The cardiovascular system consists of the heart, arteries, veins &  SA nodal Branch – supplies SA node

capillaries. The major function are circulation of blood, delivery of  Right marginal Branch – supplies the right border of
O2 & other nutrients to the tissues of the body & removal of CO2 & the heart
other cellular products metabolism  AV nodal branch – supplies the AV node
Heart  Posterior interventricular artery – supplies both
 Muscular pumping organ that propel blood into the arterial ventricles
system & receive blood from the venous system of the body.  Left Coronary
 Hollow muscular behind the sternum and between the lungs  Circumflex branch – supplies SA node in 40 % of
 Located on the middle of mediastinum people
 Resemble like a close fist  Left marginal – supplies the left ventricle
 Weighs approximately 300 – 400 grams  Anterior interventricular branch aka Left anterior
 Has heart wall has 3 layers descending(LAD)–supplies both ventricles and
 Endocardium – lines the inner chambers of the heart, valves, interventricular septum
chordate tendinae and papillary muscles.  Lateral branch – terminates in ant surface of the
 Myocardium – muscular layer, middle layer, responsible for the heart
major pumping action of the ventricles.
 Epicardium – thin covering(mesothelium), covers the outer  Coronary Veins
surface of the heart  Coronary sinus – main vein of the heart
 Great Cardiac vein – main tributary of the coronary sinus
 Pericardium – invaginated sac  Oblique vein – remnant of SVC, small unsignificant
 Visceral – attached to the exterior of myocardium
 Parietal – attached to the great vessels and diaphragm Route of Blood flow Through the Heart
1. Superior & Inferior vena cava
 Papillary Muscle 2. Right Atrium (RA)
Arise from the endocardial & myocardial surface of the 3. Tricuspid Valve
ventricles & attach to the chordae tendinae 4. Right Ventricle
5. Pulmonary semilunar valve
 Chordae tendinae 6. Pulmonary trunk
Attach to the tricuspid & mitral valves & prevent eversion 7. Pulmonary arteries
during systole 8. Lung tissue (Pulmonary circulation)
9. Pulmonary veins
 Separated into 2 pumps: 10. Left Atrium
 right heart – pumps blood through the lungs 11. Bicuspid valve
 left heart – pumps blood through the peripheral organs 12. Left ventricle
13. Aortic semilunar valves
 Chamber of the Heart 14. Aorta
 Atria 15. Body tissues (systemic circulation)
 2 chambers, function as receiving chambers, lies above the
ventricles Properties of Heart Conduction System
 Upper Chamber (connecting or receiving) • Automaticity
 Right Atrium: receives systemic venous blood through the • Excitability
superior vena cava, inferior vena cava & coronary sinus • Conductivity
 Left Atrium: receives oxygenated blood returning to the • Contractility
heart from the lungs through the pulmonary veins
Structure of Heart Conduction System
 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  Nodal
into pulmonary circulation via the aorta during ventricular tissues
systole; Right atrium has decreased pressure which is 60 –  SA
80 mmHg Node( Sino-atrial, Keith and Flack)
 Left Ventricle: propels blood into the systemic circulation  Primary Pacemaker
via aorta during ventricular systole; Left ventricle has  Between SVC and RA
increased pressure which is 120 – 180 mmHg in order to  Vagal and sympatheticervation
propel blood to the systemic circulation  Sinus Rhythms

 Heart Valves  AV Node( Atrioventricular, Kent ,and Tawara)

 Tricuspid  At the right atrium
 Pulmonic  3 zones
 Mitral  AN Zone(atrionodal)
 Aortic  N Zone (nodal)
 NH zone (nodal –HIS)
 Coronary artery – 1st branch of aorta
 Right Coronary  Internodal and Interatrial Pathways
  Connects SA and AV Node
 Ant. Internodal(Bachman) tract
 Middle Internodal(Wenckebach) 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 the 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
 Capillaries
Frank-Starling Law of the Heart - critical factor for stroke volume  The following exchanges occurs in the capilliaries
is "degree of stretch of cardiac muscle cells";  O2 & CO2
more stretch = more contraction force  Solutes between the blood & tissue
 Fluid volume transfer between the plasma & interstitial space
increased EDV = more contraction force Venules
 slow heart rate = more time to fill  Small veins that receive blood from capillaries & function as
 exercise = more venous blood return collecting channels between the capillaries & veins
Veins
Regulation of Heart Rate (Autonomic, Chemical, Other)  Low-pressure vessels with thin small & less muscles than
1. Autonomic Regulation of Heart Rate (HR) arteries; most contains valves that prevent retrograde blood flow;
 Sympathetic - NOREPINEPHRINE (NE) increases heart rate they carry deoxygenated blood back to the heart. When the
(maintains stroke volume which leads to increased Cardiac skeletal surrounding veins contract, the veins are compressed,
Output) promoting movement of blood back to the heart.
 Parasympathetic - ACETYLCHOLINE (ACh) decreases
heart rate
 Vagal tone - parasympathetic inhibition of inherent rate of Assessment of the Client with Cardiovascular Disorders
SA node, allowing normal HR Nursing History
 Baroreceptors, press receptors - monitor changes in blood Risk Factors
pressure and allow reflex activity with the autonomic nervous A. Non – Modifiable Risk Factor
system  Age
 Gender
2. Hormonal and Chemical Regulation of Heart Rate (HR)  Race
 epinephrine - hormone released by adrenal medulla during  Heredity
stress; increases heart rate B. Modifiable Risk Factor
 thyroxine - hormone released by thyroid; increases heart  Stress
rate in large quantities; amplifies effect of epinephrine  Diet
 Ca++, K+, and Na+ levels very important;  Exercise
 Sedentary lifestyle
 hyperkalemia - increased K+ level; KCl used to stop heart
 Cigarette smoking
on lethal injection
 Alcohol
 hypokalemia - lower K+ levels; leads to abnormal heart
 Hypertension
rate rhythms
 Hyperlipidemia
 hypocalcemia - depresses heart function  DM
 hypercalcemia - increases contraction phase  Obesity
 hypernatremia - HIGH Na+ concentration; can block Na+  Type A personality
transport & muscle contraction  Contraceptive Pills

