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University of Arizona
PSIO 485
Zoe Cohen

Exam 4 study: PSIO 485 Hypertension: High blood pressure 1)What is the definition of hypertension? Is it a common health problem? • Hypertension is defined as the a sustained elevation of systemic blood pressure. An increase of pressure exerted on the vasculature. If we see an elevation in systolic blood pressure greater than 120 hypertension can be the diagnosis, although the patient must have 2-3 readings before the doctor can give a diagnosis. • Hypertension is a common health problem and is one of the major factors that leads to heart failure. It accounts for 90% of developing hypertensions, and 50% have a higher risk of hypertension. 1 in 3 adults have been diagnosed with hypertension. Hypertension can also be considered silent until we can see signs. • Normal BP 120/80 systolic over diastolic • pre-hypertension 120-139/ 80-89 these people can make life style modifications to decrease the BP. • Stage 1 hypertension 140-159/90-99 life style modifications might help but medications will need to be enforced. • Stage 2 hypertension >160/>100 Life style modifications are as relevant here. Will need medication to help bring the high blood pressure back down. 2) From this lecture and others, is hypertension involved in other diseases that we’ve talked about? If so, which ones? Heart failure (not yet talked about) hypertrophy Diabetes Atherosclerosis Cerebral ischemia 3) What causes hypertension? The causes:Anything that increases blood volume • Increased Cardiac output increases blood pressure • Increased Total peripheral resistance increases blood pressure • Also have a combination of both = Mean arteriole pressure • increased viscosity - thickness of blood • increased resistance. • Increased kidney fluid retention due to kidney failure - maybe ischemia. 4) What is the difference between primary and secondary hypertension? • Primary hypertension have no known cause, where why it happened cannot be pin pointed/ idiopathic hypertension which is 90-95% of the population. Hypertension - combined systolic and diastolic; Isolated systolic hypertension is elevated systolic blood pressure accompanied by normal diastolic blood pressure. • Secondary hypertension - high blood pressure caused by another disease. Kidney problems can cause secondary hypertension. Even kidney transplants, Heart transplants, and apnea can cause secondary hypertension. This only accounts for 5-8% of all cases. 5) What’s the term that we use to describe increased aortic pressure? How does this relate to high blood pressure? How does this affect how the heart works? What cardiomyopathies could result from this? High blood pressure increases the workload of the heart. When the ventricles contract to open the semilunar valve, they must generate sufficient pressure to exceed the blood pressure in the major arteries. After load is increased so that the heart can get enough blood out. Instead of generating 120mm Hg the ventricular pressure may need to rise to 400 mmHg to force blood through the narrow aortic valve. This increases the work in the heart leading to hypertrophy.As the work increases in the heart the muscle of the heart thickens thus enlarging the diameter of the heart. This can be a good adaption but it can lead to a decreased force of contraction due to dilation which forms heart failure. 6) What factors are associated with primary hypertension? • Acombination of genetic and environmental factors. Environmental is HUGE portion of hypertension. • also a specific cause for primary hypertension has not been identified. • familial history • advancing age • gender • black race • dietary sodium intake - retain more sodium of have more sodium water follows increasing the volume of the blood volume. • obesity • cigarette smoking - nicotine is a vasoconstrictor that can elevate both diastolic and systolic pressure. Long term smoking remodels vasculature of the heart vessels. Replaces with lots of collagen which makes the heart stiff • high alcohol consumption • low potassium, calcium and magnesium intake. Without their intake sodium is retained leading to hypertension. 7) How is the sympathetic nervous system involved in blood pressure regulation? What goes wrong with hypertension? Sympathetic nervous system contributes to the pathogenesis of hypertension in many people. It helps us maintain blood pressure. Increased inotropy brings BP back to normal pressure. But a long term use of the sympathetic nervous system can cause and increase in hypertension. It does this by increasing vascular tone, catacholamines (which can change structure of vasculature; lays more collagen down making it more stiff and strong increasing BP). 