Unit 8 Cardiovascular Sytem

Question 1

What is circulatory shock?

Answer 1

An acute failure of the circulatory system to supply the peripheral tissues and organs of the body with an adequate blood supply, resulting in cellular hypoxia

Question 2

Describe manifestations of shock (fig 20.5 handout). Requested access from Alice April 14th.

Answer 2

Hypovolemic - Direct loss of effective circulating blood volume leading to:

• A rapid, weak, thready pulse due to decreased blood flow combined with tachycardia (decrease BP with increased HR)
• Cool, clammy skin due to vasoconstriction and stimulation of vasoconstriction
• Rapid and shallow breathing due to sympathetic nervous system stimulation and acidosis
• Hypothermia due to decreased perfusion and evaporation of sweat
• Thirst and dry mouth, due to fluid depletion and
• Cold and mottled skin (Livedo reticularis), especially extremities, due to insufficient perfusion of the skin
• The severity of hemorrhagic shock can be graded on a 1-4 scale on the physical signs. This approximates to the effective loss of blood volume.
• [edit]

Cardiogenic

• Distended jugular veins due to increased jugular venous pressure
• Weak or absent pulse
• Arrhythmia, often tachycardic
• Pulsus paradoxus in case of tamponade

Question 3

What are the four types of circulatory shock?

Answer 3

Hypovolemic

• Loss of whole blood
• Loss of plasma
• Loss of extracellular fluid

Obstructive

• Inability of heart to fill properly
• Obstruction to outflow from the heart

Distributive

• Loss of sympathetic vasomotor tone
• Presence of vasodilating substance in the blood
• Presence of inflammatory mediators

Cardiogenic shock

• By an alteration in cardiac function

Question 4

Be able to explain the four types of shock

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Question 5

What are the complications of shock?

Answer 5

• Acute respiratory distress syndrome
• Acute renal failure
• Gastrointestinal complications
• Disseminated intravascular coagulation
• Multiple organ dysfunction syndrome

Question 6

What is MODS?

Answer 6

• Multiple organ dysfunction syndrome
• Presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention
• Kidneys, lungs, liver, brain, and heart
• Pathophysiology: A definite explanation has not been found. Local and systemic responses are initiated by tissue damage. Respiratory failure is common in the first 72 hours after the original insult. Following this one might see hepatic failure (5–7 days), gastrointestinal bleeding (10–15 days), and renal failure (11–17 days)

Question 7

What is heart failure?

Answer 7

Failure of the heart as a pump that result in inadequate perfusion of tissues

Question 8

What are compensatory mechanisms that try to maintain cardiac output during heart failure?

Answer 8

Compensatory or adaptive mechanisms

• Activation of neurohumoral influences such as the sympathetic nervous system
• The renin–angiotensin–aldosterone mechanism
• Natriuretic peptides (refers to a peptide which induces natriuresis, the discharge of sodium through urine)
• Locally produced vasoactive substances
• Myocardial hypertrophy and remodeling

Question 9

Explain the mechansism that compensate for HF

Answer 9

• Frank-Starling mechanism: an intrinsic adaptive response which serves to adjust each ventricular output to its inflow by increasing the force of contraction of the myocardium proportionally to any increase in the length of the muscle fibers.
• RAA System
• Myocardial hypertrophy
• Sympathethic reflexes

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Question 10

How can hrt failure be described or identified?

Answer 10

• High-output or low-output failure
• Systolic or diastolic failure
• Right-sided or left-sided failure
• Chronic or acute

Question 11

Describe acute and chronic heart failure.

Answer 11

Acute heart failure

• Develops rapidly; immediately life threatening
• Results from cardiopulmonary bypass surgery, acute infection (sepsis), acute myocardial infarction, valve dysfunction, severe arrhythmias

Chronic heart failure

• Long-term condition associated with the heart undergoing adaptive responses
• Adaptive response can make heart failure worse

Question 12

What are the primary issues that cause left or right sided hrt failure?

