Exam 2 Flashcards

(243 cards)

1
Q

“Learning Objective’s” for Fluids and Electrolytes

A
  • Role of electrolytes (Na, K, Ca, Mg, PO4)
  • What are the clinical features of electrolyte imbalances? (eg HYPER vs HYPO)
  • What are the different types of IV fluids and their uses
  • Understand & interpret acidosis vs alkalosis (metabolic & resp)
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2
Q

Functions of Body Fluids

A

Transport gases, nutrients, and wastes

Help generate electrical activity needed to power body functions

Take part in the transformation of food into energy

Maintain the overall function of the body

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3
Q

ICF vs ECF

A

ICF:
- Consists of fluids contained within all the body cells
- LARGER of the two components
- Approx 2/3 of the body water in healthy adults
- Hight concentration of K+

ECF:
- Contains the remaining 1/3 of body water
- Contains all the fluids outside the cells, including interstitial or tissue spaces and Bl. vessels
- High concentration of Na+

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4
Q

Composition of ECF, Plasma and Interstitial Fluids

A

Large amounts of sodium and chloride

Moderate amounts of bicarbonate

Small quantities of K, Mg, Ca, P

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5
Q

Electrolyte Balance

A

Concentration of individual electrolytes in the body fluid compartments is normal and remains relatively constant

Electrolytes are dissolved in body fluids
Because of Na & K influence, H2O will move between compartments

Eg) if Na = High, H2O will move from intracellular space to extracellular space due to osmotic pressure

Sodium predominant EXTRACELLULAR CATION

Chloride is predominant EXTRACELLULAR ANION

Bicarbonate also in EXTRACELLULAR spaces

Potassium is predominant INTRACELLULAR CATION

Phosphates are predominant INTRACELLULAR ANION

Aldosterone works at kidney tubules to regulate sodium & potassium levels

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6
Q

Cations vs Anions

A

Cations = ACTIVELY reabsorbed

Anions = PASSIVELY follow by electrochemical attraction

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7
Q

H2O & Na+ Balance

A

Baroreceptors regulate effective volume

Modulating sympathetic nervous system outflow and ADH secretion

ANP

RAAS = Angiotensin II & Aldosterone

Gain:
- Water
- Oral intake and metabolism of nutrients
- Na+

Loss:
- Kidneys
- Skin
- Lungs
- GI tract

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8
Q

Na+ Imbalances

A

Na balance closely connected to H2O balance

HYPERnatremia:
- Na serum level >145mEq/L
- Often due to kidney disease or excessive Na intake

HYPOnatremia:
- Na serum level < 135mEq/L
- Caused by dilution of plasma or Na loss
- Most common EL imbalance in hospital

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9
Q

Regulators of Na

A

Kidney is MAIN regulator of Na

  • Monitors arterial pressure, retains Na when arterial pressure is decreased and eliminates it when arterial pressure is increased
  • Rate is coordinated by the sympathetic nervous system and RAAS
  • Atrial natriuretic peptide (ANP) may also regulate sodium excretion by kidney
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10
Q

Assessment of Body Fluid Loss

A

History of conditions that predispose to sodium and H2O losses, weight, loss and observations of altered physiologic function indicative of decreased fluid volume
-HR
- BP
- Venous volume/filling
- Cap refill rate

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11
Q

Causes of Fluid Volume Excess

A

Inadequate Na and H2O elimination

Excessive Na intake in relation to output

Excessive fluid intake in relation to output

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12
Q

Potassium Distribution and Regulation

A

Intracellular concentration 140-150mEq/L

Extracellular concentration 3.5-5.0 mEq/L

Body stores K are related to body size and muscle mass*

Play a huge role in resting membrane potential

Normally derived from dietary sources

Plasma potassium is regulated through TWO mechanisms:

1) Renal mechanism that conserve or eliminate potassium
2) Transcellular shift between the ICF and ICF compartments

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13
Q

Abnormal Potassium

A

HYPOkalemia = decrease in plasma K levels BELOW 3.5mEq/L
1) Inadequate intake
2) Excessive GI, renal and skin losses
3) Redistribution between the ICF and ECF compartments

HYPERkalemia = increase in plasma levels of potassium ABOVE 5.0mEq/L
1) Decreased renal elimination
2) Excessively rapid administration
3) Movement of K from ICF to ECF compartment

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14
Q

Diagnosis and Treatment of Potassium Disorders

A

Diagnosis:
- Based on complete history, physical examination to detect muscle weakness and signs of volume depletion, plasma K levels and ECG findings

Treatment:
- Ca antagonizes K-induced decrease in membrane excitability
- Na bicarb will cause K+ to move ICF
- Insulin will decrease ECF K+ concentration
- Curtailing intake or absorption, increasing renal excretion and increasing cellular uptake

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15
Q

Mechanisms Regulating Ca, P and Mg Balance

A

Ca, P and Mg are the MAJOR divalent cations in the body

They are:
- Ingested in the diet
- Absorbed from the intestine
- Filtered in the glomerulus of the kidnet
- Reabsorbed in the renal tubules
- Eliminated in the urine

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16
Q

Physiological Ca (3 forms)

A

ECF calcium exists in 3 forms

1) Protein Bound:
- 40% of ECF calcium is bound to albumin

2) Complexed:
- 10% is chelated w/ citrate, phosphate and sulfate

3) Ionized:
- 50% of ECF calcium is present in the ionized form

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17
Q

Ca Gain and Loss

A

Gains:
- Dietary dairy foods
- PTH and Vit D stimulate Ca reabsorption in this segment of the nephron

Losses:
- When dietary intake (and Ca absorption) is less than intestinal secretion

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18
Q

Causes and Symptoms of HYPOcalcemia

A

WATCH YOUTUBE VIDEOS ON SLIDE 22

Causes:
- Impaired ability to mobilize Ca from bone stores
- Abnormal losses of Ca from the kidney
- Increased protein binding or chelation such that greater proportions of Ca are in the nonionized form
- Soft tissue sequestration

Symptoms:
- Increased neuromuscular excitability
- Cardiovascular effect
- Nerve cells less sensitive to stimuli

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19
Q

Causes and Symptoms of HYPERcalcemia

A

CAUSES:

Increased Intestinal Absorption:
- Excessive Vit D and Ca
- Milk-alkali syndrome

Increased Bone Resorption:
- Increased Parathyroid hormone
- Malignant neoplasms
- Prolonged immobilization

Decreased Elimination:
- Thaizide, lithium therapy

SYMPTOMS:
- Changes in neural excitability
- Alterations in smooth and cardiac muscle function
- Exposure of the kidneys to high concentrations of calcium

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20
Q

Role of Phosphate in the Body

A

Plays major role in BONE FORMATION

Essential to certain metabolic processes:
- Formations fo ATP and the enzymes needed for metabolism of glucose, fat and protein

Necessary component of several vital parts of the cell

Incorporated into nucleic acids of DNA and RNA and the phospholipids of the cell membrane

Serves as an Acid-base buffer int he extracellular fluid and in the renal excretion of hydrogen ions

Necessary for delivery of O2 by RBCs

Needed for normal function of other blood cells:
- WBCs and Platelets

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21
Q

Common Causes of HYPOphophatemia and HYPERphosphatemia

A

HYPO:
- Depletion of phosphate because of insufficient intestinal absorption
- Transcompartmental shifts
- Increased renal losses

HYPER:
- From failure of the kidneys to excrete excess phosphate
- Rapid redistribution of Intracellular phosphate to ECF compartment
- Excessive intake of phosphate

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22
Q

Magnesium Balance (What Mg Does in Body)

A

Essential to all reactions that require ATP

Regulation at kidney level:
- Mg absorption in the thick ascending loop of Henle is the positive voltage gradient created int he tubular lumen by the Na+-K+-2Cl- co-transporter system

Ingested in the diet

Absorbed from intestine

Excreted by the kidneys

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23
Q

HYPERmagnesemia

A

Excessive Intake:
- IV admin of Mg for treatment of preeclampsia
- Excessive use of oral Mg-containing meds

Decreased Excretion:
- Kidney disease
- Acute renal failure

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24
Q

HYPOmagnesemia

A

Lab Values:
- Serum Mg level less than 0.65mmol/L

Neuromuscular Manifestations:
- Personality change, athetoid or choreiform movements, nystagmus, tetany, positive Babinski, Chvostek, Trousseau signs