3. Other Factors Effecting Heart Rate (HR)

normal heart rate -fetus 140 - 160 beats/minute Common Clinical Manifestations of Cardiovascular Disorders
female 72 - 80 beats/minute a. Dyspnea
male 64 - 72 beats/minute - Exertional
- Orthopnea
1. exercise - lowers resting heart rate (40-60) - Paroxysmal Noctural Dyspnea
2. heat - increases heart rate significantly - Cheyne-stokes
3. cold - decreases heart rate significantly b. Chest Pain
4. tachycardia - HIGHER than normal resting heart rate (over 100); c. Edema
may lead to fibrillation - Ascites
5. bradycardia - LOWER than normal resting heart rate (below - Hydrothorax
60); parasympathetic drug side effects; physical conditioning; - Anasarca
sign of pathology in non-healthy patient d. Palpitation
e. Hemoptysis
f. Fatigue
Vascular System g. Syncope and Fainting
 Major function of the blood vessels isto supply the tissue h. Cyanosis
with blood, remove wastes, & carry unoxygenated blood i. Abdominal Pain
back to the heart j. Clubbing of fingers
k. Jaundice
Types of Blood Vessels
Arteries Physical Assessment
 Elastic-walled vessels that can stretch during systole & recoil Inspection:
during diastole; they carry blood away from the heart & distribute – Skin color
oxygenated blood throughout the body – Neck vein distention
Arterioles – Respirations
 Small arteries that distribute blood to the capillaries & function in – Pulsations
controlling systemic vascular resistance & therefore arterial – Clubbing
pressure – Capillary refill
Palpation:  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
Heart Sounds: Stethoscope Listening 4. To determine baseline value
Overview of Heart Sounds (lub-du ; lub, dub ) 5. To monitor serum level of medications
 lubb - closure of AV valves, onset of ventricular systole 6. To assess the effects of medications
 dubb - closure of semilunar valves, onset of diastole A. Blood Studies
1. Complete Blood Count
 Tricuspid valve (lub) - RT 5th intercostal, medial a. RBC count- # of RBCs/ mm3 of blood, to diagnose anemia and
 Mitral valve (lub) - LT 5th intercostal, lateral polycythemia
 Aortic semilunar valve (dub) - RT 2nd intercostal b. Hemoglobin- # of grams of hgb/ 100ml of blood; to measure the
 Pulmonary semilunar valve (dub) - LT 2nd intercostals oxygen-carrying capacity of the blood
c. Hematocrit – expressed in %; measures the volume of RBCs in
S1 - due to closure of the AV(mitral/tricuspid) valves proportion to plasma; used also to diagnose anemia and polycythemia
- timing: beginning of systole and abnormal hydration states
- loudest at the apex d. RBC indices- measure RBC size and hemoglobin content
a. MCV (mean corpuscular volume)
S2 - due to the closure of the semi-lunar (pulmonic/aortic) valves b. MCH (mean corpuscular hemoglobin)
- timing: diastole c. MCHC (mean corpuscular hemoglobin concentration)
- loudest at the base e. Platelet count- # of Platelet/ mm3; to diagnose thrombocytopenia
and subsequent bleeding tendencies
S3 – Ventricular Diastolic Gallop f. WBC count- of WBCs/ mm3 of blood; to detect infection or
Mechanism: vibration resulting from resistance to rapid inflammation
ventricular filling secondary to poor compliance g. WBC Differential count- determines proportion of each WBC in
Timing: early diastole a sample of 100 WBCs; used to classify leukemias
Location: Apex (LV) or LLSB (RV)
Pitch: faint and low pitched Normal Values
RBC: Women – 4.2-5.4 million/mm3
S4 - Atrial Diastolic Gallop Men – 4.7-6.1 million/mm3
Mechanism: vibration resulting from resistance to late Hgb: Women – 12-16 g/dl
ventricular filling during atrial systole Men – 13-18 g/dl
Timing: late diastole ( before S1) Hct : Women – 36-42%
Location: Apex ( LV) or LLSB (RV) Men – 42-48%
Pitch: low ( use bell) WBC: 5000-10,000/mm3
Granulocytes
Heart Murmurs Neutrophils: 55-70%
Murmur - sounds other than the typical "lub-dub"; typically caused Eosinophils: 1-4%
by disruptions in flow Basophils: 0.5-1.0%
Agranulocytes
 Incompetent valve - swishing sound just AFTER the normal Lymphocytes: 20-40%
"lub" or "dub"; valve does not completely close, some Monocytes: 2-8%
regurgitation of blood Platelets: 150,000-450,000/mm3
 Stenotic valve - high pitched swishing sound when blood should
be flowing through valve; narrowing of outlet in the open state 2. Coagulation Screening Test
a. Bleeding Time – measures the ability to stop bleeding after small
Pericardial Friction Rub puncture wound
 It is an extra heart sound originating from the pericardial sac b. Partial Thromboplastin Time (PTT) – used to identify
 Mechanism: Originates from the pericardial sac as it moves deficiencies of coagulation factors, prothrombin and fibrinogen;
 Timing: with each heartbeat monitors heparin therapy.
 Location: over pericardium. Upright position, leaning forward c. Prothrombin Time (Pro-time) – determines activity and
 Pitch: high pitched and scratchy. Sounds like sandpaper being interaction of the Prothrombin group: factors V (preacclerin), VII
rubbed together (proconvertin), X (Stuart-Power factor), prothrombin and fibrinogen;
 Significance: inflammation, infection, infiltration used to determine dosages of oral anti-coagulant.
Classification of Clients with Diseases of the Heart
( Functional Capacity ) Normal Values
 Class I. Patients with cardiac disease but without resulting Bleeding Time: 2.75-8 min
limitations of physical activity. Partial Thromboplastin Time (PTT): 60 - 70 sec.
 Class II. Patients with cardiac disease resulting to slight Prothrombin Time (PT): 12-14 sec.
limitation of physical activity
3. Erythrocyte sedimentation rate ( ESR)
  It is a measurement of the rate at which RBC’s settle out of 2. QRS complex - next series of deflections, demonstrates the
anticoagulated blood in an hour depolarization of AV node through both ventricles; the ventricles
 It is elevated in infectious heart disorder or myocardial contract throughout the period of the QRS complex, with a short
infarction delay after the end of atrial contraction; repolarization of atria also
obscured
Normal Values 3. T Wave - repolarization of the ventricles (0.16 s)
Male: 15-20 mm/hr 4. PR (PQ) Interval - time period from beginning of atrial
Female: 20-30 mm/hr contraction to beginning of ventricular contraction (0.16 s)
5. QT Interval - the time of ventricular contraction (about 0.36 s);
4. CARDIAC Proteins and enzymes from beginning of ventricular depolarization to end of repolarization.
a. CK- MB ( creatine kinase)
 Most cardiac specific enzymes 2. Holter Monitoring
 Accurate indicator of myocardial dammage  A non-invasive test in which the client wears a Holter monitor and
 Elevates in MI within 4 hours, peaks in 18 hours and an ECG tracing recorded continuously over a period of 24 hours
then declines till 3 days  Instruct the client to resume normal activities and maintain a diary
 Normal value is 0-7 U/L or males 50-325 mu/ml of activities and any symptoms that may develop
Female 50-250 mu/ml
3. Stress Test
b. Lactic Dehydrogenase (LDH)  A non-invasive test that studies the heart during activity and
 Most sensitive indicator of myocardial damage detects and evaluates CAD
 Elevates in MI in 24 hours, peaks in 48-72 hours  Exercise test, pharmacologic test and emotional test
Return to normal in 10-14 days  Treadmill testing is the most commonly used stress test
 Normally LDH1 is greater than LDH2  Used to determine CAD, Chest pain causes, drug effects and
 Lactic Dehydrogenase (LDH) dysrhythmias in exercise
 MI- LDH2 greater than LDH1 (flipped LDH pattern)  Pre-test: consent may be required, adequate rest , eat a light