Answer 12

Right side - primary issue is with pulmonary semilunar valve, backup of blood to systemic system, edema of extremities

• Congenital heart diseases (VSD, PDA)
• Secondary to left sided heart failure (increase in left ventricle filling pressure is reflected back in the pulmonary circulation)
• Massive pulmonary embolism
• Chronic pulmonary disease (Cor pulmonale)

Left side - primary issue is with aortic semilunar valve, backup of blood to pulmonary vein, pulmonary hypertension

• Ischemic heart diseases
• Hypertensive heart diseases
• Cardiomyopathy
• High-output states (thyrotoxicosis, anemia)

Question 13

What are the manifestations of right and left side heart failure?

Answer 13

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Question 14

What is the pathogenesis and clinical manifestations of right-sided heart failure?

Answer 14

• fluid builds up in tissues as peripheral edema
• systemic venous congestion

1. peripheral edema
2. liver congestion – hepatomegaly
3. fluid accumulation in the body cavities
4. raised jugular venous pressure

http://postimg.org/image/runxrs9nl/

Question 15

What is the pathogenesis and the clinical manifestations of left sided heart failure?

Answer 15

• blood remains in left ventricle
• blood backs up into lungs as pulmonary edema – pulmonary congestion
• suffocation and lack of oxygen to the lung tissues

http://postimg.org/image/nqmyzadpd/

Question 16

Causes of HF

Answer 16

Myocardial disease

• Cardiomyopathies
• Myocarditis
• Coronary insufficiency
• Myocardial infarction

Valvular heart disease

• Stenotic valvular disease
• Regurgitant valvular disease

Hypertension
Congenital heart defects
Constrictive pericarditis

Question 17

What are backward and forward effects of heart failure?

Answer 17

backward heart failure a concept of heart failure emphasizing the causative contribution of passive engorgement of the systemic venous system, as a result of dysfunction in a ventricle and subsequent pressure increase behind it.

forward heart failure a concept of heart failure that emphasizes the inadequacy of cardiac output relative to body needs and considers venous distention as secondary.

Question 18

What is Cor Pulmonale?

Answer 18

refers to right sided heart failure resulting from primary lung disease and long standing pulmonary hypertension

• signs of right sided heart failure
• signs of chronic airway obstruction
• signs of polycythemia

Question 19

How does pulmonary hypertension contribute to right sided heart failure?

Answer 19

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Question 20

Compare high output and low output heart failure.

Answer 20

High output: the heart increases its output but the body’s metabolic needs are still not met

• anemia
• hyperthyroidism
• beriberi (thiamine, vitamin B1 deficiency)

Low output: common causes:

• ischemic heart disease
• cardiomyopathy

Question 21

Compare systolic and diastolic heart failure.

Answer 21

Systolic failure: a decreased in myocardial contractility
ejection failure
Causes:

• ischemic heart diseases
• valvular insufficiency
• pressure overload such as hypertension

Diastolic failure: relaxation is abnormal
conditions that impede relaxation
Causes:

• pericardial effusion, constrictive pericarditis
• aging

Question 22

Describe the cardiac cycle

Answer 22

http://en.wikipedia.org/wiki/File:Wiggers_Diagram.png

1. early diastole: DIASTOLE, AV valves open, SL valves closed
   • whole heart is relaxed
   • ventricles are expanding and filling
2. atrial systole: DIASTOLE, AV valves open, SL valves closed
   • atria contract and pump blood
   • additional 10–40% filling of ventricles
3. isovolumic ventricular contraction: SYSTOLE, AV valves closed (LUB), SL valves closed
   • ventricular myocytes begin to contract
   • ventricle volume unchanged
4. ventricular ejection: SYSTOLE, AV valves closed, SL valves open
   • ventricles fully contract
   • pump blood to rest of body
5. Isovolumic ventricular relaxation: DIASTOLE, AV valves closed, SL valves closed (DUB)
   • ventricles relax
   • ventricle volume unchanged
   • atria expand and are filling

Question 23

What is hypertension?

What is normal BP, prehypertension, stage 1 hyper tension, and stage 2 hypertension?

Answer 23

• is consistent elevation of systemic arterial blood pressure
• what is normal blood pressure and what is elevated? depends on age, gender, systolic/diastolic

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Question 24

What are the categories of hypertension?

• primary (essential hypertension)
• secondary hypertension
• malignant hypertention

Answer 24

primary (essential hypertension)

• a chronic elevation in BP that occurs without any evidence of other disease

secondary hypertension

• a chronic elevation of BP that results from some other disorder, such as kidney disease, hormonal disorder, coarctation of the aorta

malignant hypertension

• Sudden increase in BP – diastolic >120

Question 25

What are the clinical manifestations of hypertension?

