When the arteries become obstructed with plaque and cholesterol, they harden and constrict, and the
circulation of blood through the vessels becomes difficult, forcing the blood through narrower passageways.
As a result, blood pressure becomes elevated.
Arteriosclerosis occurs when lipids in the blood, including cholesterol, accumulate inside the walls of blood
vessels and reduce the size of the veins or arteries through which blood flows.
ATHEROSCLEROSIS:
A degenerative condition of the arteries characterized by thickening due to localized accumulation of fats,
mainly cholesterol. The term atherosclerosis refers to a condition in which fatty deposits build up in and on
the artery walls, interfering with the normal flow of blood and oxygen throughout the body. When this
happens, the heart has to work harder to pump blood through the narrowed blood vessels, and a heart attack
or a stroke may result.
Predisposing factors:
cigarette smoking
high fat levels in the blood
high cholesterol
high blood pressure
obesity
The symptoms of atherosclerosis depend on the part of the body where the condition is taking place. Sometimes
there aren't any noticeable symptoms until the condition has advanced to a very serious stage. When the arteries
of the heart are affected, one of the first symptoms is chest pain, often called angina. A person with clogged
arteries of the heart may also have occasional difficulty in breathing and may experience unusual fatigue after
short periods of exertion.
a. Health Teaching
b. Reduce Risk Factors
c. Restore Blood Supply
d. Pre & Post-op Care for Surgical Patients
ANGINA PECTORIS:
- insufficient coronary blood flow, thus inadequate O2 causes intermittent chest pain.
-the result of myocardial ischemia caused by an imbalance between myocardial blood supply and oxygen
demand. Angina is a common presenting symptom (typically, chest pain) among patients with coronary artery
disease. It is caused by chemical and mechanical stimulation of sensory afferent nerve endings in the coronary
vessels and myocardium.
- Angina pectoris can be relieved with rest. It lasts only for 1-5 minutes and taking up of nitroglycerine will be
beneficial for the client.
Patient experiences retrosternal chest discomfort rather than flank pain. Usually described as pressure,
heaviness, squeezing, burning and choking sensation.
It localize primarily in the epigastrium, back neck jaw or in the shoulders. The typical location for radiation
of pain is in the arms, shoulders and the neck.
Precipitating factor:
over exertion
eating
exposure to cold
emotional stress
The New York Heart Association classification is used to quantify the functional limitation imposed by patient’s
symptoms as follows: (Killips)
Class I – no limitations of physical activity (ordinary physical activity does not cause symptoms).
Class II – slight limitation of physical activity (ordinary physical activity does cause symptoms). Class III –
moderate limitation of activity (patient is comfortable at rest, but less than ordinary activity can cause symptoms).
Class IV – unable to perform any physical activity without discomfort, therefore severe limitations (patient may
be symptomatic even at rest).
Nursing Interventions:
a. ECG
b. Stress Test
c. Radioisotope Imaging
d. Coronary Angiography
Medical Management:
MYOCARDIAL INFARCTION
- process by which myocardial tissue is destroyed due to reduced coronary blood flow.
- Myocardial infarction (MI) is the rapid development of myocardial necrosis caused by a critical imbalance
between the oxygen supply and demand of the myocardium.
- This usually results from plaque rupture with thrombus formation in a coronary vessel, resulting in an acute
reduction of blood supply to a portion of the myocardium.
Causes:
1. Atherosclerotic heart
2. Coronary Artery Embolism
Pathophysiology:
- The most common cause of MI is narrowing of the epicardial blood vessels due to atheromatous plaques. .
This can result in partial or complete occlusion of the vessel and subsequent myocardial ischemia. . Total
occlusion of the vessel for more than 4-6 hours results in irreversible myocardial necrosis, but reperfusion
within this period can salvage the myocardium and reduce morbidity and mortality.
- Male predilection exists in persons aged 40-70 years. Evidence exists that women more often have MIs
without atypical symptoms. The atypical presentation in women might explain the sometimes delayed
diagnosis of MIs in women.
- MI occurs most frequently in persons older than 45 years. A positive family history includes any first-degree
male relative aged 45 years or younger.
Age , Male gender, Smoking, DM, Family history, Sedentary lifestyle, obesity, diet, stress, hypertension,
Type A personality
DIAGNOSTICS:
Lab studies:
Troponin - is a contractile protein that normally is not found in serum. It is released only when
myocardial necrosis occurs.