 Normal value is 70-200 IU/L (100 – 225 mu/ml) 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
c. Myoglobin exercise as instructed and report any pain, weakness and SOB,
 Rises within 1-3 hours monitor BP and ECG continuously, record at frequent interval
 Peaks in 4-12 hours  Post-test: instruct client to notify the physician if any chest
 Returns to normal in a day pain, dizziness or shortness of breath . Instruct client to avoid
 Not used alone taking a hot shower for 10-12 hours after the test
 Muscular and RENAL disease can have elevated myoglobin
4. Pharmacological stress test
 Use of dipyridamole
d. Troponin I and T
 Maximally dilates coronary artery
 Troponin I is usually utilized for MI
 Side-effect: flushing of face
 Elevates within 3-4 hours, peaks in 4-24 hours and persists
 Pre-test: 4 hours fasting, avoid alcohol, caffeine
for 7 days to 3 weeks!
 Post test: report symptoms of chest pain
 Normal value for Troponin I is less than 0.6 ng/mL
 REMEMBER to AVOID IM injections before obtaining 5. ECHOCARDIOGRAM
blood sample!  Non-invasive test that studies the structural and functional
 Early and late diagnosis can be made! changes of the heart with the use of ultrasound
 Client Preparation: instruct client to remain still during the test,
e. SERUM LIPIDS secure electrodes for simultaneous ECG tracing, explain that
 Lipid profile measures the serum cholesterol, triglycerides there will be no pain or electrical shock, lubricant placed on the
and lipoprotein levels skin will be cool.
 Cholesterol= 200 mg/dL
 Triglycerides- 40- 150 mg/dL 6. Phonocardiography
 LDH- 130 mg/dL  Is a graphic recording of heart sound with simultaneous
 HDL- 30-70- mg/dL ECG.
 NPO post midnight (usually 12 hours)
C. Invasive Procedure
B. Non-Invasive Procedure 1. Cardiac Catheterization ( Coronary Angiography /
1. Cardiac Monitoring / Electrocardiography (ECG) Arteriography )
A non-invasive procedure that evaluates the electrical activity of the  Insertion of a catheter into the heart and surrounding vessels
heart  Is an invasive procedure during which physician injects dye into
a. Limb Leads coronary arteries and immediately takes a series of x-ray films to
b. Precordial Leads assess the structures of the arteries
The precordial leads VI –V6 are part of the 12 lead EKG. They are  Determines the structure and performance of the heart valves
not monitored with the standard limb leads and surrounding vessels
c. 12 lead EC  Used to diagnose CAD, assess coronary atery patency and
determine extent of atherosclerosis
Deflection Waves of ECG  Pretest: Ensure Consent, assess for allergy to seafood and
1. P wave - initial wave, demonstrates the depolarization from SA iodine, NPO, document weight and height, baseline VS, blood
Node through both ATRIA; the ATRIA contract about 0.1 s after tests and document the peripheral pulses
start of P Wave.  Pretest: Fasting for 8-12 hours, teachings, medications to allay
anxiety
 Intra-test: inform patient of a fluttery feeling as the catheter  Appropriate for critically ill clients requiring more accurate
passes through the heart; inform the patient that a feeling of assessments of the left heart pressure
warmth and metallic taste may occur when dye is administered  Swan-Ganz Catheter / Pulmonary Artery Catheter is use
 Post-test: Monitor VS and cardiac rhythm  Client Preparation: obtain consent, insertion is under strict
 Monitor peripheral pulses, color and warmth and sensation of sterile technique, usually at the bedside, explain to client the
the extremity distal to insertion site sterile drapes may cover the face, assists to position client flat or
 Maintain sandbag to the insertion site if required to maintain slight T-position as tolerated and instruct to remain still during
pressure the procedure
 Monitor for bleeding and hematoma formation  Nursing Care During Insertion: Monitor and document HR,BP
and ECG during the procedure
2. Nuclear Cardiology
 Are safe methods of evaluating left ventricular muscle CARDIAC DISORDER
function and coronary artery blood distribution. CORONARY ARTERIAL DISEASE
 Client Preparation: obtain written consent, explain
ISCHEMIC HEART DISEASE
procedure, instruct client that fasting may be required for a
short period before the exam, assess for iodine allergy. Results from the focal narrowing of the large and medium-sized
 Post Procedure: encourage client to drink fluids to facilitate coronary arteries due to deposition of atheromatous plaque in the
the excretion of contrast material, assess venipuncture site vessel wall
for bleeding or hematoma. Stages of Development of Coronary Artery Disease
 Types of Nuclear Cardiology 1. Myocardial Injury: Atherosclerosis
o Multigated acquisition (MUGA) or cardiac blood pool scan 2. Myocardial Ischemia: Angina Pectoris
 Provides information on wall motion during systole and 3. Myocardial Necrosis: Myocardial Infarction
diastole, cardiac valves, and EF. I. ATHEROSCLEROSIS
o Single-photon emission computed tomography (SPECT) ATHEROSCLEROSIS ARTERIOSCLEROSIS
 Used to evaluate the myocardium at risk of infarction and to
determine infarction size.  Narrowing of artery  Hardening of artery
o Positron emission tomography (PET) scanning  Lipid or fat deposits  Calcium and protein
 Uses two isotopes to distinguish viable and nonviable  Tunica intima deposits
myocardial tissue.  Tunica media
o Perfusion imaging with exercise testing A. PREDISPOSING FACTORS
 Determines whether the coronary blood flow changes with 1. Sex: male
increased activity. 2. Race: black
 Used to diagnose CAD, determine the prognosis in already 3. Smoking
diagnosed CAD, assess the physiologic significance of a 4. Obesity
known coronary lesion, and assess the effectiveness of various 5. Hyperlipidemia
therapeutic modalities such as coronary artery bypass surgery, 6. Sedentary lifestyle
percutaneous coronary intervention, or thrombolytic therapy. 7. Diabetes Mellitus
8. Hypothyroidism
D. Hemodynamics Monitoring 9. Diet: increased saturated fats
1. CVP ( Central Venous Pressure ) 10. Type A personality
 Reflects the pressure of the blood in the right atrium.
 Engorgement is estimated by the venous column that can be B. SIGNS AND SYMPTOMS
observed as it rises from an imagined angle at th point of 1. Chest pain
manubrium ( angle of Louis). 2. Dyspnea
 With normal physiologic condition, the jugular venous column 3. Tachycardia
rises no higher than 2-3 cm above the clavicle with the client in a 4. Palpitations
sitting position at 45 degree angle. 5. Diaphoresis
 CVP is a measurement of:
- cardiac efficiency C. TREATMENT
- blood volume Percutaneous Transluminal Coronary Angioplasty and
- peripheral resistance Intravascular Stenting
 Right ventricular pressure – a catheter is passed from a  Mechanical dilation of the coronary vessel wall by
cutdown in the antecubital, subclavian jugular or basilica vein to compressing the atheromatous plaque.
the right atrium and attached to a prescribed manometer or  It is recommended for clients with single-vessel coronary
transducer. artery disease.
 NORMAL CVP is 2 -8 cm h20 or 2-6 mm Hg  Prosthetic intravascular cylindric stent maintain good
 Decrease indicates dec. circulating volume, increase indicates inc. luminal geometry after balloon deflation and withdrawal.
blood volume or right heart beat failure.  Intravascular stenting is done to prevent restenosis after
 To Measure: patient should be flat with zero point of manometer PTCA
at the same level of the RA which corresponds to the mid-axillary
line of the patient or approx. 5 cm below the sternum. Coronary Arterial Bypass Graft Surgery
 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

