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Module 3: CPR > Physiology > Flashcards

Physiology Flashcards

1
Q

What are the functions of the cardiovascular system?

A

Supply oxygen, fuel, and heat to body tissues

Remove waste and metabolic products

Remove excess heat

Transport hormones, cells, etc through the body

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2
Q

What are three control mechanisms of cardiovascular system?

A
  • Neural Control: maintains constant arteriole BP
  • Local Control: supplies nutrients to match metabolic demands
  • Neural and local Control: alters distribution of cardiac output
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3
Q

How do the ventricles contract?

A

The right ventricle contracts inward

Left ventricle contracts radially

Bulbospiral muscles around ventricle decrease diameter and height of both ventricles

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4
Q

Why are elastic properties of the aorta and other arteries so important?

A

They allow for continuous blood flow.

As the heart finishes contraction, elastic properties allow the arteries to return to regular diameter in such a way that blood flow in the body does not reach zero

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5
Q

Which vessel type as the most smooth muscle?

A

Arteries

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6
Q

Name the order in which blood flows through vessels

A

Aorta -> artery -> arteriole -> precapillary sphincter

-> capillary -> venule -> vein -> vena cava

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7
Q

Which part of the circulatory system has the lowest blood pressure in the body?

A

Right atrium

(2-4mm Hg)

  • allows for blood to flow through the body from high pressure to low pressure
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8
Q

What is the order of circulation through the cardiac and pulmonary system?

A

Vena Cava -> Right atrium -> Through tricuspid valve

  • > Right ventricle -> pulmonary valve -> pulmonary artery
  • > pulmonary capillaries -> pulmonary vein -> left atrium
  • > mitral valve -> left ventrical -> aortic valve -> aorta
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9
Q

What is ohm’s law? Why is it relevant to the circulatory system?

A

V = IR
V = voltage
I = current
R = resistance

  • It is equivalent to vascular resistance:
  • *P = QR**

P = Pressure
Q = Flow
R = vascular Resistance

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10
Q

Where is the majority of the blood stored in the body?

A

The veinous system

Low resistance, high capacitance

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11
Q

How do you calculate Pulmonary Vascular Resistance?

A

(MAP - RAP)/CO = Resistance

MAP = Mean arterial Pressure
RAP = Right atrial Pressure
CO = Cardiac Output
Resistance = resistance

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12
Q

How do nodal action potentials differ from atrial and ventricular action potentials? Why?

A
  • *Nodals are slow response**
  • Have no fast Na+ channels
  • made up of slow Ca++ channels and “funny” Na channesl
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13
Q

Differentiate between blood flow and blood velocity as related to cross sectional area.

A

Blood flow is inversely proportional to vascular cross sectional area

V = FA

Volume = flow (area)

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14
Q

What are the phases of a ventricular/atrial action potential?

A

Phase 4: Resting-diastolic membrane potiential

Phase 0: Initial action potential depolarization
Due to “fast sodium channels”

Phase 1: Brief, partial repolarization
90% closure of Na+ channels
Openting of K+ channels
Allows K+ to leave the cell

Phase 2: Plateau
K+ channel closes
slow, voltage-gated “slow” Ca++ channel opens

Phase 3: Repolarization
iKr and iKs K+ channels open, iK1 is unplugged

iKr and iKs close when repolarization is complete

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15
Q

What are the 3 refractory periods?

A

Absolute- phase 0-2- AP generation impossible

Relative- phase 2-3- AP generation possible with large stimulation

Supranormal Period- phase 3-4- reduced amplitude stimulus causes depolarization

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16
Q

Why is it easier to have an early AP during the supranormal period?

A

Most of the fast Na+ channels have reset and all rectifing K+ channels leave the cell slightly depolarized

May allow a reduced amplitude AP to occur

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17
Q

What are the stages of a nodal AP?

A

4- pacemaker potential. Funny channels (iF) open on hyperpolarization and depolarizes cell towards threshold.

0- Slow voltage gated Ca++ channels open causing a slow depolarization (upstroke)

3- K+ channel opens on depolarization and closes on hyper polarization

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18
Q

What are the vagus effects on the nodal potentials?

