Pathophysiology Exam #1 Flashcards

Question

These finger-like projections are found in all 4 chambers of the heart but especially the left ventricle. They are responsible for creating turbulence of blood flow within the chambers; keeps the blood from clotting. Another theory is they also if the chamber of the heart was smooth, when it contracted, that smooth wall would actually collapse in on itself; gives the walls a structure/ function that does not allow them to collapse onto itself during contraction

Answer 1

TRABECULAE CARNEAE

Answer 2

- fibrous pericardium | - serious pericardium

Answer 3

Fibrous pericardium is on the outer portion of the parietal pericardium and that is connective tissues that anchors the heart to adjacent structures

Answer 4

The parietal pericardium and the visceral pericardium

Answer 5

It is the outside layer of the serious pericardium that the fibrous pericardium attaches to. o Both the visceral and parietal pericardium are SEROUS pericardium § meaning they secrete a serous fluid into the pericardial cavity § normally there is only 15-20 mL of serous fluid in the pericardial cavity

Answer 6

that is the pericardial membrane that is directly attached to the heart; inseparable to the heart o When that visceral pericardium gets up to the great vessels it turns outward on itself and becomes the parietal pericardium o Both the visceral and parietal pericardium are SEROUS pericardium § meaning they secrete a serous fluid into the pericardial cavity § normally there is only 15-20 mL of serous fluid in the pericardial cavity

Answer 7

PERICARDIAL CAVTIY or PERICARDIAL SPACE

Answer 8

v that very thin layer of serous fluid allows for the pericardial membranes to glide over each other during systole and diastole o Both the visceral and parietal pericardium are SEROUS pericardium § meaning they secrete a serous fluid into the pericardial cavity

Answer 9

15-20 mls;so if you think about the heart being about the size of a human fist, that is a very thin layer of fluid surrounding the heart

Answer 10

pericarditis

Answer 11

o Infectious: such as microorganisms, bacterial, viral, and fungi o Non-infectious: idiopathic/ I don’t know why they have it, pericarditis

Answer 12

- pericardial friction rub(grating sound (two pieces of sand paper rubbing together) - Best heard over the 5th intercostal space, L sternal border

Answer 13

o MI = constant pain, radiating to the shoulder or arm, pressure pain or elephant on chest o Pericarditis = very sharp pain, varies with inspiration/ expiration, with no radiating pain to arm

Answer 14

- excessive amount of fluid within the pericardial cavity/ space - When you have pericarditis, that increases the capillary permeability in the pericardial membranes, with increase permeability, excess fluid gets within the pericardial cavity/ space; which causes a pericardial effusion

Answer 15

o At some point when the heart cannot compensate anymore and there are CV manifestations, from the pericardial effusions; this is when it becomes a cardiac tamponade o So if someone has a pericardial effusion that has accumulated over a long period of time; they are able to compensate o If that fluid accumulates very rapidly, they cannot compensate and develop cardiac tamponade

Answer 16

* “Full, Fast, Forward” * Fixed Stroke Volume 1. Avoid bradycardia 2. Avoid vasodilators 3. Optimize volume status to maximize LV filling 4. Maintain sympathetic tone 5. Spontaneous ventilation

Answer 17

- Run the risk of venodilation that will decrease preload | - Preload is everything in these cases

Answer 18

-Preload is already compromised -Positive pressure ventilation increases intrathoracic pressure that decreases preload even more and have profound cardiovascular collapse

Answer 19

CVP and R atrial pressure are not equal; there has to be a pressure gradient to move from the vena cava to the R atrium

Answer 20

The tricuspid valve

Answer 21

• The coronary sinus empties deoxygenated blood from the myocardium to the R atrium • As volume increases in the R atrium, pressure increase s/t the volume increase; at this point tricuspid valve is closed • At a certain point, R atrial pressure is higher than the R ventricle pressure; at this point the tricuspid valve leaflets open d/t the pressure gradient

Answer 22

* Blood moves with the pressure gradient from the R atrium to the R ventricle * As volume increases, pressure increases, causing the closure of the tricuspid valves * THE PRESSURE GRADIENT CLOSES THE TRICUSPID VALVE LEAFLETS

Answer 23

• At some point, the R ventricle goes into systole, increasing the pressure even more • When the R ventricle pressure becomes greater than the pulmonary artery pressure, this opens the pulmonic valve leaflets and blood is ejected into the pulmonary artery.

Answer 24

When the pulmonary artery pressure becomes greater than R ventricle pressure, this closes the pulmonic valve

Answer 25

Blood is then oxygenated and delivered back to the L side of the heart via the pulmonic veins

Answer 26

NOTICE that there are NOT any valves between the pulm veins and the L atrium; blood is continually flowing into the L atrium

Answer 27

-As volume increases in the L atrium, the pressure increases; this opens the mitral valve s/t the pressure gradient in the L atrium/ L ventricle -Blood flows into the L ventricle s/t the pressure gradient; as the volume increases in the L ventricle, so does the pressure

Answer 28

- Pressure in the L ventricle closes the mitral valve, creating even more pressure in the L ventricle - The L ventricle eventually goes into systole (which increases the pressure even more)

Answer 29

- The L ventricle eventually goes into systole (which increases the pressure even more) - When L ventricle pressure is greater than aortic pressure, this opens the aortic valve - When the pressure in the aorta is greater than the L ventricle, this closes the aortic valve leaflets

Answer 30

pressure gradient

Answer 31

~75% of preload

Answer 32

atrial kick; 75% WITH THE PRESSURE GRADIENT; THEN THE LAST 25% FROM ATRIAL SYSTOLE

Answer 33

CHORDAE TENDINEAE

Answer 34

-PREVENTS RETROGRADE BLOOD FLOW FROM RV INTO RA -The chordae tendineae are attached to papillary muscles; those papillary muscles are continuous with the myocardium of the RV • Since the papillary muscles are continuous with the myocardium of the RV; those papillary muscles contract along with the RV • When they contract, those papillary muscles shorten; and when they shorten that pulls the chordae tendineae downward and tight, which holds the tricuspid valve leaflets closed • And that prevents retrograde blood flow from RV into RA

Answer 35

No chordae tendineae or papillary muscles | associated with pulmonic or aortic valve leaflets

Answer 36

L side same as R side: PRESSURE GRADIENT = 75% and ATRIAL SYSTOLE = 25%

Answer 37

-You would lose that 25% contribution § Most people could compensate with a lose of 25% decrease in preload; but if that person were to exercise, that is when you would see CV manifestations/ complications

Answer 38

REGURGITATION § That’s why people that have had a MI have regurgitation; because those papillary muscles do not function properly

Answer 39

LA pressure

Answer 40

• Heart sounds are caused when the valve leaflets close and the blood bounces off the valve leaflets causing turbulence of the blood flow • That turbulence of blood flow causes vibrations which is transmitted to the chest wall

