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Critical Care I > test 2 > Flashcards

test 2 Flashcards

1
Q

Pressure waves are sent through body and echo waves return to the transducer elements and are processed to create ultrasound images

A

ultrasound

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2
Q

the major source of sound wave attenuation is soft tissue (the conversion of energy to heat)

A

absorption

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3
Q

occurs when sound waves encounter a boundary between two different media.

A

reflection

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4
Q

when waves are reflected off of bone an ____ _____ will be created

A

acoustic shadow

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5
Q

when us waves encounter a medium with non-homogenous surface

A

scatter

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6
Q

the consequence of scatter is

A

speckle

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7
Q

why is gel used in ultrasound

A

ensures proper contact between transducer and patient, for sound to travel through tissues

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8
Q

frequency (Hz) of the wave is measured in

A

cycles per second

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9
Q

Ultrasound imaging frequency

A

1-20 MHz

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10
Q

what frequency is better for deeper structures

A

lower frequency waves

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11
Q

frequency that provides better resolution for shallow structures

A

high frequency waves

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12
Q

Ultrasound gets _____ in tissue, signals get ____ in deeper structures, resulting in _____images.

A

Ultrasound gets attenuated in tissue, signals get weaker in deeper structures, resulting in darker images

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13
Q

_______ may prevent imaging behind solid structures

A

absorptions

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14
Q

_________may prevent imaging behind solid structures or air

A

Hard reflections

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15
Q

ultrasound transducer that provides a wide, near field image

A

Curved Array

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16
Q

when scanning for fetus or abd what type of transducer would you use

A

Curved array

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17
Q

pie shaped image, quality not as good as curved array.

A

phased array

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18
Q

what type of transducer would be better for ultrasounding the heart behind ribs

A

Phased array

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19
Q

transducer that gives the best resolution, used in vascular and superficial soft tissue studies

A

linear array

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20
Q

runs parallel to the ground separating superior from inferior

A

transverse plane

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21
Q

oriented perpendicular to ground separating pt left from right

A

Sagittal/longitudinal plane

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22
Q

separates the pt anterior from posterior

A

coronal plane

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23
Q

used to image structures that don’t line up with the other planes

A

Oblique plane

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24
Q

commonly used mode in ultrasound, different shades of gray in a 2 dimensional picture

A

B mode

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25
Q

captures returning echos along one line of the real time image. Used to quantify motion over time

A

M mode (motion mode)

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26
Q

frequency shift caused by sound waves interacting with a moving target

A

Doppler

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27
Q

used to visualize and quantify blood flow information

A

pulsed wave doppler

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28
Q

shows approx speed and direction of blood flow inside the vessel

A

color doppler

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29
Q

This color is used to identify blood flowing toward the transducer

A

red

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30
Q

This color is used to identify blood flowing away from the transducer

A

blue

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31
Q

looks at the strength or amplitude of the returning signal. assigns a color based on the strength or amplitude of the returning signal

A

power doppler

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32
Q

P on the R side of the cone image indicates what mode

A

cardiac

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33
Q

P on the L side of the cone image indicates what mode

A

standard

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34
Q

in cardiac mode the probe should be facing the

A

L shoulder

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35
Q

the Left ventricle should be on what side of the screen for cardiac mode

A

Left

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36
Q

in standard mode the probe should be facing the

A

Left hip

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37
Q

what is the optimal pt positioning for a cardiac ultrasound (Transthoracic echocardiography)

A

L lat decubitus positon which brings heart forward

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38
Q

steps for Parasternal Long Axis for Echocardiography

A

1) cardiac mode
2) Indicator to R shoulder
3) nipple line/4th intercostal space

3 Ls for success
for the PLA put the LV on the Left of the screen

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39
Q

gold standard for estimating ejection fraction in Echocardiography

A

Eyeballing EF by looking at the squeeze of the heart, and how closely the anterior mitral valve leaflet gets to the intraventricular septum
in the PLA view

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40
Q

what are the exceptions that would falsely quantify EF using the eyeball method

A

Aortic regurgitation

mitral stenosis

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41
Q

fluid is anterior to the descending aorta in the echocardiogram

A

Pericardial effusion

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42
Q

if the effusion is posterior to the descending aorta

A

Pleural effusion

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43
Q

diastolic collapse of the Rv with clinical symptoms of hypoperfusion (hypotension, tachycardia, syncope, sob, ect)

A

Pericardial tamponade

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44
Q

if you start at the PLA and rotate the probe 90 degrees clockwise towards to pt L shoulder, fan towards apex then up towards base

A

Parasternal short axis (PSA view)

“fish mouth and mercedes benz sign view”

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45
Q

to get the mid papillary on the PSA

A

fan towards apex

papillary muscles in view

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46
Q

Mitral valve view on PSA

A

fan probe towards base

“fish mouth mitral view)

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47
Q

Aortic valve view on PSA

A

Fan probe towards base

Mercedes-benz aortic valve

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48
Q

D sign on PSA

A

R ventricular strain

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49
Q

Apical 4 chamber

A

Left axilla,

Fan upwards at apex (towards pt head)

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50
Q

Subxiphoid View on Echocardiography

A

Subxiphoid region
Indicator to Left
overhand grip on probe
probe almost parallel to skin

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51
Q

IVC measurements help with

A

fluid management

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52
Q

caval index =

A

preload reserve

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53
Q

electrical path for heart

A

SA node ->AV node ->HIs purkinje system -> R and L bundle

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54
Q

electricity that moves towards a lead creates ___________ known as a ____

A

electricity that moves towards a lead creates a positive deflection known as a R wave.

