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CPR Midterm > Physiology > Flashcards

Physiology Flashcards

1
Q

Three pressures in the CV system?

A
  1. Driving (difference between two points)
  2. Hydrostatic (P of gravity and weight of blood)
  3. Transmural (P of blood on vessel wall)
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2
Q

Arteriolar resistance is regulated by the _1_ nervous system.

A
  1. Autonomic
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3
Q

Arteries are under _1_ pressure and Veins are under _2_ pressure.

A
  1. High
  2. Low
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4
Q

Blood flows from __1 (high/low)__ pressure to __2 (high/low)__ pressure. The __3__ drives blood flow.

A
  1. High
  2. Low
  3. Pressure gradient
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5
Q

Blood flow is inversely proportional to the _1_ of blood vessels. When blood flow increases, _1_ has decreased.

A
  1. Resistance (nothing is holding it back)
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6
Q

What is the equation for blood flow/cardiac output/Q?

A

CO = (Mean arterial pressure [highest P] - Right arterial pressure [lowest P]) / (Total peripheral resistance [TPR])

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7
Q

What are the factors that change the resistance of blood vessels (3)?

A
  1. Viscosity of blood (numerator)
  2. Length of blood vessel (numerator)
  3. Radius of blood vessel to the fourth power (denominator)

Resistance = (8*visc*length)/(pi*r^4)

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8
Q

What is viscosity?

A

Increased viscosity is due to increased internal friction.

  • thickness
  • the state of being thick, sticky, and semifluid in consistency
  • a measure of its resistance to gradual deformation by shear stress or tensile stress
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9
Q

Increasing viscosity by increasing hematocrit will _1_ resistance and _2_ blood flow.

A
  1. increase
  2. decrease
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10
Q

Increasing the length of a vessel will _1_ resistance. Increasing the radius of a vessel _2_ resistance.

A
  1. increase
  2. decrease
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11
Q

If a blood vessel radius decreases by a factor of 2 then resistance _1_ by a factor of _2_ and blood flow _3_ by a factor of _4_.

A
  1. increases
  2. 16
  3. decreases
  4. 16
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12
Q

_1_ resistance is illustrated by systemic circulation. Each artery in _1_ receives a fraction of the total blood flow.

A

Parallel

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13
Q

When an artery is added in parallel, the total resistance _1_. In each parallel artery, the pressure is the _2_.

A
  1. decreases
  2. same
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14
Q

_1_ resistance is illustrated by the arrangement of blood vessels in a given organ. _2_ are the largest contributers to this resistance.

A
  1. Series
  2. Arterioles
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15
Q

As blood flows through the series of blood vessels, pressure _1_. Each blood vessel in series receives the _2_ total blood flow.

A
  1. decreases
  2. same
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16
Q

_1_ flow is streamlined. _2_ flow is not and causes audible vibrations called _3_.

A
  1. Laminar
  2. Turbulent
  3. bruits
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17
Q

A _1_ number predicts whether blood flow will be turbulent or laminar.

A

Reynold’s number

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18
Q

An increased Reynold’s number increases the likelihood of _1 (laminar/turbulent)_ flow.

A

turbulent

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19
Q

What are the two factors that increase a Reynold’s number?

A
  1. Decreased blood viscosity (ex. anemia, lower hematocrit)
  2. Increased blood velocity (ex. narrowing of a vessel [decreased radius)
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20
Q

What is hematocrit?

A

the volume percentage of red blood cells in blood

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21
Q

Pulse pressure is the difference between _1_ and _2_ presures.

A
  1. systolic
  2. diastolic
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22
Q

Aging leads to a _1_ in capacitacne and an _2_ in pulse pressure.

A
  1. decrease
  2. increase
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23
Q

When is systolic pressure measured?

A

**After **the heart contracts (systole) and blood is ejected in the **arterial **system.

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24
Q

When in diastolic pressure measured?

A

When the heart is relaxed (diastole) and blood is returned to the heart via the veins.

