Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download Respiratory Distress
Transcript
RESPIRATORY DISTRESS September 8, 2005 Prepared by Christina M. Cabott D.O. RESPIRATORY DISTRESS DYSPNEA HYPOXIA HYPERCAPNEA WHEEZING COUGH HICCUPS CYANOSIS PLEURAL EFFUSION DYSPNEA Common complaint described as – “shortness of breath” – “breathlessness” – “not getting enough air” 2/3 of patients presenting to ED with dyspnea have either a cardiac or pulmonary disorder DYSPNEA Definitions: – Tachypnea: rapid breathing – Orthopnea: dyspnea in a recumbent position • Most often a result of LV failure • May be associated with diaphragmatic paralysis or COPD DYSPNEA Definitions: – Paroxysmal nocturnal dyspnea: orthopnea that awakens the patient from sleep – Trepopnea: dyspnea associated with only one of several recumbent positions • can occur with unilateral diaphragmatic paralysis • ball-valve obstruction • after surgical pneumonectomy DYSPNEA Definitions: – Platypnea: dyspnea in the upright position • Result from loss of abdominal wall muscular tone • Rarely, from left-to-right intracardiac shunting (e.g. patent foramen ovale) – Hyperpnea: hyperventilation with a minute ventilation in excess of metabolic demand DYSPNEA Pathophysiology – No defined neural pathway, derived from mechanical, chemical, and vascular receptors DYSPNEA Processes involved in sensation of dyspnea: 1. Conscious sense of voluntary peripheral skeletal and respiratory muscular efforts with increased work of breathing 2. Stimulation of upper airway mechanical and thermal receptors DYSPNEA 3. Decreased stimulation of chest all afferents 4. Stimulation of central hypercapneic chemoreceptors in the central medulla 5. Stimulation of peripheral hypoxic chemoreceptors, in carotid body and aortic arch DYSPNEA 6. Stimulation of intraparenchymal pulmonary stretch receptors, airway irritant receptors, and unmyelinated receptors, responding to interstitial edema or changes in compliance 7. Stimulation of peripheral vascular receptors • right and left atrial mechanoreceptors • pulmonary artery baroreceptor DYSPNEA Input from all of these receptors is integrated in the CNS at subcortical and cortical levels DYSPNEA Clinical features that may signify impending respiratory failure – Presentation: • • • • • shortness of breath or breathlessness tachypnea tachycardia use of accessory respiratory muscles stridor DYSPNEA Clinical features that may signify impending respiratory failure – Presentation: • inability to speak, secondary to breathlessness • agitation or lethargy • paradoxical abdominal wall movement with inspiration (abdominal wall retracts inward) DYSPNEA Clinical features – Evaluation • abnormal vital signs • ABCs – Need rapid airway control and intervention • airway obstruction • ineffective respiratory effort • changes in mental status CAUSES OF DYSPNEA Most Common Causes – Asthma & COPD – CHF/ cardiogenic pulmonary edema – Ischemic heart dz • Unstable angina &MI – Pneumonia – Psychogenic Most Immediately Life Threatening – – – – – – – – Foreign body Angioedema Hemorrhage Tension pneumo PE Myasthenia gravis Guillain-Barre Botulism Ancillary Tests Used for Dyspnea Diagnosis – pulse oximetry and ABG – CXR – EKG – peak flows – Hgb and Hct – BNP (>100 pg/ml) – spirometry – pulmonary function tests – cardiac stress tests – echocardiography – exercise testing – electromyography – V/Q scan – pulmonary biopsy DYSPNEA ED treatment – Supplemental O2: PaO2 >60 mm Hg; pulse ox >91 to 93% – CPAP or BiPAP – Bag-valve-mask ventilation – Intubation with mechanical ventilation – Patients with unclear cause of dyspnea and hypoxia require admission for monitoring HYPOXEMIA Pathophysiology – Def: inadequate delivery of oxygen to tissues – Amount of oxygen available to the tissues is a function of the arterial oxygen content (CaO2) CaO2 = 0.0031 X PaO2 + 1.38 X Hb X SaO2 – PaO2 < 60 mm Hg HYPOXEMIA Relative hypoxemia – Arterial oxygen tension is lower than expected for a given level of inhaled oxygen – Can be calculated