ARTERIOSCLEROSIS:

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

Signs and symptoms:

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.

Medical & Surgical Interventions for Athero and Arteriosclerosis:

a. Lifestyle Modification ; Reduce Risk Factors

b. Coronary Artery Bypass Graft (CABG
c. Percutaneous Transluminal Coronary Angioplasty (PTCA)
d. Directional Coronary Atherectomy (DCA)
e. Intracoronary Stents
Nursing Intervention:

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.

Signs and symptoms:

 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. Assess pain – location, character, ECG (ST elevation), precipitatingfactors

b. Help client to adjust lifestyle to prevemt angina attack – avoid excessive activity in cold weather,
avoid overeating, avoid constipation, rest after meals, exercise
c. Teach patient how to cope with angina attack – nitroglycerin every 5 mins upto 3x, if still not relieved
go to the hospital
Diagnostic Assessment:

a. ECG
b. Stress Test
c. Radioisotope Imaging
 d. Coronary Angiography
Medical Management:

a. Opiate Analgesic – MoSo4

b. Vasidilators – Nitroglygcerin, Isosorbide Mononitrate/Dinitrate
c. Calcium Channel Blockers – Dlitiazem, Nifedipine
d. Beta Blocking Agents –Propanolol

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.

- MI is a leading cause of morbidity and mortality in the United States.

- 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.

Signs and symptoms:

1. chest pain – heavy (viselike, crushing, squeezing)

 usually across the anterior pericardium typically is described as tightness, pressure, or squeezing.
 Pain may radiate to the jaw, neck, arms, back, and epigastrium. The left arm is affected more frequently;
however, a patient may experience pain in both arms.
2. Dyspnea, Orthopnea – sense of suffocation
3. Nausea and/or abdominal pain- gas pains around the heart
4. Anxiety
5. Light headedness with or without syncope
6. Cough
7. Nausea with or without vomiting
8. Cold diaphoresis, gray facial color,
9. Wheezing
10. Weakness and altered mental status – common in elderly patients.
11. Rales – may be present in congestive heart failure.
12. Neck vein distention – represents right pump failure.
13. Dysrythmias - an irregular heart beat or pulse, usually tachycardic.
14. Oliguria – urine less than 30 ml/hr
15. Apprehension
Risk factors:

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.

 Creatine kinase–MB (CK-MB)

 Myoglobin - a low-molecular-weight heme protein found in cardiac and skeletal muscle, is released more
rapidly from infarcted myocardium.
CBC – is indicated if anemia is suspected as a precipitant. Transfusion with PRBC may beindicated.

 Potassium and magnesium level – should be monitored and corrected.

 Creatinine level
 C – Reactive protein (CRP) - is a marker of acute inflammation.
 Erythrocyte sedimentation rate (ESR)
 Serum lactate dehydrogenase (LDH)

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).

 Electrocardiogram (ECG) - ST-segment elevation greater than 1 mm.

- the presence of new Q waves.

-intermediate probability of MI are ST-segment depression, T-wave inversion, and

other nonspecific ST-T wave abnormalities.

Immediate emergency intervention:

 IV access – thrombolytic agents e.g. heparin

 supplemental oxygen
 pulse oximetry – maintain oxygen saturation at >90%
 Immediate administration of aspirin en route
 Nitroglycerin for active chest pain, given sublingually or by spray
 ECG
 Treatment is aimed at:

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)

 Analgesics – reduce pain which decreases sympathetic stress.

-morphine sulfate

 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:

- All MI patients should be admitted in the ICU.

- Patient should remain on complete bed rest during his stay in the hospital and avoid straining
activities.

Nursing interventions for MI

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

Exercise program, Stress management, Teach risk factors

a. Psychological support b Long-term drug therapy

Antiarryhtmics- quinidine, lidocaine

Anticoagualnt – heparin, aspirin

Antihypertensives – propanolol, chlorathiazide

3. TRANSIENT ISCHEMIC ATTACK (TIA)

- 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:

1. Sudden loss of visual function

2. Sudden loss of sensory function
3. Sudden loss of mmotor function

Management: - Surgical Carotid Endarterectomy (bypass)

1. Post-op focus – assess neurologic deficits; avoid flexing neck

Inability to swallow, move tongue, raise arm, smile may indicate

problem in the specific cranial nerve.

