Cardiology Manual

Contents

• Basic Cardiology

1. Clinical Anatomy & Physiology

• Cardiology Case taking

1. Clinical Approach to Cardiac Patient

• Cardiology Disease

1. Congenital Heart Disease in Adult
2. Valvular Heart Disease
3. Rheumatic Fever
4. Infective Endocarditis
5. Systemic Hypertension
6. Coronary Artery Disease
7. Disease of Pulmonary Circulation
8. Heart Muscle Disease
9. Cardiac Neoplasm
10. Pericardial Disease
11. Dysrrhytmias and Conduction Defects
12. Heart Failure
13. Disease of Aorta
14. Peripheral Arterial Disease
15. Heart in Systemic Disease

[Continue reading...]

Respiratory Medicine

Contents

• Respiratory Case Taking

1. History Taking
2. Symptoms of Chest Disease- (Cough, Expectoration, Wheezes, Dyspnea, Hemoptysis, Chest Pain)
3. Investigation- (Chest X-ray, Pulmonary Function Test)

• Basic Respiratory

1. Clinical Anatomy
2. Developmental Disorder

• Respiratory Disease

1. Acute Bronchitis
2. Pneumonia
3. Pulmonary Tuberculosis- (Complication)
4. Extra Pulmonary Tuberculosis
5. Suppurative Lung Syndrome
6. Pleural Diseases
7. Bronchial Asthma
8. Hypersensitivity Pneumonitis
9. Smoking
10. Chronic Obstructive Pulmonary Disease
11. Lung Cancer
12. Disease of Mediastinum
13. Respiratory Failure
14. ARDS
15. Oxygen Therapy
16. Pulmonary Thromboembolic Disease
17. Pulmonary Hypertension
18. Pulmonary Fibrosis
19. Lung Collapse and Atelectesia
20. Disease of the Chest Wall
21. Disease of the Diaphragm
22. Uncommon Chest Diseases
23. Chest Radiology
24. Investigations in Chest Medicine

[Continue reading...]

Respiratory Alkalosis

Causes

• Stimulated respiratory drive
  • CNS
    • CVA, ICH, psychogenic
  • Hypermetabolic
    • Thyrotoxicosis
    • Pregnancy (Progesterone)(Secondary to reduced FRC)
    • Sepsis (fever) (often before metabolic acidosis)
    • DT, anxiety, pain
    • DKA and aspirin OD
  • Environmental
    • HYPERthermia (Heat tetany)
  • Drugs
    • Aspirin OD
    • Progesterone
  • Liver failure (encephalopathy) with hyperammonaemia (ammonia)
• Iatrogenic mechanical ventilation

Hypoxemia induced

• Pneumonia, PE, asthma
• Congenital heart disease
• Chronic altitude compensation
• Early in altitude acclimatisation

Compensation for metabolic acidosis

NOTE:

• Self-perpetuating process: Hyperventilation removes CO2 which causes cerebral acidosis and stimulates further increase in ventilation
• Chronic respiratory alkalosis is unique in that it CAN have full metabolic compensation (Only acid-base disorder that allows this)

Clinical

• Associated changes
  • HYPOcalcaemia, HYPOkalaemia, HYPOphosphatemia
  • Decreased Co2 reduces H+ binding, increases negative charge of proteins and increases binding of calcium to proteins
    • Thus reducing ionised calcium
  • Hypocalcaemia with tetany and carpopedal spasm
• Shift 02 dissociation curve to the left (Alkalosis) (Increased affinity of Hb for O2)

Correction

• Treat underlying cause
• Re-breather mask

[Continue reading...]

Respiratory Acidosis

Causes

• Decreased respiratory drive
  • CNS:
    • CVA, tumour, infection (encephalitis), haemorrhage
  • Drugs
    • Narcotics and sedatives
• Decreased chest wall movement
  • Neurological
    • NM disorders, Guillain-Barre
    • Myasthenia gravis, demyelinating disorders
    • Tetanus
  • Toxicity
    • Muscle relaxants, Organophosphates, fentanyl
  • Respiratory (Acute)
    • Trauma, surgery, chest wall deformity
    • Tension pneumothorax, pleural effusion
    • Upper airway obstruction
  • Equipment
    • Increased dead space, improper connection
• Obstructive pulmonary disease (chronic)
  • COPD, asthma, pneumonia

Clinical

• Vasodilation, sweaty, tachycardic, mydriasis, asterixis
• Confusion
• Drowsy and ALOC

Correction

• Renal compensation is slow and requires ventilatory changes for treatment
• Increase alveolar minute ventilation

NOTE:

• Usually the rise in pCO2 will stimulate the respiratory centre to increase minute volume.
• If this fails then rapid rise in pCO2 with sedation and failure of respiratory drive and death

[Continue reading...]

Metabolic Alkalosis

• Metabolic changes that result in the accumulation of base
• Accumulation of base occurs as a result of
  • Increased acid loss
  • Excess alkali intake

Causes

• G          GIT excess acid loss
  • Vomit (and pyloric stenosis)
  • NGT drainage
  • Diarrhoea
  • Ileostomy
  • Dehydration
• R          Renal excess acid loss
  • Bartter’s
  • Gitelman’s
  • Diuretics (Loss of H+, K+, Cl-)
• O          Overdose of base
  • Antacid OD, Laxative, Milk-alkali syndrome
  • Massive Hartmann’s transfusion
  • Iatrogenic use of HCO3
• E           Endocrine
  • Cushing
  • Steroid excess
  • Hyperaldosteronism

Clinical

• Shift O2 dissociation curve to left (increased affinity for Hb-O2)
  • Right shift with increase TEMP, 2-3 DPG, H+
• Hypokalemia, hypocalcaemia, hypochloraemia
• Symptoms related to HYPOcalcaemia and HYPOkalaemia
  • Dizzy, light-headed
  • Chest tightness
  • Anxiety, dysphasia…..laryngospasm

Correction

• Correct underlying problem
• Improve renal bicarbonate excretion (Cl, K and volume)
• Correct electrolyte imbalance
• Oxygen
• Avoid hyperventilation
• Rarely, acetazolamide or HCl infusion

[Continue reading...]