- have the greatest sensitivity and specificity in detecting MI. The test result is both diagnostic as
well as prognostic of outcome.
Imaging studies:
Chest radiography or chest x-ray – reveals pulmonary edema secondary to heart failure.
CT scan
Radionuclide Imaging
Positron Emission Imaging
Transesophagial Echocardiography
Magnetic resonance imaging (MRI) - can identify wall thinning, scar, delayed enhancement (infarction),
and wall motion abnormalities (ischemia).
1) Restoration of the balance between the oxygen supply and demand to prevent further ischemia.
2) Pain relief
3) Prevention and treatment of complications.
Drug of choice for patient with MI:
Antithrombotic agents - These agents prevent the formation of thrombus associated with myocardial
infarction and inhibit platelet function. (aspirin, -heparin)
Vasodilators - Opposes coronary artery spasm, which augments coronary blood flow and reduces cardiac
work by decreasing preload and afterload. It is effective in the management of symptoms in AMI.
- can be administered sublingually by tablet or spray, topically, or IV; nitroglycerine
Beta-adrenergic blockers - reduce blood pressure, which decreases myocardial oxygen demand. (-
metoprolol)
Platelet aggregation inhibitors – inhibits platelet aggregation.
-clopidogrel(plavix)
Angiotensin converting enzyme (ACE) inhibitors – prevents conversion of angiotensin I to ngiotensin II,
a potent vasoconstrictor. -captopril(capoten)
Complications of MI:
Dysrhytmias
Cardiogenic Shock
Heart Failure
Pulmonary Edema
Pulmonary Embolism
Recurrent MI
Complications due to Necrosis – VSD, rupture of the heart, ruptured papillary muscles
Pericarditis
Recommendations:
1. Early
a. Treat arrythmias promptly – lidocaine
b. Give analgesic- morphine
c. Provide physical rest
d. Administer O2 via cannula
e. Frequent VS
f. Nifedipine
g. Propanolo HCL
h. Emotional Support
2. Later
a. Give stool softener
b. Provide low fat, low cholesterol, low sodium diet, soft food
c. Commode
d. Self-care
e. Plan for rehabilitation
- temporary episode of neurological dysfunction lasting only a few minutes or seconds (in a day/
24hrs) due to decreased blood flow to the brain.
- A warning sign of stroke especially in first 4 weeks after TIA
Causes:
1. Atherosclerosis
2. Microemboli from atherosclerotic plaque
Manifestations:
The sinoatrial node (SAN), located within the wall of the right atrium (RA), normally generates
electrical impulses that are carried by special conducting tissue to the atrioventricular node (AVN).
Upon reaching the AVN, located between the atria and ventricles, the electrical impulse is relayed
down conducting tissue (Bundle of HIS) that branches into pathways that supply the right and left
ventricles. These paths are called the right bundle branch (RBBB) and left bundle branch (LBBB)
respectively. The left bundle branch further divides into two sub branches (called fascicles).
Electrical impulses generated in the SAN cause the right and left atria to contract first. Depolarization
(heart muscle contraction caused by electrical stimulation) occurs nearly simultaneously in the right
and left ventricles 1-2 tenths of a second after atrial depolarization. The entire sequence of
depolarization, from beginning to end (for one heart beat), takes 2-3 tenths of a second.
All heart cells, muscle and conducting tissue, are capable of generating electrical impulses that can
trigger the heart to beat. Under normal circumstances all parts of the heart conducting system can
conduct over 140-200 signals (and corresponding heart beats) per minute.
The SAN is known as the "heart's pacemaker" because electrical impulses are normally generated
here. At rest the SAN usually produces 60-70 signals a minute. It is the SAN that increases its' rate
due to stimuli such as exercise, stimulant drugs, or fever.
Should the SAN fail to produce impulses the AVN can take over. The resting rate of the AVN is slower,
generating 40-60 beats a minute. The AVN and remaining parts of the conducting system are less
capable of increasing heart rate due to stimuli previously mentioned than the SAN.
The Bundle of HIS can generate 30-40 signals a minute. Ventricular muscle cells may generate 20-30
signals a minute.
Heart rates below 35-40 beats a minute for a prolonged period usually cause problems due to not
enough blood flow to vital organs.
