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 ARTERIOSCLEROSIS:

When the arteries become obstructed with plaque and cholesterol, they harden and constrict, and thecirculation 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 bloodvessels 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 onthe artery walls, interfering with the normal flow of blood and oxygen throughout the body. When thishappens, the heart has to work harder to pump blood through the narrowed blood vessels, and a heart attackor a stroke may result.

Predisposing factors:

cigarette smokinghigh 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 Factorsb. Coronary Artery Bypass Graft (CABGc. Percutaneous Transluminal Coronary Angioplasty (PTCA)d. Directional Coronary Atherectomy (DCA)e. Intracoronary Stents

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Nursing Intervention:

a. Health Teachingb. Reduce Risk Factorsc. 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 radiationof 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’ssymptoms 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), precipitatingfactorsb. 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 relievedgo to the hospital

Diagnostic Assessment:

a. ECGb. Stress Testc. Radioisotope Imaging

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d. Coronary Angiography  Medical Management:

a. Opiate Analgesic – MoSo4b. Vasidilators – Nitroglygcerin, Isosorbide Mononitrate/Dinitratec. Calcium Channel Blockers – Dlitiazem, Nifedipined. 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 imbalancebetween the oxygen supply and demand of the myocardium.

- This usually results from plaque rupture with thrombus formation in a coronary vessel, resulting in an acutereduction of blood supply to a portion of the myocardium.

Causes:

1. Atherosclerotic heart2. 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. Anxiety5. Light headedness with or without syncope6. Cough7. Nausea with or without vomiting8. Cold diaphoresis, gray facial color,9. Wheezing10. 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.

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14. Oliguria – urine less than 30 ml/hr 15. ApprehensionRisk 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 whenmyocardial 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 morerapidly 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, andother 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

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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 myocardialinfarction and inhibit platelet function. (aspirin, -heparin)

Vasodilators - Opposes coronary artery spasm, which augments coronary blood flow and reduces cardiacwork 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:

DysrhytmiasCardiogenic ShockHeart FailurePulmonary EdemaPulmonary EmbolismRecurrent MI

Complications due to Necrosis – VSD, rupture of the heart, ruptured papillary musclesPericarditis

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. Earlya. Treat arrythmias promptly – lidocaineb. Give analgesic- morphinec. Provide physical restd. Administer O2 via cannulae. Frequent VSf. Nifedipineg. Propanolo HCLh. Emotional Support

2. Later  a. Give stool softener  

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b. Provide low fat, low cholesterol, low sodium diet, soft foodc. Commoded. Self-caree. 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. Atherosclerosis2. Microemboli from atherosclerotic plaque

Manifestations:

1. Sudden loss of visual function2. Sudden loss of sensory function3. Sudden loss of mmotor function

Management: - Surgical Carotid Endarterectomy (bypass)

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

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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 lesscapable 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 InterpretationElectrocardiogram (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.

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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.

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 attacksEnlargement of the heart  Present or impending heart attackCongenital defects Inflammation of the heart (myocarditis)Heart valve diseaseArrhythmias (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

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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:

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Normal adult 12-lead ECG 

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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 QRSo 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 waveso 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 prematurebeat, hyperkalaemia 

• normal PR intervalo 0.12 to 0.20 s (3 - 5 small squares)

for short PR segment consider Wolff-Parkinson-White syndrome or  Lown-Ganong-Levinesyndrome (other causes - Duchenne muscular dystrophy, type II glycogen storagedisease (Pompe's), HOCM)

for long PR interval see first degree heart block 

• normal QRS complexo < 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 intervalo 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 withsensorineural deafness

• normal ST segmento 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

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causes of tall T waves include hyperkalaemia, hyperacute myocardial infarction and leftbundle 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.

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d.Atrial fibrillation – rapid and chaotic firing of atrial impulses.a. fibrotic changes associated with aging process.b. AMIc. valvular diseased. 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 atrates that exceeds 300 bpm.

a. produces clinical death and must be reversed immediately.

b. AMIc.Acidosisd.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

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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; thecloser 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 beingdischarged 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 AVnode.

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.

