Lec 3 PH Disturbances and ABGs PDF

## CASE SCENARIO - A 19 year old female Medical student was brought to the ER with the complaints of feeling short of breath along with being dizzy, lightheaded, confused and with heart palpitations. - Her history revealed that she had spent all her time enjoying herself and now had to give her Ex...

## CASE SCENARIO - A 19 year old female Medical student was brought to the ER with the complaints of feeling short of breath along with being dizzy, lightheaded, confused and with heart palpitations. - Her history revealed that she had spent all her time enjoying herself and now had to give her Exams. The prospect of studying the whole course before the exams caused severe anxiety and panic attack. - On examination, her breathing was rapid, deep and uncontrolled (hyperventilation) and her mouth was dry. ## ABG - pH= 7.55 (Normal= 7.35-7.45) - PaCO2= 30mm Hg (Normal= 34-44 mm Hg) - HCO3= 18 mEq/liter (Normal= 22-26 m Eq/liter) ## RESPIRATORY ALKALOSIS ## LEARNING OBJECTIVES - RESPIRATORY ACIDOSIS - Causes - Investigation → ABG - Compensation → ABG - RESPIRATORY ALKALOSIS - Causes - Investigation → ABG - Compensation → ABG ## The Henderson-Hasselbalch Equation The Henderson-Hasselbalch Equation describes the derivation of pH as a measure of acidity in biological and chemical systems. The equation is also useful for estimating the pH of a buffer solution. $pH = pK_a + log [\frac{conjugate \ base}{weak \ acid}]$ $pH = pK_a + log[\frac{A^-}{HA}]$ $pH = pK_a + log_{10}[\frac{HCO_3^-}{H_2CO_3}]$ $7.4 = 6.1 + log_{10}(20)$ ## RESPIRATORY pH DISTURBANCES The acid-base disorders are mainly classified as: | | Acidosis | Alkalosis | |---|---|---| | | Metabolic acidosis (due to ↓ in bicarbonate) | Metabolic alkalosis (due to ↑ in bicarbonate) | | | Respiratory acidosis (due to ↑ in carbonic acid) | Respiratory alkalosis (due to ↓ in carbonic acid) | $PH = pK_a + log_{10}[\frac{HCO_3^-}{H_2CO_3}]$ ## The Four Primary Acid-Base DISORDERS | Conditions | Primary Disorder | |---|---| | ↓pH and ↓HCO3- (BEect) | Metabolic acidosis | | ↑pH and ↑HCO3- (TBEect) | Metabolic alkalosis | | ↓pH and ↑Pco2 | Respiratory acidosis | | ↑pH and ↓Pco2 | Respiratory alkalosis | ## ACIDOSIS / ALKALOSIS PRIMARY DEFECT - ACIDOSIS (↓ pH) - Respiratory (↑ H₂CO₃) - Metabolic (↓ HCO₃) - ALKALOSIS (↑ pH) - Respiratory (↓ H₂CO₃) - Metabolic (↑ HCO₃) $pH = pK_a + log_{10} [\frac{HCO_3^-}{H_2CO_3}]$ ## HOW pH IS ALTERED Determine the blood pH of an asthmatic patient, if the laboratory investigation shows the following: - HCO3- = 20 mmol/L (N=22-26mmol/l) - H2CO3 = 5 mmol/L (N= 1.2 mmol/l) - (pCO2 ×0.0301=H2CO3) $ pH = pK_a + Log [\frac{HCO_3^-}{H_2CO_3}] = 6.1 + Log[\frac{20 mmol/L}{5 mmol/L}] = 6.1 + log(4) = 6.1 + 0.6 = 6.7$ (Normal: 7.35-7.45) ## RESPIRATORY ACIDOSIS - Volatile acids (e.g. carbonic acid) are managed by respiratory control. - Non volatile acids (e.g. ketoacid, lactic acid) are managed by renal control and buffer system. ## RESPIRATORY ACIDOSIS (↓pH, ↑pCO₂) Respiratory insufficiency (asthma, COPD, narcotic poisoning) leads to: - Hypoventilation - ↑pCO₂ - ↑H₂CO₃ - ↓pH - Acidosis (Respiratory) ## RESPIRATORY ACIDOSIS... - Respiratory acidosis is the acid-base disturbance initiated by an increase in PaCO2. - The level of PaCO2 is determined by the interaction of two factors, the rate of carbon dioxide production (VCO₂) and the rate of alveolar ventilation (VA), as follows: - PaCO₂ = K x VCO₂/VA Where K is a constant. ## CAUSES - An increase in arterial pCO₂ can occur by one of three possible mechanisms: - Presence of excess CO₂ in the inspired gas - Decreased alveolar ventilation - Increased production of CO₂ by the body ## RESPIRATORY ACIDOSIS - Respiratory acidosis is a medical emergency in which decreased ventilation causes increased blood carbon dioxide concentration and ultimately