Metabolic Acidosis

Normal Anion Gap Metabolic Acidosis

• U            Ureteric diversion
• S             Small bowel fistula
• E             Extra chloride (ED resuscitation) or HCl ingestion
• D            DKA (resolving)
• C             Carbonic anhydrase inhibitors
• A             Addisons (Type 4 RTA)
• R             Renal tubular acidosis types 1, 2, and 4
• P             Pancreatic fistula

Increased Anion Gap Metabolic Acidosis

• M            Methanol (formic acid), metformin
• U            Uraemia (including aminoglycosides)
• R            Renal failure (Uric acid)
• K            Ketoacidosis (alcohol, diabetes (acute), starvation)
• L            Lactic acidosis
• E            Ethanol
• S            Salicylates
• E            Ethylene glycol (glycolic acid)
• P            Paraldehyde, propylene glycol
• T            Toluene
• I             Iron, isoniazid
• C            Cyanide and carbon monoxide

Low Anion Gap

• Increase in unmeasured cations (Increased Li, K, Ca, Mg, and IgG)
  • Lithium toxicity
  • Hypercalcaemia
  • Hypermagnesaemia
  • Hyperkalaemia
  • IgG (Multiple Myeloma)
• Decreased unmeasured anions (Decreased PO4, albumin)
  • HYPOalbuminaemia, HYPOphosphatemia
• Chloride over-estimation (anion)
  • Bromide toxicity (Read as increased chloride)
  • Iodide toxicity
  • Hypercholesterolemia

Clinical

• Respiratory
  • Hyperventilation
  • Shift of Oxy-Hb curve to right
• Cardiovascular
  • Myocardial depression
  • Tissue catecholamine resistance
  • Pulmonary vasoconstriction
  • Hyperkalaemia

Correction

• Treat underlying cause
• Supportive therapy
• IV bicarbonate controversial – usually not helpful

[Continue reading...]

Acid Base Disorders

Arterial blood gas analysis is used to determine the adequacy of oxygenation and ventilation, assess respiratory function and determine the acid–base balance. These data provide information regarding potential primary and compensatory processes that affect the body’s acid–base buffering system.

• Metabolic Acidosis
• Metabolic Alkalosis
• Respiratory Acidosis
• Respiratory Alkalosis

Interpret the ABGs in a stepwise manner:

1. Determine the adequacy of oxygenation (PaO2)
   • Normal range: 80–100 mmHg (10.6–13.3 kPa)
2. Determine pH status
   • Normal pH range: 7.35–7.45 (H+ 35–45 nmol/L)
   • pH <7.35: Acidosis is an abnormal process that increases the serum hydrogen ion concentration, lowers the pH and results in acidaemia.
   • pH >7.45: Alkalosis is an abnormal process that decreases the hydrogen ion concentration and results in alkalaemia.
3. Determine the respiratory component (PaCO2)
4. Primary respiratory acidosis (hypoventilation) if pH <7.35 and HCO3– normal.
   • Normal range: PaCO2 35–45 mmHg (4.7–6.0 kPa)
   • PaCO2 >45 mmHg (> 6.0 kPa): Respiratory compensation for metabolic alkalosis if pH >7.45 and HCO3– (increased).
   • PaCO2 <35 mmHg (4.7 kPa): Primary respiratory alkalosis (hyperventilation) if pH >7.45 and HCO3– normal. Respiratory compensation for metabolic acidosis if pH <7.35 and HCO3– (decreased).
5. Determine the metabolic component (HCO3–)
   • Normal HCO3– range 22–26 mmol/L
   • HCO3 <22 mmol/L: Primary metabolic acidosis if pH <7.35. Renal compensation for respiratory alkalosis if pH >7.45.
   • HCO3 >26 mmol/L: Primary metabolic alkalosis if pH >7.45. Renal compensation for respiratory acidosis if pH <7.35.

Additional Definitions

• Osmolar Gap
  • Use: Screening test for detecting abnormal low MW solutes (e.g. ethanol, methanol & ethylene glycol [Reference])
  • An elevated osmolar gap (>10) provides indirect evidence for the presence of an abnormal solute which is present in significant amounts [Reference]
  • Osmolar gap = Osmolality – Osmolarity
  • Osmolality (measured)
    • Units: mOsm/kg
    • Measured in laboratory and returned as the plasma osmolality
  • Osmolarity (calculated)
    • Units: mOsm/l
    • Osmolarity = (1.86 x [Na⁺]) + [glucose] + [urea] + 9  (using values measured in mmol/l)
    • Osmolarity = (1.86 x [Na⁺]) + glucose/18 + BUN/2.8 + 9 (using US units of mg/dl)
  • NOTE: even though the units of measured (mOsm/kg) and calculated (mOsm/l) are different [Reference], strictly they cannot be subtracted from one another… However, the value of the difference is clinically useful so the problem is usually overlooked!

Arterial Blood Gas (ABG) Interpretation Chart

Simple table to calculate Respiratory compensation in Acidosis and Alkalosis

Simple calculation to predict changes in HCO3– from PaCO2
	HCO3 (Baseline 24 mmol/L)
Every 10 mmHg D PaCO2 from baseline 40 mmHg	ACUTE	CHRONIC
↑PaCO2	1	4
↓PaCO2	2	5

[Continue reading...]