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Spring 2014 > Physiology - Exam 1, Deck #2 > Flashcards

Physiology - Exam 1, Deck #2 Flashcards

1
Q

Chylomicrons

A

Deliver dietary lipids to the body

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2
Q

VLDLs

A

Deliver endogenously made lipids to the body

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3
Q

LDLs

A

Deliver endogenously made cholesterol to the body

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4
Q

HDLs

A

Remove and degrade cholesterol

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5
Q

Camplobacter

A
  • Most common identified caused for food borne illness;
  • Guillain Carre Syndrome;
  • Poultry, red meat, unpasteurized milk, untreated water
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6
Q

Salmonella

A
  • Second most common food borne illness;
  • Reiter’s Syndrome, arthritis;
  • Deadly if enters the bloodstream;
  • Unpasteurized milk, eggs, raw egg products, meat, poultry
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7
Q

Listeria monocytogenes

A
  • All around environment;
  • Soft-mold ripened cheese and pates;
  • Very dangerous to PREGNANT women = miscarriage and stillbirth;
  • Infants can get sepsis and meningitis
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8
Q

E. Coli 0157

A
  • Verocytotoxin- producing (VTEC);

- Hemolytic uremic syndrome = kidney failure, brain damage, stroke

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9
Q

C. Perfringens

A
  • Meat, poultry;

- Soil, intestines, sewage and animal manure

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10
Q

Anatomical units of the Respiratory System

A
  1. Nose
  2. Pharynx to esophagus and digestive system
  3. Glottis which guards the trachea
  4. Trachea
  5. Left and right bronchi that enter each lung and branch to secondary bronchi
  6. Bronchioles
  7. Alveolar ducts
  8. Air sacs = cluster of alveoli with tons of surface area (70m^2 in a man)
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11
Q

Pulmonary artery branches

A

capillary network around the bronchioles and alveoli;

  • very abundant circulatory tree in the lungs;
  • These pulmonary capillaries reconnect to form tiny venues as blood leaves alveoli and creates the PULMONARY VEIN
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12
Q

Pulmonary Vein

A

Carries oxygenated blood BACK to the left atrium;
Exchange of O2 and CO2 takes place across alveolar epithelial tissue of our lungs into pulmonary capillaries and vice versa

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13
Q

Thoracic Cage

A
  • Neck, sternum, ribs, spinal column, and diaphragm;

- Breathing is the enlarging/contracting of the cage due to muscle

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14
Q

Pleural Cavity

A
  • Cavity formed by the thoracic cage and is entirely filled by the lungs;
  • PARIETAL PLEURA lines the inside surface of the cavity
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15
Q

Visceral Pleura

A

Lubricated membrane coverings on the lungs

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16
Q

INSPIRATION Muscles

A
  • Diaphragm;
  • External intercostal and neck muscle;
    1. Diaphragm moves down pulling the pleural cavity down and elongating it;
    2. Intercostals and neck muscles contract and lift front of thoracic cages and force ribs more forward
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17
Q

EXPIRATION Muscles

A
  • Abdominal muscles;
  • Internal intercostals
    1. Abs pull down on chest cage decreasing thoracic thickness;
    2. Abdominal contents move up against the diaphragm and decrease longitudinal dimension of the pleural cavity;
    3. Internal intercostals pull ribs down and decrease chest thickness
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18
Q

Inspiration

A
  • Thoracic cage enlarges;
  • Normal = volume increases, pressure decreases - decreased pressure of the alveoli to −3torr;
  • DRAWS AIR IN;
  • Max = breathe as hard as possible with mouth closed = −80torr
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19
Q

Expiration

A
  • Volume decreases, pressure increases to +3 torr;

- Mx = breathe inward as hard as possible = + 100 torr

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20
Q

Intrapleural Space

A

Space between lungs and thoracic cage

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21
Q

Intrapelural Pressure

A

Pressure in this space between the lungs and the thoracic cage;
**About 5 too LESS than alveoli

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22
Q

Tidal Air

A

Air that passes into and out of the lungs with each breath;

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23
Q

Tidal Volume

A

Amount of air in each breath;

-Adult male = 500mL

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24
Q

Minute Respiratory Volume

A

Tidal Volume x Normal respiration rate;

-500mLs x 12breath/min = 6000ml/min (6L/min)

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25
Q

Inspiratory Reserve Volume

A

Amount of air that can still be INSPIRED by forceful respiration after the end of a normal tidal inspiration;
-3000 ml = adult male

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26
Q

Expiratory Reserve Volume

A

Amount of air that can still be expired by forceful expiration after the end of a normal tidal expiration;
-1100 ml = adult male

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27
Q

Residual Volume

A

Volume of air remaining in the lungs after the most forceful expiration;

  • 1200 ml = adult male;
  • This volume provides air in the alveoli to allow oxygenation of the blood between breathes
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28
Q

Inspiratory Capacity

A

Tidal volume and inspiratory volume;

500 + 3000 = 3500 mls

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29
Q

Functional Residual Capacity

A

Expiratory reserve volume and residual volume;

  • Amount of air remaining in the lungs at the end of a normal expiration;
  • 2300 mls
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30
Q

Vital Capacity

A

**Most Important Medically;
-Max amount of air that a person can expel from his lungs after first fillings his lungs to their max extent then expiring to the max extent;
(Inspiratory reserve + tidal volume + expiratory reserve)
(3000 + 500 + 1100 = 4600)
**Well developed ATHLETE should be 6000-7000 mls

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31
Q

Total Lung Capacity

A

Max volume to which the lungs can be EXPANDED with the greatest possible inspiratory effort;
(Vital capacity + Residual Volume)
(4600 + 1200 = 5800mls)

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32
Q

Difference in male and female lung capacity

A

ALL pulmonary volumes and capacities are 20-25% LESS in females than in male;
-Greater in athletes

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33
Q

Oxygen consumption of an adult male at REST

A

REST = 250ml/min

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34
Q

Oxygen consumption of an adult male at MAX EXERCISE

A

Untrained = 3600 MI/min
Athetically trained avg = 4000 MI/min
Marathon runners = 5100 MI/min

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35
Q

Volumes of AIR EXCHANGED per Minutes VARIES by:

A

At rest = 6L/min;
Max exercise = 100-110 L/min;
Max breathing capacity = 150-170 L/min
**Max breathing being 50% GREATER than pulmonary ventilation at max exercise = SAFETY

