New York Heart Association (NYHA) Classification of Heart Failure


This system of classification relates to the symptoms of everyday activities and patient's quality of life.
The limitations/symptoms are in regards to normal breathing and varying degrees in shortness of breath and or angina pain.

Class
Patient Symptoms
Class I (Mild)
No limitation of physical activity. Ordinary physical activity eg. walking, climbing up stairs, does not cause undue fatigue, palpitation, or dyspnoea (shortness of breath).
Class II (Mild)
Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, palpitation, dyspnoea and/or angina.
Class III (Moderate)
Marked limitation of physical activity eg. can only walk short distances of 20-100m. Comfortable at rest, but less than ordinary activity causes fatigue, palpitation, or dyspnoea.
Class IV (Severe)
Unable to carry out any physical activity without discomfort. Mostly bedbound. Symptoms of cardiac insufficiency at rest. If any physical activity is undertaken, discomfort is increased.
Other Investigations for Respiratory Disease

1. Haematological and biochemical tests (main ones)
· Haemoglobin-anaemia/polycythaemia
· Packed call volume-secondary polycythaemia(occurs with chronic hypoxia)
· Routine biochemistry-carcinoma/infection
· D dimer-rule out PE

2. Sputum
· Colour
i. Yellow/green- inflammation(infection or allergy)
ii. Presence of blood-neoplasm/pulmonary infarct

· Microbiological studies of value in Pneumonia/TB diagnosis/Aspergillus lung disease
NOT USEFUL for URT or acute/chronic bronchitis

·
Sputum cytology- diagnosis of bronchial carcinoma

·
Transtracheal aspiration
i. needle though cricothyroid membrane
ii. catheter threaded to sit just above carina
iii. px coughs and sputum collected by aspiration
Not often required but good for LRT infection as it avoids contamination with bacteria from pharynx and mouth

3. Chest X-Ray
Take into consideration
i. Film is centred(equal space between clavicle head to spinous process)

ii. Penetration (film is not too dark)

iii. View (PA Is the norm-film is placed anterior to patient, x-Ray source posterior. AP is taken in very ill px who cannot stand up, cardiac outline bigger, scapula in the way)

iv. Look at
· Shape and bony structure of chest wall
· Trachea central?
· Diaphragm elevated/flat?
· Shape, size & position of heart
· Shape and size of hilar shadows
· Size and shape of any lung abnormalities and vascular shadowing

v. X-Ray abnormalities
· Collapse- lung lobes have habitual collapse locations
o Lower-downwards towards mediastinum
o Left upper- forward against anteriorly chest wall
o Right upper lobe- upwards and outwards(an arch)
o Right middle-anteriorly and inward, obscure right heart border
o Whole lung-mediastinal shift towards side of collapse
· Consolidation- remain the same size
· Pleural effusions
o Need to be more than 500 mL to cause problems
o Blunt costophrenic angle- a characteristic shadow with curved upper edge into axial
· Fibrosis
o Causes streaky shadowing
o Accompanying loss of lung volume causes mediastinal shift to same side
o Generalised fibrosis-honeycomb
· Round shadows-cancer/abscess/cysts/nodules/TB/anything
· Military mottling(minute opacities 1-3 mm in size) TB/Pneumoconiosis/Sarcoidosis/Pulmonary oedema

4. Computed tomography (CT)
i. Spiral scanning-done during contrast injection eg PE
ii. Conventional CT- staging of cancers
iii. CT guided biopsy
iv. High resolution in diagnosis of
· Diffuse interstitial pulmonary involvement eg. Sacoidosis
· Bronchiectasis (sensitivity & specificity >90%)
· Emphysema vs interstitial lung disease

5. Positron emission tomography (PET)-tumours take up a tracer, enabling differentiating between benign and malignant tumours

6. Scintigraphic imaging-detection of PE, though less and less as D-Dimer used to screen now
· Perfusion scan
i. Uses albumin labelled with techtium-99, aggregates in pulmonary capillaries and remain for a few hours
ii. Position is detected via gamma camera
iii. Resultant pattern indicated distribution of pulmonary blood flow

·
Ventilation-perfusion scan
i. Xenon inhaled and distribution is detected the same time as perfusion scan
ii. PE(impaired perfusion relative to ventilation)/asthma & pneumonia (both diminished)

7. Exercise tests-degree of debility produced by breathlessness
i. Uptake of oxygen/work performed/heat rate/BP/ECGs used to allow detection of lung disease and MI, allow distinction between heart and lung disease and enable assessment of fitness

8. Pleural aspiration
· Necessary for diagnosis of most effusions
i. 20 mL syringe inserted though intercostal space over an area of dullness
ii. Protein/cytology/bacteriological studies

9. Pleural biopsy- TB and malignancy

10. Fibreoptic bronchoscopy-peripheral lesions to undergo cytological examination for malignancy and appropriate staining and culturing for bacteria

9 and 10 were complex procedures that I couldn’t be bothered explaining :S

CLASSIFYING DYSPNEA:

