses, color and warmth and
 Use of dipyridamole
sensation of the extremity distal to insertion site
 Maximally dilates coronary artery
 Side-effect: flushing of face
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 Maintain sandbag to the insertion site if required to

maintain pressure
 Monitor for bleeding and hematoma formation

 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
2. Nuclear Cardiology  Decrease indicates dec. circulating volume, increase
 Are safe methods of evaluating left ventricular muscle indicates inc. blood volume or right heart beat failure.
function and coronary artery blood distribution.  To Measure: patient should be flat with zero point of
 Client Preparation: obtain written consent, explain procedure, manometer at the same level of the RA which corresponds to
instruct client that fasting may be required for a short period the mid-axillary line of the patient or approx. 5 cm below the
before the exam, assess for iodine allergy. sternum.
 Post Procedure: encourage client to drink fluids to facilitate  Fluctuations follow patients respiratory function and will fall
the excretion of contrast material, assess venipuncture site on inspiration and rise on expiration due to changes in
for bleeding or hematoma. intrapulmonary pressure. Reading should be obtained at the
 Types of Nuclear Cardiology highest point of fluctuation.
o Multigated acquisition (MUGA) or cardiac
blood pool scan 2. Pulmonary Artery Pressure ( PAP) Monitoring
 Provides information on wall motion  Appropriate for critically ill clients requiring more accurate
during systole and diastole, cardiac assessments of the left heart pressure
valves, and EF.  Swan-Ganz Catheter / Pulmonary Artery Catheter is use
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,  Client Preparation: obtain consent, insertion is under strict
assess the physiologic significance of a sterile technique, usually at the bedside, explain to client the
known coronary lesion, and assess the sterile drapes may cover the face, assists to position client
effectiveness of various therapeutic flat or slight T-postion as tolerated and instruct to remain still
modalities such as coronary artery during the procedure
bypass surgery, percutaneous coronary  Nursing Care During Insertion: Monitor and document HR,BP
intervention, or thrombolytic therapy. and ECG during the procedure

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.
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CARDIAC DISORDERS

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

Coronary Arterial Bypass Graft Surgery

I. ATHEROSCLEROSIS
ATHEROSCLEROSIS ARTERIOSCLEROSIS

 Narrowing of artery  Hardening of artery

 Lipid or fat deposits  Calcium and protein
 Tunica intima deposits
 Tunica media

A. PRESDISPOSING FACTORS
1. Sex: male
2. Race: black
3. Smoking
4. Obesity Greater and lesser saphenous veins are commonly used for
5. Hyperlipidemia bypass graft procedures
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. Objectives of CABG
 Prosthetic intravascular cylindric stent maintain good 1. Revascularize myocardium
luminal geometry after ballon deflation and withdrawal. 2. To prevent angina
 Intravascular stenting is done to prevent restenosis after 3. Increase survival rate
PTCA 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
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For Saphenous Vein Site: D. DIAGNOSTIC PROCEDURE

