Aldosterone is sensitive to low blood pressure and low blood sodium sodium increases by absorption of NaCl and blood pressure increases by absorption of water into blood stream by capillary. Excretes potassium into urine. In this manner, aldosterone increases sodium in blood and increases blood pressure. Aldosterone increase absorption of H+ into urine and secretion of bicarbonate into blood (HCO3-) Common Causes of secondary hypertension (1st cause) Overstimulation of ACE (angiotensin converting enzyme) Treatment You have to block the angiotensin converting enzyme by medicine called Captopril Captopril and Ramipril are ACE inhibitor (2nd cause) Over secretion of angiotensin 2 Leads to hypertension because AgII acts as vasoconstrictor and stimulates aldosterone secretion from adrenal cortex. Treatment Use AgII blocker which is called Valsartan (3rd Over secretion of aldosterone You need to block aldosterone receptor by medicine called Spironolactone Spironolactone is an aldosterone receptor blocker and you can control hypertension with it (4th cause) Over secretion of calcium hypercalcemia You need calcium channel blocker Use Benidipine or Felodipine (5th cause) Due to heart problem You have to go for beta I blocker use Propranolol (6th cause) Kidney does not have normal filtration rate Urine production of kidney decreases blood volume and blood pressure. Kidney produces urine and eliminates extra fluid our body has and our body uses kidney to adjust blood volume. When kidney cannot work, you have to use diuretic such as Hydrochlorothiazide this accelerates urination. (7th cause) Cushing’s syndrome - disorder of adrenal cortex Due to Tumor Infection Patient has increased aldosterone, cortisol, and androgen hormones. Cortisol Controls stress
Represents remnants of ventricular repolarization (relaxation) Prominent U waves indicate pathological conditions affecting repolarization of ventricles Ectopic foci Abnormal pacemaker sites within heart (outside of SA node) that display automaticity leads longer QRS complex After treatment of myocardial infarction, some cells spontaneously have depolarization in ventricle tissue called ectopic foci This depolarization can send signal to other part of ventricles or even atrium In EKG, we see normal P, Q, R, and S, T, P, Abnormal QRS, then T. Post myocardial infarction appears as abnormal QRS in EKG. PR interval Depolarization of AV node AV node connects and transfers the signals from atrium to ventricle Duration should be 0.12 to 0.20 seconds Longer than 0.2 seconds shows that there is a problem in AV node and interruption between atrium and ventricle which is called AV node block or AV conduction block. AV block there is no perfect connection between atrium and ventricle ST segment Means ventricle has already had (completed) contraction and is ready for relaxation phase Clinical depressed or elevated ST segment Positive sign for myocardial infarction This means there is a problem in myocardial tissue that cannot complete normal contractility phase QT interval From start of QRS to end of T wave Show ventricular contraction and relaxation depolarization and repolarization High heart rates (tachyarrhythmias) ventricular contraction duration shortens which leads to shortened QT intervals Conduction system in heart Sinoatrial node (SA node) Location In superior vena cava Normal pacemaker of the Atrioventricular node (AV node) Located on right atrium in atrial sectum