Cardiovascular:
- Tachy, Hypertension, cardiac dysrhythmias

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25
Fluid Balance
Created by matching Ins & Outs and is regulated by hormones... ADH: - Cells in hypothalamus shrink when ECF is hypertonic triggering release of ADH - ADH stimulates thirst and increases water reabsorption by kidneys Aldosterone: - Promotes reabsorption of Na+ and H2O by kidneys
26
Tonicity
Tension or effect that the effective osmotic pressure of a solution with impermeable solutes exerts on cell size because of water movement across the cell membrane Solutions can be classified according to whether of not they cause cells to shrink: ISOTONIC = neither shrink nor swell HYPOTONIC = **swell** HYPERTONIC = **shrink**
27
Fluid Replacement Agents
Dehydration is treated w/ fluid colume expanders (fluid choice depends on the cause of fluid loss) IV replacement fluids include crystalloids, colloids, and bl. products CRYSTALLOIDS: - Fludis similar to ECF, available as ISOtonic, HYPOtonic, and HYPERtonic formulations - ISOtonic crystalloids = replace lost fluid and to promote urine output** - HYPERtonic = shift fluid from ICF to ECF compartment - HYPOtonic = shift fluids from ECF to ICF compartment COLLOIDS: - Composed of proteins or starches that remain in bl. vessels (not filtered by caps), drawing fluid from ICF and interstitium into vessels to increase plasma fluid volume
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Normal Saline
ISONTONIC, crystalloid (easily passes through cell membrane) Works well w/ most hydration needs Used inconjunction w/ blood administration **Caution** in pt. w/ cardiac or renal complications, as the high sodium content can cause excess fluid retention Can be used for things like: - Bl. transfusions - Fluid replacement for DKA - Metabolic alkalosis - HypERcalcemia - HypOnatremia
29
Lactated Ringers
Sometimes works as an alt. to Saline ISOTONIC (Similar to body's natural plasma & serum concentration) Lactate commonly encountered in milk, our muscles produce it while we exercise Used in injuries and surgeries **Caution** in pt. w/ renal failure or renal complications as it can result in hypERkalemia** - liver disease as the cannot successfully metabolize the lactate - If pH level is greater than 7.5 Used to treat: - Dehydration - Burn victims - HypOvolemia resulting from third-space fluid shifts - Fluid loss in lower GI tract - Acute blood loss - Replacement of fluid and pH buffers
30
Half Normal Saline
AKA 45% NS or 0.45NaCl HYPOtonic**, crystalloid solution of NaCl dissolved in sterile water -Difference is it contains **half** the Cl concentration than 0.9 Helpful for diabetic pt who cannot handle additional glucose **AVOIDED** in burns, liver disease, or trauma, as depletes intravascular fluids which are already low, risky w/ CVD, High ICP Treat cellular dehydration and Used for: - Raising overall fluid volume - Water replacement - NaCl depletion - Gastric fluid loss - DKA after normal saline and before dextrose infusions
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Dextrose (D5W)
Sometime an alt for NS Simple sugar used in processed foods & added to baking products as a sweetner IV fluid acts as a carrier for dextrose, which acts as sugar readily available for cells to gobble up and use as energy Main versions are: 1) Dextrose in Water = raise total fluid volume, rehydration, hypERnatremia 2) Dextrose in Saline = Used for extremely specific cases** 3) Dextrose in Lactated Ringers = name implies, used for fluid and electrolyte replenishment
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Edema
Condition in which fluid accumulates in the interstitial compartment Sometimes due to blockage of lymphatic vessels or by a lack of plasma proteins or sodium retention
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Edema Formation
Physiologic mechanisms that contribute to edema include factors that: - Increase cap filtration pressure - Decrease cap colloidal osmotic pressure - Increase cap permeability - Produce obstruction to lymph flow Localized edema General edema Dependent edema
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Types of Edema
Accumulation of fluid in extracellular space: - Pitting Edema - Nonpitting edema - Brawny Edema (swelling that's dense and firm due to increased con tissue) Methods of Assessment: - Daily weight - Visual assessment - Measurement of finger pressure to assess for pitting edema
35
Acid-Base
Acid = molecule that can release an H+ Base = ion or molecule that can accept or combine w/ an H+ Physiological pH = 7.35-7.45
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Acid-Base Balance
pH regulated by chemical buffers, resp system and kidneys Imbalances are classified by effect on pH and cause: - Metabolic Acidosis/alkalosis (Related to bicarb levels) - Resp acidosis/alkalosis (related to pCO2)
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Mechanism of Acid-Base Balance
Concentration of metabolic acids and bicarb base is regulated by KIDNEY Concentration of CO2 is regulated by RESPIRATORY SYSTEM Extracellular and intracellular system buffer changes in pH that occur due to metabolic production of volatile and nonvolatile acids
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pH Regulation (3 Ways)
1) Chemical buffer systems of the body fluids: - Proteins and organic molecules 2) Lungs, which control elimination of CO2 - Bicarb buffering system 3) Kidneys, which eliminate H+ and both reabsorb and generate HCO3- - H+/K+ transcellular exchange
39
Lab Tests Used in Assessing Acid-Base Balance
Arterial blood gases and pH CO2 content and HCO3- levels Base excess or deficit Anion Gap
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Disturbances to Acid-Base Balance
Resp Acidosis Resp Alkalosis Metabolic Acidosis (lactic acidosis, ketoacidosis) Metabolic Alkalosis
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Metabolic Acidosis
Primary Disturbance: - Decrease in bicarbonate Respiratory Compensation: - Hyperventilation to decrease PCO2 Renal Compensation: - If no renal disease, increased H+ excretion and increased CHO3- reabsorption
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Causes of Metabolic Acidosis
Excess Metabolic Acids: - Excessive production of metabolic acids - Impaired elimination of " " Excessive Bicarb Loss: - Loss of intestinal secretions - Increased renal losses Increased Cl Levels
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Manifestations of Met. Acidosis
Increased extracellular H+ ion concentration Decrease in pH Decrease in HCO2- levels (<24 mEq/L)
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Metabolic Alkalosis
Primary Disturbance: - Increase in bicarb Resp Compensation: - Hyperventilate to increase PCO2 Renal Compensation: - If no renal disease, decreased H+ excretion and decreased HCO2- reabsorption
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Causes of Met. Alkalosis
Excessive gain of bicarb or alkali Excessive loss of hydrogen ions Increased bicarb retention Volume contraction
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Manifestations of Met. Alkalosis
Increase in pH due to primary excess of plasma HCO3- ions Caused by: - Loss of H+ ions - Net gain in HCO3 - Loss of Cl- ions in excess of HCO3- ions
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Signs of Compensation for Met Alkalosis
Decreased rate and depth of respiration Increased urine pH
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Respiratory Acidosis
Primary Disturbance: - Increase in PCO2 Resp Compensation: - **NONE** Renal Compensation: - Increased H+ excretion and increased HCO3- reabsorption
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Causes of Resp Acidosis
Occurs in acute or chronic conditions that impair effective alveolar ventilation and cause an accumulation of PCO2: - Impaired function of resp centre in the medulla (as in narcotic overdose) - Lung disease - Chest injury - Weakness of the resp muscles - Airway obstruction
50
Manifestations of Resp Acidosis
Characterized by decrease in pH, reflecting a decrease in ventilation and increase in PCO2
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Resp ALkalosis
Primary DIsturbance: - Decrease in PCO2 Resp Compensation: - **NONE** Renal Compensation: - Decreased H+ excretion and decreased HCO3- reabsorption
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Causes of Resp Alkalosis
**Excessive ventilation**: - Anxiety and psychogenic hyperventilation - Hypoxia and reflex stimulation of ventilation - Lung disease that reflexively stimulate ventilation - Stimulation of resp centre - Mechanical ventilation
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Manifestations of Resp Alkalosis
Decrease in PCO2 Deficit in H2CO3 pH is ABOVE 7.45, arterial PCO2 is BELOW 35mm Hg and plasma HCO3- levels usually are BELOW 24 mEq/L (24mmol/L) Neural Function: - Constriction of cerebral vessels and increased neuronal excitability CV Function: - Cardiac dysrhythmias
54
Mixed Acid-Base Disorders
Pt present w/ more than one primary disorder or a mixed disorder - Low plasma HCO3- concentration due to metabolic acidosis - High PCO2 due to chronic lung disease Presence of multiple compensatory measures
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ABG Interpretation
WATCH YOUTUBE VIDEO Slide 66 pH: Normal = 7.35-7.45 Low value = Acidosis High value = Alkalosis pCO2: Normal = 35-45 Low Value = Alkalosis High Value = Acidosis HCO3: Normal = 22-26 Low Value = Acidosis High Value = Alkalosis pO2: Normal = 80-100 Low Value = Hypoxemia High Value = O2 Therapy SaO2: Normal = 95-100% Low Value = Hypoxemia
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57
Lecture Take Aways (Cardiovascular #1)
- What are preload, afterload, and measures of cardiac function? -How does the cardiac conduction system work? - Be able to describe how BP is regulated - MOA for classes of antihypertensives & drugs for dyslipidemia - Understand atherosclerosis
58
Functions of Cardiovascular System
**Main function is transport** - Delivers O2 and nutrients to tissues - Carries wast products from cellular metabolism to kidneys, and other excretory organs - Circulates electrolytes and hormones - Transports various immune substances that contribute to the body's defense mechanisms Helps to regulate temp
59
Types of Circulation
PULMONARY CIRCULATION: - Moves blood through the lungs and creates a link w/ the gas exchange function of the resp system - **Right** heart - Pulmonary artery, caps and veins SYSTEMIC CIRCULATION: - Supplies all the other tissues of the body - **Left** heart - Aorta and its branches - Caps supplying the brain and peripheral tissues - Systemic venous system and vena cava
60
Characteristics of the Pulmonary and Systemic Circulations
Both have: - Pump - Arterial system - Capillaries - Venous system Arteries and arterioles function as a distribution system to move blood to tissues Caps serve as an exchange system where transfer of gases, nutrients, and wastes takes place Venules and veins serve as collection and storage vessels that return blood to the heart
61
Hemodynamics
**Hemo** = Blood **Dynamics** = relation b/w motion and forces Describes the physical principles governing pressure, flow, and resistance as they relate to the cardiovascular system
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Laplace's Law
Describes the relation between wall tension, transmural pressure and radius States that "wall tension becomes greater as the radius increases Wall tension is also affected by wall thickness = increases as the wall becomes thinner and decreases as the wall becomes thicker
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Cardiac Cycle
Used to describe the rhythmic pumping action of the heart Systole = period during which the ventricles are contracting Diastole = period during which the ventricles are relaxed and filling w/ blood
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2 Factors Determining the Workload of the Heart (**)
