NURS5084 Nursing the Acutely Ill Person

Week 1.1: Introduction to Nursing the Acutely Ill Person

Week 1.2: Acute coronary syndromes

Structure of the heart

Conduction system of the heart

SA and AV Node

o All myocardial cells are capable of generating an impulse (automaticity)

o Impulses begin in the SA node (located at top of right atrium)

o SA node has fastest intrinsic rate of cardiac cells

o Impulse then spreads through 3 conduction

pathways to the AV node

Delays cardiac impulse to allow for atrial

kick that helps to fill the ventricles

Controls the number of impulses reaching

the ventricles

Bundle Branches and Purkinje system

o The electrical impulse then travels from the AV

node to the left and right bundle branches

o Each bundle branch ends in a network of fibres

called the Purkinje system which stimulate

ventricular contraction

Coronary circulation

Right Coronary Artery (RCA)

o Usually supplies right atrium,

right ventricle and inferior wall of

left ventricle

o Supplies SA node in 55% of

people and AV node in 90%

Normal coronary circulation

o Left anterior descending artery:

supplies the left atrium and anterior wall of the left ventricle

o Left circumflex artery: supplies left atrium and lateral and posterior walls of the left ventricle

o Supplies SA node in 45% of people and AV node in 10%

Potential intercoronary channels between arterial branches provide possibility for collateral circulation

Risk factors for Coronary Artery Disease

Unmodifiable

o Male gender

o Post-menopausal female

o Family history

o 65+ years

Modifiable

o Smoking

o Overweight/obesity (BMI, hip:waist

ratio)

o Hypertension

o Hyperlipidaemia

o Depression

o Diabetes

o Physical inactivity

Cardiac pain

Typical cardiac pain

o Central or left-sided tightness, heaviness, discomfort

o May radiate to arms (especially left), throat, back or epigastric area

o May be associated with diaphoresis, SOB, dizziness, nausea/vomiting

Atypical cardiac pain

o Seen especially in the elderly, diabetics and women

o Epigastric pain only

o Pain or heaviness in arms only

o Pain or tightness in jaw or throat only

o Associated with fatigue and SOB

o Pleuritic pain?

Pain unlikely to be of cardiac origin

o Pain mainly located in the middle/lower abdomen

o Pain that can be localised by the tip of 1 finger – especially if over the LV apex

o Pain reproduced with movement or palpation of the chest wall or arms

o Constant pain lasting many hours with a normal ECG

o Brief episodes of pain lasting only a few seconds

o Pain that radiates into lower extremities

Coronary artery disease and stable angina

CAD = when plaque builds up on the intima (inner lining) of the arterial wall, partially occluding the artery

This may result in stable angina (predictable symptoms that occur in response to predictable stimuli)

o Deep, poorly localised chest/arm discomfort (+/- SOB)

o Comes on predictably with physical exertion, emotional stress

o Relieved promptly with rest and/or sublingual nitrates

o Not a medical emergency; patients with known stable angina should seek review if pain becomes:

More severe

Occurs more frequently

Lasts >10 minutes

Comes on at rest

o May be treated with:

Angioplasty and stenting

Coronary artery grafting

Pharmacological management

Acute Coronary Syndromes (ACS)

Pathophysiology: rupture/erosion of atheromatous plaque triggers clotting mechanism (thrombus

formation) total/partial occlusion of the artery

Unstable Angina Pectoris (UAP): chest pain/discomfort but no permanent injury

o Temporary/partial occlusion local ischaemia

o Diagnosis on clinical history and ECG

o ST segment depression >0.5mm

o T-wave inversion or flattening

o Some will have normal ECG

o Normal cardiac enzymes (Troponin)

o Patients with UAP are at high risk of death

Non ST Elevation Myocardial Infarction (NSTEMI): smaller area of infarction (permanent injury) often due

to transient/partial occlusion

o Plaque rupture

o Thrombus formation and arterial occlusion for up to 1hr

o Area of cell necrosis that does not affect all muscle layers

o Presenting symptoms and ECG patterns often identical to UAP

o But raised cardiac enzymes due to permanent damage

ST Elevation Myocardial Infarction (STEMI): indicates prolonged coronary artery occlusion and permanent