leads to decrease in the pH level. - During Alveolar hypoventilation there is an increase in CO2 thus leads to an increased PaCO₂. - **Acidosis** refers to disorders that lower cell/tissue pH to <7.35. - **Acidemia** refers to an arterial pH < 7.3. ## ACUTE RESPIRATORY ACIDOSIS - POCO₂ is elevated above the upper limit of the reference range (over 6.3 kPa or 45 mm Hg) with an accompanying acidemia (pH<7.36). ## CAUSES - occurs when an abrupt failure of ventilation occurs - failure in ventilation may be caused by depression of the central respiratory center, inability to ventilate adequately due to neuromuscular disease, or airway obstruction related to asthma or chronic obstructive pulmonary disease (COPD) exacerbation ## CAUSES OF RESPIRATORY pH DISTURBANCES - Respiratory Acidosis - Hypoventilation - COPD - Airway obstruction - Drug overdose - Chest trauma - Pulmonary edema - Neuromuscular disease ## CAUSES OF RESPIRATORY ACIDOSIS - Respiratory acidosis - Airway obstruction due to bronchitis, bronchospasm, emphysema, etc. - Lung diseases like fibrosis, pneumonia, etc. - Respiratory center depression by anesthetics, sedatives, cerebral trauma, tumors, etc. - Extrapulmonary thoracic diseases like flail chest, kyphosis and scoliosis - Neural diseases like polymyelitis, paralysis of respiratory muscles ## Regulation of Respiration **Objective:** To maintain normal levels of PO₂ & PCO₂ in arterial blood. **Respiratory control system:** Three basic elements: | Elements | Description | |---|---| | Input | - Sensors | | | - Chemoreceptors: | | | - Central | | | - Peripheral | | | - Pulmonary receptors | | | - Other receptors | | Control | - Central controller | | | - Brain stem (pons, medulla) | | | - Cortex | | | - Other parts of brain | | Output | - Effectors | | | - Resp. Muscles | | | - Diaphragm | | | - ABD. Muscles | | | - Accessory Muscles | ## CAUSES OF ACIDOSIS - HYPOVENTILATION - Drug Overdose - Pulmonary Edema - Chest Trauma - Neuromuscular Disease - ACIDOSIS - pH 17.4 - Diabetic Ketoacidosis - Salicylate OD - (ASA) - Metabolic Acidosis - (↓pH, ↓HCO₂) - Shock - Sepsis - Severe Diarrhea - Renal Failure ## SYMPTOMS OF RESPIRATORY ACIDOSIS **Clinical features** - Initial signs of acute respiratory acidosis include: - headache - anxiety - blurred vision - restlessness - Without treatment, other symptoms may occur. These include: - sleepiness - tremors - delirium ## Acidosis - Principal effect of acidosis is depression of the CNS through ↓ in synaptic transmission. - Generalized weakness. - Deranged CNS function the greatest threat. - Severe acidosis causes - Disorientation - coma - death ## CLINICAL FEATURES... Varies according to the severity and duration of respiratory acidosis, the underlying disease, and whether there is accompanying hypoxemia. 1. **Neurological:** "hypercapnic encephalopathy" include - irritability, inability to concentrate, - headache, anorexia, - apathy, confusion, combativeness, hallucinations, delirium, - transient psychosis, progressive narcosis, and coma. - Frank papilledema (pseudotumor cerebri) and motor disturbances (myoclonic jerks, flapping tremor, and seizures). The occurrence and severity of neurological manifestations depend on the magnitude of hypercapnia, the rapidity with which it develops, the severity of the acidemia, and the degree of the accompanying hypoxemia. ## Symptoms of Acidosis | Symptoms | Area| |---|---| | - Headache | Central | | - Sleepiness | Central | | - Confusion | Central | | - Loss of consciousness | Central | | - Coma | Central | | - Seizures | Muscular | | - Weakness | Muscular | | - Diarrhea | Intestinal | | - Shortness of breath | Respiratory | | - Coughing | Respiratory | | - Arrhythmia | Heart | | - Increased heart rate | Heart | | - Nausea | Gastric | | - Vomiting | Gastric | ## RESPIRATORY ACIDOSIS - **Hypoventilation** → Hypoxia - **Rapid, Shallow Respirations** - **↓ BP with Vasodilation** - **Dyspnea** - **Headache** - **Hyperkalemia** - **Dysrhythmias (TK)** - *I can't catch my breath.