2. Anticoagulant therapy: aspirin, etc.

4. Arrythmias

a. Review of Conduction System

Heart Conduction System

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.

The ECG Waves:

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.

T wave - represents ventricular repolarization and is longer in duration than depolarization.

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.

Abnormal ECG results may indicate the following:

Myocardial (cardiac muscle) defect Past heart attacks

Enlargement of the heart Present or impending heart attack
Congenital defects Inflammation of the heart (myocarditis)
Heart valve disease
Arrhythmias (abnormal rhythms)
Tachycardia (heart rate too fast) or bradycardia (too slow)
Coronary artery

How to perform ECG Using Disposable Electrodes.

Skin Preparation:
Clean with alcohol or usual skin prep, if necessary. If the patients are very hairy – shave the electrode

V1: Fourth intercostal space to the right

of the sternum.

V2: Fourth intercostal space to the Left of

the sternum.

V3: Directly between leads V2 and V4.

V4: Fifth intercostal space at

midclavicular line.
areas.

Trouble Shooting.

When no signal or a poor signal is observed the following should be considered:

1. Have the cables been correctly connected?

2. Is the equipment functioning correctly?
3. Could external electrical equipment interference be a problem?
4. Was skin preparation adequate?
5. Could the electrodes suffer from
a) gel dry out?
b) Poor adhesion?

12 Lead (10 Electrode) Placement Guide:

Normal adult 12-lead ECG
 The diagnosis through electrocardiogram is made by excluding any recognised abnormality. It's description is
therefore quite lengthy.

• normal sinus rhythm

o each P wave is followed by a QRS
o P waves normal for the subject
o P wave rate 60 - 100 bpm with <10% variation
rate <60 = sinus bradycardia , rate >100 = sinus tachycardia , variation >10% = sinus

• arrhythmia normal QRS axis

• normal P waves
o height < 2.5 mm in lead II
o width < 0.11 s in lead II
 for abnormal P waves see right atrial hypertrophy, left atrial hypertrophy, atrial premature
beat, hyperkalaemia
• normal PR interval
o 0.12 to 0.20 s (3 - 5 small squares)
 for short PR segment consider Wolff-Parkinson-White syndrome or Lown-Ganong-Levine
syndrome (other causes - Duchenne muscular dystrophy, type II glycogen storage
disease (Pompe's), HOCM)
 for long PR interval see first degree heart block
• normal QRS complex
o < 0.12 s duration (3 small squares)
 for abnormally wide QRS consider right or left bundle branch block, ventricular rhythm,
hyperkalaemia, etc.
o no pathological Q waves
o no evidence of left or right ventricular hypertrophy
• normal QT interval
o Calculate the corrected QT interval (QTc) by dividing the QT interval by the square root of the
preceeding R - R interval. Normal = 0.42 s.
o Causes of long QT interval
 myocardial infarction, myocarditis, diffuse myocardial disease
 hypocalcaemia, hypothyrodism
 subarachnoid haemorrhage, intracerebral haemorrhage
 drugs (e.g. sotalol, amiodarone)
 hereditary


Romano Ward syndrome (autosomal dominant)

 Jervill + Lange Nielson syndrome (autosomal recessive) associated with

sensorineural deafness
• normal ST segment
o no elevation or depression
 causes of elevation include acute MI (e.g. anterior, inferior), left bundle branch block,
normal variants (e.g. athletic heart, Edeiken pattern, high-take off), acute pericarditis
 causes of depression include myocardial ischaemia, digoxin effect, ventricular
hypertrophy, acute posterior MI, pulmonary embolus, left bundle branch block
• normal T wave
  causes of tall T waves include hyperkalaemia, hyperacute myocardial infarction and left
bundle branch block
 causes of small, flattened or inverted T waves are numerous and include ischaemia, age,
race, hyperventilation, anxiety, drinking iced water, LVH, drugs (e.g. digoxin), pericarditis,
PE, intraventricular conduction delay (e.g. RBBB)and electrolyte disturbance.
• normal U wave
1. Different kinds of Arrythmias

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.

b. Atrial flutter – atrial stretching or enlargement, MI, CHF.

 rate 250 – 400 beats per minute
 rhythm: regular or irregular
 P wave: not present; replaced by a saw toothed pattern (F waves).
 PR intervals: not measurable.
 QRS complex: normal shape and time.
 T wave: present but may be obscured by flutter waves.