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55
Q

electricity that moves away from a lead creates a _______ or an _____

A

electricity that moves away from a lead creates a negative deflection or an S wave

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56
Q

The leads that are placed across the chest are known as the ______-

A

Precordial leads (V1-V6, V3R, V4R)

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57
Q

Leads I, aVL, V5, V6, V7 cover the

A

L lateral side of the heart

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58
Q

Leads aVR, V3R and V4R cover the

A

R side of the heart

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59
Q

Leads II, III and aVF are classically known as the

A

inferior leads

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60
Q

V1-V4

A

anterior leads

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61
Q

V1 and V2

A

give a better idea of how the septum depolarizes

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62
Q

each small box on the EKG is

A

40 milliseconds in duration

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63
Q

in terms of the amplitude, the ECG is performed at

A

10millimeters per millivolt, 10 squares high

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64
Q

mathematical way of calculating heart rate on an EKG strip

A

Count squares between each QRS complex (each small square is 40milliseconds)

# s x 40ms = cycle length
divide 60,000 by the cycle length and this will give you the heart rate in beats per minute
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65
Q

Estimation method for calculating HR

A

find QRS closest to a thick black line and start counting at the next thick black line…300, 150, 100, 75 till you get to the next QRS
or 300 divided by 4 will give you the same

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66
Q

NSR is set by the

A

SA node

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67
Q

Atrial contraction produces what on the EKG

A

P wave

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68
Q

Ventricular contraction produces what on the EKG

A

QRS complex

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69
Q

In normal adults, electricity moves downwards and to the left towards the left ventricle.

what does this do to the ekg

A

On the EKG you will see a R wave in lead I and in aVF

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70
Q

In children, the _____ is more dominant. As a result, electricity tends to move downwards and towards the R side of the chest. This is seen in what age?

A

R ventricle

over the first 6 months it starts to shift

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71
Q

If a pt had a right axis deviation, you would see a

A

lead 1 would have Prominent S wave

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72
Q

In II, III and aV5 they all have prominent S waves so they have the negative deflections

A

Superior Axis

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73
Q

what does a Superior axis indicate and who is it seen in commonly

A

Atrioventricular canal
- common in pt with Trisomy 21

Tricuspid Atresia

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74
Q

what represents atrial depolarization (contraction)

A

P wave

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75
Q

P wave represents the

A

atrial depolarization

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76
Q

2nd half of the P wave represents the

A

L atrial contraction

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77
Q

Normal values for P wave

A

No more than 3 squares high and 3 squares wide

Less than 0.3 millivolts or duration less than 120 milliseconds

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78
Q

where is the best place to look at the P wave

A

leads II and V1 (most prominent deflections on an ECG)

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79
Q

Large peaked P wave is seen in

A

R atrial enlargement (usually >0.3 millivolts)

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80
Q

a Large notched P wave is seen in

A

L atrial enlargement

usually greater than 120 milliseconds

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81
Q

what does L atrial enlargement look like in lead V1

A

slurred terminal portion of the P waves (Biphasic P wave)

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82
Q

what part of the EKG reflects intra-atrial conduction

A

PR interval

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83
Q

A normal PR interval is less than

A

200milliseconds

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84
Q

1st degree heart block refers to a PR interval

A

greater than 200miliseconds

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85
Q

electricity from time to time gets blocked in the AV node so every now an then you have a P wave without a QRS complex

A

2nd degree heart block

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86
Q

second degree heart block that the PR intervals get longer and longer until a QRS is dropped then it starts over

A

Mobitz type 1 (Wenckebach)

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87
Q

P waves that do not have a QRS complex afterwards. Before the dropped QRS, the PR interval stays the same throughout

A

Mobitz type 2

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88
Q

which 2nd degree heart block is always pathological

A

Mobitz type 2

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89
Q

There is no impulses conducted through the AV node to the ventricles

A

3rd degree heart block

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90
Q

on the EKG strip the atrium and ventricle are beating independent of each other

A

3rd degree heart block

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91
Q

abnormal conduction through the ventricles can be seen by evaluating the

A

QRS complex

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92
Q

wide QRS complex is >

A

120 milliseconds

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93
Q

what has a wide QRS

A

R bundle branch block because electricity moves slower through the R Purkinje fibers and thus the left ventricle activates first

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94
Q

In R bundle branch block what does EKG show

A

first half of QRS complex = LV depolarization
V1 will have a small R wave
V6 will have a qR complex
(left ventricle depolarizing)
in V1 you see a tall slurred R prime (“bunny ear complex”)
V6 you see a slurred S wave as electricity moves away from V6 as the R ventricle contracts

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95
Q

L bundle branch block

A

V1 has an rS pattern

V6 has the bunny ear pattern with a tall notched R wave

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96
Q

In terms of hypertrophy the QRS deflections reflect the

A

mass of ventricles

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97
Q

what does R ventricular hypertrophy show on EKG

A

large R wave in V1
large S wave in V6
abnormal T waves in the R precordium
QR pattern in V1 or an RSR prime pattern (R prime has to be quite large) in V1 can also be used to diagnose RVH

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98
Q

L ventricular hypertrophy

A 
large R wave in V6
large S wave in V1
or 
RS ratio greater than 98% percentile
T wave inversions in the Left lateral precordium can also be looked for as can a left axis deviation
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99
Q

the end of the QRS complex to the beginning of the T wave is the

A

ST segment - isoelectric

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100
Q

changes in the ST segment can reflect

A

ischema or inflammation

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101
Q

diffuse ST elevations across all of your leads

A

Pericarditis

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102
Q

what shows ventricular depolarization and can change as the patient ages

A

T wave

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103
Q

In general the T wave follows the axis of the

A

QRS

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104
Q

T wave changes along the R precordium is observed in leads

A

v1-v3

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105
Q

from birth to seven days what do you see on the EKG

A

positive T waves noted

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106
Q

from 1 week to adolescence what happens to the T waves

A

the t waves flip over and are negative

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107
Q

After your teenage years, what happens to T waves

A

they flip over and become positive in the r precordium

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108
Q

after one week old, positive T waves seen in V1 reflect

A

RVH

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109
Q

the beginning of the QRS complex to the End of the T wave

A

QT interval

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110
Q

when measuring QT interval what leads do you use

A

Lead II and V5

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111
Q

Pt with prolonged QT interval is at risk for

A

ventricular arrhythmia and sudden death

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112
Q

Bazett’s formula

A

Divide QT interval by the sq root of the preceding RR complex (ms between QRS complexes right before the QT interval of interest)