* - **Drowsiness, Dizziness, Disorientation** - **Muscle Weakness, Hyperreflexia** - **Causes:** - ↓Respiratory Stimuli (Anesthesia, Drug Overdose) - COPD - Pneumonia **pH (↓7.35) pCO₂ (↑45mm Hg) **Retention of CO₂ by Lungs** ## ACIDOSIS(↓ pH) ALKALOSIS (↑pH) - Acidosis leads to: HYPERKALEMIA - Alkalosis leads to: HYPOKALEMIA $K^+ \rightleftharpoons H^+ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ \ H^+ \rightleftharpoons K^+$ ## HYPERKALEMIA SYMPTOMS (Normal K+ = 3.5 - 5.0 mEq/L) - Hyperkalemia & Cardiac Changes - Slows heart rate - ECG changes - Tall, peaked T wave, short QT interval -Longer PR interval, widening QRS complex - Risk for Heart Block, A-fib, or, V-fib - Severe ↑ K: - Decreased heart contraction strength - Dilated & flaccid heart - *All of these are severe and we need to fix them as soon as we can, that is, if we can. The higher the K is the worse these are. Usually associated with a K higher than 7.* ## Hyperkalemia | Area| Changes | |---|---| | V1| | | V2 | | | V3 | Peaked T waves | | V4 | Small or indiscemicle P.waves | | V5 | | | V6 | | ## Compensation Mechanisms - **Chemical buffers** - On the scene in seconds. - Already present in tissue and will handle minor changes in the acid-base balance. - **Respiratory** - Retention or elimination of CO₂ within minutes. - Respiratory compensation can handle mild to moderate acid-base shifts. - **Renal** - Regulate bicarb (HCO₂) to combat hydrogen losses and gains. - Starts in hours, but more permanent. - When the other 2 mechanisms fail, the renal system slowly gets to work and requires up to 5 days to complete. ## COMPENSATION OF RESPIRATORY ACIDOSIS - The pulmonary system and the renal will compensate for each other to return to pH to normal. - The lungs compensate for metabolic disturbances by altering the PaCO2 levels by Hyper/hypoventilation. - The kidneys compensate for respiratory disturbances by altering the HCO3- levels by reabsorbing retaining or excreting HCO3. ## Chemoreceptors - Blood pH - PaO2 - PaCO2 **Feedback Loop of Respiratory Control** | Area | Description | |---|---| | Chemoreceptors | - | | Brainstem Respiratory Centers | - | | Alveolar Ventilation Rate | - | | Breathing Muscles | - | ## COMPENSATION OF RESPIRATORY ACIDOSIS $pH = pK_a + log_{10} [\frac{HCO_3^-}{H_2CO_3}]$ **NORMAL:-** pH = 7.4, pKa = 6.1, HCO3/H2CO3 = 20, Log 20 = 1.3 | Disorder | Expected Compensation | |---|---| | Metabolic Acidosis | Expected PaCO2= HCO3 X 1.5+ 8 | | Metabolic Alkalosis | Rise in PaCO2 = Rise in HCO3 X 0.75 | | Respiratory Acidosis | Rise in HCO3 = Rise in Paco2 X 01 | | Respiratory Alkalosis | Fall in HCO3 = Fail in PaCo2 X 02 | ## COMPENSATION OF RESPIRATORY ACIDOSIS | Abnormality | pH | CO₂ | HCO₃ | Examples | |---|---|---|---|---| | Respiratory acidosis | Uncompensated | ↓ | ↑ | → | Severe Asthma | | |Partialy compensated | ↓ | ↑ | ↑ | Pneumonia | | |Fully Compensated | → | ↑ | ↑ | Hypoventilation | | Respiratory alkalosis | Uncompensated | ↑ | ↓ | → | Hyperventilation | | |Partialy compensated | ↑ | ↓ | ↓ | Panic attack | | |Fully Compensated | → | ↓ | ↓ | Aspirin Poisoning | ## RESPIRATORY ACIDOSIS (PARTIALLY COMPENSATED) | Area | Values | |---|---| | pH-value | [7.37 - 7.44] | 7.091 | | Partial pressure for CO₂| [34-44] [mmHg] | 120.1 | | Partial pressure for O₂ | [65-105] [mmHg] | 86.5 | | Standard bicarbonate | [22-26] [mmol/l] | 35.7 | | Base excess | [3+3] [mmol/l] | 2.6 | | Oxygen saturation | [95-98] [%] | 93.4 | ## Respiratory alkalosis... - Respiratory alkalosis is the acid-base disturbance initiated by a reduction in PaCO₂. - This occurs when there is excessive loss of CO₂ by hyperventilation of lungs. - Hypocapnia develops when a