by doing A-a gradient HYPOXEMIA – Simplified formula P(A-a)O2 = 145 - PaCO2 - PaO2 – Normal P(A-a)O2 is under 10 mm Hg in young, healthy patients and increases with age – Predicted A-a gradient with age • P(A-a)O2 = 2.6 + 0.21 (age in years) (+ 11) HYPOXEMIA Pathophysiology – 5 distinct mechanisms 1. Hypoventilation 2. Right-to-left shunt 3. Ventilation/perfusion mismatch 4. Diffusion impairment 5. Low inspired oxygen HYPOXEMIA Hypoventilation – Rising PaC02 displaces O2 from the aveolus PaO2 O2 diffusion gradient across the pulmonary membrane – Normal A-a O2 gradient HYPOXEMIA Right-to-left shunting – Unoxygenated blood enters the systemic circulation – May occur secondarily to under ventilated lung or with congenital heart anomalies – Increase in A-a O2 gradient – Will have failure of arterial oxygen levels to increase in response to supplemental O2 HYPOXEMIA Ventilation/Perfusion Mismatch – Regional alterations of ventilation or perfusion – Etiologies: PE, pneumonia, asthma, COPD, extrinsic vascular compression – Increased A-a O2 gradient – Hypoxemia improves with supplemental O2 HYPOXEMIA Diffusion impairment – Impairment of alveolar-blood barrier – Increased A-a O2 gradient – Hypoxemia improves with supplemental O2 HYPOXEMIA Low inspired oxygen – High altitude hypoxia – Nonobstructive asphyxia – Normal A-a O2 gradient – Hypoxemia improves with supplemental O2 HYPOXEMIA Acute compensatory mechanisms – 1. Minute ventilation – 2. Pulmonary artery vasoconstriction perfusion to hypoxic alveoli – 3. Sympathetic tone oxygen delivery by HR and cardiac output HYPOXEMIA Chronic compensatory mechanisms – 1. Red blood cell mass – 2. Tissue oxygen demand HYPOXEMIA Clinical Features – Signs and symptoms are nonspecific • Cardio-pulm: tachycardia and tachypnea • CNS: aggitation, seizures, and coma – At PaO2 < 20 mm Hg, paradoxical depression of respiratory drive – Dyspnea may or may not be present HYPOXEMIA Diagnosis and Differential – Pulse ox = screening test – ABG = defines diagnosis – Similar tests used to determine cause of dyspnea may be useful in evaluating hypoxia HYPOXEMIA ED treatment – Treatment: support, identify, and aggressively treat underlying cause – Maintain PaO2 >60 mm Hg with supplemental O2 – Arterial line if frequent ABGs Patients with persistent hypoxia require hospitalization HYPERCAPNEA Pathophysiology – def: PaO2 >45 mm Hg – Caused by hypoventilation • rapid shallow breathing • small tidal volumes • underventilation of lung reduced respiratory drive – Never due to intrinsic lung disease or increased CO2 production HYPERCAPNEA Causes of Hypercapnea – Depressed central respiratory drive • • • • Structural CNS disease: brainstem lesions Sedating drugs: opiates, sedatives, anesthetics Exogenous toxins Endogenous toxins: tetanus HYPERCAPNEA Causes of Hypercapnea – Thoracic cage disorders • Kyphoscoliosis • Morbid obesity – Neuromuscular impairment • Neuromuscular disease: myasthenia gravis, Guillain-Barre syndrome • Neuromuscular toxins: organophosphate poisoning, botulism HYPERCAPNEA Causes of Hypercapnea – Intrinsic lung disease associated with increased dead space • COPD – Upper airway obstruction HYPERCAPNEA Pathophysiology – Alveolar ventilation • Less than minute ventilation • Dependent on the tidal volume less the anatomic dead space and the respiratory rate – Efferent neuronal imput from the medulla’s chemoreceptors control tidal volume and respiratory rate HYPERCAPNEA Clinical Features – Signs and symptoms are dependent on rate and degree of elevation – Acute rise in elevation • increase in ICP, confusion, lethargy, asterixis, seizures, and coma – Acute changes to PaCO2 >100 mm Hg may lead to cardiovascular collapse HYPERCAPNEA Clinical Features – Acute retention: • For each 10 mm Hg increase of PaCO2, the pH will decrease by 0.1 U • For each 10 mm Hg increase of PaCO2, the HCO3 will increase by 1 mEq/L HYPERCAPNEA Clinical Features – Chronic retention: • May be well tolerated • Kidneys retain HCO3 • For every 10 mm Hg of