 Wear support stocking 4-6 week postop 1. History taking and physical exam
 Apply pressure dressing or sand bag on the site 2. ECG: may reveals ST segment depression & T wave
 Keep leg elevated when sitting inversion during chest pain
3. Stress test / treadmill test: reveal abnormal ECG during
3 Complications of CABG exercise
1. Pneumonia: encourage to perform deep breathing, coughing 4. Increase serum lipid levels
exercise and use of incentive spirometer 5. Serum cholesterol & uric acid is increased
2. Shock
3. Thrombophlebitis E. MEDICAL MANAGEMENT
1. Drug Therapy: if cholesterol is elevated
II. ANGINA PECTORIS  Nitrates: Nitroglycerine (NTG)
 Transient paroxysmal chest pain produced by insufficient  Beta-adrenergic blocking agent: Propanolol
blood flow to the myocardium resulting to myocardial  Calcium-blocking agent: nefedipine
ischemia  Ace Inhibitor: Enapril
 Clinical syndrome characterized by paroxysmal chest pain 2. Modification of diet & other risk factors
that is usually relieved by rest or nitroglycerine due to 3. Surgery: Coronary artery bypass surgery
temporary myocardial ischemia 4. Percutaneuos Transluminal Coronary Angioplasty
(PTCA)
Types of Angina Pectoris
 Stable Angina: pain less than 15 minutes, recurrence is less F. NURSING INTERVENTIONS
frequent. 1. Enforce complete bed rest
 Unstable Angina : pain is more than 15 mins.,but not less than 2. Give prompt pain relievers with nitrates or narcotic
30 minutes, recurrence is more frequent and the intensity of pain analgesic as ordered
increases. 3. Administer medications as ordered:
 Variant Angina ( Prinzmetal’s Angina ): Chest pain is on
longer duration and may occur at rest. Result from coronary A. Nitroglycerine(NTG): when given in small doses
vasospasm. will act as venodilator, but in large doses will act as
 Angina Decubitus: paroxysmal chest pain that occur when the vasodilator
client sits or stand.  Give 1st dose of NTG: sublingual 3-5 minutes
 Give 2nd dose of NTG: if pain persist after
A. PRESDISPOSING FACTORS giving 1st dose with interval of 3-5 minutes
1. Sex: male  Give 3rd& last dose of NTG: if pain still persist
2. Race: black at 3-5 minutes interval
3. Smoking NTG Tablets(sublingual)
4. Obesity  Keep the drug in a dry place, avoid moisture
5. Hyperlipidemia and exposure to sunlight as it may inactivate
6. Sedentary lifestyle the drug
7. Diabetes Mellitus  Change stock every 6 months
8. Hypertension  Offer sips of water before giving sublingual
9. CAD: Atherosclerosis nitrates, dryness of mouth may inhibit drug
10. Thromboangiitis Obliterans absoprtion
11. Severe Anemia  Relax for 15 minutes after taking a tablet: to
12. Aortic Insufficiency: heart valve that fails to open & close prevent dizziness
efficiently  Monitor side effects: orthostatic hypotension,
13. Hypothyroidism flushed face. Transient headache & dizziness:
14. Diet: increased saturated fats frequent side effect
15. Type A personality  Instruct the client to rise slowly from sitting
position
B. PRESIPITATING FACTORS  Assist or supervise in ambulation
4 E’s of Angina Pectoris NTG Nitrol or Transdermal patch
1. Excessive physical exertion: heavy exercises, sexual  Nitropatch is applied once a day, usually in the
activity morning.
2. Exposure to cold environment: vasoconstriction  Avoid placing near hairy areas as it may
3. Extreme emotional response: fear, anxiety, excitement, decrease drug absorption
strong emotions  Avoid rotating transdermal patches as it may
4. Excessive intake of foods or heavy meal decrease drug absorption
 Avoid placing near microwave ovens or during
C. SIGNS AND SYMPTOMS defibrillation as it may lead to burns (most
1. Levine’s Sign: initial sign that shows the hand clutching important thing to remember)
the chest
2. Chest pain: characterized by sharp stabbing pain B. Beta-blockers: decreases myocardial oxygen
located at sub sterna usually radiates from neck, back, demand by decreasing heart rate, cardiac output
arms, shoulder and jaw muscles usually relieved by rest and BP
or taking nitroglycerine(NTG)  Propanolol
3. Dyspnea  Metropolol
4. Tachycardia  Pindolol
5. Palpitations  Atenolol
6. Diaphoresis  Assess PR, withhold if [Link]
 Administer with food ( prevent GI upset )
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 Propanolol: not given to COPD cases: it causes 9. Sedentary lifestyle

bronchospasm and DM cases: it cause 10. Diabetes Mellitus
hypoglycemia 11. Hypothyroidism
 Side Effects: Nausea and vomiting, mental 12. Diet: increased saturated fats
depression and fatigue 13. Type A personality