**Preload**: - Volume of blood it pumps out - (volume in ventricles at END of diastole aka "end diastolic Pressure") - Increased in = hypervolemia, regurgitation of cardiac valves, HF **Afterload**: - The pressure it must generate to pump the blood out of the heart - (resistance left ventricle must overcome to circulate blood) - Increased in = Hypertension, Vasoconstriction - Increased Afterload = Increased cardiac workload
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Impact of Preload on Cardiac Function **
Determined largely by venous return Within physiologic limits, increasing preload will increase contractility ( + inotropic effect) Drugs may increase or decrease preload
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Impact of Afterload on Cardiac Function
Pressure that ventricles must overcome to be able to eject blood During Hypertension, afterload **increases** and heart must work harder to pump blood Antihypertensive drugs decrease afterload
67
Frank-Starling and Cardiac Reserve
**Frank-Starling Mechanism**: - The greater the volume of blood in the heart BEFORE contraction, the greater the volume of blood EJECTED from the heart -Increased contractility from EDV stretch **Cardiac Reserve**: - Maximum % of increase in cardiac output achieved above normal resting level
68
Measures of Cardiac Function
STROKE VOLUME (SV): - Amount of blood pumped by ventricle in a single contraction - Due to contractility generated by ventricle - Force of contraction can be increased by stretching cardiac muscle according to Frank-Starling Law Cardiac Output (CO): - Amount of blood pumped by a ventricle in a minute CO = HR x SV - CO is about 5L/min
69
Baroreceptors and Chemoreceptors
Baroreceptors: - Stretch sensitive receptors - Monitor BP Chemo: - Oxygenation - CO2 - pH
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Cardiac Conduction System
Cardiac function depends on coordinated contraction by atria and ventricles Conduction system ensures this happens: Auto-rhythmic pacemaker cells in sinoatrial node synchronize contraction by sending current through myocardium -> Atria contract simultaneously, then ventricles contract simultaneously -> Normal rhythm is referred to as sinus rhythm LOOK AT SLIDE 16 PICTURE** like actually 1) SA node fires a stimulus across the walls of both left and right atria, causing them to contract 2) Stimulus arrives at the AV node 3) Stimulus is directed to follow the AV bundle (bundle of His) 4) Stimulus now travels through the apex through the bundle branches 5) Purkinje fibres distribute the stimulus across both ventricles causing ventricular contraction
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Parts of the Cardiac Conduction System
Sinoatrial Node (SA): - Highest rate of autorhythmicity (approx 70bpm) - Located in RIGHT ATRIUM - Current spreads to AV node Atrioventricular Node (AV): - **Lower** rate of autorhythmicity than SA node (approx 40-60 bpm) - Current spreads along Bundle of His Bundle of His (AV bundle): - Carries impulse from atria to ventricles Purkinje Fibres: - Receive current from bundle - Rapidly carry current from inferior portion of ventricle to superior portion Dysrhythmias: - Can be due to ectopic foci (occurs when other heart regions initiate beats - Can be due to conduction problems - Can be due to increases or decreases in regular sinus rhythm
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Regulation of Cardiac Function
Regulated by ANS: - Symp nervous system increases HR, force of contraction, CO - Parasymp nervous system DECREASES HR and CO and decreases force of contraction to a lesser extent Regulated by Hormones: - Epinephrine increases HR, contractility and CO
73
Arterial BP
Represents the pressure of the blood as it moves through the arterial system CO = HR x SV Vascular resistance Mean arterial pressure (MAP) = CO x VR
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Blood Pressure Definitions
Systolic Pressure = Pressure at the height of the pressure pulse Diastolic Pressure = lowest pressure Pulse pressure = difference b/w systolic and diastolic pressure MAP = represents ave. pressure in the arterial system, during ventricular contraction and relaxation
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Factors Influencing Mean Arterial BP
Physical: - Blood volume and the elastic properties of the blood vessels Physiologic Factors: - CO - Peripheral resistance MAP = SBP + 2(DBP)/3
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Primary Factors Responsible for BP
CO: - As CO increases, so does BP Peripheral Vascular Resistance (PVR): - As blood vessels become narrower, resistance increases and BP increases PVR determined by... Blood viscosity, diameter of arterioles (symp nervous system and Angiotensin II) Blood Volume: - As blood volume increases, BP increases - (Blood volume determined by Fluid retention = dehydration, aldosterone, ADH)
77
Hemodynamics and BP
BP regulated by Nervous system through neurons in medulla = RAPID Receives info from: Baroreceptors: (stretch receptors in aortic arch and carotid sinus sense pressure) - If pressure INCREASES suddenly = HR decreases - If pressure DECREASES = HR increases Chemoreceptors: (receptors sense levels of O2, CO2, pH) - if pO2 **DECREASES**, pCO2 **INCREASES**, pH **DECREASES** = HR **increases**
78
Hormones That Regulate BP
**Longer term regulation than Nervous System** Angiotensin II: - End product of renin angiotensin aldosterone system - Potent vasoconstrictor, stimulates release of ADH and aldosterone ADH: - Potent vasoconstrictor - Stimulate thirst and increases reabsorption of H2O by kidneys - Increases BP*** Aldosterone: - Increases reabsorption of Na+ and H2O in kidneys, increasing BP ANP: - Secreted from RIGHT atrium - Enhances sodium and water excretion - Suppresses ADH and aldosterone*** - Reduces sympathetic outflow
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Normal Regulation of BP
**BP is regulated through homeostatic mechanisms** If BP increases, nervous and endocrine mechanisms become active that reduce BP Eg) CO is decreased, Arterioles dilate, Kidneys increase urine output which decreases Bl. volume
80
Types of Regulations
MINUTE TO MINUTE: Vasomotor Centre: - Regulates activity of sympathetic nervous system to alter CO and vascular tone - Baro/chemoreceptors alter CO in response to BP, pH, pO2, pCO2 Local Mediators of Vascular Tone: - Vasoconstrictors = angiotensin II, endothelin - Vasodilators = nitric oxide, prostaglandins DAY TO DAY: - Aldosterone, ADH alter blood volume
81
Systolic Vs Diastolic Factors in BP
Systolic: - Characteristics of stroke volume being ejected from heart - Ability of aorta to stretch and accommodate the stroke volume Diastolic: - Energy is stored in the aorta as its elastic fibres are stretched during systole - Resistance to the runoff of blood from peripheral bl. vessels
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Short vs Long Term Regulation of BP
SHORT = Corrects temporary imbalances in BP - Neural mechanismes - Humoral mechanisms LONG = controls the daily, weekly, and monthly regulation of BP - Renal mechanism
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Etiology of Hypertension
Consistent elevation of systemic arterial BP **Most common of cardiovascular disease** Etiology: - Primary/essential/idiopathic = 90% of cases - Secondary = other 10% (related to pathological conditions)
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Risk Factors of Hypertension
HTN develops slowly as a silent disease Diet Exercise Age Smoking Genetic factors which may alter renal function and secretion of hormones that regulate BP (angio II, aldost, ADH)
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Lifestyle Factors Contributing to HTN
High salt intake Obesity Excess alcohol consumption Dietary intake of potassium, Calcium, Mg Oral contraceptives Stress
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4 Categories of HTN
Primary HTN (Essential): - Chronic elevation of BP that occurs without evidence of other disease Secondary HTN: - Elevation of BP that results from some other disorder (eg kidney disease) Malignant HTN: - Accelerated form of HTN Systolic HTN: - Systolic pressure of 140 or greater and a diastolic less than 90
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Classifications of Essential/Primary HTN
Systolic/Diastolic HTN: - Both are elevated Diastolic HTN: - Only diastolic is elevated Systolic HTN: - Only systolic is elevated
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Most Common Causes of Secondary HTN
Kidney Disease (reno-vascular HTN) Adrenal cortical Disorders Pheochromocytoma (neuroendocrine tumor) Coarctation of the aorta (narrowing of aorta) Sleep apnea
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Complications of HTN
Heart must work harder to eject blood into circulation as BP increases contributing to... - Ventricular hypertrophy - Angina, MI, CVA (Stroke), peripheral vascular disease - HF - Kidney failure - Blindness
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Target Organ Damage
Heart = hypertrophy Brain = Dementia and cognitive impairment Peripheral Vascular = Atherosclerosis Kidney = Nephrosclerosis Retinal Complications
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Management of HTN
First approach = modify lifestyle Second is Drugs = Diuretics, ACE inhibitors, Angio II receptor blockers, calcium channel blockers, beta-blockers
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Pharmacology of HTN - Diuretics
Indications: - HTN, HF MOA: - Reduce blood volume, lowering pressure Adverse Effects: - Dehydration - Hyponatremia - Hypokalemia (thiazide, loop diuretics) - Hyperkalemia (potassium-sparing diuretics) - Nocturia (if taken late in day)
93
3 Categories for Calcium Channel Blockers
Arteriole Selective Drugs: - Relax arterial smooth muscle - Indicated for HTN, angina, Raynaud's Eg **nifedipine** Cardioselective Drugs: - Decrease HR and force of contraction - Indicated for HTN, angina, atrial dysrhythmias Eg **diltiazem** Non-selective Drugs: - Affect arterial smooth muscle and heart - Indicated for HTN, angina, certain dysrhythmias Eg **Verapamil**
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ACE Inhibitors - HTN
Indications: - HTN, HF MOA: - Reduce production of angiotensin II - Promote vasodilation, reducing periipheral resistance and BP - Reduces secretion of ADH and aldosterone, increasing urine output, decreasing bl. volume and decreasing BP - Enhance effects of diuretics Adverse Effects: - Persistent cough - Postural hypotension - Hyperkalemia - Angioedema
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Angiotensin II Receptor Blockers - HTN
Same indications as ACE Inhibitors MOA: - Inhibit effects of angio II, producing similar antihypertensive effects to ACE inhibitors Adverse Effects: - Orthostatic hypotension, hypotension - First-dose phenomenon - Dizziness, headaches - Hyperkalemia
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Beta 1 Adrenergic Antagonists - HTN
Indications: - HTN, dysrhythmias, angina MOA: - Block beta1 receptors = decreased CO - Can be non-specific as well and block beta 2 and/or alpha1 receptors Adverse Effects: - Brady, dysrhythmias - Hypotension - Bronchospasm (Blocking Beta2) - Hypoglycemia
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Alpha 1 Adrenergic Antagonists - HTN
Indications: - HTN MOA: - Block alpha 1 receptors = vasodilation Adverse Effects: - Orthostatic hypotension - Tachy, palpitations - Dizziness, headaches, flushing - Nausea, vomiting
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Alpha **2** Adrenergic Agonists
Indications: - HTN MOA: - Activate central alpha 2 receptors to reduce symp nerve impulses - Reduce pressure by decreasing HR and contractibility, promoting vasodilation Adverse Effects: - sedation, dizziness, dry mouth - Orthostatic hypotension
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Direct Vasodilators - HTN