Answer 41

Aortic--->Pulmonic Tricuspid---->Mitral(bicuspid) *All Puppies Take Mild*

Answer 42

2nd intercostal space (ICS), R sternal border

Answer 43

§ Start at the sternal notch til you find the manubrium; where the manubrium attaches to the sternum is the angle of Louis § From the angle of Louis, move your finger over and if your on a rib then move down one; if you are in an ICS, then that is the 2nd ICS

Answer 44

2nd ICS, L sternal border

Answer 45

5th ICS, L sternal border

Answer 46

5th ICS, L midclavicular line

Answer 47

Echocardiography

Answer 48

MS ARD: - Mitral valve stenosis - Aortic valve regurge ``` o Tricuspid valve stenosis o Mitral valve stenosis o Aortic valve regurgitation (murmur often not heard during auscultation; loudest point may be aortic area or along lower left sternal border) o Pulmonic valve regurgitation ```

Answer 49

MR ASS: - Mitral valve regurge - Aortic valve stenosis o Aortic valve stenosis o Pulmonic valve stenosis o Tricuspid valve regurgitation o Mitral valve regurgitation

Answer 50

o During ventricular diastole, mitral and tricuspid valves should be open § SO if the tricuspid valve should be open and we hear a diastolic murmur at the tricuspid valve auscultatory area during ventricular diastole; that would be indicative of a tricuspid valve stenosis. § Cause that valve should be open and blood flow should be easy from the atria to the ventricle § Same thing with mitral valve stenosis; if we hear a murmur (over the 5th ICS, midclavicular line) during vent diastole, that would be indicative of a mitral valve stenosis § During ventricular diastole, aortic and pulmonic valves should be closed; so if you hear a murmur at the aortic or pulmonic auscultatory area during diastole, that is indicative of an aortic/ pulmonic valve regurgitation or aortic/ pulmonic valve incompetence (you will hear it both ways) § Aortic valve regurg is often not heard during auscultation and the loudest point may actually be at the aortic area or along the lower L sternal border

Answer 51

o During systole, the aortic and pulmonic valves should be open. o If you hear a murmur at the aortic/ pulmonic valve auscultatory area during systole; that would be indicative of aortic/ pulmonic valve stenosis o Mitral and tricuspid valves should be closed = mitral/ tricuspid regurg

Answer 52

- aorta | - left ventricle

Answer 53

-diastole § When the ventricle goes into systole, that places pressure and compresses against those arteries, arterioles and capillaries; which prevent perfusion § So most perfusion occurs during ventricular diastole; when those muscles are not contracting

Answer 54

- Epi/Norepi - Alpha - Beta

Answer 55

BETA; § Many more beta-2 receptors than alpha-1 receptors § However, in states of advanced shock, when you have an excessive amount of catecholamines (or an outpouring of catecholamines) that can cause activation and predomination of the alpha-1 receptors; which would cause coronary artery constriction that would eventually lead to coronary ischemia and myocardial infarction

Answer 56

Parasympathetic/vagal stimulation ?? o The coronary arteries may or may not, possibly, maybe, but not necessarily, have parasymp stimulation or innervation o If they do, it would be thru acetylcholine and muscarinic receptors; which would have a mild dilation of the coronary arteries o Acetylcholine and muscarinic receptors o Usually minimal effect; mild dilation

Answer 57

- CORONARY ARTERY BLOOD FLOW AND MYOCARDIAL PERFUSION CONTROLLED PRIMARILY BY RATE OF MYOCARDIAL O2 CONSUMPTION !!! - Any condition that increases myocardial O2 consumption causes reflex dilation of coronary arteries. - Resting state: ~ 75% of O2 extracted from coronary blood flow; A lot greater than other tissue; usually only extract about 25 – 30% of the O2 that passes by those tissues

Answer 58

dilate; E.G., Increased strength of contraction, increased afterload, increased preload (more blood coming back to the heart, more stretch on the cardiac fibers, leading to greater strength of contraction/ EF/ CO), and INCREASED HEART RATE

Answer 59

Give them a beta-blocker

Answer 60

1. increased CO2 2. increased H+/decreased pH 3. lactate 4. adenosine

Answer 61

o CO2 is a by-product of metabolism; the more metabolism, more CO2; the more those coronary vessels need to dilate to deliver O2 to those tissues o To remove excess CO2 from the tissue spaces

Answer 62

o Maybe an outcome of anaerobic metabolism, so we hope more blood, more O2 will convert it to aerobic metabolism o as veins dilate, this removes H+ ions and other acid by-products from the tissue spaces

Answer 63

o Lactate accumulation: lactate drops the pH down towards the acid side o Lactate is a by-product of anaerobic metabolism; with a desired effect of more blood, more O2 to convert back to aerobic metabolism

Answer 64

o ATP breaks down to ADP, then to AMP, all the way back down to adenosine o VERY potent vasodilator of coronary arteries

Answer 65

- coronary sulcus | - L and R ventricle posteriorly

Answer 66

- RCA | - L circumflex

Answer 67

L CORONARY ARTERY DOMINANT

Answer 68

Left main coronary (LMC)

Answer 69

- Left anterior descending (LAD) artery | - Left circumflex artery

Answer 70

toward the apex of the heart; that LAD artery is actually sitting right on top of the interventricular septum, between the RV and LV

Answer 71

Left circumflex artery which goes around the L lateral part of the heart and continues on to the posterior surface of the heart

Answer 72

So when I say that someone is RCA dominant, all that means is the PDA is a branch of the RCA; it has nothing to do with the amount of blood flow that the RCA delivers to the myocardium ***LEFT MAIN CORONARY ARTERY PERFUSES LARGEST PERCENTAGE OF MYOCARDIUM REGARDLESS OF RIGHT OR LEFT CORONARY ARTERY DOMINANCE****

Answer 73

LAD along with the left circumflex

Answer 74

Left circumflex

Answer 75

Left circumflex and RCA(PDA)

Answer 76

Left anterior descending and left circumflex

Answer 77

left circumflex

Answer 78

LAD and the Left circumflex

Answer 79

Left circumflex and RCA(PDA)

Answer 80

mechanical contractile | fibers

Answer 81

o Form electrical conduction system through heart o Initiate and conduct action potentials through heart and to mechanical contractile fibers o Action potentials transferred to contractile fibers and coupled with mechanical contraction o Electrical impulses (action potential) MUST precede mechanical contraction § e.g., PEA

Answer 82

Cardiac contractile fibers

Answer 83

attached to actin myofilaments

Answer 84

attached to the tropomyosin

Answer 85

strongly attached to calcium ions

Answer 86

Different from skeletal muscle fibers, cardiac contractile fibers have these intercalated disks between adjacent cardiac contractile fibers that form gap junctions § These gap junctions allow for free flow of ions from muscle fiber to adjacent muscle fiber or from sarcolemma to adjacent sarcolemma; which allows for the spread of AP directly from muscle fiber to muscle fiber v remember with skeletal muscle, each muscle fiber had to be innervated by a collateral of a somatic motor neuron v cardiac muscle fiber does not because of the intercalated disk and gap junctions that allow for free flow of ions; which allow AP to spread from muscle fiber to muscle fiber, so all those muscle fibers from within a unit will depolarize and contract at about the same time

Answer 87

v Those units within the heart are called functional syncytium; there are two functional syncytia

Answer 88

atrial syncytium (R & L) and ventricular syncytium (R & L)

Answer 89

§ Right and left atria § Right and left ventricles § Separation of atria and ventricles by fibrous tissue with openings for valves and pathway for electrical fibers so impulse can be conducted from atria to ventricles § So if they are syncytium, that means that they are a unit and that all of the muscle fibers within that unit become excited and contract at about the exact same time; that allows for more efficient ejection of blood § If those muscle fibers were all contracting at different times, that would not be synchronous and would not be conducive to an effective EF, SV, CO.