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36
Q

Conditions that are covered by difference

A
  1. Exercise at high altitudes (6000ft = PO2 is 127mmHG, 84 mmHG in alveoli, 79mmHG in blood at rest);
  2. Exercise at very hot conditions
  3. Abns in respiratory system
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37
Q

Oxygen Diffusing Capacity

A

Measure of the rate at which oxygen can DIFFUSE from the alveoli into the blood;
-Can be INCREASED (better conditioned) due to increased pulmonary capillary blood flow

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38
Q

Differences in Diffusing Capacities (MI/min/m2)

A
  • Nonathlete at rest = 23;
  • Nonathlete at max exercise = 48
  • Speed skaters during max = 64;
  • Swimmers during max = 71;
  • Oarsman during max = 80
  • Almost 4x increase due to Cardio Respiratory Conditioning
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39
Q

Transfer of air between the blood and alveoli

A
  • Separated by alveolar and pulmonary membranes about 0.2-0.4 microns thick;
  • Very short diffusing distance = high diffusion rate;
  • O2 = alveoli to blood;
  • CO2 = blood to alveoli
  • *Partial pressure differences b/w the two sides of the membrane greatly determines rate of diffusion
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40
Q

Partial Pressure Concept

A 
HIGH O2 in the alveoli will move it to the blood and vice versa;
At 7600 mmHG (atmospheric) = 
- O2 air = 159 torr;
- O2 alveolar air = 104
will MOVE INTO BLOOD;
-O2 pulmonary arterial blood = 40 torr
- O2 pulmonary venous blood = 100 torr
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41
Q

Oxygen Transport

A
  • 60 times MORE O2 is carried with Hemoglobin than in blood plasma;
  • Sigmoidal curve to O2 diffusing curve due to COOPERATIVITY = As one O2 binds Hb, the subsequent binding is much easier and happens more quickly
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42
Q

Utilization Coefficient of Oxygen

A
  • 27% = 27% of oxygen is LOST to tissues each time Hb loses O2 at rest due to a 70% sat.;
  • *87% = during EXERCISE the need for O2 saturation can fall to 10% on Hb as most is released to tissue with a O2 utilization increase to 87%
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43
Q

Increases in Oxygen Utilization

A

-WITHOUT an increase in blood flow, only O2 delivery = 3 times = 77-87%;
-INCREASED blood flow (cardiac output) = 5-6 times;
BOTH increased O2 delivery and blood flow = 15-18 time increase in oxygen delivery to cells

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44
Q

Bohr Effect

A
  • Oxygen dissociation curve shifts to the RIGHT and gives rise to a DECREASED oxygen affinity by Hb with a DECREASED pH (due to lactic acid) or an INCREASE in PCO2;
  • Increases cardiac output 5-6 times
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45
Q

Transport of CO2

A

CO2 in cells at 46 torr > capillary blood at 45 torr > alveolar air at 40 torr;

  • 10% transported in BLOOD dissolved;
  • 20% with Hb
  • 70% as BICARBONATE IONS (HCO3)
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46
Q

Regulation of Respiration

A

Control center of the brain = Medulla Oblongata;

  • 2 neuronal pools are cross wired to inhibit one another when one is active;
  • Corotid Bodies and Aortic Branch respond to a drop in pH or increase in PCO2;
  • Herring Brewer Reflex keeps lungs from over-inflating
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47
Q

Parts of the Circulatory System

A
  1. Heart = 4 chambered pump;
  2. Arteries;
  3. Arterioles;
  4. Capillaries;
  5. Venules;
  6. Veins;
  7. Blood
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48
Q

What determines the amount of blood flow?

A
  • Related to the PRESSURE exerted upon it in a direct manner and to the RESISTANCE to it by the circulatory system in an INVERSE manner;
  • Pressure from the LEFT should be GREATER than the RIGHT (5-7x greater);
  • Left = Systemic circulation (a long way to go);
  • Right = Pulmonary circulation just to the lungs
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49
Q

Pulmonary Congestion

A

When the RIGHT side of the heart must exert a high amount of pressure (which it normally should’t) the heart eventually STOPS = Congestive Heart Failure

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50
Q

Anatomy of the Heart

A
  • ~300 grams;
  • Larger in men than women;
  • SEPTUM = muscle that separates the 2 sides
  • 2 Upper Chambers = Left/Right Atria (get blood from the veins);
  • 2 Lower Chambers = Left/Right Ventricles;
  • Superior Vena Cava = Veins from upper body;
  • Inferior Vena Cava = Veins from lower body;
  • *Adult repeats circulation of blood about 60-80 times/min at BASAL conditions!!
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51
Q

What happens at the RIGHT ATRIUM?

A

Receives blood that is LOW in O2 and HIGH in CO2;

  • Right atrium contracts with the left opening the TRICUSPID VALVE to the RIGHT VENTRICLE;
  • Blood moves to the RIGHT VENTRICLE;
  • Valve then closes as the Ventricle contracts
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52
Q

Chordae Tendineae

A

Attached to the PAPILLARY MUSCLES in the ventricle and prevent the Tricuspid Valve from being pushed back up into the atrium;

  • Keeps blood from going backwards!;
  • High pressure of ventricular contraction is prevented from everting AV valves by contraction of papillary muscles which are connected to AVs by chorda tendinea
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53
Q

What is the pathway once in the Right Ventricle?

A
  1. Pulmonary artery through PULMONARY SEMILUNAR VEINS;
  2. Lungs;
  3. Left Atrium via PULMONARY VEINS:
  4. Left Ventricle through MITRAL/BICUSPID VALVE (also has tendineae);
  5. Enters the DORSAL AORTA through AORTIC SEMILUNAR VALVES
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54
Q

Heart Rate by Age at Basal Conditions

A

Fetus = 160 beats/min;
3 years = 100 beats/min;
Young male adult = 70 beats/min;
Aged = 75-80 beats/min

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55
Q

Abnormal Heart Rates

A 
Bradycardia = Less than 60 beats/min;
Tachycardia = More a than 100 beats/min
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56
Q

Perfusion

A

transportation of respiratory gases, delivery of nutrients & hormones, & waste removal

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57
Q

Functions of the Circulatory System

A
  • Perfusion;
  • Include roles in temperature regulation, clotting, & immune function;
  • Homeostasis
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58
Q

Components of the Circulatory System

A

-Cardiovascular and Lymphatic System =
-Heart pumps blood thru cardiovascular system
-Blood vessels carry blood from heart to cells & back;
-Lymphatic system picks up excess fluid filtered out in capillary beds & returns it to veins
oIts lymph nodes are part of immune system
oPicks of the other excess 2 liters filtered from the plasma