Indications: - HTN MOA: - Reflex arterial smooth muscle directly causing vasodilation Adverse: - Hypotension, reflex tachy - Headache, dizzy, flushing - Fluid retention
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Managing Emergency HTN
**When diastolic is OVER 120** Fast-acting direct vasodilators Eg) **Nitroprusside sodium** MOA: - Donates nitric oxide, a direct dilators Adverse: - Hypotension - Flushing, dizziness, headache - Thiocyanate toxicity w/ extended use
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Causes of Orthostatic Hypotension
Decrease in venous return to the heart due to pooling of the blood in lower part of body Inadequate circulatory response to decreased CO and a decrease in BP Condition that Decreases Vascular Volume = dehydration Conditions that impair muscle pump function = bed rest, spinal cord injury Conditions that interfere w/ Cardiovascular reflexes: - meds - Disorders of autonomic system - Effects of aging on baroreflex function
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Common Causes of Orthostatic Hypotension Related to Hypovolemia
Excessive use of diuretics Excessive diaphoresis Loss of GI fluids through vomiting and diarrhea Loss of fluid volume assoc. w/ prolonged bed rest
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Complaints Assoc. W/ Orthostatic Intolerance
Dizziness Visual Changes Head/Neck discomfort Poor concentration while standing Palpitations Tremor, anxiety Presyncope (and in some cases syncope)
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3 Types of Lipids
Triglycerides: - Composed of 3 fatty acids attached to glycerol backbone - Major storage form of fat in body Phospholipids: - Similar structure to triglycerides but 1 fatty acid is replaced w/ phosphate group, creating a polar head group - Essential to building plasma membrane Steroids: - All steroids have a common sterol nucleus, a structure w/ four rings - Body can produce steroids from cholesterol - Steroids have two functions: 1) Hormones 2) Component of the plasma membrane - High levels of cholesterol in blood, usually transported in LDL, contribute to development of athersclerosis
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Types of Lipoproteins, Classified by Densities
Chylomicrons Very-Low Density Lipoprotein (VLDL) - Carries large amounts of triglycerides - Precursor to LDL Intermediate-Density Lipoprotein (IDL) Low-density Lipoprotein (LDL) - **Main Carrier of cholesterol** High-Density Lipoprotein (HDL): - 50% protein
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Lipoproteins
Lipid molecules are not soluble in plasma, so they are transported as lipoprotein Composed of varying proportions of protein, phospholipid, trigly., & cholesterol
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HDL vs LDL
HDL: - Transports lipids from tissues toward the liver where they can be broken down to create bile LDL: - Transports lipids towards tissues - Can lodge in areas of vascular damage, initiating the dev. of atherosclerosis - When cholesterol levels in liver are low, liver cells express receptors for LDL which reduces plasma LDL and cholesterol
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Lipoprotein Receptors
Membrane proteins that facilitate cellular uptake of LDL, VLDL, chylomicrons and IDL proteins Genetic abnormality may result in elevated levels w/ no dietary influence
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Hypercholesterolemia
Serum Cholesterol levels = > 6.2mmol/L Levels that could contribute to a heart attack, stroke, or other cardiovascular event assoc. w/ atherosclerosis PRIMARY = elevated cholesterol levels that develop independent of other health problems or lifestyle behaviours SECONDARY = assoc. w/ other health problems or behaviours
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Management of Lipid Disorders
Pts are often asymptomatic until progressing to more serious cardiovascular disorders Pharmacotherapy for hyperlipidemia focuses on reducing LDL and increasing HDL - Reducing cholesterol in liver cells can contribute to lowering LDL in plasma Non-Pharm. management of hyperlipidemia depend on: - Regular monitoring of blood lipids, HDL, & LDL - Eat a healthy diet (Reduce intake of saturated fats and cholesterol, Increase intake of soluble fibre, eliminate tobacco, alcohol, increase intake of plant sterols) - Exercise regularly
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Drugs for Dyslipidemia - Statins
Indications: - Prevention of cardiovascular disease in pts w/ elevated cholesterol - Reduction of elevated LDL, cholesterol MOA: - Statins inhibit HMG-CoA reductase, an enzyme necessary for cholesterol synthesis - Can reduce LDL cholesterol levels by 20-40%, can raise HDL levels and lower VLDL and trigly. levels Adverse Effects: - Muscle pain - Increased liver enzymes - Increased risk of DM Serious Adverse Effects: - Rhabdomylosis - Rare, breakdown of muscle fibres which can lead to acute renal failure
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Drugs for Dislipidemias - Ezetrol
Ezetimibe (Ezetrol) Blocks absorption of cholesterol in intestinal lumen Body responds to this by making more cholesterol so a statin must be administered concurrently** Adverse Effects: - Myalgia, arthralgia - Nasopharyngitic, URI
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Pathology of Arterial System
Hypercholesterolemia & Dyslipidemia Atherosclerosis Arterial disease of the extremities Arterial aneurysms
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3 Types of Lesions Assoc. w/ Atherosclerosis
Fatty Streaks: - Thin, flat, yellow intimal discolorations that progressively enlarge Fibrous Atheromatous Plaque: - Accumulation of intracellular and extracellular lipids, proliferation of vascular smooth muscle cells and formation of scar tissue Complicated Lesion: - Contains hemorrhage, ulceration and scar tissue deposits
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Major Risk Factors for Athersclerosis
Hypercholesterolemia Smoking HTN Family Hx of premature CHD in 1st degree relative Age (Men: >/= 45, Women: >/= 55) HDL cholesterol <40 CRP levels Homocysteine levels
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Major Complications of Atherosclerosis
Ischemic Heart Disease Stroke Peripheral Vascular Disease Clinical Manifestations: - Narrowing of vessel and resulting ischemia - Vessel obstruction due to plaque hemorrhage or rupture - Thrombosis and formation of emboli - Aneurysm formation
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Specific Arterial Involvement in Athersclerosis
Larger vessels = thrombus formation and weakening of vessel wall Medium-sized arteries = ischemia and infarction due to vessel occlusion are more common Arteries supplying heart, brain, kidneys, lower extremities and small intestine are most frequently involved
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Arterial Disease of the Extremities
Atherosclerotic Occlusive Disease: - Sudden event that interrupts arterial flow to the affected tissues or organ Thromboangitis obliterans: - Inflammatory arterial disorder that causes thrombus formation Raynaud Disease and Phenomenon: - Intense vasospasm of the arteries and arterioles in the fingers and less often, toes
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3 Types of Aneurysms
1) Berry: - Most often found in the circle of Willis in the brain circulation - Consists of a small, spherical vessel dilation 2) Fusiform and Saccular: - Most often found int he thoracic and abdominal aorta - Characterized by gradual and progressive enlargement of aorta 3) Dissecting: - Acute, life-threatening condition - Involves hemorrhage into the vessel wall w/ longitudinal tearing (dissection) of the vessel wall to form a blood-filled channel
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Myocardial Ischemia
Condition in which the supply of O2 to the myocardium does not meet the metabolic demands of the myocardium O2 supply depends on: - Blood flow to the myocardium (impacted by coronary artery disease aka CAD, atherosclerosis, vasospasm) Oxygenation of blood reaching myocardium: - Impacted by anemia, respiratory disease O2 demand depends on sympathetic activity, physical activity etc
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Angina Pectoris
Acute chest pain caused by myocardial ischemia Symptoms: - Crushing, painful feeling in chest (in males, pain my be referred to left arm) Types: - Stable = predictable frequency, intensity, duration (relieved by rest) - Vasospastic Angina = caused by narrowed blood vessels reducing blood supply -**Silent** = myocardial ischemia occurs but NO PAIN, asymptomatic (HIGH RISK FOR ACUTE MI) - **Unstable** = unpredictable, occurs AT REST - **Angina of effort** = occurs when client over-exerts during an activity, increasing O2 demand
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Non-pharmacological Therapy of Angina
Limit alcohol consumption Reduce cholesterol or sat. fats in diet Lower Bl. cholesterol Maintain normal BP Maintain normal Bl. glucose levels Exercise regularly Maintain healthy body weight Do no use tobacco
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Pharmacological Management of Angina
Goals of Therapy: - Reduce the frequency and intensity of angina episodes - Increase exercise tolerance - Prevent other CAD complications including dysrhythmias, HF, MI Pharmacologic Approaches: - Increase O2 supply - dilate coronary arteries to increase blood flow - Decrease O2 demand - reduce preload, afterload, HR and contractility **Organic Nitrates**: - Terminate anginal episodes by dilating coronary arteries to increase O2 supply **Beta-adrenergic blockers**: - Prevent anginal episodes by reducing cardiac workload and O2 demand **Calcium Channel Blockers**: - Prevent angina episodes by either reducing CO (decrease O2 demand), or dilating coronary arteries (increasing O2 supply) or both **LOOK AT SLIDE 10 in Cardiovascular Pt 2**
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Drug Classes for Angina - Beta Blockers
Indications: - Angina, HTN, dysrhythmias, HF (some drugs only) MOA: - Block beta1 receptors = reduces HR and contractility, decreasing O2 demand - Stabilize conductivity of heart decreasing incidence of dysrhythmias - Reduce incidence of MI
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Drugs Classes for Angina - Calcium Channel Blockers
Indications: - Vasospastic angina, stable angina** - HTN - Atrial dysrhythmias MOA: 1) **Relax muscle** - Increase O2 supply - Decreases afterload, decreasing O2 demand Eg nifedipine, diltiazem 2) **Some reduce HR and contractility - Decreases O2 demand Eg verapamil, diliazem
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Pathophysiology of MI
Etiology: - Due to advanced CAD leading to sever narrowing of coronary arteries Pathogenesis: - Plaque can block narrowed arteries (by stimulating clot formation) depriving region of myocardium of O2 - Cardiac output drops - If artery is occluding long enough, permanent myocardial damage occurs
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Pharmacotherapy of MI - Treatment Goals
1) Restore blood supply to Myocardium - Thrombocytopenia, organic nitrates 2) Reduce mycardial O2 demand - Beta blockers 3) Control MI-associated dysrhythmias - Beta blockers, calcium channel blockers 4) Reduce post-MI mortality - ASA, ACE inhibitors 5) Manage severe MI pain and anxiety - Analgesics
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MONA-TASS