Answer 90

1. AP conducted along the muscle fiber 2. AP goes down the T-Tubule 3. Sitting adjacent to the T-tubule is the terminal cisterna of the sarcoplasmic reticulum; when that AP gets there, that excites the sarcoplasmic reticulum allowing for opening of voltage-gated Ca++ channels 4. Then release of Ca++ from the sarcoplasmic reticulum into the sarcoplasm 5. Ca++ from the EC fluid increases the sarcoplasmic Ca++ concentrations 6. that interacts with troponin C which pulls troponin T and tropomyosin away from the actin binding sites 7. Myosin heads can then power-stroke, crossbridge, and shorten the sarcomere; which shortens the muscle fiber

Answer 91

- Ca++ | - extracellular fluid

Answer 92

- sarcoplasm reticulum - EC *Changes in the EC fluid would have major implications on cardiac contractility*

Answer 93

o That obliqueness allows for more effective EF, SV, and CO o Think of it as an old stringed wet mop (more effective to twist and squeeze to wring out)

Answer 94

- mitochondria | - O2

Answer 95

1. Automaticity 2. Excitability 3. Conductivity *All electrical fibers have all 3 properties, BUT some fibers have more of one than the other properties*

Answer 96

it automatically generates APs

Answer 97

becomes excited in response to APs

Answer 98

rapidly conducts APs

Answer 99

- Located in the upper part of the RA; right were the superior vena cave meets the RA - Very small, less than 0.5 cm in diameter - composed of P-cells (pacemaker cells)

Answer 100

pacemaker cells primary property are | automaticity

Answer 101

- automatically generate APs | - 60– 100 times/ min

Answer 102

Those APs are then transmitted to the | atrial intermodal pathways

Answer 103

``` Atrial internodal pathways or tracts o Run thru the tissue of the RA and the internodal pathways are hopefully lying adjacent to mechanical contractile fibers; so you can have electrical/ mechanical coupling (RA can contract) • Interatrial branch of atrial internodal pathways o You also have an interatrial branch of the atrial internodal pathway which is transmitting APs/ conducting APs from the SA node to the LA o THE ATRIAL INTERNODAL PATHWAYS JOIN BACK TOGETHER TO FORM THE AV NODE ```

Answer 104

Located in the floor of the RA and is partly composed of T-cells (transition cells)

Answer 105

1. One of the functions of the AV node is to regulate the amount of APs that can be transmitted from the atria to the ventricles 2. Another function is that it causes a slight, slight slowing of the APs; which allows for the atria to contract right before the ventricles contract

Answer 106

If you had an atrial arrhythmia like Aflutter/ A-fib, your atria is contracting at 200x a minute; do you want all those APs to be transmitted to your ventricles, and your ventricles contracting 200x a min? Nope.

Answer 107

It slows that AP down just enough so that the atria can contract and contribute that last 25% to ventricular volume before the ventricle contracts

Answer 108

o Also has pacemaker cells; those pacemaker cells can automatically generate APs o However, it does not usually do that because the SA node generates APs at a faster rate; faster than any of the other pacemaker cells of the heart o So under normal conditions, the AV node P-cells are overridden because the SA node

Answer 109

-40 – 60 times/ min.

Answer 110

bundle of His

Answer 111

- superior portion of the inter ventricular septum | - R bundle branch and the L anterior/ posterior bundle branch

Answer 112

- interventricular septum - apex of the heart - Purkinje fibers

Answer 113

- interventricular septum | - anterior and lateral aspect of the LV

Answer 114

Left Posterior Bundle Branch

Answer 115

The LV has an anterior and a posterior bundle branch because the LV has a lot more muscle that needs to depolarize

Answer 116

o You have to think of this 3-dimensionally: 1. on the anterior aspect of the RV 2. on the lateral aspect of the RV 3. on the posterior aspect of the RV

Answer 117

The primary property of Purkinje fibers are conductivity; Purkinje fibers are very good at conducting APs

Answer 118

- mechanical contractile fibers | - effective myocardial contraction

Answer 119

* Resting membrane potential (RMP) is located at -85mV * Threshold potential (TP) is about -60mV; once TP is reached,depolarization occurs * Gets up to about +20-30 mV and IMMEDIATELY REPOLARIZATION occurs and brings the AP back down to resting

Answer 120

* RMP is at -85 – -90 mV; TP is about -60mV * Depolarization occurs with a SLOOOWWWWWW REPOLARIZATION PHASE @ ~ +20mV * Then finally it rapidly goes back down to resting

Answer 121

* Look at the time difference between the two; total time is about 0.2ms for a skeletal muscle AP and 500ms for cardiac muscle AP * Cardiac muscle AP has to be longer than skeletal muscle AP to allow for contraction -Cardiac muscle has a longer repolarization time because the muscle has to have time to contract • Mechanical contraction occurs during electrical repolarization • So if this repolarization phase was very short and then another AP were to occur, that cardiac muscle fiber would not have a long time to contract • You need a long repolarization phase to allow for mechanical contraction to occur

Answer 122

- Voltage gated Na+ channels are open - Volted gated K+ channels are closed - volted gated Ca+ begin to open

Answer 123

- Voltage gated Na+ channels close - Some voltage gated K+ open, causing early repolarization - -Voltage gated Ca+ are open, slowing down repolarization

Answer 124

- Voltage gated Ca+ channels close | - Voltage gated K+ are open

Answer 125

* RMP is about -90mV (the inside of the cell membrane is -90mV more negative than the outside of the cell membrane) * What contributes to the RMP negativity? K-leak channels, Na-leak channels, and Na-K pumps

Answer 126

o K-leak channels contribute the most to RMP | o Na-K pump: 3 Na out, 2 K in

Answer 127

A stimulus

Answer 128

voltage gated Na+ channels at threshold

Answer 129

- to rise in a less negative fashion | - -40 mV

Answer 130

EARLY PHASE 0 OF DEPOLARIZATION

Answer 131

impermeable to K; so almost NO outward movement of K

Answer 132

An initial stimulus causes an influx of Na § Once that got to TP (about -60mV), we have opening of voltage-gated Na channels; which causes the MP to rise upward in a less negative fashion. § Now were at about -40mV;

Answer 133

At -40mV we initiate LATE PHASE 0 OF DEPOLARIZATION; -40mV you have opening of the slow voltage-gated Ca-Na channels

Answer 134

You now have more cations entering into the cell which brings the MP (upward in a less negative fashion) all the way up to about +20mV § Now we have the fast voltage-gated Na channels open and the slow Ca-Na channels open v there called FAST channels because they open and close really fast v there called SLOW channels because they stay open for an prolonged period of time

Answer 135

By opening of the voltage-gated Ca-Na channels at -40mV

Answer 136

Now were at +20mV; we reversed the polarity of the inside of the cell and we are at PHASE 1 OF REPOLARIZATION

Answer 137

o At this point the fast voltage-gated Na channels have snapped shut at about +20mV o However, the slow voltage-gated Ca-Na channels remain open; we have less cations moving into the cell because of the voltage-gated Na channels closing o So the MP moves from about +20mV, down to zero mV (nether + or –) o Now at some point between 0mV and here (he never gave me a #) the K channels begin to reopen; so you have influx of Ca thru the slow Ca-Na channels and some outward movement of K at this point

Answer 138

Closure of the voltage-gated Na channels as well as (at some point) the K channels begin to open up(@ ~ +20 mV)

Answer 139

PHASE 2 OF REPOLARIZATION: this is called the plateau phase of repolarization; the longest phase of repolarization. o Now we have inward movement of Ca from the slow Ca channels; the K channels have completely opened and we have outward movement of K o There is an EQUAL movement of cations inward and outward; so the membrane remains at 0mV throughout phase 2

Answer 140

PHASE 3 OF REPOLARIZATION: the slow Ca-Na channels finally close while the K channels remain fully open o That leads to outward movement of cations and minimal inward movement of cations; so the MP rapidly becomes more negative (back down to RMP)

Answer 141

PHASE 4 OF REPOLARIZATION: Is just a resting phase between APs; movements of ions are the same as during the RMP

Answer 142

- AP | - Cardiac Muscle Contraction

Answer 143

-Heart requires flow of Ca++ into sarcoplasm from SARCOPLASMIC RETICULUM and from EC FLUID.

Answer 144

the cardiac AP

Answer 145

***NO VASOCONSTRICTORS*** 1. Think fluid status 2. Thing Ca++ administration

Answer 146

o Stroke volume variance (SVV): § The more optimized your fluid status is, the less variation you have in your SV from beat-to-beat § Normally you want your SVV less than 10%; the more HYPOvolemic your pt is, the more your SV varies § And the pt has to be on positive pressure ventilation for this to all work; because that positive pressure ventilation is what’s causing that SVV § So if your HYPOvolemic, think of your vena cava as a garden hose; empty = easier to compress § SO we use SVV to assess our patient’s hemodynamic fluid volume status

Answer 147

• IF your SVV indicates adequate volume status, look at your labs and think hypocalcemia • Labs indicate hypocalcemia, the next thing I am thinking is Ca administration • Benefits of calcium administration o Increased myocardial contractility o Calcium dependent exocytosis of neurotransmitter (often forgotten) § Think about those sympathetic postganglionic fibers; for NE to be released from the postganglionic symp fibers, you have to have sufficient amounts of CA in the EC fluid § If you don’t have enough Ca in the EC fluid, you’re not going to have a large enough gradient to drive the Ca from extracellular to intracellular; you are going to have a decrease release of catecholamines (NE) § That is another way that Ca administration can improve their BP when you can’t use vasopressors or if their volume status is already adequate

Answer 148

-threshold -early and late phase of depolarization, phase 1, 2 and most of 3 of repolarization

Answer 149

when the MP gets back to threshold is the end of | the ARP

Answer 150

RELATIVE REFRACTORY PERIOD (RRP) o During the RRP, you have to have an extra strong stimulus to initiate another AP

Answer 151

SUPER NORMAL REFRACTORY PERIOD (SNP) | o Only a mild stimulus will generate another AP

Answer 152

* ARP: Cell CAN NOT depolarize again regardless of the stimulus. * RRP: If an EXTRA STRONG stimulus is applied, depolarization might occur. * SNP: Only a MILD STIMULUS applied can cause depolarization.

Answer 153