A

Releases ACh which promotes hyperpolarization by decreasing membrane Na+ and Ca++ and increasing K+ permeability.

Slows HR.

Makes phase 4 slope more shallow

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19
Q

What are the sympathetic effects on the nodal action potentials?

A

Release norepinepherine which increases membrane Na+ and Ca++ and decreases K+ permeability

Shortens phase 4 and speeds heartrate

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20
Q

What is a normal cardiac depolarization vector (what does it signifiy)?

A

+30 degrees

(it means the heart is depolarizing from the atria to the base to the apex)

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21
Q

What is a lead axis?

A

Line on the patient leading from the negative to the positive electrode.

by convention this is the right arm (-) to the left arm (+)

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22
Q

Define Mean Cardiac Vector

A

the vector sum of all myocytes

depends on the number of myocytes depolarizing (or repolarizing) and their orientation to one another.

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23
Q

What are the spontaneous depolarization rates of the cardiac conduction system?

A

SA node 70-80 AP/min

AV node 40-60 AP/min

Purkinje Fibers 15-40 AP/min

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24
Q

In what order does the heart depolarize?

A

SA node⇒AV node⇒His-Perkinje⇒left and right bundel branches

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25
Q

Why is conduction through the AV node so slow?

A

Allows atria to fully contract and empty before ventricles contract

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26
Q

What is decremental conduction and where is it observed?

A

The AV node exhibits decremental conduction wherein multiple repeated stimulation results in slower transmission of the action potential.

Fast stimulation prevents Ca++ channels from being reset

Prevents A fib from resulting in V fib

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27
Q

In what direction does cardiac repolarization occur?

What determines this?

A

Apex to base

Epicardium to endocardium

AP legnth (endocardium has longer APs)

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28
Q

In normal cardiac muscle what prevents back propagation?

A

refractory periods

(inactivation Na+ Ca++ channels to the activation of K+ channels)

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29
Q

Name the 12 ECG leads

A

Bipolar limb leads:
Lead 1 LA⇒RA
Lead 2 RA⇒LL
Lead 3 LA⇒LL

Unipolar limb leads:
aVR WCT⇒RA
aVL WCT⇒LA
aVF WCT⇒LL

Unipolar Percordial Limb leads:

V1
V2
V3
V4
V5
V6

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30
Q

What is the p-wave?

A

Atrial depolarization

+ deflection of lead I and aVF

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31
Q

What is the QRS complex?

A

Ventricular depolarization

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32
Q

What is the T-wave?

A

Ventricular repolarization

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33
Q

What is happening during the P-R interval?

What if it’s prolonged/shortened?

A

AV conduction

Prolonged=conduction failure at AV node

Shortened=ventricular preexcitation (WPW syndrome)

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34
Q

What is happening during the QRS interval?

How long should it be?

What if it’s prolonged/shortened?

A

Ventricular excitation

Should be 2.5 small blocks or narrower

Widened=slow conduction in the Purkinje fibers or ventricular muscle

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35
Q

What is the QT interval?

What is the patient at increased risk of when it is prolonged or shortened?

A

Ventricular AP duration

long or short QT interval means increased risk for arrhythmia

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36
Q

What is QTc?

What formula is used to calculate it?

A

AP duration corrected for heart rate.

Bazett’s correction:

QTc= QT/(HR0.5)

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37
Q

What is the S-T segment?

What should it be equal to?

What does it mean if it’s not?

A

Reflects the plateau phase of the ventricular AP

should be at the same height as the TP segment.

If significant injury is present S-T will be elevated or depressed.

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38
Q

What is one little ECG box equal to in the X axis? Y axis?

A

X axis:
1 small box = 40 msec (0.04 sec)
1 large box = 200 msec (0.2 sec)

Y axis:
1 small = 0.1 mV

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39
Q

What is the quick way of determining HR on an ECG?

A

HR = 300/N on a 10 second ECG

Acquire 1 target QRS wave on a solid line, subsequent QRS on dar line gives HR in given intervals:

1 box = 300
2 boxes = 150
3 boxes = 100
4 boxes = 75
5 boxes = 60
6 boxes = 50

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40
Q

What is the HR threshold for tachycardia and bradycardia?