PaCO2 over 40 mm Hg, HCO3 increases by 3.5 meq/L HYPERCAPNEA ED treatment – Identify threats to life, evaluate, and aggressively treat deficiencies in the ABCs • e.g. narcotic overdose - tx with naloxone • e.g. neuromuscular disease - tx with assisted or mechanical ventilation HYPERCAPNEA ED treatment – Supplemental oxygen should be given to maintain level normal for the patient • Don’t withhold oxygen based on worry of “decreased respiratory drive” • Hypoxia and extreme hypercapnea will kill – Bipap or CPAP - use as a bridge, not definitive care – Mechanical ventilation WHEEZES Pathophysiology – Def: musical adventitious lung sounds produced by turbulent flow through the central and distal airways – Obstruction: bronchospasm, smooth muscle hypertrophy, increased secretions, and peribronchial inflammation WHEEZES Clinical features – Usually occurs in asthma and other obstructive pulmonary diseases – “Not all that wheezes is asthma.” – Not every obstructive pulmonary disease will cause wheezing • e.g. severe asthma - quiet chest, not moving enough air to produce turbulent flow WHEEZES Causes of wheezing – Upper airway (stridor most likely, may have wheezing) • Angioedema: allergic, ACE inhibitor, idiopathic • Foreign body • Infection: croup, epiglottitis, tracheitis WHEEZES Causes of wheezing – Lower airway • Asthma • Transient airway hyperreactivity (usually due to infection or irritation) • Bronchiolitis • COPD • Foreign body WHEEZES Causes of wheezing – Cardiogenic • Cardiogenic pulmonary edema (“cardiac asthma”) • Noncardiogenic pulmonary edema – Adult respiratory distress syndrome [ARDS] • Pulmonary embolus (rare) – Psychogenic WHEEZES Diagnosis – Diagnosis is suspected in the proper clinical situation – Patient improves with relief of airway obstruction • Decreased work of breathing • Improvement of pulse ox • Decreased respiratory rate WHEEZES Diagnosis – Definitive diagnosis confirmed by spirometric testing • Cannot be done at the bedside or during an acute exacerbation – Hand held peak-flow meter used as an adjunct to gauge response to treatment • Value >80% predicted = normal • Limitations: effort and usefulness in kids WHEEZES Diagnosis – Other ancillary tests • CXR and ABG • May not be needed during an uncomplicated obstructive pulmonary disease WHEEZES ED treatment – Initial treatment: directed at identifying threats to life and aggressively treating the underlying condition – Supplemental oxygen: given if hypoxia and degree of obstruction – Monitoring WHEEZES ED treatment – Initial treatment of wheezing • inhaled beta-agonists (e.g. albuterol) and/or anticholinergic agents (e.g. ipratropium bromide) – Acute setting • steroids to help reduce airway inflammation WHEEZES ED treatment – Admission of patients • • • • Oxygen requirements Potential for quick decompensation Failed treatment Require mechanical ventilation COUGH Pathophysiology – Protective reflex that acts to clear secretions and debris from tracheobronchial tree – Initiated by stimulation of irritant receptors located in larynx, trachea, and major bronchi COUGH Pathophysiology – Receptor signal travel via vagus, phrenic, and other nerves cough center of the medulla cough pattern – Cough pattern: • deep inspiration expiration against closed glottis glottis opens forceful exhalation of air, secretions and foreign debris from tracheobronchial tree COUGH Pathophysiology – Stimulation of receptors • • • • • • • • inhaled irritants (e.g. dust) allergens (e.g. ragweed pollen) toxic substances (e.g. gastric acid) hypo- or hyperosmotic liquids inflammation (e.g. asthma) cold air instrumentation excess pulmonary secretions COUGH Categories – Acute – Chronic • Cough present more than 3 weeks without any periods of resolution COUGH Acute Causes – – – – – – – Upper respiratory infection: rhinitis, sinusitis Lower respiratory infection: bronchitis, pneumonia Allergic RXN Asthma Environmental irritants Transient airway hyperresponsiveness Foreign body COUGH Common Chronic Causes – – – – – Smoking