C. Calcium – Channel Blockers: relaxes smooth B. SIGNS AND SYMPTOMS

cardiac muscle, reduces coronary vasospasm 1. Chest pain
 Amlodipine ( norvasc )  Excruciating visceral, viselike pain with sudden
 Nifedipine ( calcibloc ) onset located at substernal& rarely in precordial
 Diltiazem ( cardizem )  Usually radiates from neck, back, shoulder, arms,
 Assess HR and BP jaw & abdominal muscles (abdominal ischemia):
 Adminester 1 hour before meal and 2 hours after severe crushing
meal ( foods delay absorption )  Not usually relieved by rest or by nitroglycerine
2. N/V
4. Administer oxygen inhalation 3. Dyspnea
5. Place client on semi-to high fowlers position 4. Increase in blood pressure & pulse, with gradual drop
6. Monitor strictly V/S, I&O, status of cardiopulmonary in blood pressure (initial sign)
fuction & ECG tracing 5. Hyperthermia: elevated temp
7. Provide decrease saturated fats sodium and caffeine 6. Skin: cool, clammy, ashen
8. Provide client health teachings and discharge planning 7. Mild restlessness & apprehension
 Avoidance of 4 E’s 8. Occasional findings:
 Prevent complication (myocardial infarction)  Pericardial friction rub
 Instruct client to take medication before indulging  Split S1& S2
into physical exertion to achieve the maximum  Rales or Crackles upon auscultation
therapeutic effect of drug  S4 or atrial gallop
 Reduce stress & anxiety: relaxation techniques &
guided imagery C. DIAGNOSTIC PROCEDURED
 Avoid overexertion & smoking 1. Cardiac Enzymes
 Avoid extremes of temperature  CPK-MB: elevated
 Dress warmly in cold weather  Creatinine phosphokinase(CPK):elevated
 Participate in regular exercise program
 Heart only, 12 – 24 hours
 Space exercise periods & allow for rest periods
 Lactic acid dehydrogenase(LDH): is increased
 The importance of follow up care
9. Instruct the client to notify the physician immediately if  Serum glutamic pyruvate transaminase(SGPT): is
pain occurs & persists despite rest & medication increased
administration  Serum glutamic oxal-acetic transaminase(SGOT):
is increased
III. MYOCARDIAL INFARCTION 2. Troponin Test: is increased
 Death of myocardial cells from inadequate oxygenation, often 3. ECG tracing reveals
caused by sudden complete blockage of a coronary artery  ST segment elevation
 Characterized by localized formation of necrosis (tissue  T wave inversion
destruction) with subsequent healing by scar formation &  Widening of QRS complexes: indicates that there is
fibrosis arrhythmia in MI
 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 4. Serum Cholesterol & uric acid: are both increased
arrhythmia leading to premature ventricular contractions 5. CBC: increased WBC
(PVC)
D. NURSING INTERVENTIONS
A. PREDISPOSING FACTORS Goal: Decrease myocardial oxygen demand
1. Sex: male
2. Race: black 1. Decrease myocardial workload (rest heart)
3. Smoking  Establish a patent IV line
4. Obesity  Administer narcotic analgesic as ordered: Morphine
5. CAD: Atherosclerotic Sulfate IV: provide pain relief(given IV because after an
6. Thrombus Formation infarction there is poor peripheral perfusion & because
7. Genetic Predisposition serum enzyme would be affected by IM injection as
8. Hyperlipidemia ordered)
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 Side Effects: Respiratory Depression g. Importance of participation in a progressive activity