injury

o Significant plaque rupture full thickness of myocardium affected

o ST elevation

≥ 1mm in 2 or more consecutive limb leads

Inferior leads II, III, aVF, high lateral leads I, aVL

≥ 2mm in 2 or more consecutive chest leads

Anterior leads V1-4, low lateral leads V5-6

Or new LBBB

o Later, deep Q waves represent necrotic areas of myocardium

o Reciprocal ST depression may be present

o Raised cardiac enzymes

Priorities in ACS

o Triage 1 or 2

o Early ECG and ECG review (within 5-10mins)

o GTN and aspirin if not given by ambulance

o Routine use of supplemental O2 is not recommended

O2 therapy if oxygen saturation <93% or if evidence of shock

In absence of hypoxia, benefit of O2 uncertain; may be harmful

o Full description of pain documented (PQRST)

o Possible cardiac pain and STEMI on ECG emergency revascularisation

Thrombolysis (e.g. TNK-Metalyse)

Or activate cardiac catheter lab team for primary angioplasty/stent

o Risk stratification of non-ST elevation ACS

High risk admit

Low risk monitor and d/c with upgraded medical therapy and early cardiology r/v

Treatment goals in ACS

o Decrease mortality, morbidity

o Decrease cardiac oxygen demand

o Improve or restore blood flow

o Limit infarct size

o Relieve pain and anxiety

Management of UAP/NSTEMI

o Soluble aspirin 300mg, SL GTN, IV access (avoid IM injections)

o Treatment of pain

Pain increases release of catecholamines (adrenaline, noradrenaline) increased HR,

BP, myocardial workload (risk of arrhythmias); coronary artery spasm further

ischaemia (give Morphine + Maxalon)

o Continuous cardiac monitoring and serial 12 lead ECGs

o Bedrest until pain resolved and ECG stable

Systems to support early revascularisation in STEMI

In STEMI, we aim to open an artery in less than 90minutes (door to balloon time)

Every 20 minutes saved 1% reduction in morality from AMI

Ambulance takes 12 lead ECG; if suspicious, sends ECG to closest cath lab hospital

o Emergency department

o Interventional cardiologist

o If ECG positive for STEMI, cath lab team called in and arrive with patient

In rural areas, either ambulance will give a clot busting drug (thrombolysis), or if ambulance delayed,

nurse-initiated thrombolysis will be given if required to save time and myocardium

Troponin to support diagnosis of myocardial damage

Early collection of blood for testing

Do not measure troponin (hs-TNT) unless clinical symptoms of ACS (or will get lots of false +)

If initial hs-TNT is elevated (≥ 14mg/L) or if there is a high clinical suspicion, repeat test after 3hrs

A positive finding should be followed up by a consideration of alternative, plausible explanations (e.g. PE,

aortic dissection, sepsis, chronic kidney disease) and cardiology consult if ACS suspected

Medications

Antiplatelet drugs (aspirin, clopidogrel)

Antithrombotic drugs (heparin); to reduce thrombus formation

Nitrates e.g. nitroglycerine (SL anginine, IV tridil)

o Potent vasodilators; dilate peripheral vessels, reduce preload (left ventricular end-diastolic

volume)

Beta-blockers (atenolol, metoprolol)

o Reduce pain and ischaemia by reducing HR, BP (therefore, myocardial workload)

ACE inhibitors (ramipril, perindopril)

o For secondary prevention where there is LV impairment

o Reduces vaso-constricting effects of renin-angiotensin system (RAS) lowered BP, left

ventricular workload

Statins (simvastatin, atorvastatin)

o Improves coronary plaque stability by increasing endothelial function, lowering vascular

inflammation, lowering platelet aggregation

o Reduces risk of coronary events and morality in CAD

Cardiac conditions can interfere with the conduction system

Acute coronary syndromes

o Ventricular arrhythmias; ischaemia results in myocardial irritability

Ventricular tachycardia

Ventricular fibrillation (especially in anterior AMI)

Scar tissue from old MI also VT

o Heart blocks/bradycardia; from poor blood supply to the SA node or AV node (especially in

inferior AMI)

o Bundle branch blocks; from poor blood supply to the bundle branches

o Sinus tachycardia; from circulating catecholamines

Other complications

Cardiogenic shock

Acute pulmonary oedema

Papillary muscle rupture

Myocardial rupture

Nursing management

Care of angioplasty access site (circ obs, bleeding)