Problems with signal conduction, due to disease or abnormalities of the conducting system, can occur
anyplace along the heart's conduction pathway.
Abnormally conducted signals , resulting in alterations of the heart's normal beating, are called
arrhythmias or dysrrythmia.
By analyzing an EKG a doctor is often able to tell if there are problems with specific parts of the
conducting system or if certain areas of heart muscle may be injured.
b. Basic ECG Interpretation
Electrocardiogram (ECG):
-An electrocardiogram (ECG) is a test that records the electrical activity of the heart.
-is used to measure the rate and regularity of heartbeats as well as the size and position of the
chambers, the presence of any damage to the heart, and the effects of drugs or devices used to
regulate the heart.
P wave - represents the wave of depolarization that spreads from the SA node throughout the atria,
and is usually 0.08 to 0.1 seconds (80-100 ms) in duration.
P – R interval - the period of time from the onset of the P wave to the beginning of the QRS complex,
which normally ranges from 0.12 to 0.20 seconds in duration. This interval represents the time
between the onset of atrial depolarization and the onset of ventricular depolarization.
QRS complex - represents ventricular depolarization. The duration of the QRS complex is normally
0.06 to 0.1 seconds.
ST segment - following the QRS is the time at which the entire ventricle is depolarized and roughly
corresponds to the plateau phase of the ventricular action potential. The ST segment is important in
the diagnosis of ventricular ischemia or hypoxia because under those conditions, the ST segment can
become either depressed or elevated.
Q – T interval - represents the time for both ventricular depolarization and repolarization to occur, and
therefore roughly estimates the duration of an average ventricular action potential. This interval can
range from 0.2 to 0.4 seconds depending upon heart rate.
Skin Preparation:
Clean with alcohol or usual skin prep, if necessary. If the patients are very hairy – shave the electrode
of the sternum.
the sternum.
midclavicular line.
areas.
Trouble Shooting.
a. Atrial tachycardia – sudden onset of atrial rates 140 – 250 per minute.
rhythm: regular
P waves: present before QRS complex.
PR interval: usually not measurable.
QRS complex: normal in shape (0.06 – 0.10 secs.)
T wave: distorted in appearance.
c. Ventricular tachycardia – life threatening dysrythmias that originates from an irritable focus
within the ventricle.
o metabolic acidosis (lactic acidosis)
o electrolyte imbalance
o digitalis toxicity
Rhythm: irregular
P wave: replaced by fibrillatory waves (“little f” waves)
PR interval: immeasurable
QRS complex: normal
T wave: normal
e.Ventricular fibrillation – random and chaotic discharging of impulses within the ventricles at
rates that exceeds 300 bpm.
a. produces clinical death and must be reversed immediately.
b. AMI
c.Acidosis
d.Electrolyte disturbance
rate: immeasurable because of absence of well formed QRS complex.
rhythm: chaotic
P wave: not present
PR interval: not present
QRS complex: bizarre, chaotic, no definite contour
T wave: not apparent
ECG TRACING OF A VENTRICULAR FIBRILLATION
a. Premature atrial contraction – ectopic beat that originates in the atria and is discharged at a
rate faster than that of the SA node
• the atrial beat occurs sooner than the next normal beat and is said to be early or
premature.
• Occurs in healthy or diseased heart (ischemia)
• Precursor of more serious dysrhytmias
rate: slow or fast
rhythm: irregular because of the early occurrence of the PAC
P wave: present for each normal QRS complex; the P wave of the premature contraction
will be distorted in shape.
PR interval: may be normal or shortened depending on where in the atria the impulses originated; the
closer the site of atrial impulse formation to the AV node, the shorter the PR interval will be.
g.Premature ventricular contraction – ectopic beat originating in the ventricle and is being
discharged at a rate faster than that of the next normally occurring beat.
• most common dysrythmias in the hospital
• AMI
• All other forms of heart disease
• Pulmonary disease
• Electrolyte disturbances
• Metabolic instability
• Drug abuse
rate: slow or fast
rhythm: irregular because of the premature firing of the ventricular ectopic focus.
P wave: absent since the impulse originates in the ventricle, bypassing the atria and the AV
node.
PR interval: immeasurable
QRS complex: QRS of the PVC will be widened (>0.12 sec.), bizarre in appearance when
compared to normal QRS complex.