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25
Q

Systolic pressure is the _1 (highest/lowest)_ arterial pressure during a cardiac cycle. Diastolic pressure is the _2 (highest/lowest)_ arterial pressure during a cardiac cycle.

A
  1. highest
  2. lowest
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26
Q

Mean arterial pressure = ?

A

MAP = 1/3 Systolic P + 2/3 Diastolic P

*because most of the cardiac cycle is spent in diastole

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27
Q

Venous pressure is very _1 (high/low)_. Veins have a _2 (high/low)_ capacitance and therefore can hold _3 (large/small)_ volumes of blood at low pressure.

A
  1. low
  2. high
  3. large

*Capacitance is proportional to volume (numerator) and inversely proportional to pressure. As a person ages, their arteries become stiffer and less distensible/stretchy therefore capacitane of arteries decreases with age.

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28
Q

what are 4 methods of regulating arterial blood pressure?

A
  1. Increase pumping force
  2. contract veins and arterioles
  3. infuse fluids
  4. administer vasoconstrictors
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29
Q

which ventricle has a thicker muscular layer? why?

A

the left ventricle. It must pump blood through to aorta to systemic circulation.

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30
Q

how does the heart contract?

A

in a spiral contraction (like wringing a washcloth)

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31
Q

what is the % ejection volume referring to?

A

the amount of blood pushed out of the ventricles

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32
Q

capillaries have (high/low) velocity, (high/low) resistance and (high/low) cross-sectional area.

A

low

low

high

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33
Q

arterioles have the (highest/lowest) resistance

A

highest

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34
Q

Describe the normal sequence of cardiac depolarization: conduction of AP atrium –> ventricle

A

SA node–>(artium)–>AV node–>bundle of His–> L/R bundle branches –> purkinje fibers –> (ventricle)

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35
Q

Describe the normal sequence of VENTRICLE repolarization

A

epicardium –>endocardium

base–>apex

**AP shorter in epicardium

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36
Q

Define the standard bipolar limb leads and Einthoven’s triangle

A

3 bipolar limb leads:

lead1: RA–>LA
lead2: RA–>LL
lead3: LA–>LL

(-) –> (+)

einthoven’s triange

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37
Q

Define the augmented unipolar limb leads and Wilson’s central terminus

A

3 unipolar limb leads:

aVR: right arm

aVl: left arm

aVf: left leg

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38
Q

basic definition of EKG

A

mean cardiac vector is assessed in several leads

records cardiac electrical activity over time

examines how action potential is generated/conducted through heart

non-invasive electrodes on skin

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39
Q

ECG: Identify the P, Q, R, S, and T waves

A

P- atrial depolaization

A-V delay

QRS- ventricular depolarization

plateau

T- ventricular repolarization

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40
Q

Identify the PR interval, QT (QTc) interval, ST segment.

A

these segments might change if A-V conduction is delayed, the ventricular action potential is prolonged, or the heart becomes ischemic.

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41
Q

Given an ECG record, determine the mean QRS axis and classify it as normal, left-, or right-deviated.

A

Left axis deviation: -30 to -90

Normal mean QRS axis -30 to +90

Right axis deviation +90 to +180

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42
Q

functional syncytium: how does cardiac eletrical activity travel through heart

A

action potential is conducted cell-to cell by direct coupling

cells connected by intercalated disks and gap junctions

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43
Q

how does a cardiac electical signal make a heart beat

A

action potential –> intracellular calcium transport –> contraction force

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44
Q

what is the “pacemaker potential” or “automaticity” in cardiac myocytes

A

specialized cells that can cause their own AP/depolarization

nodes= impulse generation sites

control heart beat

*SA node, AV node, purkinje fibers

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45
Q

how does parasympathetic neuronal input affect the heart?

A

parasympathetic–>vagus nerve–> acetylcholine –> DECREASE heart rate

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46
Q

how does sympathetic neuronal input affect the heart?

