Mr. T., a 45-year-old black man employed as a midlevel corporate manager, came to the doctor’s office seeking a physical examination. He appeared somewhat overweight. He denied taking any medications or smoking, but admitted drinking alcohol. His father and older brother have hypertension (HTN) and his paternal grandfather experienced a myocardial infarction (MI) and a CVA at a young age. Mr. T. stated, “A year ago at a health fair my cholesterol was tested. I was told later by mail that my cholesterol was 250 and I had to recheck my blood pressure.” His Bp at the time of his examination was 159/94, HR 96, weight 275, height 5’11 in.
- Explain the progressive pathophysiologic relationship between an MI and the development of left ventricular (LV) failure. What factors affect the severity of LV failure?
Hypertension is a primary cause of cardiovascular disease. Long-standing HBP leads to left ventricular hypertrophy and diastolic dysfunction that leads to rise in myocardial inflexibility. Persons with high BP are more vulnerable to ischemic heart sickness and studies have indicated that these patients might have six-fold huger risk of MI. High BP intensify the LV afterload and peripheral vascular endurance and lengthy display to an intensified load causes pressure and volume- interceded LV structural remodeling (Oh & Cho, 2020). Chronic or poorly managed HTN causes intensified afterload and hence raised cardiac workload, causing hypertrophy of the LV. Mainly this hypertrophy functions as a compensatory instrument and helps in maintaining cardiac output. However, the long-term can prevent myocardium relaxation leading to damaged cardiac filling and reduced LV production. CAD triggers direct ischemic harm to the myocardium preceding to re-modeling and scar development which reduced contractility and cardiac production.
Deep vein thrombosis (DVT) is a medical illness that transpires when a blood clot grows in a deep vein. Mostly these clots form in the arm, pelvis, lower leg or thigh. DVT risk aspects include blood coagulability, pregnancy, use of oral contraceptives leading to hyper-coagulability, and vein injury because of fractures or major surgery (Stone et al., 2017). Also, specific chronic medical sickness like cancer, lung and heart sickness causes DVT. Obesity, DVT family history, age and a catheter put in a central vein are DVT risk elements. Manifestation of DVT include pulmonary embolus, edema, tenderness and phlegmasia cerulea dolens. The goal of DVT therapy is to inhibit thrombus from enlarging and dividing, recurring thromboemboli, and post-thrombotic disorder. Management of DVT patient include using compression stockings in inhibiting DVT and easing pain and swelling (CDC, 2020). Hence these might require to be worn for two years or more after diagnosis of DVT. In acute circumstances the clot can be removed surgically. Also, endovascular management is vital when pulmonary embolism danger is risky.
Centers for Disease Control and Prevention (CDC) (2020). What is Venous Thromboembolism? https://www.cdc.gov/ncbddd/dvt/facts.html
Oh, G. C., & Cho, H. J. (2020). Blood pressure and heart failure. Clinical hypertension, 26(1), 1-8.
Stone, J., Hangge, P., Albadawi, H., Wallace, A., Shamoun, F., Knuttien, M. G., & Oklu, R. (2017). Deep vein thrombosis: pathogenesis, diagnosis, and medical management. Cardiovascular diagnosis and therapy, 7(Suppl 3), S276