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113
Q

In general the number to keep in your head for Bazett’s formula is less than

A

QTc = 450 ms

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114
Q

Anatomic presence of an accessory conduction pathway that allows for reentrant SVT

A

Wolff-Parkinson White (WPW)

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115
Q

what population is at higher risk for WPW

A

males

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116
Q

Symptoms of WPW

A 
palpitations
presyncope/syncope
sudden cardiac death
Dizziness
Chest Pain
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117
Q

characteristic ECG findings associated with WPW

A

short PR interval
delta wave which is a slurring of the P wave into the QRS
widening of the QRS complex

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118
Q

Associated congenital heart disease lesions in WPW

A

Ebstein anomaly (abnormal development of tricuspid valve)
Hypertrophic cardiomyopathy
L-transposition of great arteries (congenitally corrected transposition of great arteries, ventricular inversion)

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119
Q

diagnostics of WPW

A

ECG
Echocardiogram
Holter exercise stress ECG

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120
Q

Treatment WPW

A

B Blockade for symptomatic patients- only if not able to have ablation

Activity restriction with pts who have high risk pathways
Intracardiac catheterization for electrophysiology studies (EPS) with ablation of accessory pathway

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121
Q

meds contraindicated in WPW

A

Ketamine
Caution in reversal agents - neostigmine/atropine/glycopyrrolate - tachyarrhythmias

If pt has irregular wide complex tachycardia, these meds are highly contraindicated- at higher risk for life threatening ventricular arrhythmias
Adenosine
CCBs
B Blockers

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122
Q

genetics Long QT

A

Can be inherited in both autosomal dominant and receptive fashions

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123
Q

Symptoms Long QT

A

syncope/presyncope
Palpitations
Sudden cardiac arrest
Lightheadedness

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124
Q

Normal QTc

A

males: <440ms, females <460ms

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125
Q

For assessing QTC what leads do you use on EKG

A

II or V5

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126
Q

How do you calculate QTC

A

Step 1: Calculate the QT interval (every small box is 400ms, big box is 200ms)
Draw a tangential line along the descending slope of the T wave. Where it intersects at the baseline would be the end of the QT interval. The beginning of the QRS to the end of the T milliseconds

Step 2: Calculate the R-R interval preceding the QT interval you calculated.

STep 3: Using Bazett’s formula: The QTC is equal to the QT interval divided by the square root of the preceding R to R interval.

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127
Q

2 other arrhythmias seen in long QT

A

Torsades de point is seen in Long QT syndrome - polymorphic ventricular tachycardia that varies from a large amplitude QRS complexes to small amplitude QRS complexes and goes back and forth.
PALS algorithm
Treat with magnesium sulfate to reverse

Pseudo 2:1 AV block in the presence of a long QT
In neonates - poor prognosis with high risk of mortality. High suspicion for needing an ICD.

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128
Q

How do you treat Torsades de point in long QT

A

magnesium sulfate

PALS algorithm

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129
Q

diagnostic tools for long QT

A

ECG
Stress Testing
Holter monitor
Genetic testing

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130
Q

Probability tool used in long QT

A

Schwartz Score (probability scoring)

Less than or equal to 1 point - low (genetic testing should not be pursued)
1.5-3 points - Intermediate (genetic testing for pt and recommended ECG for relatives)
Greater than or equal to 3.5 points - High (genetic testing probability of positive is 80%)

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131
Q

what are the 3 types of long QT and what are their frequencies

A

LQTS1 -most common
LQTS2
LQTS3- least common type

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132
Q

Associated gene mutation for

LQTS1

A

Mutation in KCNQ1

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133
Q

Associated gene mutation for

LQTS2

A

Mutation in KCNH2

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134
Q

Associated gene mutation for

LQTS2

A

Mutation in SCN5A

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135
Q

LQTS1 due to loss of function in ?

A

Due to loss of function in the potassium ion gene

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136
Q

what is the key EKG feature for LQTS1

A

Early peaking T wave that comes soon after QRS complex

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137
Q

Most common trigger to lethal cardiac events in LQTS1

A

Exercise is the most common trigger to lethal cardiac event with swimming being the most common “SWIM”

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138
Q

LQTS2 due to loss of function in ?

A

Due to loss of function in the potassium ion gene

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139
Q

what is the key EKG feature for LQTS2

A

T wake is not as early peaking and has a saddleback-shaped appearance

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140
Q

Most common trigger to lethal cardiac events in LQTS2

A

Emotional stress is the most common trigger to lethal cardiac event “STARTLE”

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141
Q

LQTS3 due to increased function of ?

A

Gain of function in the Sodium ion gene

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142
Q

what is the key EKG feature for LQTS3

A

The T wave has a late peaking appearance to it

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143
Q

Most common trigger to lethal cardiac events in LQTS3

A

Periods of high vagal tone such as sleep and repose (state of tranquility) are the most common trigger to lethal cardiac event “SLEEP”

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144
Q

Treatment in LQT

A

B Blockade first line therapy (ie) propanolol, nadolol) - most effective for LQT1. Initiate even if asymptomatic.
LQT2 - less effective
LQT3 even less effective -

sodium channel blockade (Mexiletine) has shown some benefit in LQT3

Lifestyle modifications to avoid triggers
LQT1 - no competitive sports
LQT2 - normalize potassium levels and no alarms in bedroom

ICD(defibrillator): considered in specific cases

Left cardiac sympathetic denervation (LCSD) - removal of first 3-4 thoracic ganglia; benefit in high risk populations

Do not give this population medications that could increase risk for Long QT

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145
Q

atriums empty into the ventricles with contraction and blood flow through mitral and tricuspid valves

what is this?
Active or passive?

A

Diastole

Active

146
Q

Atrial kick?