 Greater and lesser saphenous veins are commonly used for 4. Excessive intake of foods or heavy meal
bypass graft procedures
Objectives of CABG C. SIGNS AND SYMPTOMS
1. Revascularize myocardium 1. Levine’s Sign: initial sign that shows the hand
2. To prevent angina clutching the chest
3. Increase survival rate 2. Chest pain: characterized by sharp stabbing pain
4. Done to single occluded vessels located at sub sterna usually radiates from neck, back,
5. If there is 2 or more occluded blood vessels CABG is done arms, shoulder and jaw muscles usually relieved by
Nursing Management: rest or taking nitroglycerine(NTG)
 Nitroglycerine is the drug of choice for relief of pain from 3. Dyspnea
acute ischemic attacks 4. Tachycardia
 Instruct to avoid over fatigue 5. Palpitations
 Plan regular activity program 6. Diaphoresis
For Saphenous Vein Site:
 Wear support stocking 4-6 week postop D. DIAGNOSTIC PROCEDURE
 Apply pressure dressing or sand bag on the site 1. History taking and physical exam
 Keep leg elevated when sitting 2. ECG: may reveals ST segment depression & T wave
inversion during chest pain
3 Complications of CABG 3. Stress test / treadmill test: reveal abnormal ECG
1. Pneumonia: encourage to perform deep breathing, coughing during exercise
exercise and use of incentive spirometer 4. Increase serum lipid levels
2. Shock 5. Serum cholesterol & uric acid is increased
3. Thrombophlebitis
E. MEDICAL MANAGEMENT
II. ANGINA PECTORIS 1. Drug Therapy: if cholesterol is elevated
 Transient paroxysmal chest pain produced by insufficient blood  Nitrates: Nitroglycerine (NTG)
flow to the myocardium resulting to myocardial ischemia  Beta-adrenergic blocking agent: Propanolol
 Clinical syndrome characterized by paroxysmal chest pain that is  Calcium-blocking agent: nefedipine
usually relieved by rest or nitroglycerine due to temporary  Ace Inhibitor: Enapril
myocardial ischemia 2. Modification of diet & other risk factors
3. Surgery: Coronary artery bypass surgery
Types of Angina Pectoris 4. Percutaneous Transluminal Coronary Angioplasty (PTCA)
 Stable Angina: pain less than 15 minutes, recurrence is less
frequent. F. NURSING INTERVENTIONS
 Unstable Angina: pain is more than 15 mins., but not less than 30 1. Enforce complete bed rest
minutes, recurrence is more frequent and the intensity of pain 2. Give prompt pain relievers with nitrates or narcotic
increases. Not relieved w/ rest or nitroglycerin analgesic as ordered
 Intractable or Refractory Angina: there’s a severe incapacitating 3. Administer medications as ordered:
chest pain
 Variant Angina ( Prinzmetal’s Angina ): Chest pain is on longer A. Nitroglycerine(NTG): when given in small doses will act as
duration and may occur at rest. Result from coronary vasospasm. venodilator, but in large doses will act as vasodilator
 Angina Decubitus: paroxysmal chest pain that occur when the  Give 1st dose of NTG: sublingual 3-5 minutes
client sits or stand.  Give 2nd dose of NTG: if pain persist after giving 1st dose with
interval of 3-5 minutes
A. PREDISPOSING FACTORS  Give 3rd& last dose of NTG: if pain still persist at 3-5 minutes
1. Sex: male interval
2. Race: black
3. Smoking NTG Tablets(sublingual)
4. Obesity  Offer sips of water before giving sublingual nitrates, dryness
5. Hyperlipidemia of mouth may inhibit drug absorption
6. Sedentary lifestyle  Relax for 15 minutes after taking a tablet: to prevent dizziness
7. Diabetes Mellitus  Monitor side effects: orthostatic hypotension, flushed face.
8. Hypertension Transient headache & dizziness: frequent side effect
9. CAD: Atherosclerosis  Instruct the client to rise slowly from sitting position
10. Thromboangiitis Obliterans  Assist or supervise in ambulation
11. Severe Anemia
12. Aortic Insufficiency: heart valve fails to open & close efficiently NTG Nitrol or Transdermal patch
13. Hypothyroidism  Nitropatch is applied once a day, usually in the morning.
14. Diet: increased saturated fats  Avoid placing near hairy areas as it may decrease drug
15. Type A personality absorption
 Avoid rotating transdermal patches as it may decrease drug
B. PRESIPITATING FACTORS absorption
4 E’s of Angina Pectoris  Avoid placing near microwave ovens or during defibrillation
1. Excessive physical exertion: heavy exercises, sexual as it may lead to burns (most important thing to remember)
activity
2. Exposure to cold environment: vasoconstriction B. Beta-blockers: decreases myocardial oxygen demand by
3. Extreme emotional response: fear, anxiety, decreasing heart rate, cardiac output and BP
excitement, strong emotions, stress  Propranolol
  Metropolol 7. Genetic Predisposition
 Pindolol 8. Hyperlipidemia
 Atenolol 9. Sedentary lifestyle
 Assess PR, withhold if dec.PR 10. Diabetes Mellitus
 Administer with food ( prevent GI upset ) 11. Hypothyroidism
 Propranolol: not given to COPD cases: it causes 12. Diet: increased saturated fats
bronchospasm and DM cases: it cause hypoglycemia 13. Type A personality
 Side Effects: Nausea and vomiting, mental depression and
fatigue B. SIGNS AND SYMPTOMS
1. Chest pain
C. Calcium – Channel Blockers: relaxes smooth cardiac  Excruciating visceral, viselike pain with sudden onset
muscle, reduces coronary vasospasm located at substernal& rarely in precordial
 Amlodipine ( norvasc )  Usually radiates from neck, back, shoulder, arms, jaw &
 Nifedipine ( calcibloc ) abdominal muscles (abdominal ischemia): severe crushing
 Diltiazem ( cardizem )  Not usually relieved by rest or by nitroglycerine
 Assess HR and BP 2. N/V
 Administer 1 hour before meal and 2 hours after meal ( foods 3. Dyspnea
delay absorption ) 4. Increase in blood pressure & pulse, with gradual drop in
blood pressure (initial sign)
4. Administer oxygen inhalation 5. Hyperthermia: elevated temp
