Renin Angiotensin Aldosterone System

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Tarang Patel
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Outline

Overview

  1. Renin Angiotensin Aldosterone System helps the body…
    1. Regulate blood pressure
    2. Regulate blood volume
    3. Regulate fluid and electrolytes
  2. RAAS is active when the kidneys sense…
    1. Hypotension
    2. Decreased blood volume (blood loss, severe dehydration)
    3. Lack of blood flow to the kidneys.
  3. Understanding RAAS helps better understand the following medication classes
    1. Angiotensin Converting Enzyme Inhibitors
    2. Angiotensin II Receptor Blockers (ARBS)
    3. Renin Antagonists

Nursing Points

General

  1. Goals of RAAS-
    1. Improve perfusion to the kidneys
    2. Increase blood pressure
    3. Increase blood volume
  2. How the RAAS works-
    1. Kidneys sense they are getting a decreased amount of blood flow
    2. Kidneys activate the RAAS by releasing the hormone renin
    3. Renin converts Angiotensinogen (an inactive protein) to Angiotensin I (active)
    4. Angiotensin I goes to the lungs where it is converted to Angiotensin II
      1. Converted by an enzyme called an angiotensin-converting enzyme (also known as ACE – a la ACE Inhibitor)
    5. Angiotensin II has a lot of functions in the body
      1. Increases sympathetic nervous system response causing vasoconstriction
        1. This increases blood pressure
      2. Causes kidneys to reabsorp more sodium which increases water retention
        1. This increases blood volume
      3. Causes the pituitary gland to increases secretion of Anti-diuretic Hormone (ADH)
        1. This increases water reabsorption in the kidneys
      4. Causes the adrenal gland to increase secretion of Aldosterone (another hormone)
        1. Causes the kidneys to increase their sodium and water retention

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Transcript

Okay, so we gonna talk about the RAA System in our body and the reason that we gonna talk about RAA system and covering it in our video, that it will help to better understand the Angiotensin Converting Enzyme Inhibitor medications, ARBs which is also called as Angiotensin II receptor blockers and Renin Antagonists. So, if you have a better understanding of the RAA system in our body, it will really help you to understand these 3 pharmacological classes of drugs and it will helpful to understand the side effects, why do we have the side effects and why do we use this medication for the particular diseases.

So, let’s go to the next slide and have a take a look at the RAA system. So, this diagram is basically presenting the RAA system. It may look complicated at first look, but it’s not really. So, if you look at the renin enzyme right here, we have a renin enzyme that gets secreted by the kidneys. When our kidney does not get enough blood flow or due to the blood pressure fall or if we have a blood loss, or it could be different reasons that the kidney is not getting enough blood flow. Or, if our body does not have enough sodium to reabsorb the water, kidney is not getting enough blood flow. Then, there’s a specialized cell in the kidney that’s gonna release renin. Now, what this renin gonna do, it’s gonna convert angiotensinogen protein which is in the inactive form in our blood to angiotensin I. So, the work of the renin, it’s gonna convert angiotensinogen to the angiotenisin I. Now, when the angiotensin I goes to the lungs, through the blood stream, the enzyme here, it’s called ACE inhibitor, right here in the lungs, gonna convert this angiotensin I into angiotensin II. So, this is the enzyme which is really important to remember. This is gonna help you in the ACE inhibitors. So, this is called Angiotensin Converting Enzyme which is present in the lung. Now, when angiotensin I gets converted into the angiotensin II, angiotensin II has many effects on our body. The first effect, when you take a look, it’s gonna increase the sympathetic system. Okay, so when it does increase the sympathetic system, nervous system, it’s gonna increase the vasoconstriction and if you really know your sympathetic nervous system. It’s gonna cause the vasoconstriction and it’s gonna increase the blood pressure. When there’s an increase in the blood pressure, kidneys gonna get enough blood flow. That’s how kidneys gonna get re-perfused. Now, the second action that angiotensin II have is on the kidney tubules. Well, it’s gonna increase the reabsorption of sodium and it’s gonna increase the excretion of potassium. Now, when it increases the reabsorption of sodium, it’s gonna increase the H2O retention, basically, the water retention. When that happens, it’s gonna increase a lot of volume, blood volume increases. When the blood volume increases, it’s gonna increase the blood pressure and that’s how it’s gonna cause, that’s how the kidneys get re-perfused which is the main problem why the renin got secreted. It also has effect on the adrenal gland as well. Angiotensin II is gonna go to the adrenal gland and it’s gonna increases the secretion of Aldosterone which is basically gonna do the same thing. Increase the sodium reabsorption, and it’s gonna increase the potassium excretion. Sodium reabsorption is gonna increase the water reabsorption as well as it’s gonna increase the blood volume. And, the final effect that angiotensin II has, it’s on the collecting ducts of the kidney. Our collecting ducts gonna, it’s main site where all the water excretion or the reabsorption happens. So, what it’s gonna do is it’s gonna go to the pituitary gland and gonna increase the secretion of ADH which is also called as antidiuretic hormone. What this antiduretic is gonna do, it’s gonna increase the water reabsorption in the kidney and it’s gonna increase blood volume. And that’s how kidney is gonna get re-perfused. So, this is how basically the RAA System works, so, have a better understanding of the RAA System and then we can understand ACE inhibitors, ARBs inhibitors and renin antagoist medication wear easily, which we’re gonna cover in the following presentation.