4. Heart Block
a. transmission of the wave of impulse from the SA node through the normal conduction
pathway is altered at the level of AV node.
b. the altered state does not allow the impulse to be conducted on time or at all.
TYPES:
a. First degree AV block – the impulse is transmitted normally but, but is delayed longer at the
level of the AV node.
b. Second degree AV block – the AV node becomes selective about which impulses are conducted
to the ventricles.
Signs and
Sypmtoms pressure, heaviness, viselike, crushing, Sudden loss of
Chest pain squeezing, burning squeezing visual function
and choking sensation
Pain may radiate to Sudden loss of
localized primarily in the jaw, neck, sensory function
the epigastrium, back arms, back, and
neck jaw or in the epigastrium. Sudden loss of
shoulders. motor function
The left arm is
The typical location affected more
for radiation of pain is frequently;
in the arms, shoulders however, a patient
and the neck may experience
pain in both arms.
=====================================================
6. Acute Respiratory Failure
Pulmonary edema
- often occurs when the left side of the heart is distended and fails to pump adequately
Clinical Manifestation
Pathophysiology
Fluid accumulation in the alveolar sacs due to hypovolemia, fluid congestions in the lungs, alveoli are
congested
Diagnostic Tests
CXR
Nursing Mgt
-------------------------------------------------------------------------------------------------------------------
7. Acute Respiratory Failure
Pneumonia
- inflammtory process of lung parenchyma assoc. w/ marked increase in alveolar and interstitial fluid
Risk factors:
Clinical Manifestation
o Chest pain, irritability, apprehensiveness, irritability, restlessness, nausea, anorexia, hx of
exposure
o Cough- productive , rusty/ yellowish/greenish sputum, splinting of affected side, chest retration
(infants)
o Sudden increased fever, chills
o Nasal Flaring, circumoral cyanosis
o Tachypnea, vomiting
Pathophysiology
Caused by infectious or non-infectious agents, clotting of an exudate rich fibrogen, consolidated lung
tissue
Diagnostic Tests
CXR, sputum culture, Blood culture, increased WBC, elevated sedimentation rate
Antibiotics
Rest
Nursing Mgt
1. Promote adequate ventilation- positioning, Chest physiotherapy, IPPB
2. Provide rest and comfort
3. Prevent potential complications
4. Health teaching
-------------------------------------------------------------------------------------------------------------------
8. Acute Respiratory Failure
Asthma
- increased responsiveness of the trachea and bronchi to various stimuli, with difficulty in breathing, caused
by narrowing of airways
Types:
** Status Asthmaticus
- a life-threatening asthmatic attack in w/c symptoms of asthma continues and so not respond to treatment
Clinical Manifestation
Pathophysiology
Bronchial smooth muscles constricts
Bronchial secretions increase
Mucosa swell and narrows airway passage
Histamine is produced in the lungs
Bronchospasm, production of large amount of thick mucous and inflammatory response contribute to resp.
obstruction
Diagnostic Tests Medical Surgical Mgt Nursing Mgt
o a group of conditions assoc. w/ chronic obstruction of airflow entering or leaving the lungs
a. Major diseases
b. Clinical Manifestation
c. Diagnostic Tests
Same w/ asthma
e. Nursing Mgt
a. Promote pulmonary ventillation
b.Facilitate expectoration
c. Health teaching
d.Breathing techniques
e.Stress management
-------------------------------------------------------------------------------------------------------------------
- noncardiogenic pulmonary infiltrations resulting in stiff, wet lungs and refractory hypoxemia in
previously healthy adult. Arf w/o hypercapnia
b. Risk Factors:
a. Primary
- Shock, multiple trauma
- Infections
- Aspirations, inhalation of chemical toxins
- Drug overdose
- DIC
- Emboli, esp Fat emboli
b. Secondary
- Overaggressive fluid administration
- Oxygen toxicity
c. Clinical Manifestation
Restlessness, anxiety, hx of risk factors, severe dyspnea – cyanosis, tachycardia, hypotension,
hypoxemia, acidosis, crackles
d. Pathophysiology
e. Diagnostic Tests
CVP, Pulmonary Wedge Capillary Pressure, ABG
g. Nursing Mgt
a. Assist in respirations
b. Prevent complications
c. Environment, fluid balance, bleeding tendencies
d. Health teaching
2. Ventilation Therapy:
- The volume of air delivered by the ventilator is relatively constant, assuring consistent adequate
breaths despite varying airway pressure.
b. Types:
1. Pressure cycled – it permits air to flow into the client’s lungs until a predetermined pressure is
reached.