A

Tachycardia: HR > 100

Bradycardia: HR < 60

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41
Q

What is Normal Sinus Rhythm (NSR)?

A
  • HR = 60-100
  • One P wave (and only one) per QRS
  • PR interval normal
  • Upright P wavves in I, II, aVf
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42
Q

What constitutes arrhythmia?

A

Anything that is not normal sinus rhythm

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43
Q

What causes regularly irregular sinus rhythm?

A

Breathing

Physical fitness

etc.

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44
Q

What is the systematic approach to interpreting ECGs?

A

Look at:

Rate

Rhythm

Intervals

Axis

Morphology

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45
Q

What are normal intervals for:
P-wave

PR

QRS

QT

A
  • *P-wave**: 0.06 - 0.1sec
    (1. 5-2.5 small boxes)

PR: 0.12 - 0.2sec
(3-5 small boxes)

  • *QRS**: 0.06 - 0.1sec
    (1. 5-2.5 small boxes)

QT: 0.4 sec
(10 small boxes)

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46
Q

What is a normal cardiac axis?

A

-30º to +90º

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47
Q

How can you estimate the cardiac axis easily?

A
  • If QRS is (+) in Lead I and (+) in Lead II ==> Normal Axis
  • If (+) in Lead I and (-) in Lead II ==> Left Axis Deviation
  • If (-) in Lead I and (+) in Lead II ==> Right Axis Deviation
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48
Q

How can you quantify the cardiac axis easily?

A

Identify the isoelectric lead and axis will be +/- 90º

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49
Q

What are common causes of axis deviation?

A
  • Incorrect lead placement
  • Heart irregularly positioned to right instead of left
  • Enlarged right ventricle
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50
Q

How do you analyze the morphology of an ECG?

A
  • Do the PQRST waves look normal?
  • P waves should be upright in Leads II, III, and aVf
  • QRS should be normal width
  • ST segments should be same level as PR
  • T waves should not be peaked or flattened
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51
Q

What is the White Parkinson Wolf pattern on an ECG?

A
  • PR interval < 120ms
  • Normal P vector
  • Presence of delta wave
  • QRS duration > 100ms
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52
Q

What is the significance of WPW?

A
  • > Found in 1-2% of normals and often goes away with age or can be fixed surgically
  • Is disqualifying for pilots
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53
Q

What is the S1 heart sound?

A

Closing of AV valves

  • slow, low pitched vibration
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54
Q

What is the S2 heart sound?

A

Closure of aortic and pulmonary valves

  • rapid, high frequency “snap”
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55
Q

What is the S3 heart sound?

A

Rapid ventricular filling, sometimes heard

56
Q

What is the S4 heart sound?

A

Atrial contraction

Infrequently heard

57
Q

What is the basic functional anatomy of the semilunar valves?

A

Semilunar valves are Aortic and Pulmonary valves

  • Do not have cordae tendineae
  • Prevent backflow during Systole
  • Close and open passively and close due to back pressure
  • More rigid due to working with more pressure
  • Strong, yet, pliable base
  • smaller than Atrioventricular valves
58
Q

Explain the relationship between cardiac anatomy and pressure development during diastole and systole

A
  • Left ventricle is large, thick, and muscular and produces 120 mmHg pressure during systole
    Diastolic pressure is 6 mmHg
  • Right antrium has a systolic pressure of 4 mmHg
    Diastolic pressure is 2 mmHg
  • Right ventricle is systolic of 25 mmHg
    Diastolic pressure is 2 mmHg
  • Left atrium is systolic pressure of
59
Q

What are the ventricles doing at 0.1sec?

A

They are beginning isovolumetric contraction.

Pulmonary and Aortic, as well as tricuspid and mitral, valves are closed, while ventricles initiate contraction.

60
Q

In what position are the aortic and pulmonic valves at 0.4?

A

They’re open and blood is entering the pulmonary artery and aorta.

61
Q

At what point do the mitral and tricuspid valves open?

A

About 1.5

They fill the ventricles with amount of blood resulting in the end diastolic volume

62
Q

What are connexons?

A

Channels in gap junctions that ellectrically couple cardiac myocytes, allowing for conduction of the action potential and subsequent cell depolarization/contraction.