A

sympathetic –> T1-4 spinal nerves –> norepinephrine –> INCREASE heart rate

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47
Q

What is the spontaneous rate of the SA node?

A

70-80 AP’s/min

**main pacemaker

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48
Q

What is the spontaneous rate of the AV node?

A

40-60 AP’s/min

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49
Q

What is the spontaneous rate of the purkinje fibers?

A

15-40 AP’s/min

*not a good pacemaker

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50
Q

what is the Frank-starling mechanism? how does it relate to the heart?

A

strength of contraction is proportional to the end diastolic volume/pressure

significance of atrial contraction: “kick” fills ventricle with blood

increased volume of blood stretches the ventricular wall, causing cardiac muscle to contract more forcefully

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51
Q

Why/HOW is conduction through the AV node very slow

A

allows for complete emptying of atrial blood into ventricle

slow Ca2+ channels take longer to develop AP and velocity reduced (versus fast Na+ channels in His/purkinje)

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52
Q
A
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53
Q

Describe the normal sequence of VENTRICLE depolarization: AP is conducted…

A

VENTRICLE depolarization: AP is conducted…

apex–>base

endocardium –>epicardium

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54
Q

total time from impulse initiation in SA node to repolarization of ventricles

A

~600 msec

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55
Q

Hexaxial Reference System

A
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56
Q

Describe the unipolar precordial/chest leads

A

all 6 (+)

V1-V6

records the AP in the horizontal plane

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57
Q

relationship of vectors to deflections of EKG: when do you have a (+) upstroke on EKG

A

when the mean cardiac vector is parallel and in SAME direction as EKG lead axis orientation

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58
Q

relationship of vectors to deflections of EKG: when do you have a (-) downward stroke on EKG

A

when the mean cardiac vector is parallel but OPPOSITE direction to EKG lead axis orientation

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59
Q

relationship of vectors to deflections of EKG: when do you have a biphasic signal on EKG

A

when the mean cardiac vector is PERPENDICULAR to the EKG lead axis orientation

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60
Q

Describe the QRS changes as the AP progresses through the unipolar precordial/chest leads

A

V1–>V6

R wave increases

S wave decreases

*zone of transition ~V3: R and S waves equal in amplitude

L ventricle has larger mass

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61
Q

how does the EKG change with decreased AV conduction (“conduction failure”)

A

prolonged PR interval

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62
Q

how does the EKG change: ventricular pre-excitation (“wolfe-parkinson-white”)

A

shortened PR interval

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63
Q

how does the EKG change: slow conduction through the ventricle or purkinje fibers (bundle branch block)

A

widened QRS duration

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64
Q

how does the EKG change: slow repolization of ventricles

A

long QT interval

*increase risk for arrhythmias

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65
Q

what is a “corrected QTc interval”

A

as heart rate increases, the AP duration decreases, the QT interval decreases

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66
Q

how does the EKG change: ischemia

A

elevation or depression of ST segment (plateau of AP)

plateau of AP is not flat bc not all cells are depolarized

K+ channels open and AP shorten

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67
Q

how does the EKG change: subendrocardial ischemia

A

ST segment depression

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68
Q

how does the EKG change: epicardial ischemia

A

ST segment elevation

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69
Q

explain excitation-contraction coupling

A

electrical stimulation of the heart results in mechanical work

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70
Q

describe the sarcolemma around myocyte

A

specialized plasma membrane

contains T-tubules, SR’s, and Ca2+ channels to trigger contractions

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71
Q

2 enzymes of the sarcoplasmic reticulum

A

calcium release channel (ryanodine receptor) and SR Ca2+-ATP-ase pump

to release and remove Ca2+ from cytoplasm during contraction

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72
Q

explain the calcium-induced-calcium release in myocytes

A

positive-feedback mechanism to amplify rise in cytoplasmic Ca

outside Ca influx triggers inside Ca release from SR

increases strength of contraction

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73
Q

describe crossbridge formation in myocytes

A

ATP hydrolyzed by myosin head

Ca binds to troponin C

conformation change of tropomyosin

reveals binding site on actin

crossbridge formation

power stroke

ADP released from myosin

new ATP binds myosin

myosin releases actin

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74
Q

the “treppe effect” or staircase phenom of cardiac muscle

A

effect of repetitive stimulation on force: increase [Ca] in SR= increase contraction force)