``` • Voltage-gated (fast) Na+ channels are inactivated in pacemaker cells • However, pacemaker cells are very leaky to Na+ ions (causes slow rise in membrane potential towards threshold) ```

Answer 154

- approximately -40 mV | - opening of voltage-gated Ca-Na channels (which initiates depolarization).

Answer 155

* When MP reaches +20mV, Ca-Na channels close and K+ channels open (which initiates repolarization). * At the end of repolarization, K+ channels close and process starts again

Answer 156

• SA node: Normal pacemaker o Rate of AP generation: 60 – 100/min. o Overrides lower, slower potential pacemakers • AV node/junction o Inherent rate: 40 – 60/min. • Ventricular Purkinje fibers o Inherent rate: 15 – 40/min. • Ectopic pacemakers can occur anywhere in conduction system o People have to come and get ablations because of the ectopic pacemaker cell activity

Answer 157

• Defined as the cardiac events that occur from the beginning of one beat, to the beginning of the next beat

Answer 158

* The P wave represents ATRIAL DEPOLARIZATION | * It does not represent atrial muscle contraction

Answer 159

Remember that ELECTRICAL DEPOLARIZATION has to occur before mechanical contraction can occur

Answer 160

-T wave represents VENTRICULAR FIBER REPOLARIZATION; there is no visible atrial repolarization because it is lost in the QRS complex

Answer 161

QRS complex represents VENTRICULAR DEPOLARIZATION; not ventricular contraction • Ventricular systole or contraction occurs after electrical depolarization; T wave represents ventricular repolarization

Answer 162

o Starting with ventricular systole; the ventricle has contracted and has injected blood into the aorta which causes a sharp rise in aortic pressure (seen here in the waveform) o Then, when the aortic pressure is greater than the LV pressure, the aortic valve closes o And when that aortic valve closes, blood falls back onto the aortic valves d/t the arch of the aorta; causing a transient rise in aortic pressure (seen as the dicrotic notch) o Then the blood moves on into the systemic circulation and the pressure in the aorta will slowly eventually decrease

Answer 163

o Starting with atrial systole, that atrial kick will provide the final 25% of LV filling volume o When the atrial kick occurs it causes a small rise in LV pressure; when LV pressure is greater than LA pressure, the mitral valve will close o The mitral valve closes, and the aortic valve has not yet opened; but the LV starts going into systole o The pressure in the LV rises sharply because the size of that chamber gets smaller during systole and because the blood is not moving in or out (because the valves are closed)

Answer 164

o LA goes into systole which causes a rise in the LA pressure waveform o Then the mitral valve closes and the ventricle goes into systole; this causes the mitral valve leaflets to balloon up into the LA, causing the (c) wave in the LA pressure wave form § This ballooning up of the mitral valve leaflets helps prevent retrograde blood flow o There are no valves from the pulm veins and the LA; so blood will continue to flow into the LA and this causes a rise in pressure (which is responsible for the (v) wave) o When the pressure in the LA is greater than the LV, the mitral valve opens and the blood passively flows into the LV; supplying the LV with 75% of LV filling pressure

