3: Respiratory physiotherapy


CHAPTER 3
Respiratory physiotherapy


Introduction


Respiratory physiotherapy is probably the least recognised and least understood treatment used in veterinary patients. The aims of treatment are to:



  • Clear chest secretions
  • Improve gaseous exchange
  • Increase lung volume
  • Reduce respiratory effort
  • Improve exercise tolerance
  • Prevent secondary complications.

These aims are achieved by using manual techniques such as percussion (coupage) and vibrations to clear secretions, and positioning to optimise gaseous exchange and prevent secondary respiratory complications.


Chest auscultation and interpretation


Chest auscultation should be carried out in a quiet area. Ideally the patient is positioned either standing or sitting; if this is not possible then he may rest in sternal recumbency. It is preferable if the patient is not panting; however, be aware that the patient may be panting because he is in respiratory distress, and closing his mouth to auscultate his chest may cause him further distress.


A systematic approach should be adopted comparing left and right sides. Dogs and cats have four lung lobes on the right side, and three lung lobes on the left side. It is not always possible to be sure which lung lobe you are auscultating over, so it is easier to divide the lung fields into zones. Each lung should be divided into three zones: the upper zone is the area of lung cranial to the heart, the mid-zone the area of lung over the heart, and the lower zone the area of lung tissue caudal to the heart.


Breath sounds


Normal breath sounds tend to be quiet, with a inspiration / expiration ratio of 1:2; inspiration is the shorter, followed without a pause by a longer expiration phase, which tends to be passive.


Diminished sounds or quiet breath sounds may be evident in areas of atelectasis caused by reduced air entry into the affected area. Diminished breath sounds may also be evident over pleural effusions, as the fluid within the pleural space will muffle the normal sounds, or if pneumothorax is present and gaseous exchange is compromised.


Added sounds


Fine crackles may be evident when auscultating towards the lower zones (or bases) of the lungs and towards the periphery of the lung zones. A fine, sharp crack may be heard at the end of inspiration just before expiration, and is caused by a small amount of fluid in the alveoli and peripheral airways when pulmonary oedema is present.


Coarse crackles are associated with retention of secretions in the larger proximal airways. Early inspiratory and expiratory coarse crackles are evident in bronchitis; late inspiratory coarse crackles are evident with pneumonia.


It is worth remembering that the worse or louder the respiratory noise is in patients with pneumonia the easier it will be to clear the secretions using manual techniques. If the secretions are not cleared and the area of lung tissue becomes consolidated, air entry and lung volume will be reduced. This will result in an increase in respiratory rate and a drop in pulse oximetry oxygen saturation (SPO2) values, and secretion clearance using manual techniques will be more difficult.


Wheeze is evident with narrowing of the airways; an expiratory wheeze with prolonged expiration is often associated with asthma. A wheeze during both inspiration and expiration may indicate an airway stricture.


Many educational websites are available with audible auscultation breath sounds, including the Colorado State University Auscultation Library (http://www.cvmbs.colostate.edu/clinsci/callan/breath_sounds.htm).


Percussion note technique and interpretation


The percussion note is tested to determine if air, fluid or solid structures are present within the lungs. The operator places a middle finger between the patients rib space and sharply taps the distal end of his finger with the other hand. The percussion note may be:



  • Resonant and therefore normal.
  • Hyperresonant, which may indicate emphysema or pneumothorax.
  • Dull, indicating areas of consolidation, collapse or pleural effusion.

The percussion note test is usually performed along with other diagnostic tests and is not a reliable diagnostic tool when used alone.


Interpretation of blood gases


Acidosis


Acidosis is an increase in blood acidity, and blood pH is determined by the blood acid–alkali balance. The PaCO2 is the measure of partial pressure of carbon dioxide in arterial blood; an increase of PaCO2 indicates respiratory acidosis; a decreased level of HCO3 (bicarbonate) in blood indicates a metabolic acidosis.


Alkalosis


Alkalosis occurs when the blood pH increases. A decrease in PaCO2 indicates a respiratory alkalosis. An increase in HCO3 indicates a metabolic alkalosis.


Base excess


Base excess assesses the metabolic component of acid–base disturbances and indicates the degree of renal compensation. A reduced base excess indicates a metabolic acidosis and an increase in base excess indicates a metabolic alkalosis (Kenyon & Kenyon, 2009) (Table 3.1).


Table 3.1 Normal blood values.