Answer 25

asymptomatic

• early stages of hypertension have no clinical manifestations. Some may have vague symptoms like headache, stiffness of the neck, and drowsiness

symptoms of complications

• most clinical manifestations are caused by complications that cause damage to the systemic organs

Question 26

What are the target organ damage casused by hypertension?

Answer 26

• chronic hypertension – damage to the walls of systemic blood vessels
• smooth muscle hypertrophy and hyperplasia – narrowing of the lumen – ischemia
• atherosclerosis
• overload on the left ventricle

Heart

• pressure load and left ventricular hypertrophy
• relative ischemia (angina)
• congestive heart failure

CNS

• CVA/strokes

Kidneys

• renal ischemia – renal failure

Retinal vessels

• ischemia, exudates and hemorrhages

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Question 27

What is orthostatic (postural) hypotension?

Answer 27

refers to a decrease in arterial blood pressure on standing

loss of reflex mechanism:

• vasoconstriction
• increased heart rate
• closure of valves in the venous system
• sympathetic activity (stimulated by upright position)

Question 28

What are the mechanisms of blood control upon assumption of an upright position?

Answer 28

action of skeletal muscle pumps

drop in blood pressure caused increase HR and vasoconstriction to return to normal levels

http://postimg.org/image/m6j2m6i0l/

Question 29

What are the two types of orthostatic hypotension?

Answer 29

acute and temporary

• drugs such as antihypertensives, antidepressants
• prolonged immobility by illness
• starvation
• volume depletion (massive diuresis)
• venous pooling (pregnancy, varicosities)

chronic orthostatic hypotension

• secondary to specific disease like diabetes mellitus, adrenal insufficiency
• idiopathic – no known cause
• aging

Question 30

What are coronary artery disease?

Answer 30

Disorders of myocardial blood flow due to stable or unstable coronary atherosclerotic plaque
1) Acute Coronary syndromes

• Unstable angina
• Non-ST-segment elevation MI
• ST-segment elevation MI

2) Chronic Ischemic Heart Disease

• Stable angina
• Variant (vasospastic) angina
• Silent myocardial ischemia

Question 31

What is stable angina?

Answer 31

Stable angina is chest pain or discomfort that usually occurs with activity or stress. Angina is chest discomfort due to poor blood flow through the blood vessels in the heart.

RISK FACTORS

Risk factors for coronary heart disease. Some include:

• Diabetes
• High blood pressure
• High LDL cholesterol and low HDL cholesterol
• Smoking

CAUSES

Anything that makes the heart muscle need more oxygen can cause an angina attack in someone with heart disease, including:

• Cold weather
• Exercise
• Emotional stress
• Large meals

Other causes of angina include:

• Abnormal heart rhythms (usually ones that cause your heart to beat quickly)
• Anemia
• Coronary artery spasm (also called Prinzmetal’s angina)
• Heart failure
• Heart valve disease
• Hyperthyroidism (overactive thyroid)

SYMPTOMS

Symptoms of stable angina are most often predictable. This means that the same amount of exercise or activity may cause your angina to occur. Your angina should improve or go away when you stop or slow down the exercise.

The most common symptom is chest pain that occurs behind the breastbone or slightly to the left of it. The pain of stable angina usually begins slowly and gets worse over the next few minutes before going away.

The pain may feel like tightness, heavy pressure, squeezing, or crushing pain. It may spread to the:

• Arm (usually the left)
• Back
• Jaw
• Neck
• Shoulder
• Some people say the pain feels like gas or indigestion.

Some patients (women, older adults, and people with diabetes) may have different symptoms, such as:

• Back, arm, or neck pain
• Fatigue
• Shortness of breath
• Weakness
• The pain of stable angina usually:

Occurs after activity or stress

• Lasts an average of 1 - 15 minutes
• Is relieved with rest or a medicine called nitroglycerin
• Angina attacks can occur at any time during the day, but a higher number occur between 6 a.m. and noon.

Question 32

What is unstable angina?

Answer 32

Unstable angina is a condition in which your heart doesn’t get enough blood flow and oxygen. It may lead to a heart attack.