63
Q

What do desmosomes do for cardiac cells?

A

They hold cells together and transmit mechanical force from cell-to-cell

  • they are called “molecular rivets”
64
Q

What are T-tubules?

How do they contribute to cardiac muscle contraction?

A

large invaginations in sarcolemma rich with voltage-gated Ca2+ channels (dihydropyridine receptors)

  • Action potential depolarization propogates down the T-tubule activating channels, allowing Ca2+ into the cell, initiating contraction
  • much less prominent in skeletal muscle
65
Q

What is the sarcoplasmic reticulum?

How does it contribute to cardiac muscle contraction?

A

storage organelle for Ca2+ which complexes with the T-tubule

  • influx of Ca2+ from T-tubule dihydropyridine receptors triggers the ryanodine receptor on the surface of the SR, inducing calcium induced calcium release (CICR)
  • this calcium binds to Troponin-C, which allows tropomyosin to roll away and expose actin-myosin binding sites, allowing for contraction
66
Q

What is the relation between myofiber, myocyte, and sarcomere?

A

Myofibers contain many myocytes, which contain many sarcomeres

  • sarcomeres are the contracting unit of the myocyte
67
Q

What is the myocyte “Triad”?

A

the site where the T tubule, Ca channel, and SR meet

  • SR wraps around sarcomeres and invaginating T tubules allow for SR and Ca channels to be closer together
68
Q

What are crucial steps in EC coupling?

A
  • Action potential plateau opens L-type Ca channel
  • Ca influx triggers release of Ca from SR (CICR)
  • Ca binding to TnC allows for cross-bridge formation
  • ATP req’d for power stroke and new cross-bridge
  • Diastolic relaxation requires reduced [Ca2+]
69
Q

How do myocytes achieve reduced Ca2+ concentration during diastole?

A

SERCA (sarco/endoplasmic reticulum Ca2+-ATPase) pumps Ca back into the SR (uses ATP)

Na/Ca2+ exchanger channels allow calcium to be released to the extracellular space

70
Q

What are the four factors of cardiac performance?

A
  1. Preload
  2. Afterload
  3. Contractility
  4. Heart Rate and Rhythm
71
Q

What is preload?

A

The tension in the myocardial wall prior to contraction

  • End Diastolic Volume (EDV) stretches the myocytes and sets the sarcomere length
  • volume difficult to measure clinically: pressure serves as surrogate
72
Q

What is the law of La Place?
Why is it used?

A

T = (P)(R)/2*(H)

T = tension
P = Pressure
R = Radius of Chamber
H= Thickness of Wall

Used to calculate tension of myocardial wall prior to contraction for Preload

73
Q

What is the afterload?

A

The tension in the chamber wall during contraction

  • also calculated by the Law of La Place
  • clinical surrogate measure is the peak pressure in that chamber (i.e. LV systolic pressure)
  • during systole, chamber radius falls, so afterload decreases during ejection –> heart is doing less work as systole progresses
74
Q

What is the correlation between preload and afterload and systolic performance?

A

Increasing preload increases the velocity and extent of shortening if afterload is constant

Increasing afterload reduces the velocity and extent of shortening for any given preload

Increased preload = increased systolic performace
Increased afterload = decreased systolic performance

75
Q

What is contractility?

A

Cardiac muslce increases strength of contraction through changing contractility

  • for any given preload and afterload, the contractile state determines:
    Velocity of muscle fiber shortening
    extent of shortening
  • Independent of preload and afterload
76
Q

What determines contractility?

A
  • [Ca2+] available to cardiac myocytes
  • In vivo, stimulation of ß-adrenergic receptors increases [Ca] and developed tension
  • this can also be achieved in vitro by increasing [Ca] of solution in which cell is contraction
  • Number of crossbridges formed between actin and myosin
  • Rapidity with which the crossbridges are formed, broken, and reformed
77
Q

How do ß-adrenergic receptors increase contractility?