MONA = 4 primary interventions performed when treating an MI TASS = Also given within 6hrs to interrupt MI evolution **M**orphine = Reduce pain and anxiety. Also a vasodilator and decreases workload of heart by reducing preload and afterload **O**2 = Provide and improve oxygenation of ischemic myocardial tissue. Enforced together w/ bedrest to help reduce myocardial oxygen consumption. Nasal Cannula 2-4L/min **N**itroglycerin = FIRST LINE of treatment for ANGINA PECTORIS and ACUTE MI. Cause vasodilation and increase blood flow to myocardium **A**spirin = Prevents formation of thromboxane A2 (which causes platelets to aggregate and arteries to constrict. Earlier pt gets ASA after symptoms onset, greater potential benefit **T**hrombolytics = Dissolve thrombus in a coronary artery allowing blood to flow through again, minimizing the size of the infarction and preserving ventricular function **A**nticoagulants = Prevent clots from becoming larger and blocking coronary arteries. Usually given w/ other anticlotting medicines to help prevent or reduce heart muscle damage **S**tool softeners = Given to avoid intense straining that may trigger arrhythmias or another cardiac arrest **S**edatives = In order to limit the size of infarction and give rest to the pt. Valium or equivalent is usually given
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Angioplasty
Watch YouTube video on Slide 16 in Cardiovascular pt 2
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Drug Classes for MI - Thrombolytics
Indication: - MI, CVA MOA: - Stimulates formation of plasmin (an enzyme that breaks down fibrin, causing active clots to dissolve) - Coronary artery opens allowing perfusion of myocardium Adverse Effects: - Severe risk of bleeding
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Drugs Classes for MI - Anticoags
Reduce likelihood of clot formation Aspirin: - Taken daily to reduce risk of clot formation - Can exacerbate GI bleeding Unfractionated Heparin, Warfarin: - Prevents clot formation until another intervention can be put in place
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Drug Classes for MI - Antiplatelets
Reduce clot formation assoc. w/ adhesion, aggregation and activation of platelets Adenosine diphosphate receptor blockers: - ADP released during aggregation, binding ADP receptors which promotes further activation and aggregation of platelets - Blocking ADP receptors inhibits aggregation Glycoprotein IIb/IIIa Receptor Antagonists: - When fibrinogen binds this receptor, platelets aggregate by forming cross bridges between cells - Blocking receptor inhibits aggregation
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Drugs Classes for MI - Beta Blockers
Indications: - Angina, MI, dysrhythmias, HTN MOA: - Reduce myocardial O2 demand by decreasing HR, contractility - Reduce conduction through AV node, reducing incidence of dysrhythmias (severe complication of MI) - Therapy usually continued for rest of clients life
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Drug Classes for MI - ACE Inhibitors, Narcotics
ACE Inhibitor: - Given within 1-2 days of onset of MI, following thrombolytic therapy - Reduce volume and afterload, decreasing myocardial O2 demand Narcotics: - Used to manage pain assoc. w/ MI, reduce anxiety Eg) Morphine, Meperidine
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Cerebrovascular Accident (Stroke)
Refers to lack of O2 supply to part of brain 2 Major Types: 1) Thrombotic/embolic = caused by presence of clot in cerebral blood vessel 2) Hemorrhagic = excessive bleeding in brain caused by damage to blood vessel S&S: - Paralysis/weakness on one side of body - Dizziness - Headache - Difficulty speaking - Vision problems
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Pharmacotherapy of Stroke
Thrombotic CVAs are treated w/ variety of drugs: - Thrombolytics to break down clot - Antihypertensive agents = CVAs are assoc. w/ HTN - Anticoags including ASA = used to reduce likelihood of clot formation - Antiplatelet Drugs = reduce incidence of clot formation
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Pathophysiology of HF
Classified based on... 1) Location: - Left-sided failure means blood backs up into pulmonary circulation = **Pulmonary edema** - Right-sided failure means blood backs up into systemic circulation = **Peripheral edema** 2) Systolic failure vs Diastolic Failure: - Systolic = decreased contractility leading to decreased ejection fraction - Diastolic = decreased filling = normal ejection fraction but less blood available to be pumped
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Responses to Decreased Cardiac Output in HF
1) Increased Sympathetic Activity: - Increases HR and force of contraction but also increases vascular resistance - Combined cardiac workload is increased and failure gets worse 2) Activation of RAAS: - Promotes vasoconstriction and volume retention which both raise BP
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LOOK AT SLIDE 27 DIAGRAM
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Forward vs Backward Signs of HF
**Forward**: - Dyspnea on exertion - Fatigue, dizziness, anxiety - Reduced BP w/ cardiac compensation (increased HR, contractility) **Backward**: - Pulmonary Congestion (Cough, orthopnea, difficulty breathing) - Peripheral edema, flushing, weight gain
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Pharmacologic Management of HF (Goals and Drug Classes)
Goals: - Reduction of preload - Reduction of systemic vascular resistance (reduction of afterload) - Inhibition of RAAS and vasocontrictor mechanisms of sympathetic nervous system Drug Classes: - ACE Inhibitors - Angiotensin II receptor blockers - Adrenergic agents, cardiac glycosides - Vasodilators
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Drugs for HF - ACE Inhibitors
Decrease vascular resistance Decrease secretion of aldosterone - Less Na+ retention, less fluid retention - Less cardiac remodeling Decrease secretion of ADH Reduce incidence of MI, protect heart during MI: - Less fluid retention - Decreased thirst (decreased intake) Adverse Effects: - Hypotension - Functional renal insufficiency - Angioedema - Cough - Hyperkalemia Angiotension receptor blockers (ARBs) similar to ACE inhibitors BUT **they are not assoc. w/ COUGH and ANGIOEDEMA**
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Drugs of HF - Angiotensin II Receptor Blockers (ARBs)
Indications: - HTN and HF - MI - Prophylaxis against stroke (CVA) MOA: - Block angiotensin II from activating target receptors in smooth muscle - Promote vasodilation = decreases BP, afterload, preload - Decrease secretion of aldosterone and ADH Adverse Reactions: - Similar to those of ACE inhibitors BUT NO COUGH OR ANGIOEDEMA** - ACE is responsible for metabolizing bradykinin = ACE **inhibitors** prevent breakdown of bradykinin which is assoc. w/ cough and angioedema - ARBs act downstream of ACE inhibitors and therefore do not share these adverse effects w/ ACE inhibs
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Drugs for HF - Adrenergic Agents
Beta1 adrenergic agonists: - Used to increase contractility of heart to produce more powerful contractions but also increase vasoconstriction and cause dysrhythmias including tachycardia Beta Blockers: - Used to decrease HR and force contraction - Some promote vasodilation as well by blocking alpha1 receptors - Prevent MI and remodeling of ventricles
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Drugs for HF - Vasodilators
Relax blood vessels through mechanism that alter amount of second messengers such as cGMP Indications: - HTN, HF MOA: - Increases intracellular cGMP promoting vascular smooth muscle relaxation through a variety of mechanisms - Reduces preload nad afterload
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Drugs for HF - Cardiac Glycosides
Indications: - HF - Can stabilize some dysrhythmias Cardiac Glycosides are positive inotropes and negative chronotropes: - Improve symptoms by decreasing HR while increasing force of contraction Require digitalization to be effective: - Becomes effective once suitable concentration of drug has built up in tissues
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Drugs for HF - Diuretics
Reduce BP and cardiac workload by reducing blood volume By reducing afterload, CO increases Used for heart failure related to fluid overload: - Loop diuretics (Eg Furosemide) are most effective
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Drugs for HF - Phosphodiesterase III Inhibitors
Breaks down cGMP and cAMP Inhibitors cause vasodilation by relaxing smooth muscles (cGMP is not broken down, smooth muscle relaxation persists) - Vasodilation reduces afterload allowing CO to increase Can increase heart contractility Used w/ clients w/ HF who have not responsed to other therapies
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Aging and the Heart
Common Causes of HF in Older Adults: - Coronary heart disease - HTN - Valvular disease - Impaired left ventricular filling due to changes in myocardial relaxation and compliance - Symptoms differ in younger pts Contributing Factors: - Reduced responsiveness to β-adrenergic stimulation - Increased vascular stiffness - Cardiac stiffness - Altered myocardial metabolism
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Dysrhythmias
Abnormalities of electrical conduction that may result in disturbances in HR or cardiac rhythm - Some are asymptomatic - Others require immediate treatment - Occur in all age groups, in healthy and diseased hearts Prodysrhythmics: - Conditions that promote formation of cardiac rhythm abnormalities
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Symptoms of Dysrhythmias
Dizziness Weakness Fatigue Decreased exercise tolerance Palpitations Dyspnea Syncope
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Classification of Dysrhythmias
Classified by different methods: - Location or type of rhythm abnormality produced is simplest method Supraventricular dysrhythmia originate in atria Dysrhythmias originating in ventricles interfere w/ heart's normal function - Atrial fibrillation: disorganizing of rhythm - Thought to be most common type of dysrhythmias
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Types of Dysrhythmias
**Premature atrial contractions**: - Extra beat originating from source other than sinoatrial, - Not normally serious **Premature Ventricular Contractions**: - Extra beat originating from source other than sinoatrial - Not normally serious **Atrial/Ventricular flutter and/or Fibrillation**: - Heartbeat faster than 150 beats/min - Ventricular more serious than atrial **Sinus bradycardia**: - Heartbeat slower than 50/min - May require pacemaker **Heart Block**: - Area of nonconduction in myocardium, ranges from 1st, 2nd, to 3rd degree
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Conditions Assoc. W/ Dysrhythmias
HTN Cardiac Valve disease CAD Low K+ levels in blood MI Stroke DM HF
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Conduction Pathways in Myocardium
Action Potentials - carry signal for cardiac muscles to contract 1) Synchronization begins in SA node "Pacemaker" - Has **automaticity** - can generate action potential on its own, no nervous system direction - Does so 75x/min = sinus rhythm 2) Action potential then travels to AV node: - Also has automaticity, used if SA node malfunctions 3) Action Potential then travels to atrioventricular bundle (Bundle of His) 4) Then to Purkinje fibres - Carry action potential to all regions of the ventricles **If SA and AV nodes fail, cells in AV bundle and Purkinje fibres can generate contractions**
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Ectopic Foci/Ectopic Pacemakers
Other regions that can initiate beats Signals may compete w/ normal conduction Can cause many of the types of dysrhythmias
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Electrocardiogram ECG
Measures the electrical activity across myocardium - Used for diagnosing many heart conditions - Produces 3 waves (P, QRS, T) - Changes in waves reveals pathologies
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Electrocardiography (ECG)
12 leads Diagnostic ECG - Each providing a unique view of the electrical forces of the heart Diagnostic criteria are lead specific Improper lead placement can significantly change the QRS morphology - Misdiagnosis of cardiac arrhythmias or the presence of conduction defects can be missed