Continuous cardiac monitoring, daily 12 lead ECGs

Early mobilisation if haemodynamically stable

Low saturated fat, salt diet

Documentation and notification of arrhythmias, chest pain, haemodynamic instability

? family screening

Cardiac rehabilitation

All ACS patients should be referred for cardiac rehabilitation

Increasing physical activity

Education sessions (nurse, psychologist, dietician, OT, physio, SW)

Screening and referral for risk factor management

Inclusion of family members

Flexible models are required to enhance access

Future pain management

Written instruction (e.g. fridge magnet)

Stop, rest, tell someone how you feel

Take sublingual nitrate

o Up to 3 anginine tablets (5 minutes apart)

o Or up to two GTN sprays (5 minutes apart)

o If pain is severe, getting worse or does not go away in 10 minutes, call ambulance

Week 1 Tutorial

Review the factors that may have caused Mr Walker to develop coronary artery disease. Are any of these factors

present in the case study?

Family history of CVA

Hypertension

Overweight; diet high in refined carbohydrates and saturated fats

Unmanaged/unstable angina

Male

Increased stress levels

List the clinical manifestations that Mr Walker exhibited and explain their pathophysiological bases.

Severe chest pain – ischaemic pain; damage to heart muscle due to lack of oxygenation

Cold extremities – vasoconstriction as blood flow is directed to heart

Tachycardia – inadequate oxygenation forces heart to pump blood faster increased HR

Ventricular gallop rhythm

Cold sweat – result of stress response

Anxiety – sympathetic nervous system activated

What are the indications that Mr Walker’s condition is worsening?

Development of Q waves suggest necrotic areas of myocardium; Q waves take hours to develop on ECG

so it suggests the patient’s condition has been worsening for a significant length of time

Symptoms worsening e.g. chest discomfort severe chest pain; apprehension anxiety

What is the significance of the laboratory tests and ECG findings?

Elevated CK-MB levels indicates MI. Serum levels begin to rise 6-8 hours post infarction

If troponin is elevated then CK-MB (creatinine kinase) can indicate reinfarction

o Troponin is only in cardiac muscle; normal levels are 0 and when cardiac muscle is damaged, it is

released into blood increased levels of Troponin

ST elevation + Q wave development – prolonged artery occlusion and permanent damage

What is your plan of care for Mr Walker; immediately and long term

Monitor BSL; potential diabetes?

Lasix? Effectiveness on hypertension

Nitro-glycerine tablets out of date? Sprays expire 30days after opening

Patient drove to hospital after 30 minutes; requires a step-by-step plan for future incidents

Immediate: attend to vital signs (every 15mins), ECG, pain assessment, determine if oxygen therapy is

needed, provide pain relief (IV 1mg/mL Morphine also vasodilates), full medication reconciliation, medical

history, neurovascular obs, full cardiac assessment, calm the patient, continuous cardiac monitoring and

12 lead ECGs, thrombolysis, bedrest, screen for depression

Long term: cardiac rehabilitation – patient education to develop a plan for future incidents, assess current

medications and provide suggestions, social worker (re: family, neighbours? Why he has not seen GP?),

dietician (pre-diabetic risks?), plan for regular physical activity

Week 1 CSL

Crisp, J. & Taylor, C. & Rebeiro, G (2013) Potter and Perry’s fundamentals of nursing (4th ed) Elsevier, Australia,

pp.1302-1306: Maintenance and promotion of oxygenation.