First determine cause:
  1. Cardiac Dyspnea-- consider mitral stenosis, IHD, LVF, esp. if ankle oedema, lung crepitations and increased JVP present.
  2. Pulmonary Dyspnea—airway and interstitial diseases. Usually diagnosis depends on circumstances in which dyspnea occurs.
  3. Anatomical Dyspnea—diseases of chest wall, muscles, pleura—also consider ascites, which restricts diaphragm movement.
  4. Shock
  5. Anemia
  6. Metabolic acidosis

Then classify by type:

- Paroxysmal nocturnal dyspnea—severe, sudden shortness of breath that wakes the patient, usually several hours after sleeping. The coughing and wheezing associated with PND can usually be relieved by sitting upright— PND due to pulmonary edema, because lying flat, fluid from other areas is reabsorbed, leading to pulmonary hypertension, then edema. Usually a sign of congestive heart failure— consider MS, AI.
-Exertional dyspnea: most common presentation. Can be caused by any disease that puts stress on the heart.
POSITIONAL DYSPNEAS
Orthopnea—breathlessness lying flat, measured in the number of pillows patient needs in order to breathe. Often a symptom of left ventricular heart failure, pulmonary edema. Other causes are asthma, chronic bronchitis, sleep apnea.
Trepopnea—SOB only when lying on one side (results from one-sided lung disease,chronic congestive heart failure, or disease of one major bronchus.) Lying on side of healthier lung, in order to prevent perfusion of diseased lung—perfusion leading to shuntingà hypoxemiaà worsened SOB.
Platypnea—opposite of orthopnea—SOB lying down, worsens when standing. Either due to hepatopulmonary syndromes, or right-to-left shunting in the heart.

Classify by grades:
Comroe grades of breathlessness:
  1. awareness of increased ventilation, SOB
  2. deep breathing associated with exercise
  3. hindered breathing
  4. suffocating feeling/need for deep inspiration
  5. breathlessness when breathholding.

Classify by rate:
-tachypnea
-eupnea
-bradypnea

DDx for breathlessness
Hematologic

  • Polycythemia
  • Shock - circulatory failure resulting in inadequate organ perfusion
    • hemorrhagic, septicemia, drugs
  • Leukemia
  • Hodgkin’s disease
  • Sickle cell anemia
  • Aplastic anemia - a syndrome of bone marrow failure characterized by peripheral pancytopenia and marrow hypoplasia
  • Methemoglobinemia - an abnormal amount of haemoglobin build up in the blood. The Hb is unable to carry oxygen effectively to the tissues.
  • Hemangioma - an abnormal buildup of blood vessels in the skin or internal organs, usually in infancy eg. Larynx
Endocrine
  • Waterhouse-friderichsen syndrome - Adrenal gland failure due to bleeding into the adrenal gland. It is caused by severe meningococcal infection or other severe, bacterial infection, leading to shock.
  • Hyperthyroidism
  • Metabolic acidosis eg. Diabetic acidosis, uremia - a clinical syndrome associated with fluid, electrolyte, and hormone imbalances and metabolic abnormalities (anion-gap metabolic acidosis), lactic acidosis
Psychogenic
  • Panic attack
Neurological and muscle disorders
  • Multiple Sclerosis
  • ALS (Amyotrophic lateral scelrosis) - A motor neuron disease involving progressive degeneration and eventual destruction of the function of nerves that control voluntary movement
  • Myasthenia Gravis
  • Certain diaphragm disorders


Cardiac causes of S.O.B

Myocardial ischaemia (IHD) – CAD, atherosclerosis, stable and unstable angina, AMI, perfusion problem to tissues, lungs.

Congestive heart failure – How? à reduced contractility, reduced stroke volume, reduced ‘spare capacity’, increased heart rate, hypertrophy, all affect à CO = HR x SV. Most can cause S.O.B by themselves!
End result. Decreasing CO and Increasing strain on the heart.
Compensatory mechanisms? MAP = CO x TPR
1.) CO decreases, MAP decreases. What now??? Increase TPR!, Baroreceptors in carotid sinus and aortic arch less stimulated More symp activity to blood vessels, vasoconstriction.
2.) ADH – symp stimulation of hypothalamus. What happens?
3.) CO decreases, MAP decreased, perceived hypovolemia! Reduced perfusion to kidneys
à RAAS : increases volume state, increases MAP!
Results of compensatory mechanisms?
Increased peripheral resistance.
Fluid overload (greater blood volume)
Both accelerate damage to myocardium!
Vasoconstriction and fluid retention
à increased hydrostatic pressure on capillaries à ODEMA!
This is really really simple, there is much more to CCF, but I’m cutting it down.

Valvular obstruction – One of the causes of CHF! What are other causes of CCF? Hypertrophy of ventricles, stiffness of walls, dilation… ineffective pumping = reduced CO

Arrhythmia – Brady à HR is too slow to provide sufficient tissue perfusion. Tachy à Inefficient pumping of the heart.

Cardiac temponade – Fluid accumulation in pericardium, external pressure on heart, prevents ventricles from filling properly, low stroke volume. Ineffective pumping of blood, shock death.