ECG TRACING OF AN ATRIAL FLUTTER

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

 rate: 140 – 220 bpm.

 rhythm: usually regular but may be irregular
 P wave: not present.
 PR interval: immeasurable. .
 T wave: usually deflected opposite to the QRS complex.
 d.Atrial fibrillation – rapid and chaotic firing of atrial impulses.
a. fibrotic changes associated with aging process.
b. AMI
c. valvular disease
d. digitalis
 rate: immeasurable because fibrillatory waves replace P waves; ventricular rate may vary from brady
to tachycardia.

 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.

 QRS and T wave: normal

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.

 T wave: usually deflected opposite to the QRS.

 ECG TRACING OF A PREMATURE VENTRICULAR CONTRACTION

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.

c. may be a sign of CAD, acute rhuematic carditis, electrolyte imbalance.

 rate: usually normal but may be slow.
 Rhythm: regular
 P wave: present for each QRS complex and is identical.
 PR interval: >20 sec.
 QRS complex: normal (0.06 – 0.10 sec.)
 T wave: normal

b. Second degree AV block – the AV node becomes selective about which impulses are conducted
to the ventricles.

c. Third degree AV block – complete heart block.

d. no relationship between the atrial and ventricular activity

Acute Inferior Myocardial Infarction

• ST elevation in the inferior leads II, III and aVF
• reciprocal ST depression in the anterior leads
 Acute Anterior Myocardial Infarction
• ST elevation in the anterior leads V1 - 6, I and aVL

reciprocal ST depression in the inferior leads

Acute Posterior Myocardial Infarction

• (hyperacute) the mirror image of acute injury in leads V1 - 3
• (fully evolved) tall R wave, tall upright T wave in leads V1 -3
• usually associated with inferior and/or lateral wall MI

Old Inferior Myocardial Infarction

• a Q wave in lead III wider than 1 mm (1 small square) and
• a Q wave in lead aVF wider than 0.5 mm and
• a Q wave of any size in lead II
Acute myocardial infarction in the presence of left bundle branch block

Features suggesting acute MI

• ST changes in the same direction as the QRS (as shown here)

• ST elevation more than you'd expect from LBBB alone (e.g. > 5 mm in leads V1 - 3)
• Q waves in two consecutive lateral leads (indicating anteroseptal MI)

5. Difference between Angina Pectoris, Myocardial Infarction, Transient Ischemic Attack

Angina Pectoris Myocardial TIA

Infarction
Definition - insufficient - process by which - tempo
coronary blood myocardial tissue is rary episode of
flow, thus destroyed due to neurological
inadequate O2 reduced coronary dysfunction lasting
causes blood flow. only a few minutes
intermittent chest or seconds (in a
pain. - not relieved with day/ 24hrs) due to
rest and decreased blood
-can be relieved nitroglycerine flow to the brain.
with rest and
nitroglycerine - needs immediate - A warning sign of
medical intervention stroke especially
in first 4 weeks
after TIA

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

Constant irritating cough, dyspnea, crackles, cyanosis

Pathophysiology

Fluid accumulation in the alveolar sacs due to hypovolemia, fluid congestions in the lungs, alveoli are
congested

Diagnostic Tests

CXR

Medical Surgical Mgt

Diuretics, low sodium diet, I&O

Nursing Mgt

1. promote effective airway clearance, breathing patterns and ventilation

2. Monitor VS
3. Psychological support
4. Administer medications

-------------------------------------------------------------------------------------------------------------------
7. Acute Respiratory Failure

Pneumonia

- inflammtory process of lung parenchyma assoc. w/ marked increase in alveolar and interstitial fluid

Risk factors:

1. Smoking, air pollution

2. URTI
3. Altered conciousness
4. Tracheal intubation
5. Prolonged immobility
6. lowered immune system
7. malnutrition, DHN,
8. Chronic Diseases:DM, Heart dse, renal dse, cancer
9. inhalation toxicity/ aspiration