increased stimulation frequency= increase in Ca release= increased tension=

increase in contractile state

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75
Q

explain the law of La Place in cardiac performance

A

increased venous return= increase in diastolic filling= greater end diastolic volume= greater wall tension

76
Q

cardiac performance: preload

A

ventricle wall tension prior to contraction

end diastolic volume stretches and determines the sarcomere length

increased preload= increased cardiac output

–pressure at end diastole used to estimate preload

77
Q

explain Frank-Starling relationship in cardiac muscles

A

increased preload/end diastolic volume= increased cardiac performance

increase diastole = increase systole= increast cardiac output

78
Q

cardiac performance: afterload

A

force aginst which the cardiac muscle is working in systole

limits ventricular performance

increased afterload= dec velocity= dec shortening of muscle fibers

–during systole, chamber radius falls, so afterload decreases during ejection

79
Q

4 major variables of effective cardiac output

A

1 contractile state

2 preload

3 afterload

4 heart rate

80
Q

effects of a (-) inotroph on myocardium contractility

A

decrease contractility

ex) Acidosis, ischemia, Ca channel blocking drugs, and Β-adrenergic blockers

81
Q

effects of a (+) inotroph on myocardium contractility

A

increase contractility

ex) NE, catechols, Digoxin, Drugs that Increase Ca availability to sarcomeres;

increase preload; increase CO

82
Q

how does the B-adrenergic receptor system affect the heart

A

autonomic nervous system increases nodal depolarization and strength of contraction

B-adrenergic stimulation: inc Ca= increase contraction

inc uptake by SR= faster relaxation

**most important single mediator of cardiac perfomance due to effects on contractility, relaxation, and rate

83
Q

Cardiac vs. Skeletal Muscle: how to vary force of contraction

A
  • Both types can vary force of contraction by changing fiber length
  • Only skeletal muscle can increase force through increasing frequency of stimulation
  • Only cardiac muscle can increase force through increasing contractility
84
Q

what is the Z-band

A

Z Band: End of sarcomere, Site of interclated disk, Site of insertion for thin filaments, Site of “triad”: (the T tubule, Ca channel, and SR meet)

85
Q

define contractility in myocardium

A

•Cardiac muscle increases strength of contraction through changing contractility
•the contractile state determines:
–The velocity of muscle fiber shortening
–Extent of shortening
•Determined by [Ca2+]i
•

86
Q

myocardium: Increasing preload

A

Increasing preload increases

the velocity and extent of shortening if afterload is constant

87
Q

myocardium: Increasing afterload

A

Increasing afterload reduces

the velocity and extent of

shortening for any given preload

88
Q

Cardiac vs Skeletal muscle: contraction

A

•Cardiac muscle contraction requires extracellular Ca2+
–CICR triggered by influx of calcium from outside cell
–skeletal muscle contraction triggered by AP directly; CICR does not require Ca influx
•Skeletal muscle can increase force by recruitment of other cells
•Cardiac muscle is a functional synctitium, all cells contract and relax together

89
Q

myocardium: what changes in the sarcome during contraction

A
  • The length of the filaments does not change
  • Z line to Z line distance gets shorter
  • H band and I band get shorter
  • A band does not change in size
90
Q

how are the semilunar and atriventricular valves opened?

A

high pressure in the ventricles and atria, respectively

91
Q

what is the difference in ventricular activity for diastole and systole?

A

diastole is ventricular filling (relaxation), systole is ventricular emptying (contraction)

92
Q

what is happening during the P wave?

