Week 10: Hypertension Flashcards
How is blood pressure regulated in the short-term?
The short-term regulation of blood pressure is managed by the Central Nervous System (CNS). The cardiovascular vasomotor control center is in the medulla and pons areas of the brainstem, with additional areas in the hypothalamus, cerebral cortex, and thalamus. The hypothalamic centers regulate cardiovascular responses to changes in temperature, and the cerebral cortex centers adjust cardiac reaction to a variety of emotional states, lastly the brainstem control center regulates heart rate and blood pressure.
The nerve fibers from the cardiovascular control center synapse with automatic neurons that influence the rate of firing of the SA node. An increased heart rate occurs with sympathetic (adrenergic) stimulation. When the parasympathetic nerves to the heart are stimulated (primarily via the vagus nerve), the heart rate slows and the sympathetic nerves to the heart, arterioles, and veins are inhibited. At rest, the heart rate in healthy individuals is primarily under the control of parasympathetic stimulation.
Messages are sent to the brain via the neural reflexes which include a collection of nerves located in the aortic arch, carotid sinuses, and other parts of the heart - these include receptors in the heart such as the baroreceptors and chemoreceptors. The brain receives theses messages and transmits commands to the circulatory system.
How is blood pressure regulated in the long-term?
See slide 22. The renin-angiotensin-aldosterone system is a key homeostatic mechanism that controls blood pressure and fluid balance. Renin is an enzyme secreted by specialized cells in the kidney when blood pressure falls or where there is a decrease in sodium flowing through the kidney tubules. Once in the blood, renin converts the inactive liver protein angiotensinogen to angiotensin I. When passing through the lungs, angiotensin I is converted to angiotensin II, one of the most potent natural vasoconstrictors known. The enzyme responsible for the final step in this system is angiotensin converting enzyme (ACE). The intense vasoconstriction of arterioles caused by angiotensin II raises blood pressure by increasing peripheral resistance. Angiotensin II also stimulates the secretion of two hormones that markedly affect blood pressure: aldosterone and ADH. Aldosterone, a hormone from the adrenal cortex, increases sodium reabsorption in the kidney. The enhanced sodium reabsorption helps the body to retain water, thus increasing blood volume and raising blood pressure. ADH, a hormone from the posterior pituitary, enhances the conservation of water by the kidneys. This raises blood pressure by increasing blood volume.
What is Primary Hypertension?
Primary hypertension is the result of a complicated interaction of genetics and the environment mediated by a host of neurohumoral effects that influence intravascular volume and PVR. Genetic predisposition to hypertension is thought to be polygenic and associated with epigenetic changes influenced by diet and lifestyle. Genetic risks include defects in renal sodium excretion, insulin sensitivity, activity of the sympathetic nervous system (SNS) and the renin-angiotensin-aldosterone system (RAAS), and cell membrane sodium or calcium transport
There is no exact known cause, but primary hypertension is responsible for 95% of all cases.
What is Complicated Hypertension?
As hypertension becomes more severe and chronic, tissue damage can occur in the blood vessels and tissues leading to target organ damage in the heart, kidney, brain, and eyes. Cardiovascular complications of sustained hypertension include left ventricular hypertrophy, angina pectoris, heart failure, coronary artery disease, myocardial infarction, and sudden death.
What is Secondary Hypertension?
Secondary hypertension is caused by an underlying disease process or medication that raises PVR or cardiac output. This form of hypertension accounts for only 5% to 10% of cases. Examples include renal vascular or parenchymal disease, adrenocortical tumors, adrenomedullary tumors (pheochromocytoma), and drugs (oral contraceptives, corticosteroids, antihistamines). If the cause is identified and removed before permanent structural changes occur, blood pressure returns to normal.
What is Malignant Hypertension?