8) How is the renin-angiotensin-aldosterone system involved in blood pressure regulation? What goes wrong with hypertension? • The RAAsystem regulates long term blood pressure and tissue perfusion. The RAA system works by increasing blood volume to increase BP. In hypertension it doesn't work properly. It just continues to increase the volume load in our body resulting in remodeling, which is a protective mechanism of high blood pressure causing remodeling which helps strengthen the vasculature and tissues of the heart. • Angiotensin II is also responsible for hypertrophy which increases hypertension. • Aldosterone not only contributes to sodium retention by the kidney but also has further deleterious effects on the cadiovascular system; remodeling. 9) How is natriuretic hormone involved in blood pressure? How do changes lead to hypertension? Anatriuretic hormone is a pathophysiologic mechanism that mediates the effects of hypertension. It is used to excrete sodium, salt and water decreasing blood pressure, but can get out of whack over a long time of hypertension. the function of these hormones can be affected by excessive sodium intake inadequate dietary intake of potassium, magnesium, calcium and obesity. When these natriuretic hormones don't function the body starts retaining salt leading to water retention and increased blood volume which increases blood sheer --> Stress --> damage in small vessels --> then constriction leading to increased blood pressure. Kidneys also become ischemic. 10)What is the role that inflammation plays in the pathogenesis of hypertension? Long term inflammation history will increase the chance of hypertension. We don't want full body inflammatory response because this leads to vasodilation which decreases renal perfusion leading to ischemia. This ischemia causes sodium retention dragging water with it increasing blood pressure. 11) How does endothelial cell dysfunction contribute to hypertension? Give some examples of diseases that are related to endothelial cell dysfunction. Endothelial cell dysfunction is characterized by a decreased production of vasodilators such as nitric oxide and increased production of vasoconstrictors such as endothelin. Some diseases that are associated with endothelial cell dysfunction is diabetes and insulin resistence. 12) What is isolated systolic hypertension and how is it different that primary or secondary hypertension? Isolated systolic hypertension: elevations of systolic pressure caused by increased cardiac output or total peripheral resistance or both.Aorta and large arteries have large relaxation problems. 13)What is complicated hypertension? What does this effect?And it what ways? Complicated hypertension is chronic hypertension damages the walls of the systemic blood vessels. Changes in the level of the vasculature where we can see physical changes. No symptoms, silent, although there are changes going on in the vessels. Target Organs for hypertension are: Brain, heart, kidney extremities and eyes. These cardiovascular complications include: ventricular hypertrophy, angina pectoris, congestive heart failure, coronary artery disease, MI and sudden death. Eye doctor can diagnose hypertension due to retina sclerosis or other eye diseases. 14)How is hypertension diagnosed? Can you measure it 1 time and go with that value? What things can you think of that might effect a blood pressure reading? • Hypertension is diagnosed by two -three readings where the systolic/ diastolic blood pressure is greater than 120/80. • Clinicians use 24-hour ambulatory blood pressure monitors to determine management modality throughout the day. Use complete medical history and assessment of life style with possible secondary cause of hypertension. • Further diagnose include: hematocrit urinalysis, biochemical blood profile and ECG. • Also white coat hypertension - associated with nervous characteristics in a health care setting. • If drunk caffeine such as coffee or an energy drink then your blood pressure will be higher than 120/80. 15)How do you treat hypertension? Treatment with pharmacologic and non-pharmacologic methods. Treatment begins with reducing risk factors, life style modifications with those who fall in the pre-hypertensive category,ACF inhibitors, andAngiotensin antagonist. You can also use Thiazide diuretics which are the safest and most effective medications for lowering BP; Beta blockers also are used to decrease BP. 16)What is hypotension? Hypotension is a decrease in pressure exerted on the vessel walls. This would mean decreased systolic over diastolic which is clinically seen as >90/>60. 17)What is orthostatic hypotension? Is this ever normal? When? Orthostatic hypotension is decrease in systolic and diastolic pressure upon standing. It is normal when postural changes are made where volume shifts initiating baroreceptor reflex activity increasing sympathetic activity. This increases HR and constricts arterioles thus BP is maintained. 