A

atrial depolarization

93
Q

What is happening during the T wave?

A

ventricular repolarization until ventricular relaxation

94
Q

what is happening during the QRS complex?

A

ventricular depolarizaton to ventricular contraction

95
Q

what are the 5 stages of the left ventricular pressure-volume loop?

A
  1. isovolumetric contraction
  2. ejection (period between aortic valve opening and closing)
  3. isovolumetric relaxation
  4. rapid ventricular filling (as soon as mitral valve opens)
  5. slow ventricular filling (right before MV closes)
96
Q

what is happening in isovolumetric contraction?

A

beginning of ventricular systole (contraction) but the aortic valve is closed therefore volume does not change but pressure is rising quickly.

*valves are closed because pressure in aorta is higher than pressure in the ventricle

97
Q

the period of rapid ejection begins when pressure within the ventricle is _1_ compared to the aorta or pulmonary artery?

98
Q

In isovolumetric relaxation, there is a _1_ in ventricular pressure.

It ends when there is what kind of relationship between the ventricle and atrium?

A
  1. decrease

when the pressure in the ventricle falls below the atrium

99
Q

What does the a wave represent in the atrium?

A

atrial contraction.

*follows P wave of EKG

100
Q

what does the c wave represent?

A

ventricular contraction

101
Q

what does the x descent represent (3)?

A
  1. ventricular emptying
  2. thoracic volume and pressure fall
  3. rapid fall in atrial pressure
102
Q

what does the v wave represent?

A

flow of blood from veins to atria.

*long period of time, AV valves are closed

103
Q

the v wave corresponds roughly with which segment of the EKG?

A

ST segment

104
Q

the *y *descent represents what?

A
  • atria draining into the ventricles
  • rapid fall in atrial pressure
105
Q

What does the S1 heart sound represent?

“LUB”

A

the mitral and tricuspid valves closing (AV valves)

*at this time the AoV and P valve are opening quietly

end diastole

slow, low pitched sound

106
Q

What are you hearing with the S2 heart sound?

“DUB”

A

aortic and pulmonary valve closure

*as MV and TV valves open quietly

end of systole

rapid, high frequency sound

107
Q

What are you hearing with the S3 heart sound?

A

mitral regurgitation (preload is high, pressure in ventricle increases and MV opens as a result of increased pressure)

108
Q

what are you hearing with the S4 heart sound?

A

atrial contraction: the left atrium pushing against a stiff left ventricle

  • high atrial pressure
  • may lead to ventricular hypertrophy
109
Q

S4 occurs during with segment of the EKG? Which part of the jugular pulse curve?

A

P-Q interval; a wave (aortic contraction)

110
Q

S1 occurs during which part of the EKG diagram? jugular pulse?

A
  • QRS complex (mainly RS when isovolumentric contraction ends)
  • c wave (ventricular contraction)
111
Q

S2 occurs during what part of the EKG?

A

at the end of the T wave when the ventricle has finished emptying

112
Q

What are the 3 types of cardiac action potentials?

A
  • ventricular- atrial- nodal
113
Q

Describe each of the phases (5) of cardiac action potentials.

A

0: rapid depolarization 1: brief, partial repolarization (absent in nodal)2: plateau (shorter in atrial, absent in nodal)3: complete repolarization (back to resting or pacemaker)4: resting potential (ventricular & atrial) or pacemaker potential (nodal)

114
Q

Nodal action potentials differ from atrial and ventricular in that they lack which phases?

A

Nodal APs lack phases 1 and 2

115
Q

Which type of cardiac APs are significantly slower (takes longer from start to finish) than the others?

A

Nodal is much slower than atrial or ventricular

116
Q

Which ion is responsible for depolarization in each of the cardiac AP types?

A

Ventricular and Atrial: Na+ influxNodal: Ca^2+ influx

117
Q

Describe the difference between resting potential (phase 4) in the 3 types of cardiac APs.