Answer 165

§ ISOVOLUMETRIC (isovolumic) CONTRACTION: the sharp rise in ventricular pressure before the aortic valve opens, with no change in volume

Answer 166

§ ISOVOLUMETRIC RELAXATION: when the LV size | increases (during diastole) without any increase in volume (from the LA

Answer 167

o Starting with atrial systole; provides the final 25% contribution; so the volume in the LV increases o The LV goes into systole and ejects blood; so the volume in the LV decreases o The aortic valve closes; then the mitral valve opens o Then the ventricle volume builds up passively from atria to ventricle (accounting for the 75% LV filling volume); then back to the atrial systole (atrial kick) for the last 25%

Answer 168

o Remember that the actual heart sounds are made from the turbulence of the blood when the valves close

Answer 169

o 1st heart sound (S1) is associated with events r/t the closure of the mitral and tricuspid valves (the AV valves)

Answer 170

o 2nd heart sound (S2) is associated with events r/t the closure of the aortic and pulmonic valves (semilunar valves)

Answer 171

1. Norepi and epi | 2. Beta 1

Answer 172

§ Norepi and epi from the POSTGANGLIONIC SYMP NERVOUS FIBERS AND THE ADRENAL MEDULLA

Answer 173

1. SA node: increased heart rate (positive chronotropic effect) (↑ permeability to Na+) 2, AV node: increased rate of transmission of those APs (positive dromotropic effect) 3. Ventricular contractile fibers: increased strength of contraction (positive inotropic effect)

Answer 174

Ø When beta−1 receptors are stimulated in the SA node; that increases the HR Ø Remember those p−cells are very leaky to Na; the way that beta−1 receptor activation works at the SA node is it actually increases the permeability of those cells to Na even more Ø So increase permeability to Na, more Na influx; so RMP potential will be reached quicker because that Na will be more permeable and the influx Ø Faster rate of upstroke means more depolarizations; more depolarizations per unit time = faster HR

Answer 175

AV node: increased rate of transmission of those APs (positive dromotropic effect)

Answer 176

v Ventricular contractile fibers: increased strength of contraction (positive inotropic effect)

Answer 177

§ The overall effect of the SNS on the heart is to increase the cardiac output (CO) § Strong SNS stimulation can increase CO up to 100%

Answer 178

the Vagus nerve?

Answer 179

- ten - Acetylcholine - Acts on Muscarinic receptors of the heart; primarily at the SA node:

Answer 180

SA node: decreased heart rate (negative chronotropic effect):

Answer 181

AV node: decreased rate of transmission (negative dromotropic effect)

Answer 182

Ventricular contractile fibers: decreased strength of contraction (negative inotropic effect)

Answer 183

Overall effect of PNS: decreased CO

Answer 184

PRIMARY PNS effect on heart (↑ permeability of those cells to K+, hyperpolarization)

Answer 185

v SA node: decreased heart rate (negative chronotropic effect): PRIMARY PNS effect on heart (↑ permeability of those cells to K+, hyperpolarization) Ø RMP of the p−cell is about –55 to –60mV Ø Those cells become more permeable to K; moves K from inside the cell to outside Ø Hyperpolarizes the cell membrane; so instead of −55mV, RMP is moved further down to about −65mV Ø Making it harder to reach threshold; slows the rate of upstroke of depolarization Ø When it takes longer to get there, that means less depolarizations over time; which will decrease the heart rate

Answer 186

- left ventricle | - venous return

Answer 187

Stretch of LV depends on volume of blood that enters during diastole o Within physiologic limits, the greater the diastolic filling volume, the greater the stretch, the stronger the contraction, the greater the systolic SV, and the greater the CO

Answer 188

• On the horizontal axis you have the atrial pressure (mm Hg); primarily determined by VOLUME • On the vertical axis you have ventricular output (L/min) • As you can see on the atrial pressure axis, up until zero, there is no CO • From 0 to +8 (on the atrial pressure axis) there is a more linear relationship • More pressure = greater ventricular output • When we get to 8 mm Hg, there is a plateau; so once the ventricles get to a certain point, giving more fluid WILL NOT HELP

Answer 189

* If you extend this curve out to about 18–22 mm HG, it starts to curve down * The ventricular fibers are over extended, thus decreasing CO

Answer 190

o Optimal volume = optimal stretch = optimal strength of contraction = optimal EF/ CO § Optimal volume status allows for optimal actin–myosin myofilaments interaction

Answer 191

o Increased volume = over stretched § Ventricular contractile fibers pulled apart and the sarcomeres are elongated; the actin and myosin myofilaments are to far apart to interact with each other; causing sub−optimal: v interaction with one another v strength of contraction v length of contraction v SV, EF, and CO

Answer 192

``` o Decreased volume = under stretched § Actin and myosin myofilaments are overlapping each other; causing sub–optimal: v interaction with one another v strength of contraction v length of contraction v SV, EF, and CO ```

Answer 193

* MEAN ARTERIAL PRESSURE = CARDIAC OUTPUT x TOTAL PERIPHERAL RESISTANCE * MAP = CO x TPR

Answer 194

CO = is the amount of blood ejected from the LV each minute o traditionally expressed in L/min o CO = HR x SV

Answer 195

§ HR and SV are affected by theANS § SNS increases HR & SV § PNS decreases HR § However, if your HR is 115−120/min; is that really going to increase your CO? NO! Not enough time for ventricular filling § SV is affected by LVEDV (preload); which is determined by the atrial volume or pressure in the vascular system § Venous return: affected by the overall blood volume and skeletal muscle pump § Sympathetic tone of the veins also affects CO

Answer 196

- Arteriolar diameter (most influential determinant of TPR vs. blood viscosity) - Blood viscosity is determined by our hematocrit (actual formed cells in the blood)

Answer 197

v Mainly the small and medium sized arteries and arterioles that have the ability to dilate and constrict, based on the amount of sympathetic tone that they have v i.e., constriction = é TPR… and vice versa

Answer 198

v Hematocrit Ø # RBCs (most abundant and biggest contributor to blood viscosity) Ø WBCs Ø Platelets v Pt’s with polycythemia often have LV hypertrophy because chronically elevated TPR because blood viscosity is up v With decreased RBC/ if your anemic, decreased HCT, decreased blood viscosity, decreased TPR

Answer 199

``` -USED TO CALCULATE CARDIA INDEX • Surface area of body. • Based on weight and height. • Expressed in square meters. • Data usually obtained from nomograms. • AVERAGE FOR 70-KG MAN: 1.73 M2 ```

Answer 200

• Volume in the left ventricle at the end of diastolic filling and available to be ejected during the next left ventricular contraction. • Determined by venous return to the heart and degree of stretch of left ventricular myocardial cells. o Increased venous return increases LVEDV and compliant myocardium allows for maximal filling. • LVEDV determines LVEDP, degree of ventricular stretch, and strength of the next systolic contraction, as stated by the Frank-Starling Law of the Heart. • NORMAL: 70 ml/m2; average 120 ml.