Goals of oxygen therapy

To prevent, relieve hypoxia

O2 is not a substitute for other treatment; should only be used when indicated. O2 should be treated as a

drug with dangerous side effects and requires monitoring or dosage/concentration

O2 can be initiated by nurses in emergencies when a patient experiences desaturation or becomes

acutely dyspnoeic; should be administered to achieve saturation level of 88-92% for the COPD patient

and ~95% for others

Safety precautions with oxygen therapy

Oxygen supports combustion; in high concentrations has a great combustion potential and readily fuels

fire. With increasing use of home O2 therapy, patients and health professionals must be aware of the

dangers and promote safety by:

o No smoking in the environment

o Determining all electrical equipment is functioning correctly and properly grounded

o Knowing the fire procedures and location of closest extinguisher

o Checking O2 level of portable cylinders before transporting to ensure there is enough oxygen

remaining in the cylinder

o Ensuring cylinders are stored in a purpose-designed holder to avoid being knocked over and

breaking the valve, thus potentially releasing oxygen under pressure

Supply of oxygen

Generally supplied to the patient’s bedside through a permanent wall-piped system but sometimes also

via oxygen cylinders

Regulators are used to control the amount of O2 delivered

Methods of oxygen delivery

Nasal cannula – oxygen is delivered via cannulas with a flow rate of up to 6L/min however flow rates

>4L/min are generally not used because of the drying effect on the mucosa and relatively little increase in

delivered oxygen concentration

Nasal catheter – used infrequently; oxygen catheter is inserted into the nose to the nasopharynx.

Securing the catheter can cause pressure on the nostril so it must be changed at least every 8 hours and

inserted into the other nostril each time. The patient may experience pain when the catheter is passed

into the naospharynx because trauma can occur to the nasal mucosa

Oxygen mask – used to administer oxygen, humidity or heated humidity; shaped to fit snugly over the

mouth and nose and secured with a strap

o Simple face mask – used for short-term oxygen therapy; fits loosely and delivers oxygen

concentrations form 30-60%. Contraindicated for patients with CO2 retention as it can worsen

o Plastic face mask with a reservoir bag – used for higher concentrations (non-rebreather = 80-

90%; re-breather = 70%); maintains a high-concentration oxygen supply in the reservoir bag.

Venturi mask can deliver oxygen 24-55% with flow rates of 2-14L/min

Mechanical ventilator

Home oxygen therapy

Indications for home oxygen therapy include an arterial oxygen partial pressure (PaO2) of 55mmHg or

less or an arterial oxygen saturation (SaO2) of 88% or less on room air at rest, on exertion or with exercise

Patients with PaO2 or 56-59 mmHg may also receive O2 if there is evidence of cor pulmonale, pulmonary

hypertension, erythrocytosis, CNS dysfunction, impaired mental status or increased hypoxaemia with

exertion

Usually delivered via nasal cannula

Three types of oxygen: compressed oxygen, liquid oxygen or oxygen concentrators

Patients require extensive teaching to be able to continue oxygen therapy at home efficiently and safely

Brown, D. & Edwards, H. (eds.) (2012) Lewis’s medical-surgical nursing (2nd ed) Elsevier, Australia pp. 808-820, 914-

919: Cardiovascular physical examination and electrocardiogram ECG).

Rhythm identification and treatment

Conduction system

o Four properties of cardiac cells enable the conduction system to start an electrical impulse, send

it through cardiac tissue and stimulate muscle contraction

Automaticity – ability to initiate an impulse spontaneously and continuously

Excitability – ability to be electrically stimulated

Conductivity – ability to transmit an impulse along a membrane in an orderly manner

Contractility – ability to respond mechanically to an impulse

o The heart’s conduction system consists of specialised neuromuscular tissue throughout the heart

o Normal cardiac impulse begins in SA node in the upper right atrium atrial myocardium via

interatrial and intermodal pathways atrial contraction atrioventricular (AV) node through the

bundle of His down the left and right bundle branches Purkinje fibres which transmit the

impulse to the ventricles

Nervous control of the heart

o ANS plays important role in the rate of impulse formation, the speed of conduction and the

strength of cardiac contraction

o ANS affects the heart via vagus nerve fibres of the parasympathetic nervous system and nerve

fibres of the sympathetic nervous system

o Stimulation of the vagus nerve decreased rate of firing of the SA node, slowed impulse

conduction of the AV node

o Stimulation of the sympathetic nerves increased SA node firing, AV node impulse conduction

and cardiac contractility

Electrocardiographic monitoring

o ECG: a graphic tracing of the electrical impulses produced in the heart; waveforms on the ECG

represent electrical activity produced by the movement of ions across the membranes of

myocardial cells, representing depolarisation and repolarisation

o High concentration of K and low concentration of Na inside the cell; low concentration of K and

high concentration of Na outside the cell. Inside the cell, at rest (polarised state) is negative

compared with the outside. When a cell/group of cells are stimulated, the cell membrane changes

permeability allows Na to move rapidly into he cell, making the inside of the cell positive

compared with the outside (depolarisation). A slower movement of ions across the membrane

restores the cell to the polarised state (repolarisation).