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59
Q

Fibrous Skeleton

A

Between atria & ventricles is layer of dense connective tissue and functionally separates the two;

  • Myocardial cells of ATRIA attach to TOP of fibrous skeleton & form 1 unit = MYOCARDIUM;
  • Cells from VENTRICLES attach to BOTTOM & form another unit;
  • ANNULI FIBROSI = Fibrous skeleton also forms rings to hold heart valves
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60
Q

Pulmonary Circulation

A

path of blood from right ventricle through lungs & back to heart

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61
Q

Systemic Circulation

A

path of blood from left ventricle to body & back to heart

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62
Q

Rate of Blood Flow

A
  • *Rate of flow through systemic circulation = flow rate thru pulmonary circuit
  • Resistance in systemic circuit GREATER than pulmonary;
  • Amount of WORK done by LEFT ventricle pumping to systemic is 5-7X greater;
  • Causing left ventricle to be more muscular (3-4X thicker)
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63
Q

Valvular Stenosis

A

narrowing of the opening in the valves (congenital or infection of strep. forming scar tissue)

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64
Q

Valvular Insufficiency

A
  • Valve is leaking and allows the backward flow of blood;
  • Don’t close properly;
  • Can be from damaged papillary muscles
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65
Q

What are the Valves of the Heart?

A
  • Blood flows from atria INTO ventricles thru 1-way atrioventricular (AV) valves;
  • Between RIGHT atrium & ventricular = TRICUSPID VALVE
  • Between LEFT atrium & ventricular is BICUSPID OR MITRAL VALVE;
  • Opening & closing of valves results from pressure differences;
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66
Q

What are the Semilunar Valves of the Heart?

A
  • During VENTRICULAR contraction blood is pumped through aortic & pulmonary semilunar valves;
  • Close during relaxation
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67
Q

Cardiac Cycle

A

Is repeating pattern of contraction & relaxation of heart;

  • SYSTOLE refers to contraction phase ;
  • DIASTOLE refers to relaxation phase;
  • Both atria contract simultaneously; ventricles follow 0.1-0.2 sec later
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68
Q

What is the End-Diastolic Volume?

A

volume of blood in ventricles at end of diastole → Not all blood is gotten rid of

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69
Q

What is Stroke Volume?

A

amount of blood EJETED from ventricles during SYSTOLE

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70
Q

What is End-Systolic Volume?

A

amount of blood left in ventricles at end of systole

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71
Q

What is an Isovolumetric Contraction?

A
  • ALL valves are CLOSED;

- As ventricles begin contraction, pressure rises CLOSING AV valves → Pressure rises and closes valves

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72
Q

What happens as pressure in VENTRICLES is greater than in the AORTA?

A
  • When pressure in ventricles EXCEEDS that in aorta, semilunar valves OPEN & EJECTION begins;
  • As pressure in ventricle falls below that in aorta, back pressure closes semilunars
  • All valves are closed & VENTRICLES undergo ISOVOLUMETRIC RELAXATION → Preparing to take on more blood
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73
Q

What happens when the pressure in the VENTRICLES falls below the atria?

A
  • When pressure in ventricles falls below atria, AVs open & ventricles fill;
  • ATRIAL SYSTOLE (contraction) sends its blood into ventricles
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74
Q

What are the sounds of the heart?

A

Closing of AV & semilunar valves produces sounds that can be heard thru stethoscope =

  • Lub (1st sound) : produced by closing of AV valves
  • Dub (2nd sound) : produced by closing of semilunars
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75
Q

What are Heart Murmurs?

A

ABN sounds produced by abnormal patterns of blood flow in heart;

  • Many caused by defective heart valves;
  • Can be of congenital origin
  • In rheumatic fever, damage can be from antibodies made in response to strep infection
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76
Q

What is Mitral Stenosis?

A
  • Mitral valve becomes thickened & calcified, impairing blood flow from left atrium to left ventricle;
  • Accumulation of blood in left atrium can cause pulmonary hypertension
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77
Q

What SEPTAL Defects cause heart murmurs?

A
  • Murmurs caused by septal defects are usually CONGENITAL;
  • Due to HOLES in septum (muscle) between left & right sides of heart;
  • Pressure causes blood to pass from LEFT TO RIGHT
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78
Q

What is the Ductus Arteriosis?

A

short broad vessel in the fetus that connects the pulmonary artery with the aorta and conducts most of the blood directly from the right ventricle to the aorta bypassing the lungs

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79
Q

What is the Foramen Ovale?

A

in the fetal heart, allows blood to enter the left atrium from the right atrium

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80
Q

What causes Blue Baby Syndrome?

A

A baby who is cyanotic (blue), due usually to a heart malformation that prevents the baby’s blood from being fully oxygenated. The bluish color reflects the deoxygenated state of the blood.

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81
Q

What is the Pacemaker System of the Heart?

A

Timing of spread of cardiac action potential =

  1. Sinoatrial (SA) Node
  2. Internodal Pathway
  3. AV Node at atrial ventricular junction;
  4. Bundle of His = AV BUndle
82
Q

What is the Sinoatrial (SA) Node Pacemaker?

A
  • Tissue in the region of the SA node spontaneously DEPOLARIZES at a FASTER rate (70-80 times/min) than any other area of the heart to threshold (Pacemaker Potential);
  • Wave of depolarization BEGINS at the SA Node;
83
Q

How do the SA Node cause a wave of DEPOLARIZATION?

A
  • Membrane voltage BEGINS at -60mV & gradually depolarizes to -40 threshold;
  • Spontaneous depolarization is caused by Na+ flowing through channel that opens when hyperpolarized (HCN channel);
  • At threshold (key value) Voltage-gated Ca2+ channels open, creating UPSTROKE & contraction → −20mV to +20mV → Calcium flows in ;
  • REPOLARIZATION is via opening of V-gated K+ channels → Returns to negative potential
84
Q

What are HCN Channels?

A

Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels are intermembrane proteins that serve as nonselective ligand-gated cation channels in the plasma membranes of heart and brain cells → pacemaker channels

85
Q

What is the Internodal Pathway?

A

Conduct the impulse from the SA node to the AV node

86
Q

What is the AV Node?

A
  • Second area where model tissue is found at the atrial ventricular junction;
  • Secondary pacemaker of the heart;
  • Depolarizes = 40-60 times/minute;
  • Assumes the pacemaker role if the rate of spontaneous discharge of the SA node is less than the rate of the AV node
87
Q

What is the Bundle of His or the AV Bundle?