If you have any question about RAA System, then you can e-mail us or contact us. Thanks.

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NP 4 Exam 2

Concepts Covered:

  • Circulatory System
  • Urinary System
  • Adult
  • Basic
  • Test Taking Strategies
  • Prefixes
  • Suffixes
  • Integumentary Disorders
  • Respiratory Disorders
  • Pediatric
  • Bipolar Disorders
  • Immunological Disorders
  • Labor Complications
  • Neonatal
  • Medication Administration
  • Disorders of Pancreas
  • Pregnancy Risks
  • Cardiac Disorders
  • Learning Pharmacology
  • Eating Disorders
  • Dosage Calculations
  • Emergency Care of the Cardiac Patient
  • Substance Abuse Disorders
  • Vascular Disorders
  • Endocrine and Metabolic Disorders
  • Shock
  • Fetal Development
  • Depressive Disorders
  • Anxiety Disorders
  • Cardiovascular Disorders
  • Liver & Gallbladder Disorders
  • Upper GI Disorders
  • Female Reproductive Disorders
  • Neurologic and Cognitive Disorders
  • Personality Disorders
  • Nervous System
  • Urinary Disorders
  • Hematologic Disorders
  • Disorders of the Posterior Pituitary Gland
  • Respiratory System
  • Renal Disorders
  • Noninfectious Respiratory Disorder
  • Shock