Answer 201

LEFT VENTRICULAR STROKE VOLUME (LVSV) • Volume ejected from the left ventricle during each left ventricular contraction. • Changes based on strength of contraction and LVEDV. • FORMULA: LVSV = CO/HR • NORMAL: 60 – 100 ml/beat

Answer 202

* Percentage of the LVEDV/preload that is ejected from the left ventricle during each contraction. * Changes based on strength of contraction and LVEDV. * FORMULA: LVEF = LVSV/LVEDV * NORMAL: 55 – 65%

Answer 203

LEFT VENTRICULAR END SYSTOLIC VOLUME (LVESV) • Volume remaining in the left ventricle after a left ventricular stroke volume is ejected. • Changes based on strength of contraction, LVEF, and LVSV. • FORMULA: LVESV = LVEDV – LVSV

Answer 204

* Resistance to flow of blood from left ventricle during contraction. * Determined by blood viscosity and SYSTEMIC VASCULAR RESISTANCE (PRIMARY DETERMINANT). * Often used interchangeably with systemic vascular resistance (see below).

Answer 205

* Pressure in the right atrium. * Determined by venous return and degree of emptying of the right atrium. * NORMAL: 2 – 8 mmHg (2 – 6 cm H2O)

Answer 206

CENTRAL VENOUS PRESSURE (CVP) • Pressure in the inferior or superior vena cava just before they join with the right atrium. • OFTEN USED SYNONYMOUSLY WITH RAP. • NORMAL: 2 – 8 mmHg (2 – 6 cm H2O)

Answer 207

``` CARDIAC OUTPUT (CO) • The volume in liters ejected by the left ventricle into the systemic circulation each minute. • FORMULA: CO = HEART RATE (HR) x LVSV • NORMAL: 4 – 8 L/MIN ```

Answer 208

CARDIAC INDEX (CI) • Cardiac output correlated with body surface area. • FORMULA: CI = CO/BSA • NORMAL: 2.5 – 4 L/min/m2

Answer 209

``` SYSTEMIC BLOOD PRESSURE • The pressure exerted on the systemic arteriolar vessels during systole (SBP) and diastole (DBP). • FORMULA: BP = CO x AFTERLOAD • NORMAL: 100 – 140/60 - 90 mmHg ```

Answer 210

PULSE PRESSURE • The difference between the systolic blood pressure (SBP) and the diastolic blood pressure (DBP) • FORMULA: PULSE PRESSURE = SBP – DBP • NORMAL: ~ 40 mmHg

Answer 211

MEAN ARTERIAL PRESSURE (MAP) • The mean or average of the systemic systolic and diastolic blood pressures. • FORMULA: MAP = SBP – DBP + DBP or 1/3(PP) + DBP 3 • NORMAL: 70 – 105 mmHg

Answer 212

SYSTEMIC VASCULAR RESISTANCE (SVR) • A major component of afterload or the resistance in the systemic arteriolar vessels that must be overcome during left ventricular contraction to eject blood into the systemic arteriolar vessels. • FORMULA: SVR = (MAP – RAP) x 80/ CO • NORMAL: 800 – 1200 dynes/sec/cm5 or 800 – 1200 dynes x sec-1 x cm-5

Answer 213

SYSTEMIC VASCULAR RESISTANCE INDEX (SVRI) • Systemic vascular resistance correlated with body surface area. • FORMULA: SVRI = MAP – RAP x 80/CI • NORMAL: 1970 -- 2400 dynes/sec/cm5/m2 or 1970 – 2400 dynes x sec-1 x cm-5/m2

Answer 214

PULMONARY ARTERY PRESSURE (PAP) • Systolic (SPAP) and diastolic (DPAP) pressures in the pulmonary artery. • Determined by right ventricular output (RVO) and pulmonary vascular resistance (PVR) (see below) and downstream pressure (e.g., pulmonary hypertension, increased left atrial pressure, mitral valve stenosis). • FORMULA: PAP = RVO x PVR • NORMAL: 15 – 30/8 – 15 mmHg