A

Fibers which arise at the AV Node and descend into the intraventricular septum through a fibrous connective tissue ring separating the atria from the ventricles;
-Top of the intraventricular septum the AV bundle divides into left and right bundles of HIS which pass to the APEX OF THE HEART

88
Q

What are Purkinge Fibers?

A

From the apex of the heart, the bundles branch into Purkinge Fibers;
-Extend to the base of the Papillary Muscles and to the rest of the musculature

89
Q

What are Ectopic Pacemakers?

A
  • Other excitable group of cells that causes a premature heart beat outside the normally functioning SA node;
  • Slower than SA node;
  • Stimulated to produce APs by SA node before spontaneously depolarize to threshold;
  • If APs from SA node are prevented from reaching these, they will generate pacemaker potentials
90
Q

Depolarization vs. Repolarization

A
  • Depolarizaton = Sodium Influx

- Repolarization = Potassium Efflux

91
Q

What are Myocardial Action Potentials?

A
  • Myocardial cells have RMP of –90 mV;
  • Depolarized to threshold by APs originating in SA node ;
  • Upstroke occurs as V-gated Na+ channels open → All due to SODIUM influx ;
  • MP rapidly declines to -15mV & stays there for 200-300 msec = PLATEAU PHASE;
  • Plateau results from balance between slow Ca2+ influx & K+ efflux;
  • Repolarization due to opening of extra K+ channels
92
Q

What are the Conducting Tissues of the Heart?

A
  • APs from SA node spread through atrial myocardium via GAP JUNCTIONS;
  • But need special pathway to ventricles because of non-conducting fibrous tissue = AV node at base of right atrium & bundle of His conduct APs to ventricles ;
  • In septum of ventricles, His divides into right & left bundle branches;
  • Give rise to Purkinje fibers in walls of ventricles → These stimulate contraction of ventricles
93
Q

What is a Block within the Heart?

A
  • If anything happens to the AV node there is not uniform conduction of nervous impulses through the heart;
  • Atria and ventricles not beating in correct sequence;
  • If the atria fail to function properly 30% of CO is LOST under normal conditions;
94
Q

What are the degrees of blockage?

A
  1. Right bundle branch block;
  2. Left bundle branch block;
  3. Complete bundle branch block
    * In nodal tissue there is a spontaneous depolarization before each contraction of cardiac muscle tissue
95
Q

What is the timing for the conduction of Action Potentials?

A

-SA node fires about 70-80 times/minute;
-APs from SA node spread at rate of 0.8 -1 m/sec;
-Time delay occurs as APs pass through AV node = slow conduction of 0.03– 0.05 m/sec;
-Delay of 0.16 sec for AP to reach AV Bundle of His;
-Rapidly reaches the APEX by 0.175 secs;
-AP speed increases in Purkinje fibers to 5 m/sec;
-Impulse spread over endocardiac surface;
-Ventricular contraction begins 0.1–0.2 sec after contraction of atria
(Top outside of RIGHT Vent by 0.21 sec; Top outside of LEFT Vent by 0.22 sec)

96
Q

What is the “Leaky Membrane Phenomenon”?

A
  • Heart contraction occurs in milliseconds after stimulation by AP;
  • APs might be spread by Ca2+ leaking into the inside of the cells of the SA node after reaching threshold and spontaneously depolarizing the tissue to threshold
97
Q

What is Excitation-Contraction Coupling?

A
  • Depolarization of myocardial cells opens V-gated Ca2+ channels in sarcolemma → membranous sheath around muscle fibers;
  • This depolarization opens V-gated & Ca2+ release channels in SR, sarcoplasmic reticulum = calcium-stimulated-calcium-release;
  • Ca2+ binds to TROPONIN & stimulates contraction (as in skeletal muscle);
  • During repolarization Ca2+ pumped out of cytoplasm & into SR
98
Q

What is Troponin?

A

a complex of three regulatory proteins (troponin C, troponin I, and troponin T) that is integral to muscle contraction[2] in skeletal muscle and cardiac muscle

99
Q

What is the Refractory Period of Heart Contractions?

A
  • Heart contracts as syncytium (all together) & thus can sustain force;
  • Its AP lasts about 250 msec;
  • Has a REFRACTORY PERIOD ALMOST as long as AP;
  • CANNOT be stimulated to contract again until has relaxed
100
Q

What controls the Heart Rate?

A
  1. Endocrine (adrenal medulla) = hormones
    - Increase Heart Rate
    - Thyroxine, Epinephrine, Norepinephrine – open Na+ channels
  2. Autonomic Nervous System
    - Sympathetic Division → Norepinephrine – Opens Na+ channels
  3. Parasympathetic Division →Acetylcholine – Opens K+ channels
101
Q

How does the Sympathetic System Control Heart Rate?

A

SA Node from cardiac nerves releases to norepinephrine and INCREASES heart rate due to opening of Ca+ channels (depolarize)

102
Q

How does the Parasympathetic System Control Heart Rate?

A
  • Vagus nerve releases Acetylcholine and SLOWS heart rate;

- Slows the rate of firing of the SA node due to the opening of K+ channels (repolarize)

103
Q

What is the Mechanism for the effect of Norepinephine (Symp) and Acetylcholine (Para)?

A

Believed to affect the rate of firing of the SA node by altering the slope of the spontaneous depolarization potential:

  • NE & Epi stimulate opening of pacemaker HCN channels = depolarizes SA faster, increasing HR
  • ACH promotes opening of K+ channels = The resultant K+ outflow counters Na+ influx, slowing depolarization & decreasing HR
104
Q

What is the Chronotropic Effect of the Symp. and Parasympathetic System on Heart Rate?

A

Affecting the rate of rhythmic movements, such as the heartbeat

105
Q

What is Vagal Tone?

A

-impulses from the vagus nerve (parasympathetic) producing inhibition of the heartbeat

106
Q

What is the Sympathetic tone of the heart?

A

Very LITTLE or no sympathetic tone of the heart;

  • Number of impulses along the vagus nerve to heart controls the normal heart at rest;
  • Control center in the MEDULLA OBLONGATA = Vasomotor Center;
  • Adjusts cardiac activity for varying needs
107
Q

Effect of Autonomic Nerve Activity on the SA Node

A 
Symp = increased diastolic depolarization; increase HR;
Para = decreased diastolic depolarization; decreased HR
108
Q

Effect of Autonomic Nerve Activity on the AV Node

A 
Symp = Increased conduction rate;
Para = Decreased conduction
109
Q

Effect of Autonomic Nerve Activity on the Atrial Muscle

A 
Symp = Increased contraction strength;
Para = No effect
110
Q

Effect of Autonomic Nerve Activity on the Ventricular Muscle

A 
Symp = Increased contraction strength;
Para = No effect
111
Q

What are the Sensory Receptors that Control Heart Rate?