A

important piece of diastole

atrial contribution to ventricular filling

147
Q

what valves are open during systole

A

Aortic and pulmonary

148
Q

what valves are closed during systole

A

Mitral and tricuspid

149
Q

full ventricles contract and pump blood to the lungs and body

A

Systole

150
Q

allows blood to flow from pulmonary vasculature to the body while in utero

A

PDA (patent ductus arteriosus)

151
Q

The heart grows …..

A

as blood flows

152
Q

Blood follows the path of

A

least resistance

153
Q

pressure leads to _____

A

Hypertrophy. If you have high BP, your heart is pumping against a high resistance so your ventricle will muscularize.

154
Q

Volume loaded heart leads to _____

A

Dilation or stretch

If you have a volume loaded heart

155
Q

umbilical vein is carrying ______ blood from ___ to ____

A

umbilical vein is carrying oxygenated blood from mom to baby

156
Q

PO2 of umbilical vein is

PO2 of the R atria -

A

30-35mmgHg

26-28

157
Q

in fetal circulation how many umbilical veins are there

A

1

158
Q

in fetal circulation how many umbilical arteries are there

A

2

159
Q

in fetal circulation from the umbilical vein….track the circulation

A

Mom to umbilical vein -> 50% travels to the ductus venosus and absorbed into hepatic blood flow/ 50% to the babys IVC where it joins in with cyanotic systemic venous return from the inferior vena cava -> Eustachian valve ushers blood to the PFO, only about 5% of the blood flows to the R ventricle and to the lungs ->from PFO to L atrium -> the 5% of venous blood returning from the lungs from the pulmonary v. joins here -> L ventricle -> ejects out systemically. Also there is a PDA which is another opportunity that made it into the RV to escape the lungs again, mixes and goes out systemically.

160
Q

Umbilical arteries carry ______ ______ from ____ to the _____

A

deoxygenated blood from the heart to the placenta (two arteries)

161
Q

What are the two places fetal circulation bypasses the lungs

A

PFO and PDA

162
Q

what ventricle works harder in utero

A

L ventricle

R ventricle gets very little blood flow

163
Q

65 % of the descending aorta output returns to the

A

placenta

164
Q

Descending aorta takes blood

A

deoxygenated blood sent to fetus and placenta through the umbilical arteries (65%)

165
Q

first few breaths in a newborn. what happens?

A

Oxygen content in the newborn raises dramatically -oxygen is a potent pulmonary vasodilator

vessels in the pulmonary artery - circulation relax and the Pulmonary vascular resistance (PVR) drops below systemic pressure.

PDA begins to close. Some will close within a few hours, sometimes days, sometimes months and some will have to have it surgically closed for them.

166
Q

CVP (central venous pressure) is the pressure in the

A

R atrium

167
Q

If pt had pulmonary htn or L atrial HTN from some obstruction the pulmonary wedge pressure would be

A

elevated

168
Q

Pulmonary wedge pressure

A

reflection of left heart’s cardiac output

169
Q

normal pressure in R atrium (CVP)

A

normal 2-6 but she says really this is more like 6-10

M=3

170
Q

normal pressure in RV

A

25/3

this is systolic/diastolic

171
Q

normal pressure in Pulmonary Artery

A

25/10

M=16

172
Q

pressure in RV is 25 and pulmonary A is 10 there is

A

Pulmonary stenosis or obstruction there

173
Q

Lv pressure

A

100/8

M=16

174
Q

aortic pressure

A

100/60

M=83

175
Q

LA pressure

A

M=8

176
Q

RV should be ___ of the pressure in the LV

A

1/4

177
Q

Pulmonary HTN - mean pulmonary artery pressure is greater than

A

25

178
Q

Pulmonary Capillary Wedge pressure normal and what does it measure

A

6-12
measures distal to the catheter so in the lung bed
actually reflects the pressure on the left side of the heart

so if the L ventricle relaxes well this will be less than 12

179
Q

If you have pulmonary HTN does your wedge pressure accurately detect the L sided heart pressure

A

no - the resistance in your lungs is high

180
Q

left ventricular end diastolic pressure (LVEDP)

A

3-12
at the end of diastole, when the LV is full of blood. In that moment before ejection starts, before contraction ejects blood across the aorta. This is the normal pressure

181
Q

If your LVEDP is high, what happens

A

blood does not want to travel into the LV - see in diastolic cardiomyopathy

182
Q

LVEDP is a measure of

A

diastolic function

183
Q

RV 80/9
Pulmonary A mean pressure is 30
what is this?

A

Pulmonary HTN

184
Q

Superior vena cava Saturations should be

A

75%

185
Q

R atrium and R ventricle saturations

A

75%

186
Q

Pulmonary artery saturations

A

75%

187
Q

L Atrium saturations

A

100%

188
Q

L ventricle saturations

A

100%

189
Q

Pulmonary veins saturations

A

100%

190
Q

Aorta saturations

A

100%

191
Q

what is the defect?
Where is it shunting?

superior vena cava 70%
R atrium 79%
R ventricle 78%

A

There is a bump in oxygen saturation in the R Atrium.

likely has an ASD
which is pulling red blood on the left side of the heart bumping our sats on the r side of the heart

192
Q

What is the defect?
where is the shunting?

Superior vena cava 70%
R atrium 70%
R ventricle 85%

A

VSD

red blood shunting across and bump up the sats

193
Q

Cardiac output components

A

preload (CVP -volume status)

contractility - is the pump able to squeeze forward

stroke volume - how much the heart is ejecting with each contraction

Afterload - systemic vascular resistance. How vasoconstricted or vasodilated is your body

194
Q

filling pressure in the ventricles at the end of diastole

A

Preload

195
Q

measure of cardiac pump performance, the degree of muscle fiber shortening

A

Contractility

196
Q

resistance the ventricle has to overcome to eject blood

A

afterload

197
Q

volume of blood pumped from one ventricle of the heart with each beat

A

stroke volume

CO/HR (50-80ml)

198
Q

Corrects Cardiac output for body surface area

A

Cardiac index

199
Q

resistance the pump must overcome to eject

A

PVR and SVR

200
Q

Qp

A

quantity of pulmonary blood flow

201
Q

Qs

A

quantity of systemic blood flow

202
Q

normal Qp:Qs ratio

A

1:1

203
Q

Qp:Qs is <1.5:1

A

small shunt

204
Q

Qp:Qs is 1.5-2:1

A

moderate shunt

205
Q

> 2:1 for Qp:Qs

A

Large shunt

206
Q

What happens when PVR goes down

what causes PVR to decrease

A

Pulmonary vasodilation

causes of PVR decrease?