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

Medical Surgical Mgt

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:

- Immunologic asthma occurs in childhood

- Non-immunologic asthma occurs in adulthood and assoc w/ recurrent resp infections.
Usually >35 y/o

- Mixed, combined immunologic and non-immunologic

** Status Asthmaticus

- a life-threatening asthmatic attack in w/c symptoms of asthma continues and so not respond to treatment

Clinical Manifestation

History of rhinitis, allergies, family hx of asthma

Increased tightness of chest, dyspnea
Tachycardia, tachypnea
Dry, hacking, persistent cough
(+) wheezes, crackles
Pallor, cyanosis, diaphoresis, Chronic barrel chest, elevated shoulders, distended neck veins, orthopnea
Tenacious, mucoid sputum

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

ABG (elevated PCO2, dec Steroids, a. Promote pulmonary

PO2 and pH) Antibiotics, ventillation
Vital capacity redued Bronchodilators, b. Facilitate expectoration
Forced expiratory expectorants c. Health teaching
Volume decreased O2, nebulization d. Breathing techniques
Residual Volume e. Stress management
increased

Chronic Obstructive Pulmonary Disease

o a group of conditions assoc. w/ chronic obstruction of airflow entering or leaving the lungs

a. Major diseases

1.Pulmonary Emphysema – airway is obstructed due to destroyed alveolar walls

2.Chronic Bronchitis- increased mucus production that obstructs airway
3.Asthma

b. Clinical Manifestation

Shortness of breath, productive cough, hypoxia, wheezes/rales, decreased exercise tolerance

c. Diagnostic Tests

Same w/ asthma

d. Medical Surgical Mgt

Antibiotics, expectorants, O2 at low flow, nebulization

e. Nursing Mgt
a. Promote pulmonary ventillation
b.Facilitate expectoration
c. Health teaching
d.Breathing techniques
e.Stress management

-------------------------------------------------------------------------------------------------------------------

1. Acute Respiratory Failure

 a. Acute Respiratory Distress Syndrome

- 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

Damage to alveolar capillary membrane

Increased Vascular Permeability to pulmonary edema
Impaired Gas exchange
Decreased surfactant prduction
Potential Atelectasis
Severe hypoxia
May lead to death

e. Diagnostic Tests
CVP, Pulmonary Wedge Capillary Pressure, ABG

f. Medical Surgical Mgt

ICU, strict monitoring, O2, suction, bronchodilator, anitibiotics, ET ventilator

g. Nursing Mgt
a. Assist in respirations
b. Prevent complications
c. Environment, fluid balance, bleeding tendencies
d. Health teaching

2. Ventilation Therapy:

a. Mechanical Ventilation – a means of augmenting respiratory gas exchange using a mechanical

device, equipped to deliver negative or positive pressure that can maintain ventilation and O2 delivery
for a prolonged period of time.

- 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:

 continues decrease in oxygenation (paO2)

 increase in arterial carbon dioxide levels (paCO2)
 persistence of acidosis (decrease in blood pH)
d. Respiratory conditions needing the aid of the mechanical ventilators:

 post operative thoracic or abdominal surgery

 drug overdose
 neuromuscular disease
 inhalation injury
 COPD
 multiple trauma
 shock
 multi-system failure
 coma
e. Mode or Breath Pattern:

- what causes the ventilator to cycle from inspiration

 Mandatory (controlled) - which is determined by the respiratory rate.

 Assisted (as in assist control) - synchronized intermittent mandatory ventilation, pressure
support.
 Spontaneous - no additional assistance in inspiration, as in CPAP.
 CMV - Conventional controlled ventilation, without allowances for spontaneous breathing.
 Many anesthesia ventilators operate in this way.
 Assist-Control - Where assisted breaths are facsimiles of controlled breaths.
 Intermittent Mandatory Ventilation - which mix controlled breath and spontaneous breath.
 Pressure Support - Where the patient has control over all aspects of his/her breath except
the pressure limit.

 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.