5. Place client on semi-to high fowlers position 6. Skin: cool, clammy, ashen
6. Monitor strictly V/S, I&O, status of cardiopulmonary fuction & 7. Mild restlessness & apprehension
ECG tracing 8. Occasional findings:
7. Provide decrease saturated fats sodium and caffeine  Pericardial friction rub
8. Provide client health teachings and discharge planning  Split S1& S2
 Avoidance of 4 E’s  Rales or Crackles upon auscultation
 Prevent complication (myocardial infarction)  S4 or atrial gallop
 Instruct client to take medication before indulging into physical
exertion to achieve the maximum therapeutic effect of drug C. DIAGNOSTIC PROCEDURED
 Reduce stress & anxiety: relaxation techniques & guided imagery 1. Cardiac Enzymes
 Avoid overexertion & smoking  CPK-MB: elevated
 Avoid extremes of temperature  Creatinine phosphokinase(CPK):elevated
 Dress warmly in cold weather  Heart only, 12 – 24 hours
 Participate in regular exercise program  Lactic acid dehydrogenase(LDH): is increased
 Space exercise periods & allow for rest periods  Serum glutamic pyruvate transaminase(SGPT): is
 The importance of follow up care increased
 Serum glutamic oxal-acetic
9. Instruct the client to notify the physician immediately if pain
transaminase(SGOT): is increased
occurs & persists despite rest & medication administration
2. Troponin Test: is increased
3. ECG tracing reveals
III. MYOCARDIAL INFARCTION  ST segment elevation
 Death of myocardial cells from inadequate oxygenation, often  T wave inversion
caused by sudden complete blockage of a coronary artery  Widening of QRS complexes: indicates that there
 Characterized by localized formation of necrosis (tissue is arrhythmia in MI
destruction) with subsequent healing by scar formation & fibrosis 4. Serum Cholesterol & uric acid: are both increased
 Heart attack 5. CBC: increased WBC
 Terminal stage of coronary artery disease characterized by
malocclusion, necrosis & scarring. D. NURSING INTERVENTIONS
Goal: Decrease myocardial oxygen demand
Types of M.I 1. Decrease myocardial workload (rest heart)
 Transmural Myocardial Infarction: most dangerous type  Establish a patent IV line
characterized by occlusion of both right and left coronary artery  Administer narcotic analgesic as ordered: Morphine
 Subendocardial Myocardial Infarction: characterized by Sulfate IV: provide pain relief(given IV because after
occlusion of either right or left coronary artery an infarction there is poor peripheral perfusion &
because serum enzyme would be affected by IM
The Most Critical Period Following Diagnosis of Myocardial injection as ordered)
Infarction  Side Effects: Respiratory Depression
 6-8 hours because majority of death occurs due to arrhythmia  Antidote: Naloxone (Narcan)
leading to premature ventricular contractions (PVC)
 Side Effects of Naloxone Toxicity: is tremors
2. Administer oxygen low flow 2-3 L / min: to prevent
A. PREDISPOSING FACTORS
respiratory arrest or dyspnea & prevent arrhythmias
1. Sex: male
3. Enforce CBR in semi-fowlers position without bathroom
2. Race: black
privileges(use bedside commode): to decrease cardiac
3. Smoking
workload
4. Obesity
4. Instruct client to avoid forms of Valsalva maneuver
5. CAD: Atherosclerotic
5. Place client on semi fowlers position
6. Thrombus Formation
 6. Monitor strictly V/S, I&O, ECG tracing & hemodynamic  Dyspnea
procedures  Weakness
7. Perform complete lung / cardiovascular assessment  Fatigue
8. Monitor urinary output & report output of less than 30 ml /  Persistent palpitation
hr: indicates decrease cardiac output  Light headedness
9. Provide a full liquid diet with gradual increase to soft diet: j. Enrollment of client in a cardiac rehabilitation program
low in saturated fats, Na & caffeine k. Strict compliance to mediation & importance of follow up care
10. Maintain quiet environment
11. Administer stool softeners as ordered to facilitate bowel IV. CARDIOGENIC SHOCK ( POWER/PUMP FAILURE )
evacuation & prevent straining  Is a shock state which result from profound left ventricular
12. Relieve anxiety associated with coronary care failure usually from massive MI.
unit(CCU)environment
 It result to low cardiac output, thereby systemic hypoperfusion.
13. Administer medication as ordered:
a. Vasodilators: Nitroglycerine TG), Isosorbide Dinitrate,
A. SIGNS AND SYMPTOMS
Isodil (ISD): sublingual
1. Decrease systolic BP
b. Anti Arrhythmicents: Lidocaine (Xylocane), Brithylium
2. Oliguria
 Side Effects: confusion and dizziness 3. Cold, clammy skin
c. Beta-blockers: Propanolol (Inderal) 4. Weak pulse
d. ACE Inhibitors: Captopril (Enalapril) 5. Cyanosis
e. Calcium Antagonist: Nefedipine 6. Mental lethargy
f. Thrombolytics / Fibrinolytic Agents: Streptokinase, 7. Confusion
Urokinase, Tissue Plasminogen Activating Factor
(TIPAF) B. MEDICAL MANAGEMENT
 Side Effects: allergic reaction, urticaria, pruritus 1. Counter pulsation ( mechanical cardiac assistance / diastolic
 Nursing Intervention: Monitor for bleeding time augmentation )
g. Anti-Coagulant  Involves introduction of the intra – aortic balloon catheter via
 Heparin the femoral artery
 Antidote: Protamine Sulfate  Intra-Aortic Balloon Pump augments diastole, resulting in
 Nursing Intervention: Check for Partial Thrombin Time increased perfusion of the coronary arteries and the
(PTT) myocardium and a decrease in left ventricular workload.
 Coumadin (Warfarin)  The balloon is inflated during diastole, it is deflated during
 Antidote: Vitamin K systole.
 Nursing Intervention: Check for Prothrombin Time (PT)  Indications:
h. Anti-Platelet: PASA (Aspirin): Anti thrombotic effect  Cardiogenic shock
 Side Effects: Tinnitus, Heartburn, Indigestion / Dyspepsia  AMI
 Contraindication: Dengue, Peptic Ulcer Disease, Unknown  Unstable Angina
cause of headache  Open heart surgery