A

Stimulation of ß-adrenergic receptors activates G-coupled proteins that activate adenylyl cyclase, increasing conversion of ATP –> cAMP

  • This allows for phosphorylation of V-gated Ca2+ channels (increasing rate of Ca entering cell)
  • Increased Ca2+ entry leads to Ca2+ release from SR and bindign to troponin C
  • Faster uptake by SR and extrusion by Na/Ca Exchanger allows for faster relaxation
78
Q

How is heart rate important for cardiac performance?

A

Increased heart rate improves cardiac performace by at least two mechanisms:

  • Increased number of systolic episodes per minute means greater volume pumped per minute
  • Direct increase in contractiliyty due to increased [Ca2+] accumulation in the SR
    (small effect in absence of ß-adrenergic receptors)
79
Q

What is the difference between cardiac and skeletal muscle in their method of increasing force of contraction?

A

Skeletal muscle can increase force through increasing frequency

Only cardiac muscle can increase force through increasing contractility

80
Q

Define cardiac output

A

Volume of blood that is pumped into the aorta per unit time (L/min)
(Normal resting = 5L/min)

CO = (HR)(Stroke Volume)

81
Q

Define Stroke volume and explain how this definition can help modify the equation for cardiac output

A

volume of blood pumped into the aorta during one cardiac cycle

CO = HR(EDV - ESV)

EDV = End Diastolic Vol.
ESV = End Systolic Vol.

(Normal = 60-100mL/beat)

82
Q

What is cardiac index?

A 
Cardiac Output (CO) adjusted for differences in Body Surface Area (BSA)
 (Normal values = 2.5-4.0 L/min/m<sup>2</sup>)

Cardiac Index = CO/BSA

83
Q

What is ejection fraction?

A

Clinical Index of Contractility

Fraction of EDV that is ejected during systole, expressed as percentage
(Normal = 55-70%)

Ejection Fraction = (EDV - ESV)/EDV
= SV/EDV

84
Q

What are ways of clinically measuring ejection fraction?

A

Echocardiogram

Cardiac Catheterization

Cardiovascular MRI

Cardiac CT

Nuclear Medicine Scan

85
Q

What is used as an index of contractility?

A

Because “contractility” is used interchangeablyl with ionotropic state, the rate of rise of ventricular pressure during isovolumetric contraction (dP/dt) is the index of contractility

  • Volume, radius, and wall thickness are constant during isovolumetric contraction, therefore, rate of rise of tension is directly proportional to dP/dt
86
Q

What is Stroke Work?

A

Amount of energy that the heart converts to work during a single cardiac cycle
(Normal = 45-75 mg-m/m2/Beat)

Best depicted by the use of ventricular pressure-volume diagrams: area within pressure-volume loop

87
Q

What are the components of Stroke Work?

A
  • External Work (99%): moves stroke volume from venous system to arterial circulation
    > Pressure work: accommodates a greater developed tension
    > Volume work: accommodates a greater stroke volume
  • Kinetic Energy of Blood Flow (1%): accelerates blood to velocity of ejection
88
Q

What is the Efficiency of Cardiac Contraction?

A

Ratio of work output to toal chemical energy expenditure
(Normal = 20-25%)

  • Most chemical energy is converted into heat rather tahn work output, and efficiency can decrease to 5-10% durign heart failure
89
Q

How is the efficiency of cardiac contraction determined?

A
  • Heart derives most chemical energy from oxidative metabolism of fatty acids (to a lesser extent lactate and glucose), therefore, oxygen consumption provides a measure of the chemical energy liberated during cardiac work
  • Wall Tension is an indicator of amount of energy needed for contraction–Dilated ventricle with increased radius will have to overcome more tension than a normal ventricle and consume more O2
90
Q

Define the four phases on the give Left ventricular Pressure-volume curves

A
  • *Phase I**: Period of Filling
  • From L atrium to ventricle
  • *Phase II:** Period of Isovolumetric Contraction
  • When all valves are closed, before ventricular pressure exceeds taht in aorta
  • *Phase III:** Period of Ejection
  • When ventricular pressure exceeds that in aorta, aortic valve opens, and blood flows out of ventricle into aorta
  • *Phase IV:** Period of Isovolumetric Relaxation
  • Wehn aortic valve closes and ventricluar pressure returns to diastolic pressure levels
91
Q

What happens to the AP of the AV if it is stimulated at a faster rate?