Answer 215

``` MEAN PULMONARY ARTERY PRESSURE (MPAP) • The mean or average of the pulmonary artery systolic and diastolic pressures. • FORMULA: MPAP = SPAP – DPAP + DPAP 3 • NORMAL: 10 – 20 mmHg ```

Answer 216

PULMONARY ARTERY WEDGE PRESSURE (PAWP) or PULMONARY ARTERY OCCLUSION PRESSURE (PAOP) • The pressure measured with a pulmonary artery catheter (e.g., Swan-Ganz catheter) when the balloon is inflated in the pulmonary artery, which reflects pressure distal to the point of occlusion. • Approximates left atrial pressure. • Also, approximates left ventricular pressure/preload as long as the mitral valve is normal. • NORMAL: 8 – 15 mmHg (NOTE: This is approximately the same as the pulmonary artery diastolic pressure. Clinically, the PA diastolic pressure is used to estimate the PAWP rather than inflating the balloon on the pulmonary artery catheter and actually performing a PAWP measurement.)

Answer 217

PULMONARY VASCULAR RESISTANCE (PVR) • The resistance in the pulmonary arteriolar vessels that must be overcome by right ventricular contraction to eject blood into the pulmonary arteriolar vessels. • FORMULA: PVR = MPAP – PCWP x 80/CO • NORMAL: 37 – 250 dynes/sec/cm5 or 37 – 250 dynes x sec-1 x cm-5

Answer 218

PULMONARY VASCULAR RESISTANCE INDEX (PVRI) • Pulmonary vascular resistance correlated with body surface area. • FORMULA: PVRI = MPAP – PCWP x 80/CI • NORMAL: 180 – 285 dynes/sec/cm5/m2 or 180 – 285 dynes x sec-1 x cm-5/m2

Answer 219

-A LV pressure-volume loop describes one complete cycle of LV contraction, ejection, relaxation, and filling. -four

Answer 220

o POINT 1: MITRAL VALVE CLOSES: § LV diastolic filling ends. § LV end diastolic volume (preload), which is 140 ml in this example, is reached.

Answer 221

o 1 → 2: isovolumetric contraction. § LV begins contraction (systole). § Initially mitral and aortic valves are closed, so no blood is entering or leaving the ventricle, that is, the LV is contracting (becoming smaller) against a closed chamber. § Thus, ventricular volume remains constant and ventricular pressure rapidly increases.

Answer 222

o POINT 2: AORTIC VALVE OPENS BECAUSE: § LV pressure exceeds aortic pressure.

Answer 223

o 2 → 3: LV EJECTION INTO AORTA: § LV volume decreases rapidly. § Volume of blood remaining in LV at POINT 3 is the LV end systolic volume, which is 70 ml in this example (140 ml – 70 ml = 70 ml; LVEDV – LVSV = LVESV). § Width of pressure-volume loop between points 2 → 3 represents volume of blood ejected (LV stroke volume), which is 70 ml in this example (140 ml – 70 ml = 70 ml; LVEDV – LVESV = LVSV).

Answer 224

o POINT 3: CLOSURE OF AORTIC VALVE BECAUSE: § Aortic pressure exceeds LV pressure (LV pressure less than aortic pressure).

Answer 225

o 3 → 4: ISOVOLUMETRIC RELAXATION. § LV relaxes (diastole) (chamber becomes larger). § Initially mitral and aortic valves are closed, so no blood is entering or leaving ventricle. § Thus, LV volume remains constant and ventricular pressure rapidly decreases.

Answer 226

o POINT 4: MITRAL VALVE OPENS BECAUSE: | § Left atrial pressure exceeds left ventricular pressure.

Answer 227

o 4 → 1: LEFT VENTRICULAR FILLING: § Initially, passive because of pressure gradient, and then active because of LA contraction. § Returns to LV end diastolic volume (preload) at point 1.

Answer 228

EFFECTS OF INCREASED LV END DIASTOLIC VOLUME (LV PRELOAD) • Venous return has increased, which increases LV end diastolic volume (preload). o Note that the distance between points 4 → 1 has increased, which represents the increased LV filling and preload. • Strength of LV contraction and LV afterload remain constant. • Based on the frank-starling relationship, increased LVEDV increases LV stretch, strength of contraction, ejection fraction, and stroke volume. • Note the increased distance between points 2 → 3, which represents increased LV stroke volume.

Answer 229

EFFECTS OF INCREASED AFTERLOAD • LV must eject blood against a higher than normal pressure, such as from aortic stenosis or arteriolar vasoconstriction. • Thus, ventricular pressure must increase higher than normal during isovolumetric contraction and during ejection. o Note the increased distance between points 1 → 2, which represents the increased pressure during isovolumetric contraction before the aortic valve opens, and the higher than normal pressure between points 2 → 3, which represents LV ejection. • As a consequence, less blood is ejected from the LV systole. o Ejection fraction/stroke volume is decreased. o LV end systolic volume is increased. o Note the decreased distance between points 2 → 3.

Answer 230

• With increased strength of LV contraction, a larger volume of blood than normal will be ejected during systole, that is, the ejection fraction and stroke volume increase. o Note the increased distance between points 2 → 3, which represents the increased ejection fraction/stroke volume. • Less blood remains in the LV. o The LV end systolic volume decreases, as indicated by point 3

Answer 231

atrial muscle depolarization

Answer 232

atrial muscle/AV node/Bundle of His depolarization

Answer 233

AV node/bundle of His depolarization

Answer 234

ventricular muscle fiber depolarization

Answer 235

phase 1 and phase 2 of ventricular repolarization

Answer 236

ventricular depolarization and repolarization

Answer 237

phase 3 and phase 4 of ventricular repolarization

Answer 238

SODIUM; influx of Na caused by an initial | stimulus

Answer 239

When we reach threshold (−60mV) we have opening of fast voltage−gated Na channels; which cause the AP to rise upward (in a less negative fashion)

Answer 240

The start of Late Phase 0 of depolarization; and slow Ca−Na channels open

Answer 241

That brings us up to about +20mV; this signifies the end of depolarization and initiates the beginning of repolarization o Fast voltage−gated Na channels close; however the slow Ca−Na channels are still open and K channels open

Answer 242

K out; Ca−Na in; same number of cations moving in as the same going out

Answer 243

- slow Ca−Na channels close and the K channels stay open | - starting the rapid repolarization; correlates with the T wave until we get to Phase 4 of repolarization

Answer 244

§ Early and Late Phase 0 of depolarization § Phase 1 of repolarization § Phase 2 of repolarization until it gets back to threshold § You can see that the ARP correlates with the upstroke of the T wave; so you will never see another depolarization on the upstroke of the T wave

Answer 245

§ Correlates with the down stroke of the T wave

Answer 246

§ Occurs at about −85mV down to −90mV; which correlates with the final downslope of the T wave • So you could see another AP on the down stroke of the T wave; which is very dangerous • Could lead to ventricular dysrhythmias

Answer 247

(3) Layers (from outside in): tunica adventitia, tunica | media, and tunica intima

Answer 248

• Tunica adventitia: o Mostly just connective tissue that provides support and structure and anchors those BVs down o Sympathetic nerve running along the outside of the nerve that innervates the smooth muscle of the BV § BVs only have sympathetic nerve fibers; post ganglionic § Predominantly alpha−1 receptors in the smooth muscle; causing vasoconstriction § NE released from the presynaptic nerve ending o BVs running on the outside of the larger BVs are called the VASO VASORUM § Large BVs cannot utilize the blood that is flowing thru them to provide O2 and nutrients to the actual BV tissue; only in the very large BVs

Answer 249

• Tunica media: o External elastic membrane: § Allows the BV to expand and helps the BV recoil to the original size o Smooth muscle: § Wrapped around the BV; the thicker the smooth muscle the more that BV can constrict and dilate § Most of the small/ medium arteries and arterioles have the thickest layer of smooth muscle; these BVs constrict and dilate the most

Answer 250

• Tunica intima: innermost layer of the BV o Internal elastic membrane: performs the same functions as the external elastic membrane o Lamina propria: composed of smooth muscle and connective tissue o Basement membrane: provides support and structure for the endothelia cells o Endothelium: lines the walls of the BVs; indirect contact with the blood itself

Answer 251

• LARGE ELASTIC ARTERIES: as you can see, this large elastic artery as mostly elastic tissue; which allows it to recoil when it is stretched • MUSCULAR ARTERIES: More like the medium and small size arteries (like mentioned earlier) that have very thick layers of smooth muscle that can constrict arteries to control the blood flow

Answer 252

VEINS • Veins are typically a lot thinner than arteries; they still have smooth muscle, so they can dilate and constrict • Veins have valves that allow for one−way blood flow (and make you look like a chump when trying to start an IV)

Answer 253

• Capillaries are known as exchange vessels; exchanges O2 and other nutrients from the blood to the interstitium • CO2 and other waste byproducts from the interstitium into the blood

Answer 254

Large arteries-> medium arteries -> small arteries ->arterioles -> metarterioles -> capillaries

Answer 255

• Very thin later of endothelia cells with a basement membrane layer wrapped around it; good for O2 delivery

Answer 256

- metarterioles | - capillary network

Answer 257

• THOROUGHFARE CHANNELS are vessels that have an unobstructed flow from the arteriole to the venous side

Answer 258

• PRECAPILLARY SPHINCTERS are bands of smooth muscles the constrict and dilate to regulate blood flow through capillaries

Answer 259

• Whether a pre capillary sphincter is constricted or | dilated mainly depends on the metabolic rate of the tissues that those capillary networks supply;

Answer 260

REGULATION OF BLOOD FLOW FROM METARTERIOLES INTO CAPILLARIES • O2 demand of tissue supplied by capillary network • Vasodilators: CO2, lactate, histamine, adenosine, K+, H+, ↓pH, ↓glucose in tissues, nitric oxide, and others

Answer 261

• As you travel down the vascular system, from the aorta down to the arteries, and arterioles; by the time we get to the capillaries, we have just one single pressure • From capillaries we have venules, veins and then the vena cava, were the pressure approaches zero • Again, there is the pressure gradient; moving blood in one single direction

Answer 262

* On the ARTERIAL side of the capillary, the objective is to filter fluid from the capillary into the interstitium; FILTRATION * ARTERIAL = FILTRATION … VENOUS = REABSORPTION

Answer 263

* On the VENOUS side, the objective is REABSORPTION; movement of fluid from the interstitium back into the capillaries * ARTERIAL = FILTRATION … VENOUS = REABSORPTION

Answer 264

1. • Starting on the arterial end with CAPILLARY HYDROSTATIC PRESSURE (CHP) 2. • The other capillary pressure we need to look at is PLASMA COLLOID OSMOTIC PRESSURE (PCOP); also called ONCOTIC PRESSURE 3. • NEGATIVE INTERSTITIAL FLUID PRESSURE (NEG. IFP) 4. INTERSTITIAL FLUID ONCOTIC PRESSURE (IFCOP);

Answer 265

• Starting on the arterial end with CAPILLARY HYDROSTATIC PRESSURE (CHP) o Hydrostatic pressure is the pressure that the fluid exerts against the walls of its container; in this example the fluid is blood and the walls of the container is the walls of the capillary o In this example the CHP is ~ 30 mmHg (you do not need to memorize these numbers, just the concepts) that favors the movement of fluid from the capillary into the interstitium; favors filtration o CHP favors FILTRATION; from the capillary to the interstitium

Answer 266

FILTRATION

Answer 267

• The other capillary pressure we need to look at is PLASMA COLLOID OSMOTIC PRESSURE (PCOP); also called ONCOTIC PRESSURE o Blood creates the PCOP from the proteins in the blood; primary plasma protein is ALBUMIN o Albumin levels are going to contribute most to the PCOP; estimated to be 28 mmHg of pressure in this example o PCOP favors REABSORPTION; from the interstitium to the capillary

Answer 268

REABSORPTION

Answer 269

• NEGATIVE INTERSTITIAL FLUID PRESSURE (NEG. IFP) o When I think of a negative pressure, I think of a vacuum; constantly sucking up fluid o Caused by the LYMPHATIC SYSTEM; terminal lymphatic vessels that lie adjacent to this interstitial fluid are constantly sucking up that interstitial fluid § that creates a negative pressure; estimated to be about 3 mmHg, and favors the movement of fluid from the capillary to the interstitium § NEG. IFP favors FILTRATION

Answer 270

Filtration

Answer 271

• Normally albumin is to large to get thru capillary membranes; however, some albumin and some proteins do get thru o Which is responsible for the INTERSTITIAL FLUID ONCOTIC PRESSURE (IFCOP); estimated to be about 8 mmHg o IFCOP favors FILTRATION

Answer 272

Filtration

Answer 273

• Back on the arterial side; o Overall goal is FILTRATION of fluid from the capillary to the interstitium o We need to compute the NET ARTERIAL FILTRATION PRESS § OUTWARD MINUS INWARD § OUT: 30 (CHP) + 3 (IFP) + 8 (IFCOP) = 41 § IN: 28 (PCOP) − 28 § NET ARTERIAL FILTRATION PRESSURE = 13 mmHg o Favors FILTRATION

Answer 274

• On the venous side: o Overall goal is REABSORPTION of fluid from the interstitium to the capillary o We need to compute the NET VENOUS REABSORPTION PRESSURE § INWARD MINUS OUTWARD § IN: 28 (PCOP) 28 § OUT: 10 (CHP) + 3 (IFP) + 8 (IFCOP) = (21) − 21 § NET VENOUS REABSORPTION PRESSURE = 7 mmHg

Answer 275

-Less fluid and less pressure in the venous capillary § Albumin has stayed in the capillary so the PCOP has stayed the same § The lymphatic system is still sucking so the NEG. IFP is still 3 mmHg; § PCOP is still the same as well

Answer 276

- terminal lymphatic vessels and the lymphatic circulation | - into the left and right subclavian veins, so fluid is eventually returned to systemic circulation

Answer 277