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Dysrhythmia Management
Asymptomatic: - Little or no benefit to treatment w/ meds Acute: - In life-threatening cases, meds warranted Prophylaxis: - Initiated for high-risk clients - Avoid drug combinations that increase QT interval WATCH VIDEO SLIDE 7 of Version 2
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Nonpharm Therapy for Dysrhythmias
Cardioversion or defibrillation - Electrical stimulation of the heart reserved for serious types Identification and destruction of myocardial cells responsible for abnormal conduction - Pacemakers - Implantable cardioverter defibrillators (ICDs) WATCH VIDEOS SLIDE 8 Version 2
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Drugs for Dysrhythmias
Alter electrophysiological properties of the heart - Blocking iron flow through ion channels - Altering autonomic activity
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5 Drugs/agents for Treating Dysrhythmias
Sodium Channel Blockers Beta-Adrenergic Antagonists Potassium Channel Blockers Calcium Channel Blockers Miscellaneous Antidysrhythmias
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Sodium Channel Blockers
INDICATIONS: Ventricular and Atrial Arrhythmias including... - Ventricular tachycardia - Atrioventricular re-entrant tachycardia - atrial fibrillation MOA: - Decreases myocardial excitability - Slows conduction velocity - May depress myocardial contractility THERAPEUTIC EFFECTS: - Suppression of arrythmias Eg) **Procainamide**
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Beta-Adrenergic Antagonists
Unlabeled Uses: - Atrial fibrillation - Ventricular arrythmias/tachycardia Therapeutic Effects: - Decreased HR and BP - Slowing of HR can help control irregular heart rhythms Eg) Metoprolol, Carvedilol, Bisoprolol
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K Channel Blockers
INDICATIONS: - Life-threatening ventricular arrhythmias unresponsive to less toxic agents MOA: - Prolongs action potential and refractory period - Inhibits adrenergic stimulation - Slows the sinus rate, increases PR and QT intervals and decreases peripheral vascular resistance (Vasodilation) THERAPEUTIC EFFECTS: - Suppression of arrhythmias Eg) Amiodarone
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Calcium Channel Blockers
Limited number approved as antidysrhythmics Effects similar to those of beta-adrenergic antagonists Safe and well tolerated by most clients Monitor bradycardia and hypotension
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Miscellaneous Antidysrhythmias
Adenosine (Adenocard, Adenoscan): - Naturally occuring nucleoside - Activates K channels in SA and AV nodes - Terminates tachycardia - Primary indication is PSVT - 10-second half life, so adverse effects are silf-limiting Digoxin (Lanoxin, Lanoxicaps): - Primarily used for HF - Can be prescribed for atrial flutter, fibrillation or PSVT - Not effective against ventricular dysrhythmias - Clients must be carefully monitored for toxicity, drug interaction and adverse effects
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Renal Lecture Takeways
Understand how renal failure is diagnosed and the accompanying electrolyte imbalances Bloodwork: Creatinine & creatinine clearance & eGFR Be able to provide education to a pt on hemodialysis, peritoneal dialysis and kidney transplant What are the overall goals of pharmacotherapy in renal failure Understand the MOAs of **5** types of diuretics What is pyelonephritis and how is it diagnosed/treated
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Review Slide 6 in Renal PP
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Renal Failure
Decrease in kidney's ability to filter the blood to remove metabolic wastes Failure can be acute or chronic Possible to maintain normal renal function w/ 50% of nephrons being functional GFR is BEST marker for estimating kidney function - Volume of waterfiltered from glomerulus into Bowman's capsule per minute - Lower rate indicates nephron dysfunction
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Acute vs Chronic Renal Failure
ACUTE: - Requires immediate treatment to prevent retention of nitrogenous wastes in blood - Most common cause is renal hypoperfusion, which can be due to HTN, dysrhythmias, HF, shock CHRONIC: - Appears over months or years - Most common causes are long-standing HTN and DM - Damage is usually irreversible
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Electrolyte Imbalances in Renal Failure
Hyperkalemia Hypermagnesmia Hyperphosphatemia HypOcalcemia
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Creatinine
Produced at a steady rate due to muscle catabolism and is not reabsorbed by the kidney tubules after filtration One of the many waste products that the kidneys filter out and excrete in the urine Chemical that is produced from creatine, a molecule of major importance for energy production in muscles Its measurement provides an indirect assessment of the glomerular filtration
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Creatinine Clearance
Creatinine is used to evaluate GFR because it is almost cleared by glomerular filtration and is neither secreted nor absorbed by the renal tubules Creatinine is not significantly metabolized or excreted anywhere else in the body, so it provides a reasonable eGFR A decrease in clearance indicates a decrease in GFR, but it cannot differentiate causes of decreased GFR due to pre-renal, renal or post-renal factors
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Renal Failure Bloodwork
Tests: - eGFR to assess kidney function - random urine sample to assess for significant persistent proteinuria
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Nonpharm Therapy for Renal Failure
Lifestyle Mods: - Altering diet to reduce protein content, sodium, K, phosphorus, magnesium Intermittent Hemodialysis/Peritoneal Dialysis - Watch Youtube video Slide 13 Kidney transplant
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Pharmacotherapy for Renal Failure
Treat primary cause of problem (often w/ cardiovascular drugs) - Discontinue nephrotoxic medications Diuretics, if kidneys have some function, are used as well to increase urinary output
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Intermittent Hemodialysis (Pros and Cons)
Pros: - Maximum solute clearance of 3 modalities - Best therapy for severe hyperkalemia - Limited anti-coagulation time - Bedside vascular access can be used Cons: - Hemodynamic instability - Hypoxemia - Rapid fluid and electrolyte shifts - Complex equipment - Specialized personnel - Difficult in small infants
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Peritoneal Dialysis (Pros and Cons)
Pros: - Simple to set up and perform - Easy to use in infants - Hemodynamic stability - No anti-coagulation - Beside peritoneal access - Treat hypothermia or hyperthermia Cons: - Unreliable ultrafiltration - Slow fluid & solute removal - Drainage failure & leakage - Catheter obstruction - Respiratory compromise - Hyperglycemia - Peritonitis - Not good for hyperammonemia or intoxication w/ dialyzable poisons
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Watch Videos on Patient Ed on Dialysis Slide 17
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Kidney Transplant
**Preferred** treatment option for most people w/ end stage Kidney disease A successful kidney transplant usually provides better quality of life because it may mean greater freedom, more energy and a less strict diet Watch video Slide 18**
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Pharmacotherapy for Renal Failure
Antidiabetic agents Antihypertensives Lipid lowering agents Erythropoiesis-stimulating agent Iron supplements Sodium bicarb Phosphate binders, calcium and Vit D Diuretics
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Erythropoiesis-stimulating Agent
Eprex aka epoetin alfa Indications: - Anemia assoc. w/ Chronic Kidney Disease (CKD) MOA: - Stimulates production of RBCs Therapeutic Effects: - Maintains and may elevate RBCs, decreasing the need for transfusions
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Loop Diuretics
Furosemide (Lasix) MOA: - Inhibits reabsorption of sodium and chloride from the loop of Henle and distal renal tubule - Increases renal excretion of water, Na, Cl, Mg, K, and Ca - Effectiveness persists in impaired renal function Therapeutic Effects: - Diuresis and subsequent mobilization of excess fluid (edema, pleural effusions) - Decreased BP Major Adverse Effect = OTOTOXICITY Potassium WASTING Loop = Loses K Monitor for HYPOkalemia
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Thiazide Diuretic
Hydrochlorothiazide (HCTZ) Indication: - Edema assoc. w/ renal impairment MOA: - Increases excretion of Na and water by inhibiting sodium reabsorption in the distal tubule - Promotes excretion of Cl, K, hydrogen, Mg, P, Ca and bicarbonate - May produce ateriolar dilation K Wasting THiazide = THrowing away K HYPOkalemia NO OTOTOXICITY**
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Potassium-Sparing Diuretic
Spironolactone (SParing = SPironolactone) Increases urine output but promotes retention of K+ (Monitor for HYPERkalemia) MOA: - Causes loss of sodium bicarbonate and Ca while saving K and hydrogen ions by antagonizing aldosterone - Blocking aldosterone receptors prevents reabsorption of water by preventing reabsorption of Na+, retaining K+
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Carbonic Anhydrase Inhibitors
Acetazolamide MOA: Blocks carbonic anhydrase at proximal tubule to inhibit reabsorption of Na+ and HCO3- in proximal convoluted tubule - Carbonic anhydrase catalyses conversion of CO2 and H2O to H2CO3 Inhibition of renal carbonic anhydrase, resulting in self-limiting urinary excretion of sodium, K, bicarb and water **Weak diuretic effect** indicated for congestive HF, mild diuresis
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Osmotic Diuretics
Mannitol Increases the osmotic pressure of the glomerular filtrate = inhibiting reabsorption of water and electrolytes Osmotic diuretics are freely filtered by kidney but not reabsorbed - Water follows the diuretic and is not reabsorbed - Na+ is not reabsorbed
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Pyelonephritis
Upper UTI and bacterial infection of the renal pelvis, tubules and interstitial tissue in one or both kidneys Bacteria reach the bladder through the urethra and ascend to kidney Frequently secondary to urine backup into the ureters usually at the time of voiding Urinary tract obstruction (stones, tumors, or prostatic hypertrophy) is another cause Pyelonephritis may be acute or chronic
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Pyelonephritis Etiology
Inflammation of the structure of the kidney Renal pelvis Renal tubules Interstitial tissue ALMOST ALWAYS caused by E. coli Kidney becomes edematous and inflamed and the blood vessels are congested Urine may be cloudy and contain pus, mucus and blood Small abscesses may form in kidney
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Clinical Manifestations and Diagnostic Tests of Pyelonephritis
Acute - may by unilateral or bilateral Causes: - Chills - Fever - Flank pain - Leukocytosis - Bacteriuria **Diagnosis** is confirmed by bacteria and pus in urine and leukocytosis - Clean-catch or catheterized urinalysis with culture and sensitivity identifies teh pathogen and determines appropriate antimicrobial therapy IV pyelogram will identify the presence of obstruction or degenerative changes caused by the infection process BUN and Creatine levels of the blood and urine may by used to monitor kidney function U/S or CT scan
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Medical Management of Pyelonephritis
Goat of treatment is to eradicate bacteria from urine Pt w/ mild S&S may be treated on an outpatient basis w/ antibiotics for 14-21 days Antibiotics are selected according to results or urinalysis culture and Sensitivity and may include broad-spectrum meds