Adapted from Waddell, L.S. (2013) The practitioner’s acid–base primer: obtaining & interpreting blood gases. Today’s Veterinary Practice, May/June. Reprinted with permission of the North American Veterinary Community.




















































Parameter Reference range canine Reference range feline
Arterial blood analysis
pH 7.395 [±0.03] 7.34 [±0.1]
PaO2 (mmHg) 102.1 [±6.8] 102.9 [±15]
PaCO2 (mmHg) 36.8 [±2.7] 33.6 [±7]
HCO3 (mmol/L) 21.4 [±1.6] 17.5 [±3]
Base excess (mmol/L) −1.8 [±1.6] −6.4 [±5]
Venous blood analysis
pH 7.352 [±0.02] 7.30 [±0.08]
PaO2 (mmHg) 55 [±9.6] 36.8 [±11]
PaCO2 (mmHg) 42.1 [±4.4] 41.8 [±9]
HCO3 (mmol/L) 22.1 [±2] 19.4 [±4]
Base excess (mmol/L) −2.1 [±1.7] −5.7 [±5]

The blood pH will be altered in uncompensated acid–base disorders, whereas pH will be normal in compensated acid–base disorders (Table 3.2).


Table 3.2 Simple acid–base disorders.





























pH PaCO2 HCO3
Respiratory acidosis
Uncompensated
Compensated		 Decreased
Normal		 Increased
Increased		 Normal
Increased
Respiratory alkalosis
Uncompensated
Compensated		 Increased
Normal		 Decreased
Decreased		 Normal
Decreased
Metabolic acidosis
Uncompensated
Compensated		 Decreased
Normal		 Normal
Decreased		 Decreased
Decreased
Metabolic alkalosis
Uncompensated
Compensated		 Increased
Normal		 Normal
Increased		 Increased
Increased

Respiratory failure


Respiratory failure occurs when blood gas values cannot be maintained within normal limits (Table 3.3). There are two types.


Table 3.3 Arterial blood gas classification of respiratory failure.
























pH PaCO2 HCO3
Acute Decreased Increased Normal
Chronic Normal Increased Increased
Acute on chronic Decreased Increased Increased

Acute or chronic relates to either type I or II respiratory failure. Acute on chronic would occur in a patient who has either chronic type I or II respiratory failure that is generally managed well medically but has an exacerbation of symptoms; e.g. when a patient with chronic emphysema is taken for a long run the chronic emphysema may become exacerbated, in which case it is termed acute on chronic.


Type I (hypoxaemic respiratory failure)


This is characterised by a decrease in the partial pressure of oxygen in arterial blood (PaO2: hypoxaemia) with a normal or slightly increased PaCO2 due to inadequate gas exchange. Causes include:



  • Pneumonia
  • Emphysema
  • Severe asthma.

Type II (ventilatory failure)


This is characterised by a decreased PaO2 with an increased PaCO2 (hypercapnia) caused by hypoventilation. Causes include:



  • Polyradiculoneuritis.
  • Asthma, chronic obstructive pulmonary disease (COPD).
  • Drug-related respiratory drive depression (Kenyon & Kenyon, 2009).

Cardiorespiratory monitoring


Cardiorespiratory monitoring and recording shows trends over time. Observing the trends over a period of time allows for early intervention to forestall a crisis situation.



  • Arterial blood pressure (ABP) is measured via an intra-arterial cannula for continuous monitoring; the cannula also provides access for arterial blood sampling for blood gas analysis.
  • Cardiac output (CO) is the volume of blood pumped into the aorta each minute (Table 3.4).
  • Central venous pressure (CVP) measures circulating blood volume and venous return via a cannula placed in the jugular vein.
  • Cerebral perfusion pressure (CPP) is used to measure blood supply to the brain.
  • Heart rate (HR) is defined as the number of times the heart beats per minute.
  • Intracranial pressure (ICP) is the pressure exerted on the brain by the cerebrospinal fluid (CSF). Hydrocephalus, cerebral haemorrhage, hypoxia and infection cause the ICP to rise resulting in a decreased blood supply to the brain. The patient may show signs of altered mentation; handling of the patient should be kept to a minimum, and ideally the head should be supported at a 15–30° angle to prevent further ICP.
  • Mean arterial pressure (MAP) is the average measure of blood in the circulatory system, related to cardiac output and systemic vascular resistance. MAP is an indicator of the tissue perfusion pressure.
  • Oxygen saturation (SPO2) is the measure of arterial blood oxygen saturation expressed as a percentage using non-invasive pulse oximetry.
  • Respiratory rate (RR) is a measure of the number of breaths in 1 minute.
  • Stroke volume (SV) relates to the volume of blood ejected from the ventricles during each systolic contraction.
  • Systemic vascular resistance (SVR) measures vascular overload in the left ventricle. Vasoconstriction will increase systemic vascular resistance, vasodilation will decrease it.