A

Decremental conduction causes a smaller, slower AP due to reduced Ca channel availability

  • AV nodal conduction slows with faster stimulation rate
92
Q

What causes the WPW Pattern on ECG?

A

Normal, intrinsic delay of AP propagation through the heart due to decremental conduction of the AV node is bypassed by an accessory pathway

The accessory pathway depolarizes the adjacent ventricle sooner than it is supposed to and earlier than the other ventricle

93
Q

What effect does decremental conduction have on atrial fibrillation?
What if a person doesn’t have proper decremental conduction?

A

Decremental conduction is able to reduce the speed of AP propagation through the ventricles

A heart in atrial fibrillation > 300bpm and working decremental conduction allows the AV node to slow ventricular contraction rate to 60-100bpm

A lack of decremental conduction will lead to ventricular rates that are too high
(WPW will be shown with a wide QRS, showing conduction is not thorugh the His-Purkinje system)

94
Q

What are the two types of tachycardia?

A

“Supraventricular tachycardia”
- atrial (or nodal) tissue is essential in maintaining rhythm
(annoying, but not usually life threatening)

  • *“Ventricular tachycardia”**
  • only vetnricular tissue essential in maintaining rhythm
95
Q

What are the three main mechanisms of tachycardia?

A

Reentry: self-perpetuating waves of depolarization

Triggered activity: secondary depolariation of a focus “triggered” by a preceding beat

Enhanced automaticity: Spontaneous depolarization of a focus outside SA node

96
Q

Describe the mechanism in which Reentry causes tachycardia?

A

Requires 3 Conditions:

  • Presence of adjacent cardiac tissue with different refractory periods
  • Unidirectional conduction block
  • Slow conduction to allow refractory tissue to recover and allow conduction where it was previously blocked
97
Q

What is the mechanism of reentry that can occur in WPW?

A
  • Can be initiated by a closely coupled premature atrial complex with blocks in the accessory pathway
  • contraction conducts through the AV
  • retrograde conduction via accessory pathway prematurely activates atrial contraction
  • Inverted P wave produced by retrograde conduction visible in ECG leads
98
Q

How does an ECG show where the reentry is occuring?

A

If QRS is narrow, conduction to the ventricle uses the AV node-His Purkinje system and reentry must be supraventricular

If QRS is wide, reentry circuit is located in ventricle

99
Q

How is reentry treated?

A

By shocking with 360 Joules

  • *- Electrical countershock depolarizes entire myocardium, blocking wavefront (reentry circuit will be reset)**
  • Sinus node should be first tissue to regain excitability, resulting in normal rhythm
  • May see pause due to “overdrive suppression” by arrhythmia
  • rapid stimulation causes activation of the NA/K-ATPase pump, hyperpolarizing SA node

- Premature stimluation can terminate reentry by inducing bi-directional block (may accelerate tachy.)

- Drugs (beta blockers, Ca channel blockers, etc) which prolong AP duration or slow conduction velocity sometimes helpful in non-life threatening situations

- Surgical destruction of pathway

100
Q

What is a sinoatrial block and how does it present on an ECG?

A

The impulse from the SA node is blocked before it enters the atrial muscle

Due to the resultant standstill of the atria, ECG shows absence of a P wave

Rate of ventricular QRS-T complex is slowed by not otherwise altered due to spontaneous AV node depolarization

101
Q

What is a atrioventricular block and how does it present on an ECG?

A

Conditions that can either decrease the rate of impulse conduction in the bundle of His (AKA A-V bundle) or block the impulse from passing from the atria to the ventricles

102
Q

What are some conditions that can cause Atrioventricular Block?

A

Ischemia of the AV node or AV bundle fibers:
Often delays or blocks conduction from atria to ventricles
Coronary insufficiency can cause ischemia of AV node and bundle

Compression of AV bundle:
Scar tissue or calcified portions of the heart can depress or block conduction from atria to ventricles

Inflammation of AV node or AV bundle:
Can depress conductivity from A to V
Inflammation results from different types of myocarditis (i.e. diphtheria or rheumatic fever)

Extreme stimulation of heart by vagus nerve:
In rare instances blocks impulse conduction through AV node. Can result from strong stim. of baroreceptors in people with carotid sinus syndrome

103
Q

What is a bradycardia?

