I need help with the two following questions in some detail. Need about two sides for each question. Also not all the patient data may be relevant to answer the questions, as there were other questions that came with the patient data, I may also need further explanation and help with those questions which are in relation to the patients myocardial infarction if anyone can help and can send them once these have been answered. thank you in advance
Question 1. In relation to the blood gas data below discuss the pathophysiological mechanisms which can lead to hypoxemia. Explain the potential benefits and hazards in relation to respiratory control mechanisms of oxygen therapy in the patient. Briefly explain what is meant by CPAP and BiPAP inhaled gas delivery system and why it may help this patient.
Question 2. discuss the mechanisms of action and clinical use of nitrates such as isosorbide mononitrate and beta-adrenergic receptor antagonists such as bisoprolol in the management of chronic heart failure.
60 year old male, had an myocardial infarction several years ago.
Bilateral leg edema up to his calf and shortness of breath on exercise.
Has a heart rate of 100 beats per minute, and arterial blood pressure of 100/60 mmHg. Patient has an enlarged heart.
Arterial blood sample of patient:
Pco2 = 7.2 kPa (4.8 - 6.1)
P02 = 7.0 kPa (10.0 - 13.3 )
Ph = 7.29 (7.36 - 7.44)
Echocardiography revealed severe left ventricular dysfunction with an ejection fraction of 32%. Coronary angiography showed complete occlusion of the right coronary artery 40mm distal to its origin, and diffuse, non occlusive disease in the major branches of the left artery.
Patient family history: both parents died at around 60 years of age. Two brothers who are smokers have been admitted to hospital for cardiac problems.
Patient has been smoking 30 cigarettes a day since he was 17 .
Patient has been suffering from from angina pain on mild exertion and been radiating down left arm even at rest. Need to sleep at night with raised pillows but wakes up due to feeling breathless.
Please see attached file.
Heart failure results from myocardial dysfunction that impairs the heart's ability to circulate blood at a rate sufficient to maintain the metabolic needs of peripheral tissues and various organs. It follows myocardial damage when the compensatory hemodynamic and neurohumoral mechanisms are overwhelmed or exhausted and results from the loss of a critical amount of functioning myocardium, which in this patient is due to myocardial infarction, coronary artery disease and hypertension.
When an excessive workload is imposed on the heart by increased systolic blood pressure (pressure overload), increased diastolic volume (volume overload), or loss of myocardium, normal myocardial cells hypertrophy in an effort to enhance contractile force of the normal areas. The subsequent alterations in biochemistry, electrophysiology, and contractile function lead to mechanical alterations of myocardial function: The rate of contraction slows, the time to develop peak tension increases, and myocardial relaxation is delayed. Peak force development may be well preserved with enough viable myocardium and adequate time for the development of force. Thickening of the ventricular ...