 Antidote: Naloxone (Narcan) program
 Side Effects of Naloxone Toxicity: is tremors h. Resumption of ADL particularly sexual intercourse: is 4-
2. Administer oxygen low flow 2-3 L / min: to prevent respiratory 6 weeks post cardiac rehab, post CABG & instruct to:
arrest or dyspnea & prevent arrhythmias  Make sex as an appetizer rather than dessert
3. Enforce CBR in semi-fowlers position without bathroom  Instruct client to assume a non weight bearing
privileges(use bedside commode): to decrease cardiac position
workload  Client can resume sexual intercourse: if can climb
4. Instruct client to avoid forms of valsalva maneuver or use the staircase
5. Place client on semi fowlers position i. Need to report the ff s/sx:
6. Monitor strictly V/S, I&O, ECG tracing & hemodynamic  Increased persistent chest pain
procedures  Dyspnea
7. Perform complete lung / cardiovascular assessment  Weakness
8. Monitor urinary output & report output of less than 30 ml / hr:  Fatigue
indicates decrease cardiac output  Persistent palpitation
9. Provide a full liquid diet with gradual increase to soft diet: low  Light headedness
in saturated fats, Na & caffeine j. Enrollment of client in a cardiac rehabilitation program
10. Maintain quiet environment k. Strict compliance to mediation & importance of follow up
11. Administer stool softeners as ordered:to facilitate bowel care
evacuation & prevent straining
12. Relieve anxiety associated with coronary care IV. CARDIOGENIC SHOCK ( POWER/PUMP FAILURE )
unit(CCU)environment
 Is a shock state which result from profound left ventricular
13. Administer medication as ordered:
failure usually from massive MI.
a. Vasodilators:Nitroglycirine (NTG), Isosorbide Dinitrate,
 It result to low cardiac output, thereby systemic
Isodil (ISD): sublingual
hypoperfusion.
b. Anti Arrythmic Agents: Lidocaine (Xylocane), Brithylium
 Side Effects: confusion and dizziness
A. SIGNS AND SYMPTOMS
c. Beta-blockers: Propanolol (Inderal)
1. Decrease systolic BP
d. ACE Inhibitors: Captopril (Enalapril)
2. Oliguria
e. Calcium Antagonist: Nefedipine
3. Cold, clammy skin
f. Thrombolytics / Fibrinolytic Agents: Streptokinase,
4. Weak pulse
Urokinase, Tissue Plasminogen Activating Factor
5. Cyanosis
(TIPAF)
6. Mental lethargy
 Side Effects:allergic reaction, urticaria, pruritus 7. Confusion
 Nursing Intervention: Monitor for bleeding time
g. Anti Coagulant B. MEDICAL MANAGEMENT
 Heparin 1. Counterpulsation ( mechanical cardiac assistance /
 Antidote: Protamine Sulfate diastolic augmentation )
 Nursing Intervention: Check for Partial  Involves introduction of the intra – aortic
Thrombin Time (PTT) balloon catheter via the femoral artery
 Caumadin(Warfarin)  Intra Aortic Balloon Pump augments
 Antidote:Vitamin K diastole, resulting in increased perfusion of the
 Nursing Intervention: Check for Prothrombin coronary arteries and the myocardium and a
Time (PT) decrease in left ventricular workload.
h. Anti Platelet: PASA (Aspirin): Anti thrombotic effect  The balloon is inflated during diastole, it is
 Side Effects:Tinnitus, Heartburn, Indigestion / deflated during sytole.
Dyspepsia  Indications:
 Contraindication:Dengue, Peptic Ulcer Disease,  Cardiogenic shock
Unknown cause of headache  AMI
14. Provide client health teaching & discharge planning  Unstable Angina
concerning:  Open heart surgery
a. Effects of MI healing process & treatment regimen
b. Medication regimen including time name purpose, C. NURSING INTERVENTIONS
schedule, dosage, side effects 1. Perform hemodynamic monitoring
c. Dietary restrictions: low Na, low cholesterol, avoidance 2. Administer oxygen therapy
of caffeine 3. Correct hypovolemia. Administer IV fluids as ordered
d. Encourage client to take 20 – 30 cc/week of wine, 4. Pharmacology:
whisky and brandy:to induce vasodilation a. Vasodilators: Nitroglycerine
e. Avoidance of modifiable risk factors b. Inotropic agents:Digitalis, Dopamine
f. Prevent Complication c. Diuretics : Furosemide
 Arrhythmia: caused by premature ventricular d. Sodium Bicarbonate, Relieve lactic acidosis
contraction 5. Monitor hourly urine output, LOC and arrhythmias
 Cardiogenic shock: late sign is oliguria 6. Provide psychosocial support
 Left Congestive Heart Failure 7. Decrease pulmonary edema
 Thrombophlebitis: homan’s sign a. Auscultate lung fields for crackles and wheezes
 Stroke / CVA b. Note for dyspnea, cough , hemoptysis and
 Dressler’s Syndrome(Post MI Syndrome):client is orthopnea
resistant to pharmacological agents: administer c. Monitor ABG for hypoxia and metabolic acidosis
150,000-450,000 units of streptokinase as ordered d. Place in fowler’s position to reduce venous return
e. Administer during therapy as ordered:
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 Morphine sulfate to reduce venous 1. Administer oxygen