A
  1. Baroreceptors;

2. Chemoreceptors

112
Q

What are Baroreceptors?

A
  • Stretch receptors stimulated by DISTENTION:
  • Located in the walls of the heart, aortic arch, carotid sinus (arterial) = Stimulate the cardiac INHIBITORY center;
  • Located in the walls of the superior/inferior vena cava (venous)= Stimulate the ACCELERATORY center
113
Q

What are Chemoreceptors?

A

Carotid and aortic bodies that are sensate to elevated PCO2 = increased heart rate

114
Q

What is the Vasomotor Center?

A
  • In the Medulla Oblongata or brain stem;
  • 2 neuronal pools that act in reciprocation to inhibit the activity of the other;
  • Innervate the pacemaker system of the heart by the sympathetic and parasympathetic branches of the nervous system;
    1. Para = cardiac inhibitory;
    2. Symp = cardiac acceleratory
115
Q

What is an Electrocardiogram (ECG/EKG)?

A
  • A recording of electrical activity of heart conducted thru ions in body to surface;
  • First waves PRECEEDE the contraction of the atrium
116
Q

What is a typical EKG Pattern?

A

Interpretation of the actions of the heart caused by a flow of current in the chest around a partially depolarized heart and depolarization passing through the chambers of the heart

117
Q

What are the significant parts of a wave in an EKG Pattern?

A
  1. Isoelectric Line;
  2. P wave;
  3. QRS Complex;
  4. T wave
118
Q

Isoelectric Line

A

the entire heart myocardium is in the RESTING state = polarized

119
Q

P wave

A

the weak depolarization of the ATRIA just before they contract

120
Q

QRS Complex

A

Ventricular depolarization which occurs just before the ventricles contract

121
Q

T Wave

A

rises to a round peak as the ventricular cells depolarize and falls back to zero when all the cells are repolarized

122
Q

What are Bipolar Leads of an EKG?

A

Bipolar leads record voltage between electrodes placed on wrists & legs (right leg is ground)

  1. Lead I records between right arm & left arm
  2. Lead II: right arm & left leg
  3. Lead III: left arm & left leg
    - All 3 are EKG Positive
123
Q

What are Unipolar Leads of an EKG?

A
  • Unipolar leads record voltage between a single electrode placed on body & ground built into ECG machine;
  • Limb leads go on right arm (AVR), left arm (AVL), & left leg (AVF);
  • The 6 chest leads allow certain abnormalities to be detected
124
Q

What are the Chest Unipolar Leads ( = precordial leads)?

A

Indifferent electrode connected to right arm, left arm, left leg at the same time;

  • 6 different standard chest leads from the anterior (front) wall;
  • Right leg lead is the GROUND;
  • V1-V6
125
Q

What are the 3 diseases of the Heart and Circulatory System?

A
  1. Coronary Artery Disease;
  2. Congenital Cardiac Dysfunction and acquire vascular disease;
  3. Congestive Heart Failure
126
Q

Coronary Artery Disease

A

Limit coronary blood flow and hence O2 supply to the heart muscle = Atherosclerosis

127
Q

Congenital Cardiac Dysfunction and acquire vascular disease

A

Structural imperfections arising during the embryological development of the heart or as a result of disease

128
Q

Congestive Heart Failure

A

Gradual profession toward a state in which the heart is unable to maintain an output adequate for body requirements

129
Q

Myocardial Ischemia

A
  • Temporary lack of blood supply in the heart tissues;
  • Usually from CAD;
  • Reduced O2 carrying capacity of the blood occurs in ANEMIA = lack of RBC or of Hb in the RBC;
  • Deficiencies in arterial O2 saturation (chronic pulmonary disease);
  • Marked hypertrophy of ventricular muscle fibers b/c ratio of capillary are to fiber in decreased;
  • Advanced stages of valvular insufficiency
130
Q

Arteriosclerosis

A
  • Late stage atherosclerosis when vessels become constricted by plaque’
  • Most common cause of ISCHEMIA is arteriosclerosis due to impaired blood flow by mechanical obstruction of coronary artery
131
Q

Atherosclerosis

A
  • Cardiac Thrombosis = gradually limits blood thru heart;
  • Metabolic disease;
  • Prime incidence in men past 40, but can occur at any age;
  • Begins as lipid deposits in blood vessels that are elevated above the vascular surface;
  • Later lipids coalesce (combine), become filled with cholesterol, and covered with HYALINE tissue = Atherosclerotic Plaque;
  • Fills blood vessels and hinders their ability to contract;
132
Q

What happens due to Arteriosclerosis and Atherosclerosis?

A
  1. Resistance to blood flow increased;
  2. Pressure of blood getting past the plaque is lowered;
  3. Blood flow reduced (and velocity of blood flow beyond the lesion reduced leading to THROMBUS;
133
Q

Thrombus

A

A fibrous clot in the coronary thrombosis

134
Q

Angina Pectoris

A

Inadequate coronary flow;

  • Anterior chest pain develops during exercise or excitement and radiates to the neck and arms;
  • Typically angina relieved by rest or nitroglycerine
135
Q

Coronary Occlusion

A

Sudden occlusion followed by development of acute MYOCARDIAL INFARCTION (death of heart tissue);
-Ventricular fibrillation is a leading cause of death during the period immediately following the occlusion

136
Q

AST and ALT Transaminases

A

Degree of infarction;

-Infarcted area replaced by fibrous non-contractile connective tissue

137
Q

Mortality Rate of Myocardial Infarction

A
  • 1st month after infarction = 25%;
  • In survivors = physical limitation based upon degree of infarction area
  • *Cardiac tissue CANNOT divide and regenerate itself — connective tissue forms a scar and limits usage ability
138
Q

What is the Coronary Circulatory System?

A

Ascending limb of the aorta → left and right coronary arteries → arterioles → capillary beds → venules → venous blood → coronary sinus → right atrium

139
Q

What is Bypass Surgery (remedy for heart problems)?