Also known as a Hypertensive Crisis, (malignant hypertension) is rapidly progressive hypertension in which systolic pressure is ≥180mm Hg and/or diastolic pressure is ≥120mm Hg and is associated with advanced bilateral retinopathy, encephalopathy, or microangiopathy. It can occur in those with primary hypertension, but the reason some people develop this complication and others do not is unknown. Other causes include complications of pregnancy, cocaine or amphetamine use, reaction to certain medications, adrenal tumors, and alcohol withdrawal. High arterial pressure renders the cerebral arterioles incapable of regulating blood flow to the cerebral capillary beds. High hydrostatic pressures in the capillaries cause vascular fluid to exude into the interstitial space. Retina exhibit hemorrhages, cotton wool spots, and papilledema. If blood pressure is not reduced, cerebral edema and cerebral dysfunction (encephalopathy) increase until death occurs.
Identify the modifiable and non-modifiable risk factors in the development of hypertension
Modifiable Risk Factors:
- Socioeconomic status
- Sleep apnea
- Psychosocial stressors
- Increased sodium intake
- Glucose intolerance/Insulin Resistance
- Heavy Alcohol use
- Obesity (increases water retention & inflammation)
- Cigarettes & vapes
- Decreased potassium, magnesium, and calcium
Non-Modifiable Risk Factors:
- Family history (some evidence of genetic influence)
- Race (more prevalent in South Asian & Black communities)
- Gender (females >70, Male >55)
- Advancing age
Explain the pathophysiology of hypertension
See slide 20. Multiple mechanisms contribute to the pathophysiology of hypertension; genetic and environmental risks lead to changes in neurohormones and dysfunction of the SNS and RAAS, insulin resistance and obesity, and inflammation.
Obesity contributes to hypertension through changes in adipokines and increased inflammation. The combination of obesity, insulin resistance, SNS and RAAS dysfunction, and inflammation cause sodium and water retention and peripheral vasoconstriction leading to sustained hypertension and organ damage.
Increased vascular volume is related to a decrease in renal excretion of salt, often referred to as a pressure shift in the pressure-natriuresis relationship. Increased SNS activity causes accelerated heart rate and systemic vasoconstriction - these changes increase both cardiac output and peripheral vascular resistance, thus raising blood pressure.
Sustained hypertension results in structural changes in the blood vessels (vascular remodeling) that contributes to hyaline sclerosis and atherosclerosis which can cause retinal changes, renal disease (nephrosclerosis), cardiac disease (coronary artery disease, congestive heart failure), and neurologic disease (stroke, dementia, encephalopathy)
Discuss dietary requirements for hypertension and the non-pharmacological treatment of clients with hypertension including nutritional modifications
- Healthy diet in accordance with the DASH (Dietary Approaches to Stop Hypertension) diet: high in fresh fruits and vegetables and low-fat dairy products; low in saturated fat and salt
- Regular physical activity: 30 to 60 minutes of moderate cardiorespiratory activity (such as walking, jogging, cycling, or swimming) four to seven times per week
- Limited alcohol intake: no more than 2 standard drinks per day (less than 14 per week for men and less than 9 per week for women)
- Healthy weight: maintain an ideal body weight (body mass index [BMI] of 18.5 to 24.9 kg/m2; waist circumference <102 cm for men and <88 cm for women)
- Restricted salt intake: less than 100 mg/day for individuals who are considered salt-sensitive (such as those over age 45 years, of African descent, or with impaired renal function or diabetes)
- Smoke-free environment
- Stress management
What is Hypertension?
Hypertension is consistent elevation of systemic arterial blood pressure. It results from a sustained increase in peripheral vascular resistance (PVR), an increase in circulating blood volume and cardiac output, or both. Hypertension is defined as a SUSTAINED systolic blood pressure (SBP) of 140mm Hg or a diastolic blood pressure (DBP) of 90mm Hg or greater after multiple measurements made over several visits.
A client with a SUSTAINED BP on 120-139/80-89 mm Hg is said to be pre-hypertensive.