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
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 CONGESTIVE HEART FAILURE
inflammatory thickening of the pericardium compresses the heart
so that it is unable to fill normally during diastole. Inability of the heart to pump blood towards systemic circulation to
meet the needs of the tissues for oxygen and nutrients

A. SIGNS AND SYMPTOMS I. LEFT-SIDED HEART FAILURE

1. Pain in the anterior chest, aggravated by coughing, yawning, A. PREDISPOSING FACTORS
swallowing, twisting and turning the torso, relieved by upright, 1. 90% - Mitral valve stenosis
leaning forward position.  RHD
2. Pericardial friction rub – scratchy, grating or cracking sound  Inflammation of mitral valve
3. Dyspnea  Anti-streptolysin O titer (ASO) – 300 todd units
4. Fever, sweating, chills  Penicillin, PASA, steroids
5. Joints pains  Aging
6. Arrhythmias 2. MI
3. IHD
B. NURSING INTERVENTIONS 4. HPN
1. Elevate head of bed, place pillow on the overbed table so that the 5. Aortic valve stenosis
patient can lean on it.
2. Bed rest B. SIGNS AND SYMPTOMS
3. Administer prescribed pharmacotherapy. 1. Pulmonary edema/congestion
a. ASA to suppress inflammatory process  Dyspnea, PND (awakening at night d/t difficulty in
b. Corticosteroids for more severe symptoms breathing), 2-3 pillow orthopnea
4. Assist in pericardiocentesis if cardiac tamponade is present.  Productive cough (blood tinged)
5. Pericardiocentesis is aspiration of blood or fluid from pericardial  Rales/crackles
sac.  Bronchial wheezing
 Frothy salivation
VI. CARDIAC TAMPONADE 2. Pulsus alternans (A unique pattern during which the
Also known as pericardial tamponade, is an emergency condition in amplitude of the pulse changes or alternates in size
which fluid accumulates in the pericardium (the sac in which the with a stable heart rhythm.)This is common in severe
heart is enclosed). left ventricular dysfunction.)
If the fluid significantly elevates the pressure on the heart it will 3. Anorexia and general body malaise
prevent the heart's ventricles from filling properly. 4. PMI displaced laterally, cardiomegaly
This in turn leads to a low stroke volume. 5. S3 (ventricular gallop)
The end result is ineffective pumping of blood, shock, and often
death. C. DIAGNOSTICS
1. CXR – cardiomegaly
A. PREDISPOSING FACTORS 2. PAP – pulmonary arterial pressure
1. Chest trauma ( blunt or penetrating )  Measures pressure in right ventricle
2. Myocardial ruptured  Reveals cardiac status
3. Cancer 3. PCWP – pulmonary capillary wedge pressure
4. Pericarditis  Measures end-systolic and end-diastolic pressure (elevated)
5. Cardiac surgery ( first 24 – 48 hours )  Done through cardiac catheterization (Swan-Ganz)
6. Thrombolytic therapy 4. Echocardiograph – reveals enlarged heart chamber
5. ABG analysis reveals elevated PCO2 and decreased PO2
B. SIGNS AND SYMPTOMS (respiratory acidosis)  hypoxemia and cyanosis
1. Beck’s Triad Tracheostomy  for severe respiratory distress and laryngospasm 
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 BP on ALLEN’S test – collateral circulation
inspiration ) Cardiac Tamponade: pulsus paradoxus, muffled heart sounds, HPN
3. Tachycardia
4. Breathlessness II. RIGHT SIDED HEART FAILURE
5. Decrease in LOC A. PREDISPOSING FACTORS
1. Tricuspid valve stenosis
C. NURSING INTERVENTIONS 2. COPD
1. Administer oxygen 3. Pulmonary embolism (char by chest pain and dyspnea)
2. Elevate head of the bed, place pillow on the overbed table so that 4. Pulmonic stenosis
the patient can lean on it. 5. Left sided heart failure
3. Bed rest
4. Administer prescribed pharmacotherapy. B. SIGNS AND SYMPTOMS (Venous congestion)
c. ASA to suppress inflammatory process 1. Jugular vein distention
d. Corticosteroids ore severe symptoms 2. Pitting edema
5. Assist in pericardiocentesis and thoracotomy 3. Ascites
6. Pericardiocentesis is aspiration of blood or fluid from pericardial 4. Weight gain
sac. 5. Hepatosplenomegaly
6. Jaundice
7. Pruritus/ urticaria
 8. Esophageal varices  Prevent complications : Arrhythmia, Shock,
9. Anorexia Thrombophlebitis, MI, Cor pulmonale – RV
10. Generalized body malaise hypertrophy
 Regular adherence to medications