  • normal ventilation
  • Oxygen
  • Nitric Oxide
  • Hypocarbia
  • Sildenafil
  • AcetylcholinePGE
  • Milrinone
  • Calm
207
Q

What causes PVR to increase

A 
Sympathetic stim
Stress
Agitation
Hyperinflation
Hypercarbia
Acidosis
Viscosity
Vasopressin

(vasoconstriction)

208
Q

What causes SVR to go up or down

A 
Neural control
autonomic system
hormones
catecholamines
vasoactive agents (vasopressin - causes SVR to go up, milrinone vasodilator so causes SVR to go down)
inotropes
environmental temp
exercise
viscosity
209
Q

infants myocardium resembles a

A

failing adult heart. neonatal heart relies on extracellular calcium for excitation-contraction coupling. low number/size of myocytes and type 1 stiff collagen. The heart progresses as the child ages.

210
Q

determines cardiac rate and rhythm

A

impulse conduction

211
Q

cardiac rate is determined by the cell with the fastest intrinsic rate. All slower cells have their rates suppressed.

A

overdrive suppression

212
Q

What CNS mediated reflexes control cardiac rate and contractility resulting in homeostasis of the aforementioned parameters.

A

CNS mediated reflexes take afferent information regarding atrial volume (Bainbridge reflex), arterial blood pressure (Baroreceptor reflex) and blood or CSF levels of carbon dioxide, pH or oxygen (chemoreceptor reflex) and control cardiac rate and contractility

213
Q

humeral control of the heart affecting cardiac rate and contractility include what

A

adrenal gland secretion of adrenaline and norepinephrine.

214
Q

drugs that are inotropic effecting cardiac rate and contractility

A

adrenocortical steroids
thyroid hormones
glucagon

215
Q

the difference between the pressures at the arterial and venous ends

what is this estimated at

A

capillary hydrostatic pressure

estimated at 32 and 15 mmHg

216
Q

what hydrostatic pressure is usually 0

A

tissue hydrostatic pressure

217
Q

The oncotic pressure averages ____ in the capillary and less than ___ in the tissue

A

25mmHg

5mmHg

218
Q

Because Hydrostatic forces push fluid _____ the tissue and oncotic forces _______, more fluid is filtered at the arterial end then is reabsorbed at the venous end. The result is ___

A

out into the tissue
pull it back
lymphatic flow and the volume in a 24 hour period approximates the total body plasma volume.

219
Q

what is increased when the plasma proteins are low, capillary permeability is high or there is an increase in hydrostatic pressure across the capillary

A

Lymphatic flow

220
Q

what happens when the total lymphatic flow exceeds the capability of the lymphatic system, when there are lymphatic obstructions or high CVPs

A

Edema

221
Q

the resistance to flow is determined only by the radius and length of the vessel and the viscosity of the blood

A

Poiseuille’s law

222
Q

term used to describe the distensibility of blood vessels

A

Capacitance

223
Q

a term to denote the ability of the distal vascular bed to accept flow

A

Capacity

224
Q

reflexes that involve humeral modulation of vascular tone

A

RAAS (vasoconstrictive)
arginine vasopressin hypothalamic osmoreceptor system
Vasodilator effects by ANP and BNP

225
Q

R ventricular impulse is located

A

under the xiphoid sternum

226
Q

if the r ventricular impulse is more prominent than the ________ after —- hours of age, it is abnormal and requires evaluation

A

left apical impulse after 12 hours of age

227
Q

A2 is always loudest where?

A

at the Lower left sternal border

228
Q

All high frequency murmurs occur at the _____ in systole

A

apex

229
Q

A qR pattern in V1 denotes

A

r ventricular hypertrophy

230
Q

when qR pattern is absent in V6, it is highly associated with

A

hypoplastic L heart

231
Q

in utero when does the heart develop

A

3rd week and is complete by day 45

232
Q

means that the atria and main stem bronchi have developed in the usual relationship to each other
(RA is to the right of the LA)

A

Situs solitus

233
Q

when the atria and main stem bronchi develop opposite

A

Situs inversus

234
Q

The absence of lateralization of the atria nd the thoracic organs

A

Situs ambiguous

235
Q

When there are 2 r or 2 left atrial chambers

A

Atrial isomerism

236
Q

when the atria connects to the ventricles in the way they should. RA connects to RV and LA connects to LV

A

concordant

237
Q

When the RA connects to the LV and the RA to the LV

A

discordant

238
Q

The atria connect to only one ventricle

A

univentricular

239
Q

AV is straddling and committed to whichever ventricle is receiving more than 50% of output

A

ambiguous

240
Q

when the RV connects with the PA and the LV with the aorta

A

concordant ventriculoarterial connections

241
Q

When the aorta arises from the RV and the PA from the LV

A

transposition of the great arteries

242
Q

if the pulmonary or aortic valve is overriding a VSD. It is considered to arise from the ventricle which greater than 50% of the valve is committed.