18)What are the differences between acute and chronic hypotension? Acute hypotension is associated with known diseases or problems in the body. Whereas chronic hypotension is associated with long term problems that are not known. Heart Failure: 1) What does the term “heart failure” actually mean? • The inability of the heart to supply the demands of the body; thus referring to the cardiac output. The heart can't keep pace with the body's demands for supplies and removal of waste. The demands of the body can also need more blood than the heart can pump out. • It affects 5 million where 50% will die within four years of diagnosis. • Types of heart failure - left ventricular dysfunction (systolic and diastolic heart dysfunction), right ventricular dysfunction ( dysfunctional in pulmonary disease), Some condition cause inadequate perfusion despite normal of elevated cardiac heart failure. • Prime defect in heart failure - Decreased heart contractility, Inotropy. 2) What are the 2 most common causes of heart failure? What happens in the heart in each of these cases prior to development of heart failure? • Damage to the heart muscle - following a myocardial infarction no contraction of the damaged muscle leading to ischemia which decreases oxygen to heart and decreases the ability to pump --> heart failure. • Prolonged pumping of the ventricles against a chronically increased afterload. This prolonged pumping causes a stenotic aortic valve leading to heart failure. Increased pumping leads to high blood pressure causing heart failure. Some hypertrophy may also result which thickens the walls of the heart leading to remodeling of the vasculature because it has to stretch with the huge muscle mass; this also leads to heart failure. 3) During the early stages of heart failure, the heart will try to compensate. What does it do?And how does this affect cardiac output? • Sympathetic activity to the heart is reflexly increased, where the sympathetic system affects CO and TPR. It increases Inotropy to maintain CO, and increases HR to also maintain CO. However with long term sympathetic activity there is a less response to norepinephrin where the heart stops listening to the norepinephrin. • Kidneys use their salt retention mechanisms to retain water to expand blood volume when there is reduced CO. When the heart is weaker the ejection fraction decreases which decreases organ blood flow. The kidneys are very much affected with less amounts of blood. Thus kidneys will increase blood volume. However the increased blood will stretch the heart decreased contractility leading to Heart failure. 4) What are some causes of heart failure (there are 12 listed in your slides)? Think about how these could lead to heart failure. • Myocardial infarction - damaged muscle decreases contractility, ischemia to heart, heart weakens causing heart failure. • coronary artery disease - blockage in the heart causes ischemia which decreases blood to the heart and decreases inotropy, even less blood gets to heart leading to heart failure. • Valve disease - stenotic aortic valve which increases afterload due stiff valve which increases inotropy thickening the muscle causing heart failure. • idiopathic cardiomyopathy - unknown causes that may cause heart failure • Viral or bacterial cardiomyopathy - Causing infections and diseases that can flow in the blood stream leading the heart causing infections their leading to damaged heart tissue leading to heart failure. • Myocarditis - infected myocardium of the heart • Pericarditis - infected heart sac. • Arrhythmias - Disorder of the HR or pulse, such as beating too fast. • Chronic hypertension - increased blood pressure • Thyroid disease - hypothyroidism increases heart rate • Pregnancy - more demand for blood increases chance of Heart failure • Septic shock - overwhelming infection leading to low blood pressure, which can affect any part of the body including the heart. 5) What does the term “decompensated heart failure” mean? As disease progresses the contractility of the heart deteriorates further. The heart reaches its maximum point at which it no longer is able to pump out a normal stroke volume despite compensatory measures. 6) Why is left sided heart failure more serious than right sided heart failure? Left sided failure - backwards left sided failure leads to pulmonary edema because blood dams up in the lungs due to heart not being able to pump out blood and more volume is returning into the heart from the lungs. Left atria dilates, the lungs get dammed up. Venous damming. Blood doesn't move forward but backward. Lungs get filtration too much and there is no reabsorption which leads to fluid in the lungs --> pulmonary edema. One of the more serious consequences is inadequate blood flow to the kidneys, which causes a twofold problem. 