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ECG TRACING OF A PREMATURE VENTRICULAR CONTRACTION

4. Heart Block

a. transmission of the wave of impulse from the SA node through the normal conductionpathway 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

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 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

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 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

Infarction

TIA

Definition - insufficientcoronary bloodflow, thusinadequate O2causesintermittent chestpain.

-can be relievedwith rest andnitroglycerine

- process by whichmyocardial tissue isdestroyed due toreduced coronaryblood flow.

 - not relieved withrest andnitroglycerine

- needs immediatemedical intervention

- temporary episode of neurologicaldysfunction lastingonly a few minutesor seconds (in aday/ 24hrs) due to

decreased bloodflow to the brain.

- A warning sign of stroke especiallyin first 4 weeks

after TIA

Signs andSypmtomsChest pain

pressure, heaviness,squeezing, burningand choking sensation

localized primarily inthe epigastrium, backneck jaw or in theshoulders.

The typical locationfor radiation of pain is

in the arms, shouldersand the neck

viselike, crushing,squeezing

Pain may radiate tothe jaw, neck,arms, back, andepigastrium.

 

The left arm isaffected morefrequently;

however, a patientmay experiencepain in both arms.

Sudden loss of visual function

Sudden loss of sensory function

Sudden loss of motor function

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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 MgtDiuretics, low sodium diet, I&O

Nursing Mgt

1. promote effective airway clearance, breathing patterns and ventilation2. Monitor VS3. Psychological support4. 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 pollution2. URTI3. Altered conciousness4. Tracheal intubation5. Prolonged immobility6. lowered immune system

7. malnutrition, DHN,8. Chronic Diseases:DM, Heart dse, renal dse, cancer 9. inhalation toxicity/ aspiration

Clinical Manifestationo Chest pain, irritability, apprehensiveness, irritability, restlessness, nausea, anorexia, hx of 

exposureo Cough- productive , rusty/ yellowish/greenish sputum, splinting of affected side, chest retration

(infants)

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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 lungtissue

Diagnostic Tests

CXR, sputum culture, Blood culture, increased WBC, elevated sedimentation rate

Medical Surgical Mgt

AntibioticsRest

Nursing Mgt

1. Promote adequate ventilation- positioning, Chest physiotherapy, IPPB2. Provide rest and comfort3. Prevent potential complications4. Health teaching

-------------------------------------------------------------------------------------------------------------------8. Acute Respiratory Failure

Asthma

- increased responsiveness of the trachea and bronchi to various stimuli, with difficulty in breathing, causedby 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 asthmaIncreased tightness of chest, dyspneaTachycardia, tachypneaDry, hacking, persistent cough(+) wheezes, cracklesPallor, cyanosis, diaphoresis, Chronic barrel chest, elevated shoulders, distended neck veins, orthopneaTenacious, mucoid sputum

Pathophysiology

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Bronchial smooth muscles constrictsBronchial secretions increaseMucosa 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, decPO2 and pH)

Vital capacity reduedForced expiratoryVolume decreasedResidual Volumeincreased

Steroids,Antibiotics,Bronchodilators,

expectorantsO2, nebulization

a. Promote pulmonaryventillation

b. Facilitate expectorationc. Health teachingd. Breathing techniquese. Stress management

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 walls2.Chronic Bronchitis- increased mucus production that obstructs airway3.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 ventillationb.Facilitate expectorationc.Health teachingd.Breathing techniquese.Stress management

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1. Acute Respiratory Failure

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a. Acute Respiratory Distress Syndrome

- noncardiogenic pulmonary infiltrations resulting in stiff, wet lungs and refractory hypoxemia inpreviously 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 embolib. Secondary- Overaggressive fluid administration- Oxygen toxicity

c. Clinical ManifestationRestlessness, anxiety, hx of risk factors, severe dyspnea – cyanosis, tachycardia, hypotension,hypoxemia, acidosis, crackles

d. Pathophysiology

Damage to alveolar capillary membraneIncreased Vascular Permeability to pulmonary edemaImpaired Gas exchangeDecreased surfactant prductionPotential AtelectasisSevere hypoxiaMay lead to death

e. Diagnostic TestsCVP, Pulmonary Wedge Capillary Pressure, ABG

f. Medical Surgical MgtICU, strict monitoring, O2, suction, bronchodilator, anitibiotics, ET ventilator 

g. Nursing Mgta. Assist in respirationsb. Prevent complicationsc. 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 adequatebreaths despite varying airway pressure.

b. Types:

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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

comae. 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, pressuresupport.