(see matrix and stages…)

B. Classification of Shock

Classification Etiology

1. Hypovolem Blood loss: Massive Trauma, GI Bleeding, Ruptured Aortic

ic Shock
- due to inadequate
circulationg blood volume
Aneurysm, Surgery, Erosion of Vessesl due to lesion,
tubes or other devices, DIC
Plasma loss: Burns, Accumulation of intra-abdominal fluid,
malnutrition, severe dermatitis, DIC

Crystalloid loss: Dehydration, Protracted Vomiting, Diarrhea,

nasogastric suction
 2. Cardiogeni Myocardial disease: Acute MI, Myocardial Contusion,
c Shock Cardiomypathies

- due to inadequate Valvular Disease or injury: Ruptured Aortic Cusp, Ruptured

pumping action of the
heart because of primary
cardiac muscle dysfunction
or mechanical obstruction
of blood flow caused by MI
or valvular insufficiency
Papillary muscle, Ball thrombus
External Pressure on the Heart interferes with heart filling or emptying:
Pericardial Tamponade due to Trauma, aneurysm,
cardiac surgery, pericarditis, massive
pulmonary embolus, tension pneumothorax

Cardiac Dysrhtymias: Tachyarrhythmias, Bradyarrythmias,

Electromechanical dissociation

3. Neurogenic Spinal: Spinal anesthesia, spinal cord injury

Shock
- interference with Vaso-vagal reaction: Severe pain, severe emotional stress
nervous system
control of the blood
vessels

4. Anaphylacti Allergy to food, medicines, dye, insect bites or stings

c Shock
- severe
hypersensitivity
reaction resulting in
massive systemic
vasodilation.

5. Septic Gram-negative septicemia but also caused by other organisms

Shock
- systemic reaction
vasodilation due to
infection

MATRIX: PATHOPHYSIOLOGY OF SHOCK

Myocardial disease Blood loss Plasma loss Crystalloid loss

External Pressure on the Heart interferes with heart filling or emptying Spinal cord injury

Cardiac Dysrhtymias Vaso-vagal reaction Severe pain Severe emotional stress

Valvular Disease or injury septicemia Allergy to medicines, food, dye,

insect bites or stings

CIRCULATORY SYSTEM

HEART LARGE BLOOD VESSELS MICROCIRCULATION

(peripheral circulation)
 Non-progressive Stage

Compensated Decompensated

(body is able to maintain tissue (systemic circulation & microcirculation

perfusion to the vital organs) no longer work in unison)

Normal State vasoconstriction continues

microcirculation dilates

decreased venous return decreased circulation of

reoxygenated blood
Inadequate tissue perfusion

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.

- body responds to compensate for the hypovolemia

to maintain blood pressure.

cardiac output sympathetic stimulation

capillary blood flow epinephrine and

hydrostatic pressure within norepinephrine released
capillaries lower than
surrounding tissues vasoconstriction

fluid moves from tissues tachycardia systemic vascular

into vascular system resistance

circulating volume blood pressure maintained

2. Progressive Stage - the compensatory mechanisms are not adequate to

compensate for the loss of 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

arterial blood pressure

venous pooling coronary artery
tissue perfusion filling
pooling of blood
in microcirculation damage to microcirculation myocardial function

accumulation of cellular hypoxia and release of

metabolites in cell vasoactive substances

metabolic acidosis capillary permeability

venous return

3. Irreversible Stage – occurs if the cycle of inadequate tissue perfusion is

not interrupted

- cellular ischemia and necrosis lead to organ failure

D. Physiologic Manifestations of Shock

Early signs

1. tachycardia
2. tachypnea
3. oliguria

Late signs

4. cold moist skin

5. color ashen: pallor
6. hypotensive, tachycardia
E. Effects of Shock in Different Organs
a.Respiratory system

- shock leads to hypoxia, with blockage of normal aerobic metabolism.

- lactic acid accumulates, resulting to tissue acidosis.

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

F. Medical Surgical Management

1. Improve oxygenation
- supplemental oxygen is administered to protect against hypoxemia
- via O2 cannula, ET tude, tracheostomy tube

2. Restore and maintain adequate perfusion

3. Administer vasoactive medications or emergency drugs

- Atropine, dopamine, epinephrine, isoproterenol ( to increase Stroke volume), Lidocaine
(for dysrrhythmias), Metaraminol ( promotes vasoconstriction), Levophed, Na bicarbonate

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