1. vital kidney function is depressed. 2. kidneys retain even more salt and water. Congested heart failure - can either be systolic or diastolic heart failure or both. 7) What is the difference between systolic heart failure and diastolic heart failure? Systolic heart failure is defined as an inability for the heart to generate an adequate cardiac output. In systolic dysfunction chambers are too large. Diastolic heart failure is inability of the ventricles to fill in relaxation decreases cardiac output leading to systolic heart failure. Chambers are two small and don't allow for enough blood to fill in the relaxation time. 8) How does preload affect heart function? How could it lead to heart failure? Preload or left ventricular end diastolic volume is increased with decreased contractility or in excess blood plasma. increased volume and decreased contraction stretches out the chambers. From this we can get ischemia of the kidneys and then heart failure.Also we can get a regurgitation of the mitral valve causing heart failure. 9) How does afterload affect heart function? How could it lead to heart failure? Increased afterload is most commonly a result of increased peripheral vascular resistance seen with hypertension. Due to resistance the pressure it takes to push open the valves is very high. This can lead to a stenotic valve which leads to heart failure, hypertrophy can also be caused by this leading to heart failure. We can also see increased contraction due to sympathetic stimulation from the angiotensin-aldosterone system. 10)What are some important mediators of heart function (there are 8 of them listed)? If I name each one, could you tell me if it improves or hinders cardiac function if it’s high? If it’s Low? 1. Catecholamines - used in sympathetic nervous system to increase heart rate and peripheral vascular resistance. However it can act on tissue and remodel it.Also toxic in large numbers causing cardiomyocytes to die. 2. Angiotensin II - increases preload and afterload and has a direct effect of toxicity to the myocardium. 3. Aldosterone - causes salt and water retention but also contributes to myocardial fibrosis, remodeling of the heart, dysrhythmias, and autonomic dysfunction. 4. Arginine vasopressin - (ADH) antidiuretic hormone causes peripheral vasoconstriction, and renal fluid retention. These can cause low blood sodium and congestive heart failure. Low blood sodium causes water intoxication with too much fluid and less electrolytes. 5. Natriuretuc peptides - increased in CHF and may have protective effect by decreasing preload. used in hypertension. 6. endothelial hormones - Potent vasoconstrictor and is associated with patients with a poor prognosis of CHF. 7. Endotoxin - People with CHF have been found to have high levels of this substance, especially with significant edema. Used in vasodilation. 8. Cytokines - Protein made by the cell that can act on neighboring cells. Remodels cell and degrades nitric oxide. 11) What are some clinical signs that could lead you to suspect that a person has heart failure? Pulmonary vascular congestion, abnormal breathing excessive fluid in lings being coughed out, blue skin (adema), and displaced apex due to large heart/dilated heart, swelling of feet, lack of energy, confusion/ impaired memory, increased urination at night, swollen abdomen. 12)How do you treat systolic left heart failure? Is this the same or different than treating chronic left heart failure? To treat left systolic heart failure we need to break the cycle increasing preload and afterload as well as blocking the neurohumoral mediators of myocardial toxicity. BREAK THE CYCLE, catch it early before we see remodeling of the heart. WE NEED to INCREASE O , inotropi2 drugs, Ca , diuretics ( reduce preload),AndACE inhibitors (reduce preload and afterload by reducing aldosterone levels).Also beta blockers can help slow heart rate down by increasing relaxation which increasing coronary flow in the heart. Treatment of left systolic heart failure and chronic left heart failure both need to reduce preload and afterload, while increasing contractility. There are some differences in that salt restriction, avoidance of inflammatory medications, and institution of exercise training can help the symptoms get better. 13)What is diastolic heart failure? Diastolic heart failure is defined as pulmonary congestion despite normal stroke volume and cardiac output. This results from decreased compliance and abnormal diastolic relaxation allowing the normal left ventricular end diastolic volume results in an increase in increased Left ventricular end diastolic pressure. This pressure pushes on theAV valve pushing blood backward into the lungs creating pulmonary edema. Use beta blockers to increase diastole. 14)What is right hea
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