Study Plan Lessons

EKG (ECG) Course Introduction
Fluid & Electrolytes Course Introduction
Life Support Review Course Introduction
12 Points to Answering Pharmacology Questions
CPR-BLS (Basic Life Support)
Electrical A&P of the Heart
54 Common Medication Prefixes and Suffixes
Advanced Cardiovascular Life Support (ACLS)
Electrolytes Involved in Cardiac (Heart) Conduction
Fluid Pressures
Vitals (VS) and Assessment
Fluid Shifts (Ascites) (Pleural Effusion)
Pediatric Advanced Life Support (PALS)
Therapeutic Drug Levels (Digoxin, Lithium, Theophylline, Phenytoin)
Essential NCLEX Meds by Class
Isotonic Solutions (IV solutions)
Neonatal Resuscitation Program (NRP)
6 Rights of Medication Administration
Hypotonic Solutions (IV solutions)
Hypertonic Solutions (IV solutions)
Preload and Afterload
Performing Cardiac (Heart) Monitoring
The SOCK Method – Overview
The SOCK Method – S
The SOCK Method – O
The SOCK Method – C
The SOCK Method – K
Basics of Calculations
The EKG (ECG) Graph
Nursing Care and Pathophysiology of Angina
Dimensional Analysis Nursing (Dosage Calculations/Med Math)
EKG (ECG) Waveforms
Sodium-Na (Hypernatremia, Hyponatremia)
Calcium-Ca (Hypercalcemia, Hypocalcemia)
Calculating Heart Rate
Nursing Care and Pathophysiology of Myocardial Infarction (MI)
Oral Medications
Chloride-Cl (Hyperchloremia, Hypochloremia)
Injectable Medications
Nursing Care and Pathophysiology of Coronary Artery Disease (CAD)
IV Infusions (Solutions)
Magnesium-Mg (Hypomagnesemia, Hypermagnesemia)
Complex Calculations (Dosage Calculations/Med Math)
Phosphorus-Phos
Normal Sinus Rhythm
Normal Sinus Rhythm
Nursing Care and Pathophysiology for Heart Failure (CHF)
Sinus Bradycardia
Sinus Bradycardia
Sinus Tachycardia
Sinus Tachycardia
Atrial Flutter
Pacemakers
Atrial Fibrillation (A Fib)
Atrial Fibrillation (A Fib)
Premature Atrial Contraction (PAC)
Supraventricular Tachycardia (SVT)
Premature Ventricular Contraction (PVC)
Premature Ventricular Contraction (PVC)
Ventricular Tachycardia (V-tach)
Ventricular Tachycardia (V-tach)
Ventricular Fibrillation (V Fib)
Ventricular Fibrillation (V Fib)
1st Degree AV Heart Block
2nd Degree AV Heart Block Type 1 (Mobitz I, Wenckebach)
2nd Degree AV Heart Block Type 2 (Mobitz II)
3rd Degree AV Heart Block (Complete Heart Block)
Benzodiazepines
Nursing Care and Pathophysiology of Hypertension (HTN)
Cardiac (Heart) Disease in Pregnancy
Nursing Care and Pathophysiology for Cardiomyopathy
Nursing Care and Pathophysiology for Thrombophlebitis (clot)
Dehydration
Nursing Care and Pathophysiology for Hypovolemic Shock
Nursing Care and Pathophysiology for Cardiogenic Shock
Nursing Care and Pathophysiology for Distributive Shock
Fetal Circulation
MAOIs
SSRIs
TCAs
Congenital Heart Defects (CHD)
Defects of Increased Pulmonary Blood Flow
Defects of Decreased Pulmonary Blood Flow
Insulin
Obstructive Heart (Cardiac) Defects
Mixed (Cardiac) Heart Defects
Histamine 1 Receptor Blockers
Histamine 2 Receptor Blockers
Renin Angiotensin Aldosterone System
ACE (angiotensin-converting enzyme) Inhibitors
Angiotensin Receptor Blockers
Calcium Channel Blockers
Cardiac Glycosides
Metronidazole (Flagyl) Nursing Considerations
Ciprofloxacin (Cipro) Nursing Considerations
Vancomycin (Vancocin) Nursing Considerations
Anti-Infective – Penicillins and Cephalosporins
Atypical Antipsychotics
Autonomic Nervous System (ANS)
Sympathomimetics (Alpha (Clonodine) & Beta (Albuterol) Agonists)
Parasympathomimetics (Cholinergics) Nursing Considerations
Parasympatholytics (Anticholinergics) Nursing Considerations
Diuretics (Loop, Potassium Sparing, Thiazide, Furosemide/Lasix)
Epoetin Alfa
HMG-CoA Reductase Inhibitors (Statins)
Magnesium Sulfate
NSAIDs
Corticosteroids
Hydralazine (Apresoline) Nursing Considerations
Nitro Compounds
Vasopressin
ABG (Arterial Blood Gas) Interpretation-The Basics
ABG (Arterial Blood Gas) Oxygenation
ABG Course (Arterial Blood Gas) Introduction
ABGs Nursing Normal Lab Values
ABGs Tic-Tac-Toe interpretation Method
Acute Coronary Syndrome (ACS) Module Intro
Base Excess & Deficit
Blood Flow Through The Heart
Cardiac A&P Module Intro
Cardiac Anatomy
Cardiac Course Introduction
Cardiovascular Disorders (CVD) Module Intro
Coronary Circulation
Fluid Compartments
Heart (Cardiac) Failure Module Intro
Heart (Cardiac) Failure Therapeutic Management
Heart (Cardiac) Sound Locations and Auscultation
Hemodynamics
Hemodynamics
Lactic Acid
Metabolic Acidosis (interpretation and nursing diagnosis)
Metabolic Alkalosis
MI Surgical Intervention
Nursing Care and Pathophysiology for Aortic Aneurysm
Nursing Care and Pathophysiology for Arterial Disorders
Nursing Care and Pathophysiology for Cardiogenic Shock
Nursing Care and Pathophysiology for Cardiomyopathy
Nursing Care and Pathophysiology for Distributive Shock
Nursing Care and Pathophysiology for Heart Failure (CHF)
Nursing Care and Pathophysiology for Hypovolemic Shock
Nursing Care and Pathophysiology for Thrombophlebitis (clot)
Nursing Care and Pathophysiology for Valve Disorders
Nursing Care and Pathophysiology of Angina
Nursing Care and Pathophysiology of Coronary Artery Disease (CAD)
Nursing Care and Pathophysiology of Endocarditis and Pericarditis
Nursing Care and Pathophysiology of Hypertension (HTN)
Nursing Care and Pathophysiology of Myocardial Infarction (MI)
Nursing Care and Pathophysiology of Myocarditis
Pacemakers
Performing Cardiac (Heart) Monitoring
Potassium-K (Hyperkalemia, Hypokalemia)
Preload and Afterload
Proton Pump Inhibitors
Respiratory Acidosis (interpretation and nursing interventions)
Respiratory Alkalosis
ROME – ABG (Arterial Blood Gas) Interpretation
Shock Module Intro
Venous Disorders (Chronic venous insufficiency, Deep venous thrombosis/DVT)