Angina is a type of chest discomfort caused by poor blood flow through the blood vessels (coronary vessels) of the heart muscle (myocardium).

CAUSES

Coronary artery disease due to atherosclerosis is by far the most common cause of unstable angina. Atherosclerosis is the buildup of fatty material called plaque along the walls of the arteries. This causes arteries to become narrowed and less flexible. The narrowing interrupts blood flow to the heart, causing chest pain.

People with unstable angina are at increased risk of having a heart attack.

Rare causes of angina are:

• Abnormal function of tiny branch arteries without narrowing of larger arteries (called microvascular dysfunction or Syndrome X)
• Coronary artery spasm

RISK FACTORS

Risk factors for coronary artery disease include:

• Diabetes
• Family history of early coronary heart disease – a close relative such as a sibling or parent had heart disease before age 55 (in a man) or before age 65 (in a woman)
• High blood pressure
• High LDL cholesterol
• Low HDL cholesterol
• Male gender
• Not getting enough exercise
• Obesity
• Older age
• Smoking

SYMPTOMS

Symptoms of angina may include:

• Chest pain that you may also feel in the shoulder, arm, jaw, neck, back, or other area
• Discomfort that feels like tightness, squeezing, crushing, burning, choking, or aching
• Discomfort that occurs at rest and does not easily go away when you take medicine
• Shortness of breath
• Sweating
• With stable angina, the chest pain or other symptom only occurs with a certain amount of activity or stress. The pain does not occur more often or get worse over time.
• Unstable angina is chest pain that is sudden and often gets worse over time. You may be developing unstable angina if the chest pain:

Starts to feel different, is more severe, comes more often, or occurs with less activity or while you are at rest
Lasts longer than 15 - 20 minutes
Occurs without cause (for example, while you are asleep or sitting quietly)
Does not respond well to a medicine called nitroglycerin
Occurs with a drop in blood pressure or shortness of breath

Unstable angina is a warning sign that a heart attack may happen soon. It needs to be treated right away. If you have any type of chest pain, see your doctor.

Question 33

Missing Coronary Atery Disease Handout (requested from Alice April 12th)

Question 34

What is variant (vasospastic) angina?

Answer 34

Coronary artery spasm is a temporary, sudden narrowing of one of the coronary arteries (the arteries that supply blood to the heart). The spasm slows or stops blood flow through the artery and starves part of the heart of oxygen-rich blood.

CAUSES

The spasm often occurs in coronary arteries that have not become hardened due to plaque buildup (atherosclerosis). However, it also can occur in arteries with plaque buildup.

These spasms are due to a squeezing of muscles in the artery wall. They usually occur in just one area of the artery. The coronary artery may appear normal during testing, but it does not function normally.

About 2% of patients with angina (chest pain and pressure) have coronary artery spasm.

Coronary artery spasm occurs most commonly in people who smoke or who have high cholesterol or high blood pressure. It may occur without cause, or it may be triggered by:

• Alcohol withdrawal
• Emotional stress
• Exposure to cold
• Medications that cause narrowing of the blood vessels (vasoconstriction)
• Stimulant drugs such as amphetamines and cocaine
• Cocaine use and cigarette smoking can cause severe spasms of the arteries, and can cause the heart to work harder. In many people, coronary artery spasm may occur without any other heart risk factors (such as smoking, diabetes, high blood pressure, and high cholesterol).

SYMPTOMS

Spasm may be “silent” – without symptoms – or it may result in chest pain or angina. If the spasm lasts long enough, it may even cause a heart attack.

The main symptom is a type of chest pain called angina, which most often is felt under the chest bone (sternum) or left side of the chest, and is described as:

• Constricting
• Crushing
• Pressure
• Squeezing
• Tightness
• It is usually severe. The pain may spread to the neck, jaw, shoulder, or arm.

The pain of coronary artery spasm:

• Often occurs at rest
• May occur at the same time each day, usually between midnight and 8:00 AM
• Lasts from 5 to 30 minutes
• The person may lose consciousness.

Unlike angina that is caused by hardening of the coronary arteries, chest pain and shortness of breath due to coronary artery spasm are often not present when you walk or exercise.

Question 35

Describe the pathophysiology of Coronary Artery Diseases (CAD).