return. 2. Elevate head of bed, place pillow on the overbed table
 Aminophylline to reduce bronchospasm so that the patient can lean on it.
caused by severe congestion. 3. Bed rest
 Vasodilators to reduce venous return 4. Administer prescribed pharmacotherapy.
 Diuretics to decrease circulating volume c. ASA to suppress inflammatory process
d. Corticosteriods for more severe symptoms
V. PERICARDITIS / DRESSLER’S SYNDROME 5. Assist in pericardiocentesis and thoracotomy
 Is the inflammation of the pericardium which occurs 6. Pericardiocentesis is aspiration of blood or fluid from
approximately 1 – 6 weeks after AMI. pericardial sac.
 Results as an antigen – antibody response. The necrotic
tissues play the role of an antigen, which trigger antibody
formation. Inflammatory process follows. CONGESTIVE HEART FAILURE
 Constrictive Pericarditis is a condition in which a chronic
Inability of the heart to pump blood towards systemic circulation
inflammatory thickening of the pericardium compresses the
heart so that it is unable to fill normally during diastole.
I. LEFT-SIDED HEART FAILURE
A. SIGNS AND SYMPTOMS
A. PREDISPOSING FACTORS
1. Pain in the anterior chest, aggravated by coughing,
1. 90% - Mitral valve stenosis
yawning, swallowing, twisting and turning the torso,
 RHD
relieved by upright, leaning forward position.
 Inflammation of mitral valve
2. Pericardial friction rub – scratchy, grating or cracking
 Anti-streptolysin O titer (ASO) – 300 todd units
sound
 Penicillin, PASA, steroids
3. Dyspnea
 Aging
4. Fever, sweating, chills
2. MI
5. Joints pains
3. IHD
6. Arrhythmias
4. HPN
5. Aortic valve stenosis
B. NURSING INTERVENTIONS
1. Elevate head of bed, place pillow on the overbed table
B. SIGNS AND SYMPTOMS
so that the patient can lean on it.
1. Pulmonary edema/congestion
2. Bed rest
 Dyspnea, PND (awakening at night d/t difficulty in
3. Administer prescribed pharmacotherapy.
breathing), 2-3 pillow orthopnea
a. ASA to suppress inflammatory process
 Productive cough (blood tinged)
b. Corticosteriods for more severe symptoms
 Rales/crackles
4. Assist in pericardiocentesis if cardiac tamponade is
 Bronchial wheezing
present.
 Frothy salivation
5. Pericardiocentesis is aspiration of blood or fluid from
2. Pulsus alternans (A unique pattern during which the
pericardial sac.
amplitude of the pulse changes or alternates in size with
a stable heart rhythm.)This is common in severe left
VI. CARDIAC TAMPONADE
ventricular dysfunction.)
 Also known as pericardial tamponade, is an emergency
3. Anorexia and general body malaise
condition in which fluid accumulates in the pericardium (the
4. PMI displaced laterally, cardiomegaly
sac in which the heart is enclosed).
5. S3 (ventricular gallop)
 If the fluid significantly elevates the pressure on the heart it
will prevent the heart's ventricles from filling properly. C. DIAGNOSTICS
 This in turn leads to a low stroke volume. 1. CXR – cardiomegaly
 The end result is ineffective pumping of blood, shock, and 2. PAP – pulmonary arterial pressure
often death.  Measures pressure in right ventricle
 Reveals cardiac status
A. PREDISPOSING FACTORS 3. PCWP – pulmonary capillary wedge pressure
1. Chest trauma ( blunt or penetrating )  Measures end-systolic and end-diastolic pressure
2. Myocardial ruptured (elevated)
3. Cancer  Done through cardiac catheterization (Swan-Ganz)
4. Pericarditis 4. Echocardiograph – reveals enlarged heart chamber
5. Cardiac surgery ( first 24 – 48 hours ) 5. ABG analysis reveals elevated PCO2 and decreased
6. Thrombolytic therapy PO2 (respiratory acidosis)  hypoxemia and cyanosis
B. SIGNS AND SYMPTOMS Tracheostomy  for severe respiratory distress and laryngospasm
1. Beck’s Triad  performed at bedside within 10-15 minutes
 Hypotension
 Jugular venous distension CVP  reveals fluid status; Normal = 4-10cm H2o; right atrium
 Muffled heart sound PAP – cardiac status; left atrium
2. Pulsus paradoxus ( drop of at least 10 mmHg in arterial ALLEN’S test – collateral circulation
BP on inspiration ) Cardiac Tamponade: pulsus paradoxus, muffled heart sounds, HPN
3. Tachycardia
4. Breathlessness
5. Decrease in LOC