Table 3.4 Cardiorespiratory monitoring equations.






















Parameter Equation
Cardiac output (CO) (L/min) CO = HR × SV
Cerebral perfusion pressure (CPP) (mmHg) CPP = MAP− ICP
Mean arterial pressure (MAP) (mmHg) MAP = (diastolic BP × 2) + (systolic BP)/3
Stroke volume (SV) (mL) SV = (CO × 1000)/HR
Systemic vascular resistance (SVR) (mmHg) SVR = (MAP − CVP/CO) × 79.9

BP, blood pressure (mmHg); CVP, central venous pressure (mmHg); ICP, intracranial pressure (mmHg).


Electrocardiograms


Electrocardiograms (ECGs) detect the sequence of electrical events that occur during the contraction (depolarisation) and relaxation (repolarisation) cycle of the heart. Depolarisation is initiated by the sinoatrial node, the heart’s natural pacemaker, which transmits the electrical stimulus to the atrioventricular (AV) node. From here the impulse is conducted through the bundle of His and along the bundle branches to the Purkinje fibres, causing the heart to contract.


Normal sinus rhythm is characterised by:



  • Regular rhythms and rates.
  • A P wave, QRS complex and T wave are all present; and all similar in size and shape (Figure 3.1).
c3-fig-0001

Figure 3.1 Electrocardiogram of normal sinus rhythm.


Sinus tachycardia (Figure 3.2) occurs with sinus rhythm and an elevated resting heart. Causes include:



  • Sepsis
  • Anaemia
  • Pulmonary embolism
  • Hypovolaemia
  • Drugs (salbutamol).
c3-fig-0002

Figure 3.2 Electrocardiogram of sinus tachycardia.


Sinus tachycardia can also occur in high emotional states such as:



  • Pain
  • Anxiety
  • Fear.

Premature ventricular contractions (PVCs) are characterised by early beats (ectopic), usually caused by electrical irritability in the ventricular conduction system or myocardium. They can be asymptomatic. However, they can indicate impending fatal arrhythmias in patients with heart disease. ECG findings include:



  • An irregular rhythm during PVC; however, underlying rhythm and rate are usually regular.
  • The P wave is absent, the QRS complex is wide and early, and the T wave is in the opposite direction from the QRS complex during PVC (Figure 3.3).
c3-fig-0003

Figure 3.3 Electrocardiogram of premature ventricular contractions.


Atrial fibrillation is characterised by rapid unsynchronised electrical activity generated in the atrial tissue. Transmission of the impulses to the ventricles via the AV node is variable and unpredictable, leading to an irregular heartbeat. ECG findings include:



  • Absent P waves replaced by fine baseline oscillations.
  • Irregular ventricular complexes.
  • Ventricular rate varies between 100 and 180 bpm but can be slower (Figure 3.4).
c3-fig-0004

Figure 3.4 Electrocardiogram of atrial fibrillation.


Respiratory presenting conditions


Chronic obstructive pulmonary disease (COPD)


Chronic obstructive pulmonary disease (COPD) is an umbrella term used to describe several relatively common respiratory diseases affecting humans, in which it is often associated with tobacco smoking or contact with fine particles that may be inhaled into the lungs, such as asbestos. Domestic animals may be subjected to passive smoking, which may contribute to COPD in these species (Figure 3.5).

c3-fig-0005

Figure 3.5 Chronic obstructive pulmonary disease.


Asthma


Asthma tends to be seen more commonly in feline patients. Diagnosis is usually reached by eliminating other diseases and by the response seen to treatment (anti-inflammatory steroids). Symptoms include increased respiratory rate and effort in the expiratory phase as the patient attempts to clear CO2

Only gold members can continue reading. Log In or Register to continue

Related posts:

  1. answers
  2. 4: Hydrotherapy
  3. 1: Musculoskeletal physiotherapy
  4. 2: Neurology

Stay updated, free articles. Join our Telegram channel
Tags:
Jul 18, 2021 | Posted by in NURSING & ANIMAL CARE | Comments Off on 3: Respiratory physiotherapy

Full access? Get Clinical Tree
Get Clinical Tree app for offline access