sufficiently strong ventilatory stimulus causes CO₂ output in the lungs to exceed its metabolic production by the tissues. - As a result, partial pressure of CO₂ and H+ conc, falls and so there is a decrease in bicarbonate levels. ## RESPIRATORY ALKALOSIS (↑pH, ↓pCO₂) - Increased Respiration (anxiety, hypoxia, anemia, pregnancy) - Hyperventilation - ↓Pco₂ - ↓H.CO₃ - ↑pH - Alkalosis (Respiratory) ## CAUSES **Respiratory Alkalosis** **ETIOLOGY and PATHOGENESIS** - Develops when a sufficiently strong ventilatory stimulus causes CO₂ output in the lungs to exceed its metabolic production in the tissues. - May be due to stimulation of CNS (e.g. pain, anxiety), peripheral chemoreceptors (e.g. hypoxemia, pneumonia), chest receptors (e.g. PTE). ## CAUSES **Respiratory Response to High Altitude** - Hypoxemia causes hyperventilation. - Hyperventilation causes decreased in Pco₂ & respiratory alkalosis (RA). - These 2 inhibit CNS respiratory centre ('offsetting' ++ drive of hypoxemia). - **Body's solution:** - Renal HCO₃ excretion increased - RA resolved (via increased excretion of CSF HCO₃). - Hyperventilation now will not be 'offset' because now, O₂ is the drive* via PCRI. ## CAUSES OF RESPIRATORY ALKALOSIS - Respiratory Alkalosis - Hyperventilation - Hypoxia - Anxiety - High altitude - Pregnancy - Fever ## SYMPTOMS OF RESPIRATORY ALKALOSIS **RESPIRATORY ALKALOSIS** | Symptoms | Description | |---|---| | Seizures | - | | Deep, Rapid Breathing | - | | Hyperventilation | - | | Tachycardia | - | | Lor Normal BP | - | | Hypokalemia | - | | Numbness & Tingling of Extremities | - | | Lethargy & Confusion | - | | Light Headedness | - | | Nausea, Vomiting | - | pH (↑7.45) Pco₂ (↓35mm Hg) ↑ Loss of CO₂ from Lungs **Causes:** - Hyperventilation (Anxiety, PE, Fear) - Mechanical Ventilation ## HYPOKALEMIA - Normal Potassium= 3.5 and 5.0 mEq/L) - Potassium is an important electrolyte for nerve and muscle cell functioning, especially for muscle cells in the heart. - ↓K+ - feeling tired, leg cramps, weakness and constipation. - abnormal heart rhythm, which is often too slow, and can cause cardiac arrest ## HYPOKALEMIA | Area | Changes | |---|---| | | Slightly prolonged PR interval | | | ST depressed and prolonged | | | Sighly peaked Pwave | | | Prominent U wave | | | Depressed Twave (may be inverted) | ## ABG | ABG | pH | PaCO2 | HCO3 | |---|---|---|---| | Respiratory Acidosis | ↓ | ↑ | normal | | Respiratory Alkalosis | ↑ | ↓ | normal | | Metabolic Acidosis | ↓ | normal | ↓ | | Metabolic Alkalosis | ↑ | normal | ↑ | ## COMPENSATION OF RESPIRATORY ALKALOSIS $pH = pK_a + log_{10} [\frac{HCO_3^-}{H_2CO_3}]$ | Disorder | Expected Compensation | |---|---| | Metabolic Acidosis | Expected PaCO2= HCO3X1.5+ 8 | | Metabolic Alkalosis | Rise in PaCO2 = Rise in HCO3 X 0.75 | | Respiratory Acidosis | Rise in HCO3- = Rise in Paco2 X 01 | | Respiratory Alkalosis | Fall in HCO3- = Fail in PaCO2 X 02 | ## TABLE 1 The Four Primary Acid-Base Disorders and Their Compensatory Changes [HCO₂1 PH = PK + log10 [H₂CO₃] | Conditions | Primary Disorder | Compensation | |---|---|---| | ↓pH and IHCO₃- (18Eect) | Metabolic acidosis | ↓P002 | | ↑pH and ÎHCO₃- (ÎBEect) | Metabolic alkalosis | ↑PCO₂ | | IpH and IPco₂ | Respiratory acidosis | THCO, - (BEect) | | TpH and IPco₂ | Respiratory alkalosis | ↓HCO₃- (BEect) | ## COMPENSATION pH = pK + log10 [HCO,1 [H₂CO₃]/ | Acid-base disorder | Primary change | Compensatory change | Timescale of compensatory change | |---|---|---|---| | Metabolicacidosis | ↓ plasma bicarbonate | ↓ pCO) (hyperventiation) | Minutes hours | | Metabolic alkalosis | ↑ plasma bicarbonate | ↑ pCO (Phypoventiation) | Minuteshours | | Respiratory acidosis | TpCO₂ | I renal bicarbonate generation: | Days | | | | ↑ plasma bicarbonate | | | Respiratory akalosis | ↓pCO₂ | renal bicarbonate reabsorption: | Days | | | | ↓ plasma bicarbonate | |