Water flows through the horizontal branching pipe shown in Fig. P3.103 at a rate of 10 ft3 /s. If viscous effects are negligible, determine the water speed at section (2), the pressure at section (3), and the flowrate at section (4)
KIN 408 - Advance Exercise Prescription Exam 2 Study Guide Ch.23 Indications for Clinical Exercise Test - Diagnosis: assessment of symptoms caused by CAD, symptom-limited graded exercise test with ECG only - Prognosis: how long they’ll live Pretest: Contradictions Mode of Exercise: -Protocols: Bruce treadmill protocol =pros- physician familiarity, time efficient; cons=can’t touch handrails because change workload; At 1 report of chest pain=continue test Termination: age predicted maxHR to stop is different to justify If stop at 85% will miss ischemic abnormalities Post Exercise Recovery: Put in supine position=more stress on heart Hemodynamic response: -Decrease systolic blood pressure=decrease cardiac output and unequivocal criteria to terminate an exercise -failure to recover HR promptly after exercise Respiratory Gas Exchange: more accurate measurement of exercise capacity Ch. 24 Diagnostic Procedure -Diagnosis: Medical history, physical exam, ECG, stress test, Exercise physiologist makes the general decision making process and specific procedures Clinical Workup gap- between ACC/AHA guideline and common practices -echocardiography- no imaging test, has more sensitivity and specificity Ch. 25 Lung disease: obstructive, restrictive, vascular -shortness of breath in all of them +Inhale: diaphragm contracts and moves downward; rib cage moves upward; negatives pressure in thorax + Exhalation: diaphragm relaxes and moves upward; rib a\cage moves inward allowing air to move from lungs to mouth size of airway decreases, cartilage is reduced COPD- Chronic Obstructive Progressive Disease : progressive and persistent airflow limitation; diaphragm flattens= increase difficulty to move air non-uniform narrowing of airways ; loss of elastic recoil; alveoli not open -Emphysema is destruction of lung parenchyma and smaller airways because of protease-antiprotease imbalance, chronic inflammation, pulmonary vascular wall thickening and smooth muscle proliferation; inflammation result of exposure to cigarette smoke; Lung loses elasticity and elastic recoil, small alveolar walls lose traction and easily collapsible; reduced capacity of lungs to do their work; non- uniform ventilation; Reduced capacity of lungs to do their work; nonuniform ventilation; increase deadspace; increase minute ventilation increase respiratory rate; diagnosed based on patient history reduced FEV/FVC ratio diffusing capacity for Carbon Monoxide Test of emphysema : Chronic Bronchitis Type of COPD characterized by chronic cough and mucus produced primary involves large airways, elastic recoil is normal but airways injury and inflammation cells and mucus glands cause repair process =deposition of collagen in air ways, increase airway resistance = receive little ventilation perfusion imbalance of vascular beds Lead to arterial hypoxemia ; not able to ventilate lungs = reduce O2 in blood = increase heart workload to move blood; have low minute ventilation, even slower at night, FEV1 is reduced; bronchodialators don’t work -Astham is a type of obstructive pulmonary disease, complex airflow obstruction, bronchial hyperactivity Airway reactivity-episodic and often response to stimuli Antibody response to a stimuli Abnormal collagen depostition and subepithelial fibrodid delepment and results in persistent airway narrowing Common shortness of breath due to inflammation and wheezing Reduced residual volume and total lung capacity increases Clinical Features of COPD Risk factors: most cigarette smokers experience effects 20 years later Family history of lung disease Women develop earlier than men @ childhood – initially no abnormalities , later wheezing, decreased breathing sounds, dec diaphragm movement and heart sounds , lean forward to reduce breathing work and will lose weight overtime due to muscle washing and wasting disease Flat diaphragm enlargement of pulmonary artery Exercise Intolerance: gas exchange is abnormal at rest that becomes worst with exercise Ventilation – perfusion imbalance Loss of lung parenchyma Alveolar hypoventilation increase dead space Ventilator and peripheral muscle dysfuction = loss of strength and endurance Pulmonary function test (PFT) = FEV1 is best correlated within morbidity and mortality