A

Slowing of heart rate
(< 60bpm)

  • may be caused by increased vagal tone, ischemia, or degenerative disease of conduction
103
Q
A
104
Q

What is a first-degree AV block?

A

Prolonged P-R interval
( > 200ms)

ECG shows only one P wave for each QRS

Usually due to enhanced vagal tone causing slow conduction through the AV node

Sometimes called a first-degree incomplete heart block because conduction is delayed, not actually blocked

Not usually treated pharmacologically

105
Q

What is second-degree AV block (Mobitz 1)?

A

Conduction through AV bundle is slowed enought to increase PR interval to 0.25 - 0.45s - AP is somtimes strong enough to pass through bundle and sometimes not

More P waves than QRSs
PR interval gets progressively longer before dropped QRS

Usually due to increased vagal tone and disappears with exercise (benign form)

(AKA: Wenkebach)

106
Q

What is second degree AV block (Mobitz 2)?

A

Slowed conduction through AV bundle to increase PR interval, AP is sometimes strong enough to conduct through to ventricles and sometimes not

PR interval does not change prior to dropped QRS
Note wide-complex QRS, suggesting diffuse disease in conduction system

His-Purkinje system has become undependable (think frayed wire) and can progress unexpectedly to complete heart block

107
Q

What is a third-degree AV block?

A

Also known as complete AV block

When condition causing poor conduction in AV node or bundle becomes severe, complete block of impulse from atria to ventricles occurs - Atria is no longer connected to ventricles

Atrial depolarization rate faster than ventricluar (more P waves than QRS)
PR interval changes constantly without altering ventricular rhythm

Can become asystole without warning

108
Q

What are the two types of reentry?

A
  • *Anatomic** - reentry occurs around fixed, non-conducting structure
  • *ECG monotonous**
    (i. e. atrial flutter, atrioventricular reciprocating tachy, V tachy around dead tissue from previous MI)
  • *Functional** - reentry occufrs around area which is temporarily non-conductiong but may move
  • *ECG chaotic**
    (i. e. atrial fibrillation, ventricular fib)
109
Q

What is premature ventricular contraction (PVC)?

A
  • Arises from ectopic focus in ventricles
  • Early QRS not preceded by P wave
  • Will have unusual QRS shape:
    Odd vector
    Prolonged QRS duration
  • Will have a compensatory pause
110
Q

What is Poiseuille’s Law?

A

Q = k(r^4)(P)/L

Q = flow
k = π/(8n)
n = viscosity
P = change in pressure
L = length

111
Q

What does Poiseuille’s law teach about the relationship between flow and:

a) radiius
b) length

A

a) Q is proportional to r^4
b) Q is proportaional to 1/L

112
Q

What are Poiseuille’s assumptions?

A
  • Flow is laminar
  • Flow is through smooth cylindrical rigid tubes
  • Flow is steady and constant
  • viscosity of the fluid is constant
113
Q

What is laminar flow?

A

When fluid flows at a steady rate through along, smooth cylindrical tube, it flows in streamlines

It is laminar flow when each layer of blood remains the same distance form the vessel wall and the central most portion of fluid stays in the center of the vessel

Results in a parabolic velocity profile

114
Q

What is turbulent flow?

A

Turbulent flow can result from an obstruction during laminar flow

the fluid, instead of flowing in streamlines, flows in all directions in the vessel and continually mixes

115
Q

What can cause turbulent flow in the circulatory system?

A
  • Branching of vessels
  • Arterial plaques
    (disrupt smooth arterial walls, cause bruits)
  • Valves in the heart (aortic and mitral)
116
Q

How can an increase in blood viscosity interrupt circulation?

A

Due to Poiseuille’s law:
Increased viscosity –> Increased resistance –> Decreased flow

Also, if blood is too viscous, it won’t perfuse organs as well and can lead to a lack of O2 availability

Increased viscosity can be due to increased hematocrit and proteins in blood (or decreased water)

117
Q

How do you add resistances in series?

In parallel?