- the volume of air or O2 can vary as the client’s airway resistance changes.
Birds
Bennett
2. Volume cycled – delivers a predetermined volume of gas into the patient’s lungs with each breath.
- preset volume of air, ordered by the physician.
Engstron
Bennett
Ohio and Emerson
c. Indications:
Positive End Expiratory Pressure (PEEP) – a method of maintaining a pressure higher than
the atmospheric pressure in the lungs in the end of each expiration.
Continues Positive Airway Pressure (CPAP) – a non mechanical means of ventilation. It
provides a continues positive airway pressure in the lungs at the end of expiration.
Bennett MA-1 Bennett Puritan
=====================================================
3. SHOCK
- is defined as failure of the circulatory system to maintain adequate perfusion of vital organs.
A. Pathophysiology of Shock
The three major components of the circulatory system are the heart, large blood vessels and
microcirculation. As long as two of these factors canmaintain a satisfactory compensatory action,
adequate blood circulation can be maintained even if the third factor is not functioning normally.
However, if compensatory mechanisms fail or if more than one of these three factors necessary for
adequate circulation malfunction, circulatry failure results and shock develops.
B. Classification of Shock
Classification Etiology
External Pressure on the Heart interferes with heart filling or emptying Spinal cord injury
CIRCULATORY SYSTEM
Compensated Decompensated
Progressive Stage
Cellular Ischemia
Necrosis
Organ Failure
C. Stages of Shock DEATH
1. Nonprogressive Stage - cardiac output is slightly decreased because of
loss
of actual or relative blood volume.
- blood declines to a very low level that is not adequate to maintain blood flow to the cardiac
muscle thus heart begins to deteriorate.
persistent compensatory vasoconstriction
dilation in microcirculation
venous return
cardiac output
venous return
Early signs
1. tachycardia
2. tachypnea
3. oliguria
Late signs
b. Cardiovascular System
1. Myocardial deterioration
2. Disseminated Intravascular Coagulation
c. Neuroendocrine System
1. General Adaptation Response
- neuroendocrine responses during shock are defensive reactions that
occur during the body’s stage of resistance
2. Adrenal Response
- increase in adrenocortical mineralocorticoid hormones occurs
- helps increase intravascular fluid volume by stimulating the kidneys
to retain sodium and water
3. Pituitary response
-ADH is released and carried to the kidneys where it causes the body
to retain water
4. Metabolic Response
- during the initial phase of shock, the body’s small stores of available
carbohydrates are rapidly depleted. Protein and fats are then
metabolized to meet body’s energy requirements.
d. Immune System
- all forms of shock depresses the macrophages located both in the
bloodstream and tissues.
- A person in a state of shock is more susceptible to bacterial endotoxins.
e. GI Sysytem
- vagal stimulation to the GI tract slows down or stops, resulting to
absence of peristalsis
- liver loses ability to detoxify and may release vasoactive substances .
- during shock, pooling of blood occurs in the liver or portal bed
f. Renal System
1. Altered Capiillary blood pressure and glumerular filtration
2. Renal Ischemia
1. Improve oxygenation
- supplemental oxygen is administered to protect against hypoxemia
- via O2 cannula, ET tude, tracheostomy tube
4. Assist circulation
-use of intra aortic balloon pump, medical anti shock trousers (MAST suit)
- modified trendelenberg position
- administer blood products properly typed and crossmatched
5. Fluid replacement –Colloid or balanaced salt solution, colloid solution, blood,
6. Prevent complications such as renal impairment and GI bleeding
G. Nursing Intervention
1. Assessment:
• Vital signs, Airway, breathing, circulation, LOC, state of hydration, Pane, presence of
any laceration or deformity (if any)
2. Diagnosis
• Ineffective airway clearance, impaired gas exchange, decreased cardiac output, etc..
3. Planning
• Plans of intervention R/T diagnosis and state of the client
4. Intervention
• Assess and monitor client, stop bleeding (if present), Administer medications and
fluids, Refer accordingly, position client appropriately, maintain safety of the patient
5. Evaluation