What is blood pressure and how is it measured?
Blood pressure is the pressure of circulating blood against the walls of blood vessels. Most of this pressure results from the heart pumping blood through the circulatory system. When used without qualification, the term “blood pressure” refers to the pressure in a brachial artery, where it is most commonly measured.
Blood pressure is measured using the systolic and diastolic pressures. The systolic pressure is the pressure exerted when the ventricles contract and blood is pumped out into the circulation. Diastolic pressure is measured when the ventricles relax and fill with blood.
Blood pressure is impacted by cardiac output (i.e., increased stroke volume or heart rate), peripheral resistance (i.e., sympathetic nervous system activity, renin/angiotensin II, increase in blood viscosity), and blood volume (i.e., fluid loss/dehydration, fluid retention from increased aldosterone or increased anti-diuretic hormone) - increases in these factors will increase BP.
Blood pressure = Cardiac output x Peripheral Resistance
What is Pulse Pressure?
The pulse pressure is the difference between the systolic pressure and the diastolic pressure (Ps - Pd) and is typically between 40-50 mm Hg. It is directly related to arterial wall stiffness and stroke volume. A large pulse pressure tells us that possibly the vessels are very rigid.
What is Mean Arterial Pressure (MAP)?
MAP is the average pressure in the arteries throughout the cardiac cycle, it depends on the elastic properties of the arterial walls and the mean volume of blood in the arterial system. MAP can be approximated from the measured values of the systolic and diastolic pressures and is an overall indicator of tissue perfusion. The normal range for MAP is 70 to 110mm Hg.
What is Cardiac Ouput?
The cardiac output (minute volume) of the heart can be changed by alterations in the heart rate, stroke volume (volume of blood ejected during each ventricular contraction), or both. An increase in cardiac output without a decrease in peripheral resistance will cause the MAP and flow rate to increase. The higher arterial pressure increases blood flow through the arterioles. On the other hand, a decrease in the cardiac output causes a drop in the MAP and arteriolar flow if peripheral resistance stays constant
Amount of blood pumped by a ventricle in 1 minute and is increased by any condition that increases heart rate or stroke volume.
CO = HR X SV
(heart rate x stroke volume)
What is Stroke Volume?
The amount of blood pumped by the left ventricle in one contraction. Stroke volume could be impacted by a weak ventricle, a prolapsed valve or an incompetent valve. Stroke volume is controlled by preload, contractility and afterload.
What is Systemic Vascular Resistance (SVR)?
It is the force opposing movement of blood within vessels. To elaborate, Total resistance in the systemic circulation, known as either SVR or TPR, is primarily a function of arteriolar diameter. If cardiac output remains constant, arteriolar constriction raises the MAP by reducing the flow of blood into the capillaries, whereas arteriolar dilation has the opposite effect. Reflex control of total cardiac output and peripheral resistance includes (1) sympathetic stimulation of the heart, arterioles, and veins; and (2) parasympathetic stimulation of the heart
What is Preload?
Preload involves the filling of the ventricles but is actually a measure of stretch in the fibers; how much blood is going in and what is the degree of stretch - through this measurement, we understand the ventricles ability to RECOIL.
Preload is the volume and pressure inside the ventricle at the end of diastole (ventricular end-diastolic volume [VEDV] and pressure [VEDP]). Preload is determined by two primary factors: (1) the amount of blood left in the ventricle after systole (end-systolic volume) and (2) the amount of venous blood returning to the ventricle during diastole. End-systolic volume is dependent on the strength of ventricular contraction and the resistance to ventricular emptying. Venous return is dependent on blood volume and flow through the venous system and the atrioventricular valves.
What is Afterload?
Afterload is how hard the ventricle has to work to eject blood, it is a measure of CONTRACTILITY.
Ventricular afterload is the resistance to ejection of blood from the ventricle. It is the load the muscle must move during contraction.