A

Atrial and ventricular (resting potential) is constant at about -80 mVNodal (pacemaker potential) slowly depolarizes toward threshold (max hyperpolarization is -60 mV) due to the “funny” Na+ that open on hyperpolarization

118
Q

Why is pacemaker potential not constant?

A

Pacemaker potential in nodal APs slowly depolarizes because the “funny” Na+ channels are open during hyperpolarization

119
Q

How to cardiac APs control heart rate?

A

the frequency of nodal APs control heart rate (the duration of phase 4 will lengthen or shorten)

120
Q

In general, what ion conductances does the autonomic nervous system alter to change heart rate? (3)

A
  1. Na+2. K+3. Ca^2+
121
Q

How does the parasympathetic nervous system slow the heart rate?

A

Vagus nerve: releases ACh- depolarize the threshold - decreases Na+ and Ca^2+ permeability and increases K+ permeability during pacemaker potential (hyperpolarization)

122
Q

How does the sympathetic nervous system increase heart rate?

A

Release of norepinephrine during pacemaker potential- increases Na+ and Ca^2+ potential and decreases K+ permeability (depolarizes)

123
Q

normal EKG values: PR interval

A

PR interval=

120-200ms,

.12-.20s

124
Q

normal EKG values: P wave

A

P wave:

60-100ms,

.06-.10s

125
Q

normal EKG values: QRS duration

A

QRS duration

60-100ms,

.06-.10s

126
Q

Normal EKG values: QT interval

A

QT interval

450ms, .

45ms

127
Q

myocardium: ischemia vs infarction

A

ishemia- restriction in blood supply/can be reversed

infarction- necrosis/damage/not reversible

128
Q

stable vs unstable angina

A

no ekg changes, can have changes in lab values for cardiac enzymes

stable: predictable pain, on exertion, goes away with rest
unstable: changes from usual pattern, at rest

129
Q

normal heart rates by age

A

Infants: 100 to 160 beats per minute
Children 1 to 10 years: 70 to 120 beats per minute
Children over 10 and adults: 60 to 100 beats per minute
Athletes: 40 to 60 beats per minute

130
Q

types of aortic stenosis (3)

131
Q

signs of severe aortic stenosis (3)

A
  1. delayed, small volume carotid upstroke (turbulance= shuddering of valve)
  2. loss of A2
  3. late peaking murmur

on top of common aortic stnosis sx: CP, DIB, syncope, heart failure signs, JVD, S4

132
Q

in the clinic: why do we make patients stand or valsalva

A

reduce venous return

reducec systolic

decrease aortic pressure

increase heart rate

shrink heart

make murmurs worse (HCM and MVP)

133
Q

hypertrophic cardiomyopathy

A

buldging of septum into outflow tract

occurs as midsystolic murmur

heard best at LLSB

brisk carotid upstrokes, no ejection sound

murmur increases with standing/valsalva

most common in young people with sudden loss of consciousness

134
Q

describe pulmonic stenosis and associated heart sound

A

obstruction of flow from the right ventricle of the heart to the pulmonary artery

inc resistance to blood flow causes right ventricular hypertrophy

midsystolic ejection murmur that does NOT radiate to carotids

widened S2 split

varies with respiration

135
Q

describe an innocent systolic murmur

A

caused by high flow in outflow tracts

“stills murmur” in children

crescendo-decrescendo ejection murmur

common in pregnancy, anemia, fever, high output state

localized to pulmonic or aortic area

136
Q

describe a holosystolic or “pansystolic” murmur

(2 types)

A

begins with SA and end after S2

caused by high flow

harsh, blowing, well heard with diaphragm

  1. AV valve leakage
  2. interventricular shunt
137
Q

chronic mitral regurgitation and associated heart sound

A

caused by mitral valve prolase

leads to chronic volume overload of L ventricle

can hear at axilla and base

increases with inceased afterload (squatting)

holosystolic murmur (from S1 through S2; pansystolic)