o ECG has 12 recording leads

6 measure electrical forces in the frontal plane; these are bipolar (+ or -) leads I, II, and

III; and unipolar (+) leads aVr, aVl and aVf

Remaining 6 unipolar leads (V1 to V6) measure electrical forces in the horizontal plane

(praecordial leads)

o 12 lead ECG may show changes suggesting structural changes, conduction disturbances,

damage, electrolyte imbalance or drug toxicity and useful assessment of arrhythmias

o One or more ECG leads can be used to continuously monitor a patient (usually II and V1)

Telemetry monitoring

o Observation of a patient’s HR and rhythm at a site distant from the patient

o Can help rapidly diagnose arrhythmias, ischaemia or infarction

Assessment of cardiac rhythm

o Normal sinus rhythm: a rhythm that starts in the SA node at

a rate of 60-100 times per minute and follows the normal

conduction pathway

Electrophysiological mechanisms of arrhythmias

o Arrhythmias result from disorders of impulse formation, conduction of impulses, or both

o Normally the SA node is the pacemaker of the heart. A secondary pacemaker from another site

may fire in two ways

If the SA node fires more slowly than a secondary pacemaker, the electrical signals from

the secondary pacemaker may ‘escape’; the secondary pacemaker will then fire

automatically at its intrinsic rate. These secondary pacemakers may start from the AV

node at a rate of 40-60 times per minute or the His-Purkinje system at a rate of 20-40

times per minute

Secondary pacemakers can fire more rapidly than the normal pacemaker of the SA node.

Triggered beats (early or late) may come from an ectopic focus or accessory pathway

(area outside the normal conduction pathway) in the atria, AV node or ventricles

arrhythmia which replaces normal sinus rhythm

o Common causes:

Cardiac conditions e.g. accessory pathways, cardiomyopathy, HF, MI, valve disease

Other conditions e.g. acid-base imbalance, caffeine, metabolic conditions, drugs

Types of arrhythmias

Sinus bradycardia – the conduction pathway is the same as that in sinus rhythm but the SA node fires at a

rate less than 60BPM

o May be normal in aerobically trained athletes and in some people during sleep

o Can also be in response to carotid sinus massage, hypothermia, increased intraocular pressure,

certain drugs

o Common diseases states associated: hypothyroidism, increased ICP, hypo, inferior MI

o Treatment may consists of administration of atropine (anticholinergic)

Sinus tachycardia – discharge rate from the sinus node increases because of vagal inhibition or

sympathetic stimulation (>100BPM)

o Associated with physiological, psychological stressors (exercise, pain, MI etc.)

o Can also be an effect of drugs e.g. adrenaline, noradrenaline, atropine, caffeine etc.

o Treatment is based on underlying caused

Premature atrial contraction (PAC) – a contraction starting from an ectopic focus in the atrium (outside of

the SA node) and coming sooner than the next expected sinus beat; the ectopic signal starts in the L or R

atrium and travels across the atria by an abnormal pathway distorted P wave. At the AV node is may

be stopped (non-conducted PAC), delayed (lengthened PR) or conducted normally

o Can result from emotional stress, physical fatigue, caffeine, tobacco, alcohol, hypoxia

o Disease states e.g. hyperthyroidism, COPD, CAD

o ECG: HR varies with underlying rate, frequency of the PAC and rhythm is irregular. P wave is

differently shaped from regular P wave.

o In health hearts, isolated PACs are not significant. In people with heart disease, frequent PACs

may indicate enhanced automaticity of the atria or a re-entry mechanism

Paroxysmal supraventricular tachycardia (PSVT) – arrhythmia starting in an ectopic focus anywhere

above the bifurcation of the bundle of His. Occurs because of a re-entrant phenomenon (re-excitation of

the atria when there is a one-way block)

o In normal heart, PSVT is associated with overexertion, emotional stress, deep inspiration, deep

stimulants like caffeine and tobacco.