``` INCREASED CHP: • Increased systemic blood pressure • Increased vascular volume • Heart failure/increased CVP • Arterial side of capillary bed o Favors filtration • Venous side of capillary bed o Opposes reabsorption ```

Answer 278

``` INCREASED IFCOP: • Leaky capillaries and loss of albumin into interstitial fluid o Sepsis, major trauma, burns, etc • Arterial side of capillary bed o Favors filtration (because that albumin has moved into the interstitial fluid and is pulling volume along with it, from the vascular to interstitium) • Venous side of capillary bed o Opposes reabsorption ```

Answer 279

• Decreased systemic blood pressure • Decreased vascular volume • Arterial side of capillary bed o Opposes filtration (less CHP to push that fluid from the vascular compartment to the interstitium) • Venous side of capillary bed o Favors reabsorption (again CHP to oppose filtration, favors reabsorption)

Answer 280

``` DECREASED IFCOP: • Hypoalbuminemia o Liver dz, burns, etc • Arterial side of capillary bed o Favors filtration (because there is not the osmotic gradient pulling fluid back into the compartment) • Venous side of capillary bed o Opposes reabsorption ```

Answer 281

• Net effect o Interstitial edema § this is a compensatory mechanism to decrease the volume in the vascular compartment § especially with CHF; way for that person the decrease vasc vol and displace it into the interstitial compartment § same with overload a pt with crystalloids; pt gets puffy because the ↑ CHP o Decreased vascular volume

Answer 282

• Net effect o More volume stays in the systemic circulation o another compensatory mechanism

Answer 283

• Net effect o Interstitial edema o Decreased vascular volume

Answer 284

• Net effect o Interstitial edema o Decreased vascular volume • Be careful giving albumin to the septic, trauma or burn pt’s because that cause even greater vascular fluid loss and edema d/t the leaky capillary beds

Answer 285

LYMPHATIC OBSTRUCTION: • Obstruction caused by a tumor or lymphadenectomy (from breast CA) • Because of the proteins in the interstitial fluid; those terminal lymphatic vessels are constantly sucking up that interstitial fluid protein • And decreasing the protein level as well as the volume in the interstitium that is compensating for that net arterial pressure being greater than the net venous reabsorption pressure • When you have lymphatic obstruction, that creates edema because those lymphatics can’t compensate for the net arterial filtration pressure and net venous reabsorption pressure • Albumin accumulation in interstitial space • Net effect o Remember: NET ARTERIAL FILTRATION PRESSURE = 13 AND NET VENOUS REABSORPTION PRESSURE = 7 !!! o Interstitial edema