S3

harsh/ blowing sound

138
Q

describe mitral valve prolapse and associated heart sound

A

mitral leaflet moves into LA suring systole

causes mild systolic “click”

can cause regurgitation

139
Q

describe mitral stenosis and associated heart sound

A

narrowing of the heart’s mitral valve= decreased blood to L ventricle

turbulent, high velocity flow in diastole

mainly caused by rheumatic heart disease

can cause atrial fibrillation

rumbling diastolic murmur: opening snap, loud S1

OS= sharp

140
Q

signs of severe mitral stenosis

A

long diastolic rumble (pandiastolic)

short A2-OS interval

pulmonary hypertension= loud P2 and RV lift

artial fibrillation

CHF

141
Q

aortic regurgitation and associated heart sound

A

incompetant aortic valve

loss of cardiac output backwards from aorta into LV

LLSB with diaphragm (high frequency): S3

midsystolic murmur (MSM) and blowing, decrescendo early diastolic murmur (EDM)

best heard when pt leans forward and breathes out

bounding carotid pulse palpable (increased systolic arterial pressure)

142
Q

PE findings: “water hammer pulses”

A

wide pulse pressure with low diastolic

Due to the large stroke volume and “aortic runoff” of blood from the aorta back into the left ventricle, there is a sudden rise and abrupt collapse of peripheral arterial pulse.

143
Q

PE findings: Durrosiez’s sign

A

to and fro bruit at femoral artery

144
Q

PE findings: Hill’s sign

A

popiteal arterial pressure > 20 mmHg more than brachial

145
Q

PE findings: Quinke’s sign

A

Quincke’s: pulsating capillary refill in slightly compressed fingernail bed

nailbed flush with systole

146
Q

PE findings: de Musset’s sign

A

deMusset’s sign: bobbing of head with each heart beat

147
Q

signs of severe aortic regurgitation

A

diastolic BP less than 50

enlarged LV (large regurgitant volume)

S3

CHF sx

bounding (Corrigan’s) pulses

148
Q

in the clinic: why do we make patients squat during cardiac exam

A

increase venous return

increase venous return

increase murmurs (AS and MR)

149
Q

physiological splitting of S2

A

normal sound

asynchronous A2 aortic and P2 pulmonic valve closure
heard on inspiration over pulmonic valve

inspiration draws more blood into expandedlungs and RA/RV

increased duration of left ventricular systole

*these change with respiration

150
Q

abnormalities of S2

A 
loud P2/ audible at apex= hypertension
single S2 (A2 OR P2 MISSING)
WIDE S2 SPLITTING
PARADOXIAL SPLITTING (P2 before A2)
\*these not change with respiration
151
Q

abnormalities of S2: what can cause a wide S2 splitting

A

pulmonic stenosis, mitral regurgitation, R bundle branch block, atrial septal defect

152
Q

abnormalities of S2: what can cause a loud S2 heard even at the apex

A

loud P2/ audible at apex= hypertension

153
Q

what disease does hearing an S3 indicate?

A

volume overload
rapid filling of diastole

154
Q

what disease does hearing an S4 indicate?

A

hypertension
hypertrophic cardiomyopathy
aortic stenosis

155
Q

grading murmurs

A

1/6= less than S1/S2
2/6= murmur is equal S1/S2
3/6=murmur is greater than S1/S2
4/6= palpable thrill
5/6= heard with stethoscope
6/6= audible with naked ear

156
Q

murmur patterns (4)

A

holosystolic
crescendo
decrescendo
crescendo-decrescendo

157
Q

Corrigan’s pulse

A

visibly bounding arterial pulse

common in carotid, brachial and femoral arteries with increased systolic arterial pressure

158
Q

describe aortic stenosis and its related heart sound

A

aortic valve narrows

listen ay 2RICS: harsh crescendo-decrescendo midsystolic murmur (MSM)

S2 split

3LICS: sharp ejection sound (ES)

159
Q

describe a holosystolic murmur

A

(HSM) fills the entire systole, and may even obscure the two heart sounds.