 Diet modifications
C. DIAGNOSTICS  Importance of ffup care
1. CXR – cardiomegaly
2. CVP – measures pressure in right atrium; N = 4-10cc H2O
 During CVP: trendelenburg  to prevent pulmo HYPERTENSION
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
 Hypovolemia – fluid challenge two 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, cataract.
 Acyanotic  Brain: CVA, encephalopathy
 PDA – machine-like murmur  Kidneys : renal insufficiency, RF
 DOC: indomethacin SE: corneal cloudiness  Peripheral Bloods Vessels – aneurysm, gangrene
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 A. CLASSIFICATION
 Aminophylline (theophylline)  Essential / Idiophatic / Primary HPN, accounts for 90 –
 Tachycardia, palpitations 95% of all cases of HPN, cause is unknown
 CNS hyperactivity, agitation  Secondary HPN, due to known causes ( Renal failure,
 Narcotic analgesics Hypertension )
 Morphine sulfate – induces vasodilation  Malignant Hypertension, is severe, rapidly progressive
 Vasodilators elevation in BP that causes rapid onset of end organ
 NTG and ISDN complication
 Anti-arrhythmic agents  Labile HPN, intermittently elevated BP
 Lidocaine (SE: dizziness and  Resistant HPN, does not respond to usual treatment
confusion)  White Coat HPN, elevation of B only during clinic or
 Bretyllium hospital visits
 YOU DON’T GIVE BETA-BLOCKERS TO  Hypertensive Crisis, situation that requires immediate
THESE PATIENTS blood pressure lowering 240mmHg / 120 mmHg
2. Administer O2 inhalation at 3-4 L/minute via NC as
ordered  high flow B. RISK FACTORS
3. High fowler’s, 2-3 Pillows 1. Family history
4. Restrict Na and fluids 2. Age
5. Monitor strictly VS and IO and Breath Sounds 3. High salt intake
6. Weigh pt daily and assess for pitting edema 4. Low potassium intake
7. abdominal girth daily and notify MD 5. Obesity
8. provide meticulous skin care 6. Excess alcohol consumption
9. provide a dietary intake which is low in saturated fats 7. Smoking
and caffeine 8. Stress
10. Institute bloodless phlebotomy
 ROTATING TOURNIQUET C. SIGNS AND SYMPTOMS
 Rotated clockwise every 15 minutes to 1. Headache
promote a decrease in venous return 2. Epistaxis
11. Health teaching and discharge planning 3. Dizziness
4. Tinnitus
5. Unsteadiness
 6. Blurred vision  Bisoprolol - Penbutolol
7. Depression  Carteolol - Pindolol
8. Nocturia  Carvedilol - Propranolol
9. Retinopathy  Esmolol - Timolol

Vasodilator
 Direct vasodilators
D. TREATMENT STRATEGIES  Diazoxide - Hydralazine
Non-pharmacologic therapy  Minoxidil - Nitroprusside
1. Low salt diet.  Fenoldopam
2. Weight reduction.  Calcium channel blockers
3. Exercise.  Amlodipine - Nifedipine
4. Cessation of smoking.  Diltiazem - Nimodipine
5. Decreased alcohol consumption.  Felodipine - Nisoldipine
6. Psychological methods: Relaxation/meditation.  Isradipine - Nitrendipine
7. Dietary decrease in saturated fat.  Manidipine - Nicardipine
Drug therapy  Lacidipine - Verapamil
Stepped Care  Lercanidipine - Gallopamil
o Progressive addition of drugs to a regimen, starting with one,
usually a diuretic, and adding, in a stepwise fashion, a AGENTS THAT BLOCK THE PRODUCTION OR
sympatholytic, vasodilator, and sometimes an ACE inhibitor. ACTION OF ANGIOTENSIN
Monotherapy  ACE inhibitors
o Advantageous because of its simplicity, better patient  Benazepril - Moexipril
compliance, and relatively low incidence of toxicity.  Captopril - Quinapril
 Enalapril - Perindopril
CATEGORIES OF ANTI-HYPERTENSIVE DRUGS  Fosinopril - Ramipril
 Lisinopril - Trandolapril
Drugs that alter sodium and water balance à Diuretics.  AT1-receptor blockers
 Loop diuretics  Irbesartan - Losartan
 Thiazides  Telmisartan - Valsartan
 Spironolactone and Triamterene  Candesartan - Eprosartan
 Olmesartan
Drugs that alter sympathetic nervous system function à
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

Sympatholytic drugs.
 Centrally-acting sympatholytics
 Clonidine
 Guanabenz
 Guanfacine
 Methyldopa
 Peripherally-acting sympatholytic
 Guanadrel
 Guanethidine
 Reserpine
 a-blockers
 Doxazosin
 Prazosin
 b-blockers
 Acebutolol - Labetalol
 Atenolol - Metoprolol
 Betaxolol - Nadolol
  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