A
  1. Bypass surgery =a surgical procedure performed to relieve angina and reduce the risk of death from coronary artery disease. Arteries or veins from elsewhere in the patient’s body are grafted to the coronary arteries to bypass atherosclerotic narrowings and improve the blood supply to the myocardium (heart muscle)
140
Q

What is Angioplasty? (remedy for heart problems)

A
  1. Angioplasty =procedure used to open narrow or blocked coronary (heart) arteries. The procedure restores blood flow to the heart muscle;
    - a thin, flexible catheter (tube) with a balloon at its tip is threaded through a blood vessel to the affected artery. -the balloon is inflated to compress the plaque against the artery wall;
    - Restores blood flow through the artery.
141
Q

What is Cardiac Output?

A

[CO = SVxHR in mLs/min]

  • mLs of blood pumped by each ventricle of the heart per minute;
  • SV = stroke volume;
  • HR = heart rate in beats per minute;
  • Total blood volume = 5.5L
142
Q

What is the Cardiac Control Center?

A
  • Vasomotor control center in the Medulla Oblongata coordinates input from sympathetic and parasympathetic receptors and then sends messages to the heart;
  • HR increase to 180BPM increases cardiac output; ABOVE 180 BPM, CO decreases b/c decreased stroke volume
143
Q

What regulates Heart Rate?

A
  • Vasomotor Center
    1. Automatic rhythm set by rate of sinoatrial node firing — primary pacemaker of the heart; automoticity;
    2. Sympathetic = release norepineprhine and other cathecolamines that increae spontaneity of the pacemaker by opening Ca2+ channels;
    3. Parasympathetic = releases Ach to decrease firing by K+ channels
144
Q

What regulates STROKE VOLUME?

A
  1. Frank-Starling law of the heart = Intrinsic Control;

2. Extrinsic control of contractility – sympathoadrenal system

145
Q

What are the 3 variables in determining stroke volume?

A
  1. End diastolic volume (EDV) = volume of blood in ventricles at end of diastole;
  2. Total peripheral resistance (TPR) = impedance to blood flow in arteries — after load;
  3. Contractility = strength of ventricular contraction
146
Q

What is the “Preload”?

A
  • Frank-Starling:
  • End-diastolic volume on heart PRIOR to contraction (systole) determined the work load imposed by the ventricle muscle just prior to contraction;
  • SV is directly proportional to preload & contractility;
  • As EDV decreases the myocardial muscles are stretched leading to increased force of contraction
147
Q

What is the “Afterload”?

A
  • Mean arterial pressure that impedes ejection from ventricle that is imposed on the ventricles after contraction has begun;
  • SV= (alpha)(1/afterload)
148
Q

What is the Ejection Fraction?

A

= SV/ EDV;

-Normally is 60%; useful clinical diagnostic tool

149
Q

What is the Frank-Starling Law of the Heart?

A
  • States that strength of ventricular contraction varies directly with EDV
  • Is an intrinsic property of myocardium;
  • As EDV increases, myocardium is stretched more, causing greater contraction & SV — actin and myosin interact more allowing more force development
150
Q

What is the EXTRINSIC Control of of Contractibility for regulation of Stroke Volume?

A
  • At any given EDV, contraction depends upon level of SYMPATHOADRENAL ACTIVITY;
  • NE & Epi produce an increase in HR & contraction (positive inotropic effect)
  • Due to increased Ca2+ in sarcomeres;
151
Q

What is the Sympathoadrenal System?

A
  • Sympathetic = norepinephrine;
  • Arenal medulla = epinephrine and norepinephrine;
  • Cathecholamines = increase in contraction strength — positive isotropic effect of cathecholamines
152
Q

What is the Venous Return?

A

-Is return of blood to heart via veins
-Controls EDV & thus SV & CO
Dependent on:
1. Blood volume & venous pressure
2. Vasoconstriction caused by Symp
3. Skeletal muscle pumps
Pressure drop during inhalation

153
Q

What affects the Venous Return?

A

The end-diastolic volume and thus the stroke volume and cardiac output is controlled by factors that affect the venous return of blood to the heart;

  • Rate at which the atria are filled with venous blood depends on the:
    1. Venous blood pressure
    2. Blood volume – Total blood volume = 5.5 liters
154
Q

Blood within the VEINS

A
  • Veins hold most of blood in body (70%) & are thus called CAPACITANCE VESSELS = Have thin walls & stretch easily to accommodate more blood without increased pressure (=higher compliance)
  • Have only 0-10 mm Hg pressure
155
Q

What are the regulators of the Venous Return to the Heart?

A
  1. Sympathetic nerve activity — vasoconstriction;
  2. Skeletal muscle pumps w/ one way valves;
  3. Pressure difference b/w thoraces (chest) and abdominal cavity
156
Q

What is the effect of Blood Volume?

A
  • EDV and thus SV and Cardiac Output are influenced by Blood Volume;
  • Total = 5.5L (amount to be circulated);
  • Determined by:
    1. Steady state distribution of water
    2. Flux of water per day
157
Q

Water Distribution in the Body

A
  • Blood constitutes small fraction of total body fluid;
  • 2/3 (66%) of body H20 is inside cells = INTRACELLULAR — 27-30L;
  • 1/3 (34%) total body H20 is in extracellular compartment = 80% (11-13L) of this is interstitial fluid and 20% (3-3.5L)is blood plasma
158
Q

What is the Flux of water per day?

A 
Influx = drink, metabolic, and food — 1.5-2.5L/day;
Efflux = Water Loss:
-Kidneys - 0.6-1.5L
-Lungs - 0.3-0.4L
-Skin/glans - 0.2-1L
-Feces - 0.1-0.2L
159
Q

What is Transcapillary Fluid Exchange or Dynamic Equilibrium?

A
  • Occurs across the capillary beds;
  • Driven by a DROP in BP;
  • Fluid leaves the capillaries at the arteriolar end
  • Some fluid returns to the capillaries at the venuolar end
  • Some excess fluid returns via the LYMPH drainage
  • If there is too much excess interstitial fluid EDEMA results
160
Q

What is Hydrostatic Pressure?

A 
(Classical Treatment of Exchange)
-Forces fluid from high to low pressure;
-Pushing and pulling of fluid;
1. Blood pressure — OUT of capillary
= Arteriolar end – 30 mm Hg (high to…)
= Venuolar end – 10 mm Hg (…low)
161
Q

What is the Interstitial Fluid Pressure?

A
  • Interstitial fluid pressure – OUT of capillaries;

- Draws fluid into the interstitial fluid compartment = 5.3 mm Hg out

162
Q

What is the Net Hydrostatic Pressure?