160
Q

What dx alters the QRS on EKG

A

bundle branch blocks

abrnomal depolarization (VPC’s)

myocardial disease

161
Q

what is happening here?

A

increased venous return

162
Q

what is happening here?

A

atrial contraction

increased venous return

increased pressure in right atrium

163
Q

what is happening here?

A

no a wave

filling from right atrium to ventricle is high (sharp y curve)

x is small because atria doesn’t relax

164
Q

what is happening here?

A

increase PR interval. for the curve, nothing has changed from sinus rhythm because a first degree block is asymptomatic.

165
Q

what is happening here?

A

high atrial contraction

166
Q

what is happening here?

A

ventricle is not contracting

167
Q

what is happening here?

A

atria are contracting but nothing else is working because the signal cannot get past the AV node.

168
Q

two functions of the venous system?

A

blood storage/liberation, regulat return of blood to heart

169
Q

% of the total blood volume is contained in the venous system (think about earth)

170
Q

what is the effect of sympathetic stimulation on venous tone? how does that change blood flow?

A

venous tone increases, less blood is held in the veins.

171
Q

CVP is also equal to what?

A

venous pressure equal right atrial pressure

172
Q

Myocardial ischemia

A

insufficient blood flow

O2 delivery< O2 demand

Leads to: heart failure (loss of systole/diastole), arrhythmia, tissue damage, dyspnea, angina pectoris

173
Q

Collateral vessel

A

After a coronary artery occlusion, collateral vessels often develop to shunt blood around the blockage.

174
Q

Physiologic role of conduit vessels in coronary circulation

A

Arteries and veins that supply the myocardium

175
Q

Physiologic role of resistance vessels in coronary circulation

A

Precapillary arterioles that regulate flow to myocardium

176
Q

Physiologic role of exchange vessels in coronary circulation

A

Capillaries that allow gas/nutrient exchange at myocardium

177
Q

Physiologic role of capacitance vessels in coronary circulation

A

Venules that return blood from the myocardium to the heart

178
Q

rate of Normal coronary blood flow

A

1ml/min/g myocardium at rest, and 4 ml/min/g with exercise

179
Q

Acute vs subacute vs sustained state of myocardial ischemia

A

Acute is reversible (<10min),

subacute is slowly reversible/”stunned” (10min-10hrs),

Sustained is irreversible/”infarcted”(>10 hrs)

180
Q

Name some mechanisms that control coronary blood flow

A

metaboliuc regulation- meet myocardium’s demands

physical factos- pressure on vessel

physioligical response- changes due to NO or NE release

181
Q

What happens if the MAP (mean arterial pressure drops below 50mmHg?

A

loss of blood flow to the coronary blood vessels and myocardium

vital organs will not get enough Oxygen perfusion, and will become hypoxic, a condition called ischemia.

182
Q

what can happen if the diastolic intraventricular pressure is too high or if diastole is too short (ex due to rapid heart rate)

A

lack of blood flow to the coronary arteries and myocardium

myocardium perfusion occurs in DIASTOLE

183
Q

What is MAP?

A

[MAP] is considered to be the perfusion pressure seen by organs in the body.

average arterial pressure during a single cardiac cycle

[MAP}= {2/3}(DP) + (1/3}(SP)]

[MAP = (CO *SVR) + CVP]

184
Q

describe this calculation for coronary afteries: Functional flow reserve (FFR)

A

Calculates pressure gradient in coronary artery before and after an obstruction/stenosis

FFR= P(distal)/P(aorta)

**FFR<.75 is BAD

185
Q

describe this calculation: Coronary artery stenosis gradient

A

Measure perfusion pressure in coronary artery before and after an obstruction/stenosis

∆P= P(aorta)-P(distal)

CPR Midterm (15 decks)

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