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GI & Enteral/Parenteral Nutrition
What is the purpose of each part of the GI tract (upper/lower) as well as accessory organs? Eg) main function/action Be able to define gastritis, peptic ulcer disease, GI bleeds, GERD, IBD, IBS, pancreatitis, constipation, diarrhea, nausea & vomiting What is H. pylori and how is it diagnosed and treated? Pharm: Understand in what cases different drugs are used and why (antidepressants are used in IBS - why?) Nutritional support: what causes would we use EN vs PN Different routes and types of feeding (Frequency, formula types)
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Overview of Digestive System
2 Basic Anatomic Divisions: 1) GI tract or Alimentary Canal - Mouth, esophagus, stomach, small intestine, large intestine, rectum 2) Accessory Organs of digestion: - Teeth, tongue, salivary glands, liver, pancreas Physiologic Functions: - Digestion - Absorption - Secretion - Motility
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Physiology of the Upper GI Tract: Mouth
**Digestion** - Mechanical = chewing to break down food - Chemical = salivary amylase and salivary lipase break down carbs and lipids **Absorption** - Little absorption of food - Buccal and sublingual absorption of some drugs **Secretion** - Saliva by salivary glands **Motility** - Chewing/swallowing - DYSPHAGIA = difficulty swallowing - ODYNOPHAGIA = painful swallowing - ACHALASIA = failure of the esophageal sphincter to relax
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Upper GI Tract: Stomach
DIGESTION: - Mechanical = churning motion - Chemical = pepsin and HCl break down protein, including protein drugs (enteric coating) ABSORPTION: - Very little absorption of food or drugs SECRETION: - Chief cells = secrete pepsinogen (converted to active pepsin by HCl) - Parietal cells = secrete HCl and intrinsic factor (IF; necessary for absorption of Vit B12) - Goblet Cells = secrete mucous - Enteroendocrine cells = secrete gastrin (helps to regulate secretion and motility) MOTILITY: - Churning of stomach by 3 muscle layers - Helps to convert food into chyme as it enters small intestine
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DO REQUIRED READINGS FOR WEEK 8
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Lower GI Tract Physiology
SMALL INTESTINE: 3 Sections = duodenum, jejunum, iluem Digestion: - Chemical - secretions from pancreas and small intestine break down proteins, carbs, lipids and nucleic acids Absorption: - Proteins, carbs, lipids, nucleic acids - Most drugs taken through enteral route - Ileum - Vit B12, Vit A, D, E, K and long-chain fatty acids - Villi increase surface area for absorption Secretion: - Intestinal juice includes enzymes to digest macromolecules and mucous to protect lining of SI acidic chyme Motility: - Smooth muscles of SI contracts in a coordinated rhythmic manner (peristalsis) to move nutrients through alimentary canal - Controlled by hormones, enteric nervous system and parasymp nervous system Blood vessels that drain from SI merge into hepatic portal vein which carries absorbed nutrients and drugs directly to the liver Liver enzymes can metabolize drugs at this point (first pass metabolism) Liver can regulate usage of nutrients, especially glucose under influence of insulin
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Large Intestine Physiology
LARGE INTESTINE: Digestion: * Little, if any, digestion occurs in large intestine Absorption: * Water and electrolytes *Enterohepatic recirculation of bile Secretion: * Mucous to lubricate fecal matter Motility: * Peristalsis to move chyme through large intestine * Coordinated contraction of sphincter muscles to eliminate fecal matter * Can impact time for drug to be absorbed by increasing or decrease rate of peristalsis Contains host flora that synthesize: * B-complex vitamins (essential for development of red blood cells and as cofactors for metabolic processes) * Vitamin K –key requirement for producing many clotting factors
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Accessory Organs of Digestion Physiology
LIVER: **Metabolic functions:** *Regulates serum levels of glucose, cholesterol and triglycerides *Detoxifies potentially harmful substances *Synthesizes bile, plasma proteins, clotting factors *Storage of iron, Vitamins A, D, E, K **Pharmacological Importance:** * Drugs taken through enteral route are subject to first-pass metabolism, by cytochrome P450 enzyme system* Hepatic function can be altered by certain drugs (increase or decrease activity) * Drugs that damage hepatic tissues can have wide-ranging impacts physiologically and pharmacologically **Enterohepatic recirculation:** * Reabsorption of bile and some drugs occurs in large intestine, transported back to liver * Recycling drug extends half-life * Loss of bile can alter absorption of drugs GALLBLADDER: * Stores bile until receiving hormonal signal to release bile into duodenum * Bile supports lipid digestion and absorption PANCREAS: * Exocrine –secretion of digestive enzymes and bicarbonate into small intestine * Endocrine –secretion of insulin and glucagon to coordinate metabolism of glucose
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Regulation of Digestive Processes
**Autonomic nervous system (ANS):** *Parasympathetic nervous system (PNS) **Enteric nervous system (ENS):** * Vast network of neurons in the submucosa that has sensory and motor functions * Influenced by PNS and hormones secreted by structures of GI tract * Gastrin *Incretins –gastric inhibitory protein (GIP), glucagon-like peptide 1 (GLP-1)
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Acid Production by the Stomach
**Cardiac sphincter** prevents stomach contents from moving back up the esophagus (AKA esophageal reflux) **Pyloric sphincter** regulates substances leaving the stomach * In stomach * Chief cells secrete pepsinogen to chemically break down proteins * Parietal cells secrete hydrochloric acid, to break down food, kill microbes, and activate pepsinogen
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Regulation of Acid Secretion
Parietal cells secrete hydrochloric acid through activity of H+/K+ proton pump Acid secretion is increased by activity of: * Gastrin receptors * Histamine 2 receptors (H2 receptors) * PNS –acetylcholine receptors Acid secretion is decreased by activity of: * Prostaglandin receptors (PGE2 receptors)
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Protection from Acid Secretion
Goblet cells produce mucous which protects the lining of the stomach Mucous production is stimulated by agonists of PGE2 receptors Pancreas secretes bicarbonate ions into duodenum to neutralize acid to protect mucosa
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Types of Gastritis
ACUTE: * A transient inflammation of the gastric mucosa * Most commonly associated with local irritants such as bacterial endotoxins, alcohol, and aspirin CHRONIC: * Characterized by the absence of grossly visible erosions and the presence of chronic inflammatory changes * Leads eventually to atrophy of the glandular epithelium of the stomach
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Peptic Ulcer Disease (PUD)
Characterized by erosion of mucosal lining of stomach and/or duodenum Etiology: * H. pylori infection (85% of cases) * Chronic use of NSAIDs (reduce production of prostaglandins) * Zollinger-Ellison Syndrome (ZES) * Tumour that secretes gastrin; gastrin promotes acid secretion by parietal cells* Gastric ulcers less common than duodenal ulcers: - Pain often relieved with food, but returns 1–3 hours after meal Stress, mediated by the sympathetic nervous system, leads to vasoconstriction of blood vessels to stomach: *Reduced secretion of mucous and bicarbonate ions
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Helicobacter pylori
Colonize the mucus-secreting epithelial cells of the stomach Produce enzymes and toxins that have the capacity to interfere with the local protection of the gastric mucosa against acid Produce intense inflammation Elicit an immune response
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Methods for Est. Presence of H. pylori Infection
**Watch Video** Slide 23 C urea breath test using a radioactive carbon isotope Stool antigen test Endoscopic biopsy for urease testing Blood tests to obtain serologic titers of H. pylori antibodies
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Pharmacotherapy of H. pylori
Antibiotics usually given with drug that reduces acid secretion (PPI or H2 blocker) Two or more antibiotics usually given at same time to prevent development of resistance to antibiotics Beta-lactamase, macrolides and tetracyclines are used together
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Complications of Peptic Ulcer
**Hemorrhage:** *Caused by bleeding from granulation tissue or from erosion of an ulcer into an artery or vein **Obstruction:** * Caused by edema, spasm, or contraction of scar tissue and interference with the free passage of gastric contents through the pylorus or adjacent areas **Perforation:** * Occurs when an ulcer erodes through all the layers of the stomach or duodenum wall
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GI Tract Bleeding
**Hematemesis:** * Blood in vomit * May be bright red or have coffee ground appearance Melena * Blood in the stool * Ranges in color from bright red to tarry black * May be occult (hidden)
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Gastroesophageal Reflux Disease (GERD)
Chronic condition characterized by persistent heartburn due to weakening of lower esophageal sphincter Symptoms: * Heartburn, chest pain * Nausea, belching * Dysphagia, early satiety
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Pharmacotherapy for PUD and GERD
Change lifestyle factors that may be contributing to severity Goals of PUD pharmacotherapy: * Relieve symptoms * Promote healing * Prevent complications * Prevent future recurrence * Eliminate causative factors
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Drugs that Reduce Acid Secretion
H2 Receptor antagonists: - occupy the histamine receptors and prevent acid secretion Proton Pump Inhibitors (Eg Pantoprazole): - Binds to enzyme H+, K+ -ATPase and prevents acid from being secreted Anticholinergics Prostaglandins
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Drugs that Neutralize Acid and Antibiotics for PUD/GERD
Neutralize: Antacids = Chemically combine w/ acids to raise the stomach pH Antibiotics: - Eradicate H. pylori (primary cause of peptic ulcers) Eg) - Amoxicillin - Clarithromycin - Tetracycline - Metronidazole
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Pharmacotherapy w/ H2 Receptor Antagonists
Available OTC and by prescription Pharmacokinetic Properties: - Rapid absorption in SI - 30-minute Onset - Half-life = 1-4hr - **Antacids diminish absorption of H2 receptor antagonists** Eg) FamotiDINE, CimetiDINE
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Pharmacotherapy w/ Proton Pump Inhibitors (PPIs)
PPIs H+/K+ pump on parietal cells, reducing acid secretion in the therapy of PUD & GERD Should be taken 30min before meals Eg) Pantoprazole Na and Pantoprazole Mg
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Pharm w/ Antacids & Adverse Effects
Composed of carbonate, hydroxide, and bicarb compounds that neutralize stomach acid - Calcium carbonate, aluminum carbonate - Aluminum hydroxide, Mg hydroxide - Na bicarb Can affect absorption of drugs, especially those that require an acidic environment ADVERSE EFFECTS: Ca Antacids = Constipation, aggravation of kidney stones, Milk alkali syndrome (hypercalcemia) Al Antacids = Constipation, hypophosphatemia Na Antacids = Fluid retention Mg Antacids = hypermagnesemia (fatigue, dysrhythmias, hypotension)
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Miscellaneous Drugs Used for PUD & GERD