A
  • Arteriolar end – 35.3 mm Hg out;

- Venuolar end – 15.3 mm Hg out

163
Q

What is Colloidal Osmotic Pressure?

A
  • Due to plasma proteins;
  • Draws fluid toward that compartment;
    1. Plasma = 6-8g/100ml = 28mm Hg into capillary
    2. Interstitial = 2g/100 ml = 6 mm Hg out of capillary
    3. Net = 22 mm Hg into plasma
164
Q

What are the Overall Pressure Changes for Transcapillary Exchange (Dynamic Equilibrium)?

A
  1. Arteriolar end – 35.3 mm out – 22 mmHg in = 13.3 mm Hg out
  2. Venuolar end -15.3 mm Hg out – 22 mm Hg in = 6.7 mm Hg in
165
Q

What is the Overall Fluid Movement per day?

A
  • 20 L filtered out of capillaries per day
  • 18 L returned to capillaries per day
  • 2 L returned via the lymphatic vessels
166
Q

What are the functions of the Lymphatic System?

A
  1. Transports interstitial fluid (lymph) back to blood through the lymph capillaries;
  2. Transports absorbed fat from small intestine to blood - chylomicrons
  3. Helps provide immunological defenses against pathogens
167
Q

What are the Lymphatic Capillaries?

A
  • Lymphatic capillaries are closed-end tubes that form vast networks in intercellular spaces = Very porous, absorb proteins, microorganisms, fat;
  • Lymph is carried from lymph capillaries to lymph ducts to lymph nodes
168
Q

What is the function of the Lymph Nodes?

A
  • Lymph nodes filter lymph before returning it to veins via thoracic duct or right lymphatic duct;
  • Nodes make lymphocytes & contain phagocytic cells that remove pathogens;
  • Lymphocytes also made in tonsils, spleen, thymus
169
Q

How is the movement of Lymph (fluid) accomplished?

A

Lymph movement is accomplished by:

  1. One-way valves
  2. Muscle pumps
  3. Contractile vessels
170
Q

What is Edema and its causes?

A
  • Excessive accumulation of interstitial fluid;
  • Causes of edema =
    1. High blood pressure or venous obstruction
    2. Leakage of plasma proteins into interstitial fluid – inflammation or tissue allergic reaction
    3. Decreased plasma protein concentration
  • Liver disease
  • Kidney disease
  • Third degree burns
    4. Pregnancy
    5. Obstruction of lymphatic drainage - elephantiasis (Wucheraria bancrofti round worm from mosquitoes)
171
Q

What regulates the Blood Volume by the Kidneys?

A
  1. Glomerular filtration rate = in man =125 mls/min = 180 L/day
  2. In woman = 115 mls/min
  3. Glomerular filtrate fluid is plasma ULTRAFILTRATE:
    - Blood volume = 5.5 L
    - Plasma volume = 3-3.5 L
    - Cells = 2 – 2.5 L
    * *98 > 99% of the plasma is filtered into the nephrons and reabsorbed back into the blood
    - 0.6 – 1.5 L is lost as urine
172
Q

How is Urine formed from the filtered plasma?

A
  • Urine formation begins with filtration of plasma in the GLOMERULUS;
  • Filtrate passes through & is modified by the nephron (kidney);
  • Volume of urine excreted can be varied by changes in REABSORPTION of the filtrate = Adjusted according to needs of body by action of HORMONES
173
Q

What are the 4 hormones that regulate blood volume?

A

Similar to autoregulation of glomerular filtration rate (Excretory System)

  1. Antidiuretic Hormone (ADH);
  2. Aldosterone;
  3. Renin-Angiostensin System;
  4. Atrial Natiuretic Peptide (ANP)
174
Q

Antidiuretic Hormone (ADH)

A
  • ADH is synthesized by neurons in the HYPOTHALAMUS and transported within axons to the posterior pituitary gland (neurohypophysis);
  • Released into the blood when OSMORECEPTORS in the hypothalamus detect an INCREASE in plasma osmolality due to:
    1. Dehydration
    2. Excessive salt intake;
  • Inhibited by LOW osmolality
175
Q

Mode of Action of ADH

A

**Target tissue of ADH = collecting duct - AQUAPORINS → H2O reabsorption into circulation

176
Q

Aldosterone

A
  • Steroid hormone secreted by the ADRENAL CORTEX which stimulates the active reabsorption of Na+ from the kidneys with Cl- following it electronically;
  • Indirectly promotes the osmotic reabsorption of H2O by the ADH mechanism
  • Secretion of aldosterone is stimulated by SALT DEPRIVATION AS a consequence of an intermediate mechanism known as the Renin- Angiotensin system
177
Q

Renin Angiotensin System

A

-REDUCED blood flow and pressure or REDUCED Na+ concentration in the renal artery causes Release of renin from the JUXTAGLOMERULAR APPARATUS of the nephrons;

178
Q

Mode of Action of the Renin Angio System

A
  1. Renin converts angiotensinogen → angiotensin I (10 AA long)’;
  2. Angiotensin Converting Enzyme in the lungs alters angiotensin I →angiotensin II ( 8 AA long) due to a SALT DEFICIT:
  3. Angiotensin II → adrenal cortex where it stimulates the release of ALDOSTERONE and increased peripheral resistance of the efferent arterioles;
    - Raises BP by Vasoconstriction, aldosterone secretion, thirst, increased GFR
179
Q

Atrial Naturetic Peptide (ANP)

A
  • 28 AA peptide that is released from the ATRIA of the heart in response to stretching from increased blood volume;
  • ANP acts as a ENDOGENOUS DIURETIC by lowering blood volume through Na+ secretion at the glomeruli to reduce BP;
  • Expanded blood volume is detected by stretch receptors in left atrium & causes release of ANP;
  • Inhibits aldosterone, promoting salt & water excretion to lower blood volume
  • Promotes vasodilation
180
Q

What Circulatory changes take place during exercise?

A
  • At beginning of exercise, Symp activity causes VASODILATION of certain vascular beds via Epi & ACh release;
  • Blood flow is shunted away from periphery & visceral organs to active skeletal muscles — 20x increase;
  • Blood flow to BRAIN stays same;
  • As exercise continues, intrinsic (Frank-Starling) regulation is major vasodilator;
  • Symp effects cause SV & CO to increase = HR & ejection fraction increases vascular resistance
181
Q

What are the changes in cardiac output due to exercise?