PERIPHERAL ARTERY DISEASE
- Involve thickening of artery wall, which results progressive
narrowing of arteries of upper/lower extremities
- This can lead to ischemia (reduction blood flow of tissues)
- “Severe peripheral arterial occlusive disease” – can lead to skin
ulceration & gangrene
-
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
PRINCIPLES OF DRUG THERAPY  Fusiform Aneurysm , involves outpouching of the both side
 Monotherapy is generally reserved for mild to moderate HPN; it of the artery
has gained popularity because of its simplicity, fewer side effects,  Saccular Aneurysm , outpouching of only one side of the
and improved patient compliance. artery.
 More severe HPN may require treatment with several drugs that  Dissecting Aneurysm, involves separation or tear in the
are selected to minimize adverse effects of combined regimen. tunica intima and tunica media
 Treatment is initiated with any of 4 drugs depending on individual B. RISK FACTOR
patient: Diuretic, b-blocker, ACEI, and a Ca-channel blocker; if 1. Age
BP is inadequately controlled, a 2nd-drug is then added. 2. Tobacco use
 HPN may co-exist with other disease that may be aggravated by 3. HPN
some of the anti-HPN agents. 4. Atherosclerosis
 Lack of patient compliance is the most common reason for failure 5. Race
of anti-HPN therapy; it is important to enhance compliance by 6. Gender
carefully selecting a drug regimen that minimizes adverse effects. 7. Family history
 Therapy is directed at preventing disease that may occur in the C. SIGNS AND SYMPTOMS
future, rather than in relieving present discomfort of the patient. 1. Pulsating mass over abdomen (AAA)
2. Presence of the bruit sound
E. NURSING INTERVNTIONS 3. Low back pain
1. Patient Teaching and Counselling 4. Lower abdominal pain
 Teaching about HPN and its risk factors 5. Flank pain
 Stress therapy 6. Shock
 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 D. MEDICAL / SURGICAL MANAGEMENT
 Avoid very warm bath 1. Hypertensive Medication
 Avoid prolonged sitting and standing 2. Surgery if aneurysm is greater than 4 cm
 Teflon graft
  Dacron graft  Avoid barefoot walking
 Gortex graft  Straight nails
 Lanolin cream for feet
E. NURSING INTERVENTIONS  (-) constricting clothes
1. Monitor the following 5. Assist in surgery: BKA
 VS
 Hemodynamic measurements
 Urine output II. REYNAULD’S DISEASE – characterized by acute episodes of
 BUN and creatinine arterial spasms involving the digits of hands and fingers
 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
THORACIC AORTIC ANEURYSM A.PREDISPOSING FACTORS
- Tear develops in the inner layer or aorta, blood surges in this tear 1. High risk group  women 15-40 years old up
into the middle layer of aorta, causing the inner and middle layers 2. Smoking
to separate (dissect) 3. Collagen diseases
- Opioids and sedatives (administer as ordered)  SLE
ABDOMINAL AORTIC ANEURYSM  RA
- Atherosclerosis (most common cause of this condition) 4. Direct hand trauma
- Weakening in the wall of a portion of the aorta results in a balloon-  Piano playing
like bulge as blood flows through aorta.  Excessive typing
- Oxycodone & morphine sulfate (to decrease oxygen demand)  Carpal tunnel syndrome
 Operating chainsaw
 Writing
ARTERIAL ULCERS 2 CLASSIFICATION OF RAYNAUD’S PHENOMENON
1. Primary/Idiopathic Raynaud’s (Raynaud’s disease)
I. THROMBOANGITIS OBLITERANS ( Buerger’s Dse. ) - Occurs in the absence of underlying disease
– acute inflammatory condition affecting the smaller and 2. Secondary Raynaud’s (Raynaud’s Syndrome)
medium sized arteries and veins of the lower extremities. - Occurs in association with underlying disease, usually
IDIOPATHIC connective tissue disorder such as systemic lupus
erythematosus , rheumatoid arthritis, trauma etc.
A. PREDISPOSING FACTORS B. SIGNS AND SYMPTOMS
1. High risk group  men 30 years old above 1. Intermittent claudication
2. Chronic smoking 2. Cold sensitivity and skin color changes
B. SIGNS AND SYMPTOMS  Consistent to all arterial  White/pallor  bluish/cyanosis  red/rubor
diseases  (+) especially post smoking
1. Intermittent claudication – leg pain upon strenuous walking 3. Trophic changes
r/t temporary ischemia 4. Ulceration
2. Cold sensitivity and skin color changes 5. Gangrene formation
 White/pallor  bluish/cyanosis  red/rubor C. DIAGNOSTICS
 (+) especially post smoking 1. Oscillometry – reveals a decrease in peripheral pulse
3. Decreased peripheral pulses’ volume particularly in volume
dorsalis pedis and posterior tibial 2. Angiography – site and extent of malocclusion
4. Trophic changes
5. Ulceration D. NURSING MANAGEMENT
6. Gangrene formation 1. Administer medications as ordered
 Analgesics
C. DIAGNOSTICS  Vasodilators
1. Oscillometry – reveals a decrease in peripheral pulse 2. Encourage pt to wear gloves
volume 3. Instruct: avoid smoking and exposure to cold environment
2. Doppler UTZ – decrease in blood flow to affected extremity
3. Angiography – site and extent of malocclusion VENOUS ULCERS

D. NURSING MANAGEMENT I. VARICOSE VEINS – abnormal dilation of the veins of the

1. Encourage slow progressive physical activity lower extremities d/t incompetent valves leading to increased
 Walking 3-4x/day venous pooling and venostasis  decreased venous return
 Out of bed 3-4x/day A. PREDISPOSING FACTORS
2. Medications as ordered 1. Hereditary
 Analgesics 2. Congenital weakness of veins
 Vasodilators 3. Thrombophlebitis
 Anticoagulants 4. Cardiac diseases
3. Instruct patient to avoid smoking and exposure to cold 5. Pregnancy
environment 6. Obesity
4. Institute foot care management 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

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)
A. PREDISPOSING FACTORS
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
11. Sedentary lifestyle

B. SIGNS AND SYMPTOMS

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

D. NURSING MANAGEMENT
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
5. Administer medications as ordered
 Analgesics
 Anticoagulants – heparin
6. Prevent complications
 Pulmonary embolism