Sucralfate = stimulates mucous, bicarb, and prostaglandin Misoprostol = prostaglandin agonist, promotes mucous secretion and inhibition of acid secretion Bismuth compounds = Used for dyspepsia (indegestion), heartburn, and diarrhea
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Inflammatory Bowel Disease (IBD)
Watch YouTube video (Slide 37) Includes: **Crohn's Disease** = ulcers in distal portion of SI - Recurrent, granulomatous type of inflammatory response that can affect any area of the GI tract from mouth-anus **Ulcerative Colitis** = mucosal erosions in LI - Nonspecific inflammatory condition of the colon Etiology: - Hypothesized to be due to hypersensitivity response to normal flora, prompting chronic inflammation - Smoking, GI infection, NSAIDS are trigger for IBD
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Pharm of IBD
Treated w/ immunosuppressants and anti-inflammatory drugs Expected outcomes: - Reduce acute symptoms of active disease by induction therapy - Keep the disease in remission w/ maintenance therapy Therapy similar for both Crohn's and UC: 1) **5-aminosalicylic acid (5-ASA or Mesalazine)** - FIRST LINE THERAPY - Reduces production of prostaglandins which are assoc. w/ inflammation 2) **Corticosteroids (Eg Prednisone)** - Used if client not responsive to 5-ASA 3) **Immunosuppressants** - Used as maintenance once disease in remission from 5-ASA or corticosteroids
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IBS & Pharmacotherapy
Characterized by: - Abdominal pain, colicky cramping - Visible bloating, excessive gas - Alternate bouts of constipation & diarrhea - Mucous in stool - Defecation providing relief from syptoms Non-pharm therapies: - Relaxation techniques, reduce stressors - Avoid foods that cause bloating - Avoid drugs that promote constipation PHARM: Laxatives and antidiarrheal agents may be used depending on what predominates: - IBS-C - psyllium - IBS-D - loperamide, alosetron (5HT3 antagonist) Antidepressant Therapy: - Tricyclic antidepressants (Not first-line***, better if depression comorbid in pt)
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IBD vs IBS
IBD: 1) **Chronic inflammatory** disease involving the GI tract 2) Immune cells cause inflammation and ulceration in the lining of the intestines which can lead to frequent/urgent BMs, ab pain, diarrhea and bleeding 3) GI tract is DAMAGED. Symptoms can be different for everyone and depend on the type of IBD and where the inflammation is located 4) **Anemia MAY by present** 5) INFLAMMATION (redness, ulceration, bleeding seen), imaging shows bowel wall inflammation IBS: 1) **Functional GI disorder** that causes recurrent ab pain and changes in BMs 2) Symptoms may include bloating, constipation, diarrhea, or mixed D/C 3) Pts w/ IBS have these symptoms WITHOUT DAMAGE to GI tract 4) Endoscopy and radiology tests DO NOT show inflammation (calprotectin NOT elevated) 5) **NO anemia present** 6) NO INFLAMMATION** in imaging or endoscopy
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Diagnostic Procedures to Confirm IBD
**Blood Tests**: - Looking for inflammation - Levels of RBCs, WBCs, Platelets, & C-Reactive Protein - Can help identify possible risks for complications **Stool Tests**: - Checking for infection/inflammation (looking at levels of fecal calprotectin, protein in stool) **Endoscopic Procedures**: UPPER ENDOSCOPY (go through mouth)= Crohn's Only** SIGMOIDOSCOPY = UC only**, shows extent of inflammation in lower colon and rectum COLONOSCOPY (through anus) = BOTH** **Internal Imaging Procedures**: - CT or MRI
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Pancreatitis
Digestive enzymes remain in the pancreas rather than being released into duodenum ACUTE: * More common in middle-aged adults * Associated with gallstones in females, alcoholism in males CHRONIC: * Associated with alcoholism Etiology * Alcoholism * Infections * Genetic (cystic fibrosis) S&S: * Left upper quadrant pain when eating * Nausea and vomiting (when eating) Treatment * Replacement therapy with pancreatic enzymes
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Constipation
More frequent in older adults Can be a symptom of underlying disease Diagnosis requires at least two of the following symptoms. * Two or fewer bowel movements per week * Lumpy or hard stools at least 25% of time * Straining to pass stools at least 25% of time * Feeling of incomplete evacuation at least 25% of time Many causes including: * Lack of exercise * Insufficient diet, lack of dietary fibre * Lack of fluid intake * Drugs that reduce GI motility Severe constipation can lead to: * Fecal impaction * Complete obstruction of bowel Non-pharmacological approaches: * Regular exercise promotes more regular GI activity * Eating a sufficient amount of food to meet requirements of body * Healthy diet including insoluble dietary fibre * Adequate hydration, drinking recommended amount of water every day Occasional episodes can be resolved quickly with medication
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Pharmacotherapy w/ Laxatives (4 Classes)
**Bulk-forming (Eg. psyillium)** * Fibre that absorbs water, forming bulkier stool that passes more easily * Must be taken with lots of water **Stool softeners (i.e. docusate)** * Surfactant that lowers surface tension of stool allowing more water to enter stool * Often given when constipation poses a risk **Stimulants (i.e. bisacodyl)** * Irritate bowel, promoting peristalsis * Can cause diarrhea and cramping **Osmotics (i.e. magnesium hydroxide)** * Draw water into GI tract * Can cause dehydration
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Diarrhea
Colon doesn't reabsorb enough water** Often secondary to another condition Etiology: - GI infection - Drugs (Antibiotics, NSAIDs, orlistat, digoxin) - Inflammation of bowel - Foods - Disease of SI and pancreas = leading to malabsorption of food Therapeutic focus is to eliminate primary cause and manage symptoms through pharmacotherapy - If infection is primary cause, antibiotics wil be most effective treatment BUT can be combined w/ antidiarrheals
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Prolonged Diarrhea
- Imbalances in fluid, acid-base, electrolytes - Indication for pharmacotherapy - Symptom of underlying disorder Can Cause: - Fluid imbalance - pH imbalance - Electrolyte imbalance
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Pharmacotherapy for Diarrhea
Opioids (**Most effective**): - Decrease GI motility via mu receptors, providing more time for water absorption Eg) Codeine Diphenoxylate w/ atropine (Lomotil) Loperamide (Imodium) Non-Opioids: - Bismuth subsalicylate (Pepto-bismul) (Draws fluid out of bowel, anti-inflammatory) - Psyllium - absorbs water to form bulk
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Nausea and Vomiting
N = unpleasant feeling of need to vomit accompanied by weakness, diaphoresis, dizziness, and hyperproduction of saliva V (emesis) = Controlled by vomiting centre of the brain that receives signals from digestive tract, inner ear, chemoreceptor trigger zone, cortex Usually secondary to another condition Treatment outcomes should focus on removal of cause Causes: - Motion sickness - Drugs, toxins - GI infection - Stress, pain - Preggos Complications from Chronic Vomiting: - Dehydration - Electrolyte imbalances - Weight loss - Vascular collapse - Metabolic alkalosis
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Pharmacotherapy for N&V
**Anticholinergics**: Cause = Motion Sickness Eg) Scopolamine **Antihistamines**: Cause = Motion sickness Side effect = Significant drowsiness Eg) Dimenhydrinate aka Gravol **Serotonin (5HT3) receptor antagonists**: Cause = Chemo-induced N&V Eg) Ondansetron **Phenothiazides (D2 Receptor antagonists)**: - Antineoplastic therapy Eg) Prochlorperazine **Cannabinoids**: - Antineoplastic Therapy **Corticosteroids**: - Antineoplastic Cause = Post-surgical N&V Eg) Dex
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Enteral vs Parenteral Nutrition
Provide Nutrition Support = Delivery of formulated nutrients via feeding tube or IV E = supplying nutrients using GI tract, including tube feedings or oral diets P = IV provision of nutrients BYPASSING GI Tract
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Enteral Nutrition Support
Wide selection of formulas, designed to meet variety of medical and nutritional needs Can be used alone OR with other foods **Requires intact and normal GI function** Classified according to macronutrient composition **Preferred over IV feedings
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Types of Enteral Formulas
Standard = for pt's who can digest & absorb nutrients WITHOUT difficulty (contains protein & carb sources) Hydrolyzed = For pt's with compromised digestive or absorptive functions (Macronutrients are partially or fully broken down & require little, if any, digestion before absorption) Disease-specific = Designed to meet nutrient needs of pt's w/ particular disorders (Liver, Kidney, lung, glucose intolerance, metabolic stress etc) Modular = contain only 1 or 2 macronutrients (used to enhance other formulas)
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Candidates for Tube Feedings
Major Dysphagia Little or no appetite for extended periods (especially if malnourished) GI obstructions, impaired motility of upper GI tract After intestinal resection, beginning enteral feedings Mentally incapacitated due to confusion, dementia, neurological disorders Coma People w/ extremely high nutrient requirements People on mechanical ventilators
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Feeding Routes
Based on: - Condition - Expected duration - Potential complications MAIN ROUTES: 1) Transnasal (temporary) = Nasogastric, nasoduodenal, nasojejunal 2) Gastrostomy 3) Jejunostomy
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3 Frequencies of Enteral Nutrition
Bolus = delivery of prescribed volume in less than 15min Intermittent = delivery of prescribed volume over 20-40min Continuous = sow delivery at a constant rate over 8-24hrs
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Meeting Water Needs
Estimating Fluid Requirements: Adults = 30-40mL/kg Older Adults = 30mL/kg Child = 50-60mL/kg Baby = 150mL/kg Fluid intake may be restricted for pts w/ kidney, liver or heart disease Fluid intake may be increased w/ fever, high urine output, diarrhea, excessive sweating, severe vomiting, fistula drainage, high-output ostomies, blood loss, open wounds Standard formulas contain 85% water (850mL/L) Nutrient Dense Formulas contain 69-72% water Meet fluid needs with additional water flushes
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Parenteral Nutrition Support
Indicated for pts who do not have functioning GI tract & are malnourished*** Used when enteral formulas cannot be used or intestinal function is inadequate Life-saving option for critically ill persons 2 Main access sites = peripheral or central vein
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Peripheral Parenteral Nutrition (PPN)
* Can only provide limited amounts of energy & protein * Peripheral veins can be damaged by overly concentrated solutions * Limited to patients who do not have high nutrient needs or fluid restrictions * Used most often for short-term nutrition support (7-10 days) * Rotation of vein sites may be necessary
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Total Parenteral Nutrition (TPN)
* Can reliably meet complete nutrient requirements * Provides nutrient-dense solutions for patients with high nutrient needs or fluid restrictions * Preferred for long-term intravenous feedings * Inserted directly into a large central vein
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Parenteral Solution
Customized formulations Highly individualized (often recalculated on daily basis until pt's condition stabilizes) Contents: - Amino acids (both essential and non for proteins) - Carbs (dextrose) - Lipid emulsions - Fluids & Electrolytes - Vitamens & trace minerals