A
  • Cardiac output is 5-6 L/min = REST, but it is not distributed equally to different organs
  • Cardiac output INCREASES 5-6 fold during exercise to 25 – 30 L/min.
  • Most of the increase in cardiac output during exercise goes to skeletal muscles (20x increase) and the heart (5x increase)
182
Q

Organ Blood Flow Changes due to Exercise

A
  1. Skeletal at rest = 21%, exercise = 80-85%;
  2. Heart at rest = 4%, exercise = 5%;
  3. Brain at rest = 13%, exercise = 4%;
  4. GI and liver at rest = 24%, exercise = 4%
183
Q

Cardiac Output in a Marathoner vs. Non-athlete

A 
REST:
-Non-Ath: SV = 75; HR = 75;
-Marathoner: SV = 105; HR = 50
MAX EX.:
-Non-Ath: SV = 110; HR = 1956;
-Marathoner: SV = 162; HR = 185
184
Q

How does MUSCLE BLOOD FLOW change at max exercise?

A
  • Resting blood flow – 3.6 ml O2/ 100g muscle/min
  • Maximal exercise – 90 ml O2/ 100g muscle/min
  • *25X INCREASE in O2 delivery to the muscles
185
Q

What is Vascular Resistance to Blood Flow?

A

Determines how much blood flows through a tissue or organ

  • VASODILATION decreases resistance, increases blood flow;
  • VASOCONSTRICTION does opposite
186
Q

What is the Physical Law Describing Blood Flow (Qualitative)?

A
  • Blood flow% = (α)P1 –P2/ Resistance;
  • Blood flows through vascular system when there is pressure difference (DP) at its two ends ;
  • Flow rate is directly proportional to difference (DP = P1 - P2)
187
Q

What is the Poiseuille – Hagan Equation?

A 
*Quantitative;
{Vb = ∆Pπr4/8nL}
Where:
Vb = blood flow rate
∆P = pressure difference
r    = vessel radius
n   = blood viscosity
L   = vessel length
 π =  3.1416
188
Q

What is the Peripheral Resistance of Blood Flow?

A

Resistance = Peripheral Resistance;
-Directly proportional to L and n
-Inversely proportional to r4
Peripheral resistance {(α)Ln/r4}

189
Q

How does size of the vessel effect the Peripheral Resistance?

A
  • If one vessel has twice the radius of another, and if all other factors are the same, flow in the larger vessel would be 16 x greater than in the smaller vessel (r4)
  • Doesn’t apply to arteries – flow is turbulent;
  • Changes in vascular resistance = mostly in small arteries and arterioles
190
Q

What is Total Peripheral Resistance?

A
  • Total peripheral resistance is the SUM of all of the vascular resistances within the systemic or pulmonary circuits (mostly muscular arteries/arterioles);
  • Changes in resistance within one organ directly effects blood flow to only that organ if the resistance to all other organs remains constant
  • **Regional distribution of blood flow is controlled in large part by changes in peripheral resistance to blood flow
191
Q

What is the EXTRINSIC Regulation of Blood Flow?

A
  • SYMPATHOADRENAL ACTIVATION CAUSES increased CO & resistance in periphery & viscera;
  • Blood flow to skeletal muscles is INCREASED
  • Because their arterioles dilate in response to Epi & their Symp fibers release ACh which also dilates their arterioles;
  • Thus blood is shunted AWAY from visceral & skin to muscles
192
Q

How is the heart mostly AEROBIC?

A
  • Heart (& brain) must receive adequate blood supply at all times;
  • Heart is most aerobic tissue–each myocardial cell is within 10 µm of capillary
  • Lots of mitochondria & aerobic enzymes;
  • During SYSTOLE, coronary vessels are occluded;
  • Heart gets around this by having lots of MYOGLOBIN = 02 storage molecule that releases 02 to heart during systole
193
Q

Blood Pressure

A
  • *Variations in the radius of the arterioles simultaneously affects blood flow through the capillaries and the upstream systemic arterial pressure;
  • Blood pressure is routinely determined with a SPHYGMOMANOMETER
194
Q

BP Regulation by the Arterioles

A
  • Arterioles play role in blood distribution & control of BP;
  • Blood flow to capillaries & BP is controlled by aperture of arterioles ;
  • BP in the medium and large arteries is INCREASED;
  • Capillary BP is decreased because they are DOWNSTREAM of high resistance arterioles;
  • Capillary BP is also low because of large total cross-sectional area
195
Q

What controls Blood Pressure?

A
  • Mainly by HR, SV, & peripheral resistance;
  • INCREASE in any of these = increased BP;
  • Sympathoadrenal activity raises BP by arteriole vasoconstriction & by increased CO;
  • Kidney plays role in BP by regulating blood volume & thus stroke volume
196
Q

How doe the Kidneys (renal) regulate Blood Pressure?

A
  • Controlled by sensory impulses to the Medulla Oblongata from BARORECEPTORS in the circulatory system;
  • Autonomic innervation of the heart’s pacemaker system and smooth muscles controlling arteriole radius
197
Q

What is the Baroreptor Reflex?

A

-Activated by changes in BP
Which is detected by baroreceptors (stretch receptors) located in aortic arch & carotid sinuses;
-Increase in BP causes walls to stretch, increasing frequency of APs;
-Baroreceptors send APs to vasomotor & cardiac control centers in medulla;
-Is most sensitive to decrease & sudden changes in BP

198
Q

What are Atrial Stretch Receptors?

A
  • Activated by increased venous return & act to reduce BP;
  • Stimulate reflex TACHYCARDIA (increase in HR);
  • Inhibit ADH release & promote secretion of ANP
199
Q

How is BP Measured?

A
  • AUSCULTATION (to examine by listening);
  • No sound is heard during laminar flow (normal, quiet, smooth blood flow);
  • KOROTKOFF SOUNDS can be heard when sphygmomanometer cuff pressure is greater than diastolic but lower than systolic pressure
200
Q

How does the BP cuff generate sound?

A
  1. Blood pressure cuff is inflated above systolic pressure, occluding artery
  2. As cuff pressure is lowered, blood flows only when systolic pressure is above cuff pressure, producing Korotkoff sounds
  3. Sounds are heard until cuff pressure equals diastolic pressure, causing sounds to disappear
201
Q

What it HTN?

A
  • BP in EXCESS of the normal range for the persons age and sex;
  • Borderline pressure = 140/90
  • Severe hypertension can produce pressures of 250/130-150;
  • HTN effects 20% of the adults in the U.S.

Spring 2014 (22 decks)

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