o Associated with heart disease, digitalis toxicity, CAD and cor pulmonale

o ECG: HR is 150-220 BPM and rhythm is regular or slightly irregular

o Treatment includes vagal stimulation (carotid massage, coughing) and drug therapy (IV

adenosine)

Atrial flutter – atrial tachyarrhythmia identified by recurring, regular, sawtooth-shaped flutter waves that

originate from a single ectopic focus in the right (or left; less common) atrium

o Rarely occurs in a healthy heart; hence associated with CAD, HTN, PE, chronic lung disease, cor

pulmonale and use of drugs such as digoxin and adrenaline

o ECG: atrial rate is 200-350 BPM; atrial rhythm is regular and ventricular rhythm usually regular

o High ventricular rates (>100BPM) and loss of the atrial ‘kick’ that are associated with atrial flutter

decrease CO. This can cause serious consequences e.g. HF especially if underlying heart

disease

o Increased risk of stroke because of the risk of thrombus formation in the atria from the stasis of

blood

o Primary goal of treatment is to slow the ventricular response by increasing AV block (e.g. Ca

channel blockers)

Atrial fibrillation – characterised by a total disorganisation of atrial electrical activity because of multiple

ectopic foci, resulting in loss of effective atrial contraction

o Arrhythmias may be paroxysmal (beginning/ending spontaneously) or persistent (lasting >7 days)

o Occurs in patients with underlying heart disease e.g. CAD, HF and pericarditis; often develops

acutely with alcohol intoxication, caffeine use, stress and cardiac surgery

o Results in a decrease in CO because of ineffective atrial contractions and/or a rapid ventricular

response

o Goals of treatment include a decrease in ventricular response, prevention of stroke and

conversion to sinus rhythm, if possible

Junctional arrhythmias – arrhythmias that start in the area of the AV node

o Result because the SA node fails to fire or the signal is blocked AV node becomes the

pacemaker of the heart; the impulse from the AV node usually moves in a retrograde (backwards)

fashion.

o Often associated with CAD, HF, cardiomyopathy, inferior MI and rheumatic heart disease

First-degree AV block

Second-degree AV block

o Type I (Mobitz I/Wenckebach heart block)

o Type II (Mobitz II heart block)

Third-degree AV block – complete heart block; no impulses from the atria are conducted to the ventricles

Premature ventricular contraction (PVC) – contraction coming from an ectopic focus in the ventricles;

premature occurrence of a QRS complex

Ventricular tachycardia – occurs when there are three or more consecutive PVCs

o VT is associated with MI, CAD, significant electrolyte imbalances, cardiomyopathy, drug toxicity

and CNS disorders

o Ventricular rate is 150-250BPM

Accelerated idioventricular rhythm

Ventricular fibrillation (VF) – a severe derangement of the heart rhythm characterised on ECG by irregular

waveforms of varying shapes and amplitude

o VF occurs in acute MI and myocardial ischaemia and in chronic diseases such as HF and

cardiomyopathy

o HR is not measurable; rhythm is irregular and chaotic

o VF results in an unresponsive, pulseless and apnoeic state

o Treatment consists of immediate initiation of CPR and advanced life support

Asystole – total absence of ventricular electrical activity

o Usually a result of advanced cardiac disease, a severe cardiac conduction system disturbance or

end-stage HF

o Generally the patient has end-stage heart disease or has a prolonged arrest and cannot be

resuscitated

Pulseless electrical activity (PEA) – organised electrical activity is seen on the ECG but there is no

mechanical activity of the ventricles and the patient has no pulse

Brown, D. & Edwards, H. (eds.) (2012). Chapter 25: Assessment of the Respiratory System, 570-586

Subjective data

Important health information

o Past health history: frequency of upper respiratory problems, allergic reactions, asthma, COPD

o Medications: reason for taking medication, length, side effects

o Surgery or other treatments

Functional health patterns

o Health perception-health management pattern (how do your breathing problems affect self-care?)

o Nutritional-metabolic (have you recently lost weight because of difficult eating secondary to

respiratory problems?)

o Elimination (does your respiratory problem make it difficult for you to get to the toilet?)

o Activity-exercise (are you ever SOB during exercise?)

o Sleep-rest (do breathing problems cause you to awaken during the night?)

o Cognitive-perceptual (do you have difficulty remembering things?)

o Self-perception-self-concept (describe how your respiratory problems have changed your life?)

o Role-relationship (has your respiratory problem caused any difficulties in your work, family or

social relationships?)

o Sexuality-reproductive (has your respiratory problem caused a change in your sexual activity?)

o Coping-stress tolerance (how often do you leave your home?)

o Value-belief (what do you believe causes your respiratory problems?)