A

Double outlet

243
Q

If the connection consists of only one great vessel or a common arterial trunk

A

Single outlet

244
Q

fetal blood flow

A

Nutrients and oxygen supplied by placenta ->through umbilical vein ->ductus venosus ->inferior vena cava ->r atrium where the blood mixes with blood returning to the heart from the upper body in the superior vena cava and from the lower body in the inferior vena cava ->a small amount of blood flows to R ventricle while the rest goes through the foramen ovale -> L atrium -> L ventricle -> aorta - > body

blood from R ventricle -> pulmonary artery (lungs are fluid filled) -> pulmonary has high resistance and systemic has low resistance. The blood pumped into pulm A. is more likely to flow to ductus arteriosus -> aorta -> body -.umbilical arteries ->placenta

245
Q

when the placenta is removed form the circulation what begins to rise?

A

systemic vascular resistance

pulmonary pressures begin to decrease

246
Q

at what age does pulmonary vascular resistance decrease to normal levels after birth

A

6-8 weeks

247
Q

when does the foramen ovale finally close

A

within 3 months

fibrin fuses septal wall together

it may not close

248
Q

normally the ductus closes in

A

4-10 days

249
Q

ductus venosus usually closes within

A

3-7 days then becomes ligamentum venosum

250
Q

3 important parts to a patient history when evaluating cardiac

A

1) Gestational and perinatal history
2) Postnatal and present history
3) Family History

251
Q

Relevant maternal history

A

Healthy while pregnant?

Receive prenatal care?

Routine Ultrasound? did they show anything of concern?

252
Q

Relevant Maternal Infections to Cardiac History

A

TORCH

Toxoplasmosis
Other
Rubella
Cytomegalovirus
Herpes
253
Q

Maternal medications relevent to Cardiac history

A

Did she take any meds

Phenytoin
Lithium
Retinoic acid
warfarin

254
Q

Postnatal and present history

A

Are they growing along their growth curve?

if not, have they at least consistently gained weight or have they been loosing weight

are they meeting developmental milestones

feeding problems?

cyanosis

when they are running on the playground, are they able to keep up with their peers or are they falling back?

Have they ever fainted or felt like they were going to?

have they ever had chest pains or palpitations (does it feel like they have had extra beats or skipped beats)

255
Q

In infants for cardiac history feeding is actually a ____ test

A

exercise - if they are able to feed and grow, it is not usually a cardiac issue

256
Q

family history for cardiac

A

has anyone in your family ever been born with a heart problem (congenital heart disease)

Has anyone passed away suddenly or from an unexplained cause?

Also can ask about car accidents or drownings? can be electrical problems with heart

anyone with hypertrophic or dilated cardiomyopathy

anyone in the family require a pacemaker or implanted defibrillator

257
Q

physical exam cardiac

A

do they look well nourished or malnourished

are they breathing easily or quickly and with difficulty

Place hand on their chest to feel their precordium to see if they are hyperdynamic. is the point of maximal impulse displaced and do you feel a thrill?

feel upper brachial pulse and feel the lower femoral pulse. Are they bounding or is there a difference between the upper and lower pulses

BP - take a upper extremity BP and a lower extremity BP to make sure there is no gradient. A systolic bp of > 10mmHg higher in arm then leg may signify a coarctation in the aorta.

Auscultation - S1 - mitral (M1) and tricuspid (T1) valve closure
S2 - Aortic (A2) and pulmonic (P2) valve closure

splitting of S2 - variation with respiration is normal

258
Q

when S2 sounds are widely split

what does it mean

A

Abnormal splitting can be reflective of volume overload or electrical delay in a bundle branch block

259
Q

S2 narrowly split means

A

Pulmonary HTN

aortic stenosis

260
Q

S2 is entirely stenosis can mean

A

severe aortic stenosis

severe pulmonary HTN

261
Q

Abnormal heart sounds are categorized into

A 
systolic murmurs
diastolic murmurs
continuous murmurs
Gallops
Clicks
262
Q

murmur barely audible

A

Grade I/VI

263
Q

murmur soft but easily audible

A

Grade II/VI

264
Q

murmur moderately loud but no thrill

A

Grade III/VI

265
Q

murmur loud and accompanied by a thrill

A

Grade IV/VI

266
Q

murmur audible with stethoscope barely on chest

A

Grade V/VI

267
Q

murmur audible with stethoscope off the chest

A

Grade VI/VI

268
Q

3 categories of murmurs

A

Ejection
Late Systolic
Holosystolic

269
Q

murmur usually reflective of pulmonary stenosis or aortic stenosis

A

Ejection

270
Q

murmur usually reflective of Mitral valve prolapse

A

Late systolic murmur

271
Q

Murmur usually reflective of Tricuspid regurgitation, mitral regurgitation, VSD

A

Holosystolic murmur

272
Q

Midsystolic murmur described

A

Ejection systolic

Crescendo/decrescendo murmur…starts soft, gets loud then soft again

273
Q

murmur heard throughout systole between S1 and S2

A

Holosystolic murmur

274
Q

murmur that is short and heard right at the beginning

A

early systolic murmur

275
Q

murmur that is accompanied by a mitral click

A

Late systolic murmur

276
Q

Diastolic murmurs are always ________

A

pathologic

systolic may be benign or pathologic

277
Q

Early pitched diastolic murmur

A 
higher pitched
Aortic regurgitation (radiates to apex)
pulmonary regurgitation (radiates along left sternal border)
278
Q

Mid diastolic murmur

A

lower pitched
use bell of stethoscope
mitral stenosis (apex)
tricuspid stenosis (left lower sternal border)

279
Q

Continuous murmurs are reflective of

A

PDA
AV fistula
Shunt murmur post surgery
Venous hum

280
Q

aortic valve stenosis murmur would be best appreciated in the

A

aortic valve area - in the Right upper sternal border

281
Q

Pulmonary murmurs are best appreciated in the

A

Left upper sternal border

282
Q

Mitral murmurs are usually heard along the

A

apex

283
Q

VSD , tricuspid regurgitation or Stills murmur are best heard at the

A

left lower sternal border

284
Q

Gallops are broken down to

A

S3

S4

285
Q

S3 is usually heard at the

A

apex if produced by dilated or dysfunctional L ventricle or along the Left lower sternal border if produced by a dilated or dysfunctional R ventricle

286
Q

is S3 normal?