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 exceptthe pressure limit.

Positive End Expiratory Pressure (PEEP) – a method of maintaining a pressure higher thanthe atmospheric pressure in the lungs in the end of each expiration.

Continues Positive Airway Pressure (CPAP) – a non mechanical means of ventilation. Itprovides a continues positive airway pressure in the lungs at the end of expiration.

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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

ic Shock

- due to inadequatecirculationg blood volume

Blood loss: Massive Trauma, GI Bleeding, Ruptured Aortic

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

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2. Cardiogeni c Shock

- due to inadequatepumping action of the

heart because of primarycardiac muscle dysfunctionor mechanical obstructionof blood flow caused by MIor valvular insufficiency

Myocardial disease: Acute MI, Myocardial Contusion,Cardiomypathies

Valvular Disease or injury: Ruptured Aortic Cusp, RupturedPapillary muscle, Ball thrombus

External Pressure on the Heart interferes with heart filling or emptying:Pericardial Tamponade due to Trauma, aneurysm,

cardiac surgery, pericarditis, massivepulmonary embolus, tension pneumothorax

Cardiac Dysrhtymias: Tachyarrhythmias, Bradyarrythmias,Electromechanical dissociation

3. NeurogenicShock- interference withnervous system

control of the bloodvessels

Spinal: Spinal anesthesia, spinal cord injury

Vaso-vagal reaction: Severe pain, severe emotional stress

4. Anaphylacti c Shock- severehypersensitivityreaction resulting inmassive systemicvasodilation.

Allergy to food, medicines, dye, insect bites or stings

5. Septic

Shock- systemic reactionvasodilation due toinfection

Gram-negative septicemia but also caused by other organisms

MATRIX: PATHOPHYSIOLOGY OF SHOCK

CIRCULATORY SYSTEM

HEART LARGE BLOOD VESSELS MICROCIRCULATION

(peripheral circulation)

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,

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Compensated Decompensated

(body is able to maintain tissue (systemic circulation & microcirculationperfusion to the vital organs) no longer work in unison)

 

C. Stages of Shock

1. Nonprogressive Stage - cardiac output is slightly decreased because of 

lossof actual or relative blood volume.

- body responds to compensate for the hypovolemia

to maintain blood pressure.

cardiac output sympathetic stimulation

capillary blood flow epinephrine andhydrostatic pressure within norepinephrine releasedcapillaries lower thansurrounding 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 cardiacmuscle thus heart begins to deteriorate.

Non-progressive Stage

vasoconstriction continuesmicrocirculation dilatesNormal State

decreased venous return decreased circulation of reoxygenated blood

Inadequate tissue perfusion

Pro ressive Sta e

Cellular IschemiaNecrosis

Organ FailureDEATH

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persistent compensatory vasoconstriction

dilation in microcirculation

venous return

cardiac output

arterial blood pressurevenous pooling coronary artery

tissue perfusion fillingpooling of bloodin 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. tachycardia2. tachypnea3. oliguria

Late signs

4. cold moist skin5. color ashen: pallor  6. hypotensive, tachycardia

E. Effects of Shock in Different Organsa.Respiratory system

- shock leads to hypoxia, with blockage of normal aerobic metabolism.- lactic acid accumulates, resulting to tissue acidosis.

b. Cardiovascular System1. Myocardial deterioration2. Disseminated Intravascular Coagulation

c. Neuroendocrine System1. General Adaptation Response

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- neuroendocrine responses during shock are defensive reactions thatoccur during the body’s stage of resistance

2. Adrenal Response- increase in adrenocortical mineralocorticoid hormones occurs- helps increase intravascular fluid volume by stimulating the kidneysto 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 availablecarbohydrates are rapidly depleted. Protein and fats are thenmetabolized 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 toabsence 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 System1. Altered Capiillary blood pressure and glumerular filtration2. 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 Intervention1. 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

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• Plans of intervention R/T diagnosis and state of the client4. Intervention

• Assess and monitor client, stop bleeding (if present), Administer medications andfluids, Refer accordingly, position client appropriately, maintain safety of the patient

5. Evaluation