Answer 35

Depends on the location and extent of damage

Transmural infarcts

• Involve the full thickness of the ventricular wall
• Occur when there is obstruction of a single artery

Subendocardial infarcts

• Involve the inner one third to one half of the ventricular wall
• Occur more frequently in the presence of severely narrowed but still patent arteries
• Wall thinning, healing, hypertrophy, dilation
• Ventricular remodelling – anuerysm formation
• Impairment of ventricular function
• Arrhythmias – heart failure

Question 36

What is cardiac output?

Answer 36

The amount of blood ejected from each ventricles into the aorta/pulmonary trunk in one minute

CO = SV ml/min X HR beats/min
= 70 ml X 75
= 5.25 L/min

Question 37

Calc. the CO of a patient with a SV of 50 ml/min and HR of 60 beats per minute.

Question 38

What are the typical values for the following?

• end-diastolic volume (EDV)
• end-systolic volume (ESV)
• stroke volume (SV)
• ejection fraction (Ef)
• heart rate (HR)
• cardiac output (CO)

Answer 38

• end-diastolic volume (EDV) 120 mL
• end-systolic volume (ESV) 50 mL
• stroke volume (SV) 70 mL
• ejection fraction (Ef) 58%
• heart rate (HR) 75 bpm
• cardiac output (CO) 5.25 L/minute (range 4.0–8.0 L/min)

Question 39

How is CO related to other measurable variables of the heart?

Answer 39

CO = SV x HR = (contractility x EDV - ESV) x HR

SV: The amount of blood pumped out of each ventricle with each contraction
= (EDV minus ESV)
= 135 – 65 = 70 ml (approximately)

FACTORS THAT AFFECT SV

1) Intrinsic control
- Pre-load

• End diastolic volume (EDV) - the volume of blood to be ejected out from the hrt (systolic volume)
• Venous return
• Strength of cardiac contraction (contractility - force with which the heart contracts)
• After-load (end systolic volume, ESV) - pressure or force hrt must overcome to eject blood from hrt

2) Extrinsic control
- Sympathetic activity

Question 40

What factors affect the hrt rate?

Answer 40

Sympathetic activity
Parasympathetic activity
Other factors that increase or decrease heart rate

• physiological factors – age, activities
• Diseases – high fever, thyrotoxicosis
• Drugs – aspirin, beta blockers

Question 41

Define the following:

• blood pressure (BP)
• pulse pressure (PP)
• mean arterial pressure (MAP)

Answer 41

blood pressure (BP)

• Is the hydrostatic pressure exerted by blood against a vessel wall
• Systolic pressure - Maximum pressure in the artery when blood is ejected during systole
• Diastolic pressure - Minimum pressure in the artery during diastole

pulse pressure (PP)

• The pressure difference between systole and diastole
• The pulse can be felt close to the surface of the skin due to pulse pressure

mean arterial pressure (MAP)

• the average pressure responsible for driving blood forward into the tissues throughout the cardiac cycle
• the average pressure in the arterial system during ventricular contraction and relaxation
• It equals the difference in pressure between the beginning and the end of systemic circulation
• MAP is a good indicator of tissue perfusion and BP reflexes (neural reflexes) respond to changes in MAP.

Mean arterial pressure= diastolic pressure + 1/3 pulse pressure

OR

MAP = VR x CO
If BP = 120/80 = 80+1/3 of 40 = 93 mmHg
Range : 80 – 100 mm Hg

Question 42

Calc the MAP for the following BP 120/80.

Answer 42

Mean arterial pressure= diastolic pressure + 1/3 pulse pressure
If BP = 120/80 = 80+1/3 of 40 = 93 mmHg
Range : 80 – 100 mm Hg

Question 43

What is an arterial blood pressure?

Answer 43

Represents the pressure of the blood as it moves through the arterial system

Cardiac output = HR x SV
 Vascular resistance (VR)
 Mean arterial pressure = CO x VR

Question 44

What factors affect BP?

Give examples on each factor

Answer 44

Cardiac output
Resistance to the flow of blood through small vessels (peripheral resistance) – which depends on

• blood viscosity (polycthemia)
• blood vessel length (obesity)
• blood vessel radius (vasodilation)

Give examples on each factor

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Question 45

What hormones affect BP? Explain how they affect BP.