A

Series: Rtotal = R1 + R2 + R3…

Parallel: 1/Rtotal = 1/R1 + 1/R2 + 1/R3…

118
Q

How is the mean pressure of pulsatile flow determined?

A

Mean pressure is 1/T multiplied by the integral from T1-T2 of Pdt

==> Mean pressure = DPr + (Pulse Pressure)/3

DPr = diastolic pressure
Pulse Pressure = SPr - DPr
SPr = systolic pressure

119
Q

Define microcirculation

A

Part of the vascular system comprised of small arterioles, capillaries and small venules

120
Q

What is the function of microcirculation?

A

to regulate blood flow and nutrient exchange between blood and tissue

121
Q

What part of microcirculation controls blood flow and what controls where microflows go?

A

arterioles control blood flow and they are able constrict precapillary sphincters to control microflows

122
Q

How does blood flow through capillary beds?

A

There is no one-way flow

Blood flows according to open and closed precapillary sphincters

123
Q

How is fluid flux across capillary membranes altered?

A

Forces favoring Fluid loss:

  • *Pc** = capillary hydrostatic pressure
  • *πif** = Interstitial fluid colloid osmotic pressure

Forces favoring Reabsorbtion:

  • *Pif** = Interstitial fliud hydrostatic pressure
  • *πc** = capillary colloid osmotic pressure
124
Q

What is Starling’s law of transcapillary fluid equilibrium?

A

Net fluid movement = Forces favoring fluid loss - Forces favoring reabsorbtion

F = (Pc + πif) - (Pif + πc)

F > 0: Forces fluid out of vessel
F < 0: Forces fluid into vessel

125
Q

How does lymphatic circulation work?

A

Pressure on capillaries (by skeletal muscle) moves fluid through the lymph system

Valves throughout the vessels prevent back flow of lymph

Pores vessel walls make the system good for picking up large, cellular debris

Pores also have valves that are opened by pressure to move lymph into the lymph system
- these valves are anchored to the ECM by anchoring filaments

126
Q

What is the function of the lymph system?

A
  • Remove unabsorbed interstitial fluid
  • Remove interstitial protein
  • Remove cellular debris
  • Minimize interstitial fluid presssure to prevent edema
127
Q

What are some factors contributing to edema?

A
  • Increased capillary permeability
  • Decrease in plasma colloid osmotic pressure
  • Elevated capillary pressure
  • Lymphatic obstruction
128
Q

What are some factors that can affect diffusion of nutrients in capillary system?

A

- Thickness of vessel wall
Increased thickness = decreased diffusion

- Available surface area
Decreased SA = decreased diffusion

- Particle size
Increased particle size = slower equilibration

- Solubility of particle
Increased solubility = faster equilibration

- Charge of particle
Charged particle = decreased diffustion
(membranes in vivo are lipid)

129
Q

What are challenges to vascular homeostasis?

A
  • Postural changes
  • Local changes (exercise)
  • Hemorrhage
  • Return from space
  • Sexual activity
130
Q

What is the baroreceptor reflex?

A

Reflex initiated by stretch receptors located at specific points in the walls of several large systemic arteries

  • A rise in arterial pressure stretches baroreceptors and casues them to transmit signals into the CNS
  • “Feedback” signals are then sent through the autonomic nervous system to the circulation to reduce arterial pressure
131
Q

Where are baroreceptors most abundant?

A
  1. Wall of the internal carotid arteries slightly above the carotid bifurcation (area known as carotid sinus)
  2. Wall of the aortic arch
132
Q

How do baroreceptors respond to pressure change?

A

As blood pressure rises, baroreceptors initiate sinus nerve stimulation, resulting in the lowering of blood pressure.

  • receptors respond rapidly to changes in arterial pressure
  • Rate of impulse firing increases in fracion of a second during each systole and decreases during diastole
  • Receptors also respond much more to rapidly changing pressure than to stationary pressure
133
Q

What are the net effects of the baroreceptors?

A
  1. Vasodilation of veins and arterioles throughout peripheral circ. sys.
  2. Decreased HR and Strength of Contraction

==> Causes arterial pressure to decrease
(Conversely, low pressure has opposite effect)

134
Q
A

Module 3: CPR (10 decks)

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