and/or chronic bronchitis Postnasal drainage Asthma: reactive airway disease - worse at night Gastroesophageal reflux Angiotensin-converting enzyme inhibitor - b/c accumulation of bradykinin and substance P – Angiotensin II receptor blocker COUGH Less Common Chronic Causes – – – – – – – – Congestive Heart Failure Bronchiectasis Lung cancer or other intrathorcic mass Emphysema Occupational and environmental irritants Recurrent aspiration or chronic foreign body Cystic fibrosis Interstitial lung disease COUGH Diagnosis – Most acute cough does not require routine ancillary tests • CXR: if purulent sputum and/or fever • Spirometry: evaluation of airflow obstruction in asthmatics COUGH Diagnosis – Chronic cough • Treatment based on clinical assessment first • Ancillary tests performed only if symptoms persist – Nasolaryngoscopy - document mucosal inflammation and excessive mucous drainage – Sinus radiographs or CT - check for sinusitis – Spirometry - check for airflow obstruction COUGH Acute treatment – Cough suppressants • opioids: dextromethorphan, codeine, and oxycodone – Demuculants COUGH Chronic treatment 1. Reduce lung irritant exposure 2. Discontinue use of ACE inhibitors, ARBs, and B-blockers 3. Treat post-nasal drainage with oral antihistamine-decongestant and/or nasal steroid COUGH Chronic treatment 4. Evaluate and treat for asthma 5. Obtain CXR and sinus x-ray 6. Evaluate and treat GE reflux 7. Refer patient for bronchoscopy HICCUPS Hiccups a.k.a singultus – Def: an involuntary respiratory reflex with spastic contraction of the inspiratory muscles against a closed glottis, producing the characteristic sound – There is no specific protective purpose known for hiccups HICCUPS Pathophysiology – Afferent: phrenic and vagus nerves and thoracic sympathetic chain – Intensive interconnection among the hypothalamus, medullary reticular formation, respiratory center, and cranial nerve nuclei – Efferent: phrenic nerve, recurrent laryngeal branch of the vagus nerve, and the motor nerves to the anterior scalene and intercostal muscles HICCUPS Pathophysiology – 30 to 40 msec after the onset of inspiration, glottic closure is stimulated – In cases where a specific cause can be assigned, hiccups appear to result from stimulation, inflammation, or injury to one of the nerves of the reflex arc HICCUPS Causes of Hiccups – Acute: benign, self-limited • Gastric distention - from food, drinking (especially carbonated drinks), or air • Alcohol intoxication • Excessive smoking • Abrupt change in environmental temperature • Psychogenic - excitement or stress HICCUPS Causes of Hiccups – Chronic: persistent, intractable • • • • • Central nervous system structural lesions Vagal or phrenic nerve irritation Metabolic: uremia, hyperglycemia General anesthesia Surgical procedures: thoracic, abdominal, prostate, urinary tract, craniotomy HICCUPS Diagnosis – Benign hiccups • Resolves spontaneously or with simple maneuvers • Do not seek medical attention • Do not require specific diagnosis HICCUPS Diagnosis – Persistent hiccups • History to determine specific event associated with the onset • Persistence during sleep – Suggests organic cause • Resolution during sleep – Suggests psychogenic cause – Most patients with benign hiccups • Inquiries about general anesthesia, surgical procedures, and metabolic diseases HICCUPS Diagnosis – Persistent hiccups • Evaluate external auditory canal – hair in canal can press up against the tympanic membrane and stimulate the auricular branch of the vagus nerve • CXR – evaluate for intrathoracic pathology • Fluoroscopy – evaluate unilateral vs bilateral diaphragmatic movement during hiccups HICCUPS Treatment with physical maneuvers – Stimulating the pharynx will block vagal portion of reflex arc and abolish hiccups Treatment with medications – – – – – chlorpromazine metoclopramide nifedipine valproic acid baclofen HICCUPS chlorpromazine – 25 to 50 mg IV, with repeated dose in 2 to 4 hours, if needed – If improvement, 25 to 50 mg po tid or qid – May cause extrapyramidal symptoms – Usually works within 30 min metoclopramide – 10 mg IV or IM – If effective, 10 to 20 mg po qid for 10 days – May cause extrapyramidal symptoms or hypotension – Usually works within 30 min HICCUPS nifedipine – 10 to 20 mg po tid or qid valproic acid – 15 mg/kg per day po tid baclofen – 10 mg po tid These all work more gradually CYANOSIS Pathophysiology – Indicated by the bluish color of the skin and mucus membranes – Resulting from an increased amount of deoxyhemoglobin – Usually 5 g/ 100 mL of deoxyhemoglobin must be present for cyanosis to occur – Amount of oxyhemoglobin does not matter CYANOSIS Pathophysiology – Various factors affect the presence or absence of cyanosis • • • • • Skin pigmentation Skin thickness Subcutaneous microcirculation Lighting Ambient temperature CYANOSIS Clinical Features – Presence of cyanosis signals tissue hypoxia, but not always • Sensitive indicator = tongue • Less sensitive indicators = earlobes, conjunctiva, and nail beds – Cause either central or peripheral cyanosis CYANOSIS Clinical Features – Central cyanosis • Result of unsaturated arterial blood or abnormal hemoglobin (e.g. methemoglobin) – Peripheral cyanosis • Caused by decreased peripheral circulation and clinical situations that lead to an increased arterial oxygen extraction CYANOSIS Central cyanosis – Hemoglobinopathies • Methemoglobin: acquired; hereditary • Sulfhemoglobinemia: acquired – Decreased arterial oxygen saturation • Pulmonary etiologies: shunt , diffusion, V/Q mismatch • Hypoventilation • High altitude CYANOSIS Central cyanosis – Anatomic right-to-left shunts • Cardiac: Ventricular Septal Defect (VSD), Atrial Septal Defect (ASD), and Tetralogy of Fallot (TOF) • Intrapulmonary • Intrapulmonary shunts CYANOSIS Peripheral cyanosis – Decreased cardiac output – Distributive shock – Cold exposure on extermities – Venous congestion – Arterial thrombosis or embolus CYANOSIS Diagnosis – Presence of cyanosis must be taken in context with clinical situation – Tests • • • • • ABG: will confirm the diagnosis Hematocrit: check for polycythemia or anemia CXR EKG Abnormal hemoglobin tests PSEUDOCYANOSIS Blue, gray, or purple cutaneous discoloration that may mimic cyanosis Causes – Heavy metals: iron (hemochromatosis), gold, silver, lead, and arsenic – Drugs: phenothiazines, minocycline, amiodarone, and chloroquine PSEUDOCYANOSIS Chrysiasis – Gray, blue, or purple pigmentation of areas exposed to light – Rare-dose dependent complication of gold treatment that causes permanent discoloration of the skin PSEUDOCYANOSIS Argyria – Slate blue to gray coloration of skin – Results of chronic ingestion or local application of silver salts or colloidal silver, CYANOSIS True cyanosis DOES blanch when direct pressure is applied to skin Pseudocyanosis DOES NOT blanch when direct pressure is applied to skin CYANOSIS Diagnosis – Methemoglobin, sulfhemoglobin, and carbon monoxide poisoning must be kept in mind • Artificially alter peripheral pulse oximetry, secondary to pigment formation in the blood CYANOSIS Diagnosis – Methemoglobin, • Causes – Drugs: most commonly by benzocaine and nitrates – Hereditary: rare genetic disorder affecting NADH • Visible cyanosis with as little as 1.5 g/dL • Incapable of binding oxygen • Symptoms related to hypoxia CYANOSIS Diagnosis – Methemoglobin • Severity of symptoms related to quantity, rapidity of onset, and pts cardiovascular system • Need to consider if oxygen supplementation does not correct hypoxia • Venous blood looks chocolate brown • Treatment: methylene blue CYANOSIS Diagnosis – Sulfhemoglobin • • • • • Caused commonly by phenacetin or acetanilid Inert as an oxygen carrier Can produce deep cyanosis at level < 0.5 g/dL Irreversible Treatment – symptomatic and supportive care – identification and removal of suspected causes CYANOSIS ED treatment – Central cyanosis • Supplemental oxygen • supplied in appropriate conditions – Methemoglobinemia • Methylene blue 1 to 2 mg/kg of body weight IV over 