Objective data

Physical examination (vital signs, nose, mouth, pharynx, thorax, lungs, neck)

o Inspection – pursed-lip breathing, tripod position, accessory muscle use, splinting, increased AP

diameter, tachypnea, Kussmaul respirations, cyanosis, finger clubbing, abdominal paradox

o Palpation – tracheal deviation, altered tactile fremitus, altered chest movement

o Percussion – hyperresonance, dullness

o Auscultation – fine/coarse crackles, Rhonchi, wheezes, stridor, absent breath sounds, pleural

friction rub, Bronchophony, whispered pectoriloquy, Egophony

Normal breath sounds

o Vesicular – relatively soft, low pitched, gentle, rustling sounds

o Broncho-vesicular – medium pitch and intensity; heard anteriorly over the mainstem bronchi on

either side of the sternum and posteriorly between the scapulae

o Bronchial – louder, higher pitched and resemble air blowing through a hollow pipe

Abnormal breath sounds

o Bronchial or bronchovesicular sounds heard in the peripheral lung fields

o Adventitious sounds – extra breath sounds that are abnormal e.g. crackles, wheezes

Brown, D. & Edwards, H. (eds.) (2012). Chapter 27: Lower Respiratory Problems: Acute Bronchitis and

Pneumonia, 615–622

Acute bronchitis

An inflammation of the bronchi in the lower respiratory tract

Up to 90% of acute bronchial infections are viral in origin

Cough (most common symptom) lasts for up to 3 weeks

Clear, mucoid sputum is often present, although some patients produce purulent sputum

Associated symptoms: headache, fever, malaise, hoarseness, myalgias, dyspnea and chest pain

Assessment may reveal normal breath sounds or rhonchi, rales or wheezes, usually with expiration and

exertion

Evidence of consolidation (e.g. fremitus, rales, egophony), which is suggestive of pneumonia, is absent

with bronchitis (consolidation in the lungs occurs when fluid accumulates, causing the lung tissue to

become stiff and unable to exchange gases)

Acute bronchitis is usually self-limiting, and treatment is supportive (e.g. bronchodilators, cough

suppressants, inhaled corticosteroids)

Pertussis (whooping cough)

Highly contagious infection of the respiratory tract caused by Gram-negative bacillus Bordella pertussis

Characterised by uncontrollable, violent coughing

Despite improved childhood vaccination rates in developed countries, the incidence of pertussis has been

steadily increasing since the 1980s, with the largest increase noted in adults

Immunity resulting from childhood vaccination with DPT may wane over time milder infection that is still

distressing and contagious

Signs and symptoms occur in stages

o First stage: mild upper respiratory tract infection (URI) with a low-grade or no fever, runny nose,

watery eyes and mild non-productive cough

o Second stage (paroxysmal): paroxysms of cough; inspiration after each cough produces typical

‘whooping’ sound as the patient tries to breathe in air against an obstructed glottis; vomiting may

also occur with coughing

Treatment: course of Abx

Pneumonia

Acute infection of the lung parenchyma

Pneumonia is more likely to occur when the defence mechanisms (of the airway distal to the larynx e.g.

air filtration, cough reflex, mucociliary escalator mechanism) become incompetent or are overwhelmed by

the virulence or quantity of infectious agents

Decreased consciousness depresses cough/epiglottal reflexes; tracheal intubation interferes with cough

reflex; air pollution, some medications, cigarettes etc.

Organisms that cause pneumonia reach the lung in three ways:

o Aspiration of normal flora from the nasopharynx or oropharynx; many of the organisms causing

pneumonia are normal inhabitants of the pharynx in healthy adults

o Inhalation of microbes in the air

o Haemotogenous spread from a primary infection elsewhere in the body e.g. Staph aureus

Types of pneumonia