A

it can be normal in children and young adults and it can also be reflective of pt with dilated ventricles and decreased compliance

287
Q

S4 is heard where and is it bad?

A

heard at apex and always pathologic associated with decreased ventricular compliance associated with myocardial ischemia and ventricular hypertrophy

288
Q

3 types of clicks

A

Ejection click
mid-systolic click
Diastolic opening snap

289
Q

Ejection click is appreciated where and reflective of what

A

apex

aortic stenosis or if bicuspid aortic valve

290
Q

Mid systolic clicks are appreciated where and reflective of what

A

apex

mitral valve prolapse

291
Q

diastolic opening snap are appreciated where and reflective of what

A

Apex or Left lower sternal border

mitral stenosis

292
Q

Pericardial friction rub

A

heard when 2 walls of pericardium rub together producing audible friction

described as grating, scratching and rasping sound
systolic and diastolic components

appreciated between apex and sternum and can be indicative of pericarditis

293
Q

what is the most common congenital heart defect

A

VSD

294
Q

As far as coronary defects or obstructions, which side would be worse

A

L side

295
Q

where do the coronary arteries branch off of

A

Aorta

296
Q

Circumflex artery branches off of

A

L coronary artery

297
Q

3 categories of CHD circulation problems

A

Too much pulmonary blood flow

too little pulmonary blood flow

Too little systemic blood flow

298
Q

Too much pulmonary blood flow, you have what symptoms

A 
Tachypnea
increased wob
murmur
diaphoresis
fatigue
poor feeding
FTT
cardiomegaly
hepatomegaly
pulmonary edema

example would be VSD

299
Q

In too much pulmonary blood flow what is the relationship with Qp and Qs

A

Qp>Qs

Qp is quantity of blood to lungs
Qs is Quantity of blood to body

Qs is always 1 all the time

300
Q

Too little pulmonary blood flow, what is the relationship with Qp and Qs

A

Qp

301
Q

what symptoms for too little pulmonary blood flow

A 
cyanosis
clubbing
murmur
Polycythemia
Fatigue
302
Q

cyanosis in extremities

A

Acrocyanosis. in infants normal finding from immature circulation

303
Q

Too little systemic blood flow
Qp vs Qs

example

A

Qp> Qs

Qp is quantity of blood to lungs
Qs is Quantity of blood to body

quantity of blood to lungs >quantity of blood to body

classic example is aorta coarctation

304
Q

symptoms for too little systemic blood flow

A 
tachypnea
increased wob
cool extremities
pallor
murmur
diaphoresis
fatigue
poor feeding
FTT
cardiomegaly
hepatomegaly
305
Q

in aortic coarctation before the narrowing the pressures are

A

high

306
Q

in aortic coarctation after the narrowing (distal) the pressures are

A

lower

307
Q

screening tool/assessment for coarctation

how would you perform

what would signify reason for concern

A

4 extremity blood pressure

  • perform sequentially (do not wait in between)
  • R arm first (pre-coarctation arm)
  • if R arm SBP >15mmHg more than lower extremity SBP consider further evaluation
308
Q

If the 4 extremity blood pressures are positive then what do you do?

A

echo

refer to cardiology

309
Q

most severe form of coarctation

A

interrupted aortic arch

310
Q

in transposition of the great arteries what other defect is essential for mixing to prevent heart failure

A

ASD

311
Q

Transposition babies are sometimes put on what to keep the ductus open

A

PGE

312
Q

patho for ASD

A

left to right shunting (atrial) 🡪 R atrial dilation, R ventricle volume overload

313
Q

presentation for ASD

A

fatigue + dyspnea, systolic ejection murmur at left sternal border (large → diastolic murmur) split s2

314
Q

Plan of Care ASD

A

Echo for diagnosis
RV, RA, and PA dilation
Many have spontaneous closure (secundum ASD’s/PFO’s)
Surgical or interventional cath closure if signs of HF

315
Q

Patho for VSD

A

RV shunting (increased pulmonary blood flow) with LA/LV dilation

With time, causes changes to pulmonary vascular bed d/t increased pressures

If PA pressure > systemic pressure, the shunt reverses (R→L) and causes cyanosis (Eisenmenger syndrome)

316
Q

murmur for VSD

A

systolic regurgitant murmur along the left sternal border (louder the murmur, smaller the defect)

317
Q

plan of care VSD

A

Surgical closure if S/S of HF, growth failure, PH, or LV volume overload

Spontaneous closure possible for perimembranous/muscular defects – medically managed

318
Q

patho coarctation of aorta

A

narrowing of the aorta (location determines severity of illness)

319
Q

presentation coarctation of aorta

A

LV hypertension + hypertrophy, can acutely present after closure of ductus arteriosus (NEC, end-organ hypo-perfusion, AKI), grade 2-3 systolic ejection murmur at the left upper sternal border +/- gallop, discrepancy between BP on upper and lower extremities

320
Q

plan of care coarctation of aorta

A

emergent infusion of PGE (restore ductal patency) and surgical repair of coarctation – in older children, able to perform elective non-emergent repair

321
Q

interrupted aortic arch patho

A

Ductal dependent lesion

Patho: disruption between ascending and descending aorta, blood flows from L ventricle to aortic arch, at disruption blood flows through ductus arteriosus which shunts R to L

322
Q

presentation interrupted aortic arch

A

cardiovascular decompensation at time of ductal closure, requires CT/MRI or echo to diagnose

323
Q

interrupted aortic arch plan of care

A

emergent PGE infusion to maintain ductal patency until surgical intervention can be made

324
Q

aortic stenosis patho

A

thickened, rigid valve causing outflow obstruction from the L ventricle

325
Q

aortic stenosis presentation

A

can range from mild to moderate symptoms, severe are dependent on PDA, can have signs of HF, irritability, poor feeding, hypotension/tachycardia and poor perfusion, systolic murmur at the left upper sternal border, R arm BP higher than left arm