Answer 45

Hormones that affect on BP by influencing on heart rate and blood volume:

• epinephrine/norepinephrine
• RAA (renin-angiotensin-aldosterone system)
• ADH
• ANP

The kidneys provide a hormonal mechanism for the regulation of blood pressure by managing blood volume.

• The renin-angiotensin-aldosterone system of the kidneys regulates blood volume. In response to rising blood pressure, the juxtaglomerular cells in the kidneys secrete renin into the blood. Renin converts the plasma protein angiotensinogen to angiotensin I, which in turn is converted to angiotensin II by enzymes from the lungs. Angiotensin II activates two mechanisms that raise blood pressure:
• Angiotensin II constricts blood vessels throughout the body (raising blood pressure by increasing resistance to blood flow). Constricted blood vessels reduce the amount of blood delivered to the kidneys, which decreases the kidneys’ potential to excrete water (raising blood pressure by increasing blood volume).
• Angiotensin II stimulates the adrenal cortex to secrete aldosterone, a hormone that reduces urine output by increasing retention of H2O and Na+ by the kidneys (raising blood pressure by increasing blood volume).

Various substances influence blood pressure. Some important examples follow:

• Epinephrine and norepinephrine, hormones secreted by the adrenal medulla, raise blood pressure by increasing heart rate and the contractility of the heart muscles and by causing vasoconstriction of arteries and veins. These hormones are secreted as part of the fight-or-flight response.
• Antidiuretic hormone (ADH), a hormone produced by the hypothalamus and released by the posterior pituitary, raises blood pressure by stimulating the kidneys to retain H2O (raising blood pressure by increasing blood volume).
• Atrial natriuretic peptide (ANP), a hormone secreted by the atria of the heart, lowers blood pressure by causing vasodilation and by stimulating the kidneys to excrete more water and Na+(lowering blood pressure by reducing blood volume).

Question 46

Describe the mechanisms that control BP in the short and long term.

Answer 46

Short-term regulation: corrects temporary imbalances in blood pressure

• Neural mechanisms
• Humoral mechanisms

Long-term regulation: controls the daily, weekly, and monthly regulation of blood pressure

• Renal mechanism

The endogenous regulation of arterial pressure is not completely understood, but the following mechanisms of regulating arterial pressure have been well-characterized:

Baroreceptor reflex: Baroreceptors in the high pressure receptor zones detect changes in arterial pressure. These baroreceptors send signals ultimately to the medulla of the brain stem, specifically to the Rostral ventrolateral medulla (RVLM). The medulla, by way of the autonomic nervous system, adjusts the mean arterial pressure by altering both the force and speed of the heart’s contractions, as well as the total peripheral resistance. The most important arterial baroreceptors are located in the left and right carotid sinuses and in the aortic arch.[31]

Renin-angiotensin system (RAS): This system is generally known for its long-term adjustment of arterial pressure. This system allows the kidney to compensate for loss in blood volume or drops in arterial pressure by activating an endogenous vasoconstrictor known as angiotensin II.

Aldosterone release: This steroid hormone is released from the adrenal cortex in response to angiotensin II or high serum potassium levels. Aldosterone stimulates sodium retention and potassium excretion by the kidneys. Since sodium is the main ion that determines the amount of fluid in the blood vessels by osmosis, aldosterone will increase fluid retention, and indirectly, arterial pressure.

Baroreceptors in low pressure receptor zones (mainly in the venae cavae and the pulmonary veins, and in the atria) result in feedback by regulating the secretion of antidiuretic hormone (ADH/Vasopressin), renin and aldosterone. The resultant increase in blood volume results an increased cardiac output by the Frank–Starling law of the heart, in turn increasing arterial blood pressure.

These different mechanisms are not necessarily independent of each other, as indicated by the link between the RAS and aldosterone release. Currently, the RAS is targeted pharmacologically by ACE inhibitors and angiotensin II receptor antagonists. The aldosterone system is directly targeted by spironolactone, an aldosterone antagonist. The fluid retention may be targeted by diuretics; the antihypertensive effect of diuretics is due to its effect on blood volume. Generally, the baroreceptor reflex is not targeted in hypertension because if blocked, individuals may suffer from orthostatic hypotension and fainting.