C. NURSING INTERVENTIONS
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II. RIGHT SIDED HEART FAILURE 2. Administer O2 inhalation at 3-4 L/minute via NC as
ordered  high flow
A. PREDISPOSING FACTORS 3. High fowler’s, 2-3 Pillows
1. Tricuspid valve stenosis 4. Restrict Na and fluids
2. COPD 5. Monitor strictly VS and IO and Breath Sounds
3. Pulmonary embolism (char by chest pain and dyspnea) 6. Weigh pt daily and assess for pitting edema
4. Pulmonic stenosis 7. abdominal girth daily and notify MD
5. Left sided heart failure 8. provide meticulous skin care
9. provide a dietary intake which is low in saturated fats
B. SIGNS AND SYMPTOMS (Venous congestion) and caffeine
1. Jugular vein distention 10. Institute bloodless phlebotomy
2. Pitting edema  ROTATING TOURNIQUET
3. Ascites  Rotated clockwise every 15 minutes to
4. Weight gain promote a decrease in venous return
5. Hepatosplenomegaly 11. Health teaching and discharge planning
6. Jaundice  Prevent complications : Arrhythmia, Shock,
7. Pruritus/ urticaria Thrombophlebitis, MI, Cor pulmonale – RV
8. Esophageal varices hypertrophy
9. Anorexia  Regular adherence to medications
10. Generalized body malaise  Diet modifications
 Importance of ffup care
C. DIAGNOSTICS
1. CXR – cardiomegaly
2. CVP – measures pressure in right atrium; N = 4-10cc HYPERTENSION
H2O
 During CVP: trendelenburg  to prevent pulmo
embolism and to promote ventricular filling  Is an abnormal elevation of Bp, systolic pressure above 140
 Flat on bed post CVP, check CVP readings mmHg and or diastolic pressure above 90mmHg at least two
 Hypovolemia – fluid challenge readings
 Hypervolemia – diuretics (loop)  WHO: BP >160/95 mmHg
3. Echocardiography – reveals enlarged heart chamber
 AHA: BP >140/90 mmHg
 Muffled heart sounds  cardiomyopathy
 In hypertension, vasoconstriction – vasospasm – increases
 Cyanotic heart diseases
PVR – decrease blood flow to the organ.
 TOF  “tet” spells  cyanosis with
hypoxemia  Target Organs:
 Tricuspid valve stenosis  Heart : MI, CHF, Dysrhythmias
 Transposition of aorta  Eyes: blurred / impaired vision, retinopathy,
 Acyanotic cataract.
 PDA – machine-like murmur  Brain: CVA, encephalopathy
 DOC: indomethacin SE: corneal  Kidneys : renal insufficiency, RF
 Peripheral Bloods Vessels – aneurysm, gangrene
cloudiness
4. Liver enzymes
CLASSIFICATION OF BP FOR ADULTS 18 YRS AND OLDER
 SGPT up
(PHIL. SOCIETY OF HPN)
 SGOT up
 Optimal
D. NURSING MANAGEMENT
o <120 mmHg / <80 mmHg Recheck in
Goal: increase myocardial contraction  increase CO; Normal
CO is 3-6L/min; N stroke volume is 60-70ml/h2o 2 years.
 Normal
1. Administer medications as ordered o 120-129 mmHg / 80-84 mmHg Recheck in
 Cardiac glycosides 2 years.
 Digoxin (N=.5-1.5, tox=2)  High normal
 Tox: Anorexia, N&V; A: Digibind o 130-139 mmHg / 85-89 mmHg Recheck in
 Digitoxin – given if (+) ARF; metabolized in 1 year.
liver and not in kidneys  Stage 1 (mild) HPN
 Loop diuretics o 140-159 mmHg / 90-99 mmHg Confirm in
 Lasix – IV push, mornings 2 months.
 Bronchodilators  Stage 2 (moderate) HPN
 Aminophylline (theophylline) o 160-179 mmHg / 100-109 mmHg Evaluate
 Tachycardia, palpitations within a month.
 CNS hyperactivity, agitation  Stage 3 (severe) HPN
 Narcotic analgesics o 180-209 mmHg / 110-119mmHg Evaluate
 Morphine sulfate – induces vasodilation within a week.
 Vasodilators  Stage 4 (very severe) HPN
 NTG and ISDN o 210 mmHg / >/=120 mmHg Evaluate
 Anti-arrhythmic agents
 Lidocaine (SE: dizziness and confusion) A. CLASSIFICATION
 Bretyllium  Essential / Idiophatic / Primary HPN, accounts for
 YOU DON’T GIVE BETA-BLOCKERS TO THESE 90 – 95% of all cases of HPN, cause is unknown
PATIENTS
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 Secondary HPN, due to known causes ( Renal  Guanfacine