326
Q

plan of care aortic stenosis

A

Echocardiogram + doppler to measure pressures in the aorta + left ventricle, repair with valvuloplasty, valve replacement, or resection of membrane causing obstruction

327
Q

do you have normal or decreased spo2 in ASD and VSD

A

normal

328
Q

boot shaped heart on xray is consistent with

A

Tetralogy of fallot

329
Q

4 components of Tetralogy of Fallot

A

Pulmonary stenosis

VSD

Aortic override

RV is hypertrophied (thickened) - it is seeing high pressure because its pumping against the high pressure from pulmonary stenosis

330
Q

snowman sign on xray is consistent with what

A

Total anomalous Pulmonary venous return (TAPVR)

331
Q

Total anomalous Pulmonary venous return

A

pulmonary veins (2 from left and 2 from R) miss the left side of the heart so the oxygenated blood is going back to the right side of the heart, going to the lungs again. You have to have ASD or they dont have any systemic circulation…if they have a restricted ASD they have very little systemic circulation.

332
Q

Highest risk TAPVR

A

infradiaphragmatic TAPVR

vein travels beneath the diaphragm and high risk for obstruction

333
Q

How do you keep the ductus arteriosus patent

A

Prostaglandin E1 (Alprostadil)

if a newborn is crashing, while your going through the list…no harm in giving this. If pt has a ductal dependent lesion. Can make them apneic or give them a low temp, but your in the EC, you can intubate, you may buy them time

334
Q

if you have too little systemic blood flow

A 
order echo
start PGE (may or may not be helpful but the lesion is ductal dependent it will save their life)

if they have a ductal dependent lesion - they need volume! push fluids
maximize their preload

335
Q

what genetic syndromes are highly associated with congenital cardiac defects

A

Trisomy 21, 18, 13

22q11 deletion

williams syndrome

Alagille syndrome

Noonan syndrome

336
Q

in utero that is associated with congenital cardiac defects

A

Maternal diabetes (not just gestational, also with Type I or poorly controlled)
Antiepileptic drugs (ie) Depakote)
psychiatric medications
thyroid dysfunction
maternal autoimmune disease (lupus and Sjogren’s)
alcohol abuse
smoking
HTN
infectious illness (less likely to be structural, more likely for myopathies)

337
Q

3 types of Cardiomyopathy

A

Dilated - most common (Volume overloaded)

Hypertrophic (this is the stories you hear where the basketball player drops during a game)

Restrictive (Diastolic problem where it wont relax, filling inhibited so cant eject well)

338
Q

Pressure overload lesions

A

aortic stenosis
pulmonary stenosis
coarctation of aorta
hypoplastic left heart

339
Q

increased RV outflow tract obstruction -> increased RV pressure -> increased preload ->increased RA pressure -> R to L shunting ->cyanosis

A

Pulmonary stenosis

340
Q

to separate aortic stenosis from hypoplastic left heart syndrome

A

get an ECG

341
Q

if there is an obstruction such as aortic stenosis, what do pressures look like in LV?

A

LV pressure 150

pressure above valve may only be 50 or 75

342
Q

Her RV is systemic means what about the LV

A

RV is same pressure as the LV

343
Q

If someone is in Heart failure and their RV pressure is 3/4 systemic. …what does this tell you

A

whats their PA pressure?
Do they have pulmonary hypertension or maybe pulmonary stenosis?
Hows their RV function

344
Q

Resistance that the pump must overcome to eject blood into pulmonary circulation

A

Pulmonary Vascular resistance (PVR)

345
Q

Resistance pump must overcome to eject blood into systemic circulation

A

Systemic Vascular Resistance (SVR)

346
Q

In VSD what is the problem

A

Too much pulmonary blood flow

347
Q

blood flow in Transposition of Great Arteries

A

Comes in R Atrium to R Ventricle to the transposed aorta and pulmonary artery to the body with opportunity for mixing with an ASD.

Left side of the heart just keeps circulating to the lungs

348
Q

what do Transposition of Great Arteries babies Saturations look like until repair and how do they fix?

A

upper 70s, low 80s

Arterial switch operation

349
Q

5 common Cyanotic Heart Defects

A

Transposition of the Great Arteries

Tetralogy of Fallot (TOF)

Truncus Arteriosus

Total Anomalous Pulmonary Venous Connection (TAPVR)

Tricuspid Valve Abnormalities

350
Q

With an ASD or VSD, what do your Saturations do

A

normal

351
Q

Do most ASDs cause alot of shunting?

A

no

352
Q

Now if you have ASD with Pulmonary HTN, what do your sats look like

A

Now your R heart pressure is similar to your left heart pressure or even higher. Then that would cause the shunting to go this way…R to left, then you may have a cyanotic problem

353
Q

PDA is a source of what kind of shunt

A

L to R shunt

354
Q

Complete AV canal (AV septal defect) is common in children with what genetic syndrome

A

Down Syndrome

355
Q

what heart defect has no or maybe a very small L ventricle. ductal dependent

A

Hypoplastic L Heart

356
Q

Ductal dependent Pulmonary blood flow lesion

A

Pulmonary Atresia with Intact ventricular Septum (IVS)

Atresia means there is no blood flow there

357
Q

if you have too little systemic blood flow in an infant start

A

PGE

358
Q

If you have too little pulmonary blood flow in an infant….their hypoxic with severe pulmonary stenosis or a ductal dependent lesion closing

A

Volume (Fluids)
PGE

fluids maximize their preload to force blood across obstruction

359
Q

what med class is the enemy for inadequate pulmonary blood flow lesions

A

Diuretics

You want to maximize their preload to push past that obstruction

360
Q

L to R shunt VSD

tachypneic

A

Lasix

remember this is the big volume dilated heart

361
Q

what screening is done after the first 24 hours of life to screen for Congenital heart disease

A

Pulse ox screening

362
Q

Mickey mouse ears on echo is characteristic of

A

Restrictive Cardiomyopathy

Critical Care I (27 decks)

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