5 minutes PLEURAL EFFUSION Result from fluid accumulating in potential space between visceral and parietal pleura Most common causes in developed countries – CHF – Pneumonia – Cancer PLEURAL EFFUSION Pathophysiology – Normally, small amount of fluid is secreted from parietal pleura into pleural space, where it is absorbed by visceral pleural microcirculation – Small amount of fluid decreases friction between the pleural layers and allows for smooth lung expansion and contraction during respiration PLEURAL EFFUSION Pathophysiology – Transudates • Result of imbalance in hydrostatic or oncotic pressure • Produces an ultrafiltrate across the pleural membrane • Low protein content PLEURAL EFFUSION Pathophysiology – Exudates • Result of pleural disease, usually inflammation or neoplasm • Active fluid secretion or leakage • High protein content COMMON CAUSES OF PLEURAL EFFUSION Transudates – CHF Transudate or exudate – Diuretic therapy Exudates – Cancer: primary or metastatic – Bacterial pneumonia with parapneumonic effusion – Pulmonary embolism LESS COMMON CAUSES OF PLEURAL EFFUSION Transudates – Cirrhosis with ascites – Peritoneal dialysis – Nephrotic syndrome Transudate or exudate – Pulmonary embolism Exudates – Viral, fungal, mycobacterial or parasitic infection – SLE or RA – Uremia – Pancreatitis – Post-cardiac surgery or radiotherapy – Amiodarone PLEURAL EFFUSION Clinical features – May be clinically silent – Detected by symptoms of underlying disease – Increase in volume of effusion with dyspnea – Development of inflammation and associated pain with respiration PLEURAL EFFUSION Physical exam – Percussion dullness in dependent portions of the lung – Decreased breath sounds at lung base PLEURAL EFFUSION Diagnosis – Upright CXR: in an adult, 150-200 mL of pleural fluid in hemithorax required to produce signs – Supine CXR: haziness in posterior pleural space – Diagnostic thoracentesis • analyzed to determine cause PLEURAL EFFUSION Detection of exudative pleural effusion – Pleural fluid/serum protein ratio > 0.5 – Pleural fluid/serum LDH ratio > 0.6 – Pleural fluid LDH > 2/3 of upper limit for serum LDH PLEURAL EFFUSION Additional tests – Gram stain and culture - detect bacteria – Cell count • Neutrophils- parapneumonic, PE, pancreatitis • Lymphocytes- cancer, TB, post-cardiac sz – Glucose: low in parapneumonic, malignancy, TB, and RA PLEURAL EFFUSION Additional tests – Cytology for malignancy • Highest yield: adenocarcinoma • Lower yield: squamous cell, lymphoma, or mesothelioma – Pleural fluid pH • Normal: around 7.46 • Parapneumonic: <7.10, predicted development of or persistence of empyema PLEURAL EFFUSION Additional tests – Pleural fluid amylase • Elevated in pancreatitis or esophageal rupture – Mycobacterial and fungal stains and cultures – Tuberculosis pleural fluid markers: • PCR for mycobacterial DNA • Pleural fluid adenosine deaminse • Pleural fluid interferon- PLEURAL EFFUSION Treatment – Dyspnea at rest • Therapeutic thoracentesis with drainage of 1 to 1.5 L of fluid – Empyema (gross pus or organisms on Gram stain) • Drainage with large bore thoracostomy tubes PLEURAL EFFUSION Treatment – Parapneumonic effusions • Thoracostomy tube drainage if + cultures, +Gram stain, or pleural fluid pH < 7.10 – CHF pleural effusions • Diuretic therapy • Usually resolves 75% of effusions within 2 to3 days QUESTIONS 1. Causes of central cyanosis 2. Causes of peripheral cyanosis 1. B, D, F. 2. A, C, E, G A. Decreased cardiac output B. Methemoglobin C. Hypothermia D. Right-to-left shunt E. Venous congestion F. High altitude G. Embolus QUESTIONS 3. Causes of upper airway obstruction 4. Causes of lower airway obstruction 3. A, C, D, G. 4. B, C, E, F A. Angioedema B. Bronchiolitis C. Foreign body D. Croup E. COPD F. Asthma G. Epiglotitis QUESTIONS 5. If PaO2 < 20 mm Hg, what happens to the respiratory drive?. A. Increases B. Decreases 6. In an acute setting, what should the pH be for a patient with a PaCO2 of 60? C. 7.15 D. 7.25 E. 7. 35 F. 7.55 G. 7.65 5. B 6.C