Respiratory Examination (Lionel)
General inspection
· Breathing patterns
o Bradypnoea
§ CO2 narcosis (excess O2 administration)
§ Drugs (e.g. opiates, alcohol, benzodiazepines, muscle relaxants)
§ Raised intracranial pressure
§ Head injury or cervical cord trauma
§ Acute neuromuscular disease (e.g. Guillain-Barré syndrome)
§ Severe hypothermia
o Tachypnoea
§ Hypoxia (e.g. CO poisoning, exertional, anaemia)
§ Shock
§ Sepsis
o Accessory muscle use
§ Dyspnoea
o Pursed-lip breathing
§ COPD
o Cheyne-Stokes breathing
§ LVF
§ Brain damage
§ High altitude
o Kussmaul’s breathing
§ Metabolic acidosis
o Hyperventilation
§ Anxiety
o Ataxic breathing
§ Brainstem damage
o Apneustic breathing
§ Pontine damage
o Paradoxical respiration
§ Diaphragmatic paralysis
· Cough
o Bovine cough
§ Vocal cord paralysis
o Muffled, wheezy, ineffective cough
§ Obstructive pulmonary disease
o Loose, productive cough
§ Excessive bronchial secretions (chronic bronchitis, pneumonia, bronchiectasis)
o Dry, irritating cough
§ Chest infection
§ Asthma
§ Carcinoma of bronchus
§ LVF
§ Interstitial lung disease
§ Drugs (ACE-I)
· Stridor
o Obstruction of larynx, trachea, large airways
§ Foreign body
§ Tumour
§ Infection (e.g. epiglottitis)
§ Inflammation
· Hoarseness
o Recurrent laryngeal nerve palsy
§ Carcinoma of lung (usually left sided)
§ Laryngeal carcinoma
§ Laryngitis
§ Hypothyroidism
· Cyanosis
o Central
§ Ventilation/perfusion imbalance (reduced arterial O2 saturation)
· Pneumonia
· COPD
· PE
Hands
· Clubbing
o Hypertrophic pulmonary osteoarthropathy
o Lung carcinoma
o Chronic pulmonary suppuration (bronchiectasis, lung abscess, empyema)
o Idiopathic pulmonary fibrosis
o Cystic fibrosis
o Asbestosis
o Pleural mesothelioma or pleural fibroma
· Staining
o Cigarette smoking
· Wasting and weakness
o Compression of and infiltration of brachial plexus by peripheral lung tumour
· Pulse rate
o Tachycardia
§ Asthma
§ Drugs (β-agonists)
o Pulsus paradoxus
§ Obstructive pulmonary disease
o Asterixis
§ COPD
Face
· Eyes
o Horner’s syndrome
§ Apical lung tumour compressing cervical sympathetic nerves)
· Nose
o Nasal polyps
§ Asthma
o Engorged turbinates
§ Allergies
o Deviated septum
§ Nasal obstruction
· Mouth
o Reddened pharynx, tonsillar enlargement, pus
§ URTI
· Sinuses
o Tenderness
§ Sinusitis
Trachea
· Displacement
o Upper lobe collapse
o Upper lobe fibrosis
o Pneumonectomy
o Massive pleural effusion
o Tension pneumothorax
o Retrosternal goitre
· Tracheal tug
o Airflow obstruction causing overexpansion of chest
Chest
· Inspection
o Barrel chest
§ Severe asthma
§ Emphysema
o Pectus carinatum
§ Childhood respiratory illness
o Harrison’s sulcus
§ Severe childhood asthma
§ Rickets
o Subcutaneous emphysema
§ Pneumothorax
§ Oesophageal rupture
§ Pneumomediastinum
o Reduced chest wall movement
§ Unilateral
· Localised pulmonary fibrosis
· Consolidation
· Collapse
· Pleural effusion
· Pneumothorax
§ Bilateral
· COPD
· Diffuse pulmonary fibrosis
· Palpation
o Reduced chest expansion
§ Lesion on reduced side
o Apex beat
§ Displacement towards lesion
· Collapse of lower lobe
· Localised pulmonary fibrosis
§ Displacement away from lesion
· Pleural effusion
· Tension pneumothorax
§ Impalpable
· COPD
o Vocal fremitus
§ See vocal resonance
o Ribs
§ Localised pain
· Fracture
· Percussion
o Hyperresonance
§ Pneumothorax
§ COPD
o Dullness
§ Pneumonia
· Auscultation
o Breath sounds
§ Quality
· Bronchial breath sounds
o Consolidation
o Localised pulmonary fibrosis
o Pleural effusion
o Collapsed lung
§ Intensity
· Reduced
o COPD
o Pleural effusion
o Pneumothorax
o Pneumonia
o Large neoplasm
o Pulmonary collapse
§ Adventitious sounds
· Wheezes
o Asthma
o COPD
o Bronchial obstruction
· Crackles
o Early inspiratory
§ COPD
o Late or pan-inspiratory
§ Alveolar disease
o Fine crackles
§ Pulmonary fibrosis
o Medium crackles
§ LVF
o Coarse crackles
§ Bronchiectasis
· Pleural friction rub
o Pleurisy
§ Vocal resonance
· Aegophony
o Consolidation