failure, Hypertension )  Methyldopa
 Malignant Hypertension, is severe, rapidly  Peripherally-acting sympatholytics
progressive elevation in BP that causes rapid onset of  Guanadrel
end organ complication  Guanethidine
 Labile HPN, intermittently elevated BP  Reserpine
 Resistant HPN, does not respond to usual treatment  a-blockers
 White Coat HPN, elevation of B only during clinic or  Doxazosin
hospital visits  Prazosin
 Hypertensive Crisis, situation that requires  b-blockers
immediate blood pressure lowering 240mmHg / 120  Acebutolol - Labetalol
mmHg  Atenolol - Metoprolol
 Betaxolol - Nadolol
B. RISK FACTORS  Bisoprolol - Penbutolol
1. Family history  Carteolol - Pindolol
2. Age  Carvedilol - Propranolol
3. High salt intake  Esmolol - Timolol
4. Low potassium intake
5. Obesity Vasodilators
6. Excess alcohol consumption  Direct vasodilators
7. Smoking  Diazoxide - Hydralazine
8. Stress  Minoxidil - Nitroprusside
 Fenoldopam
C. SIGNS AND SYMPTOMS  Calcium channel blockers
1. Headache  Amlodipine - Nifedipine
2. Epistaxis  Diltiazem - Nimodipine
3. Dizziness  Felodipine - Nisoldipine
4. Tinnitus  Isradipine - Nitrendipine
5. Unsteadiness  Manidipine - Nicardipine
6. Blurred vision  Lacidipine - Verapamil
7. Depression  Lercanidipine - Gallopamil
8. Nocturia
9. Retinopathy AGENTS THAT BLOCK THE PRODUCTION OR
ACTION OF ANGIOTENSIN
D. TREATMENT STRATEGIES  ACE inhibitors
 Benazepril - Moexipril
Non-pharmacologic therapy  Captopril - Quinapril
1. Low salt diet.  Enalapril - Perindopril
2. Weight reduction.  Fosinopril - Ramipril
3. Exercise.  Lisinopril - Trandolapril
4. Cessation of smoking.  AT1-receptor blockers
5. Decreased alcohol consumption.  Irbesartan - Losartan
6. Psychological methods: Relaxation / meditation.  Telmisartan - Valsartan
7. Dietary decrease in saturated fat.  Candesartan - Eprosartan
 Olmesartan
Drug therapy
Stepped Care DRUGS FOR HYPERTENSIVE EMERGENCIES OR CRISES
o Progressive addition of drugs to a regimen, starting
with one, usually a diuretic, and adding, in a  Trimethaphan
stepwise fashion, a sympatholytic, vasodilator, and o 1 mg/ml IV infusion; titrate;
sometimes an ACE inhibitor.
instantaneous onset
Monotherapy
 Sodium nitroprusside
o Advantageous because of its simplicity, better
o 5-10 mg/L IV infusion; titrate;
patient compliance, and relatively low incidence of
instantaneous onset
toxicity.
 Diazoxide
CATEGORIES OF o 300-600 mg Rapid IV push;
ANTI-HYPERTENSIVE DRUGS instantaneous onset
 Nifedipine
Drugs that alter sodium and water balance  Diuretics. o 10-20 mg Sublingual or chewed;
 Loop diuretics onset within 5-30 min.
 Thiazides  Labetalol
 Spironolactone and Triamterene o 20-80 mg IV at 10-minute intervals ([Link]:
300mg); immediate onset

Drugs that alter sympathetic nervous system function 

Sympatholytic drugs.
 Centrally-acting sympatholytics
 Clonidine
 Guanabenz
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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
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 Inform the client that absence of symptoms does

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

D. NURSING MANAGEMENT
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

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

B. SIGNS AND SYMPTOMS

1. Pain after prolonged standing
2. Dilated tortuous skin veins which are warm to touch
3. Heaviness in the legs