Pressure waves are sent through body and echo waves return to the transducer elements and are processed to create ultrasound images
ultrasound
the major source of sound wave attenuation is soft tissue (the conversion of energy to heat)
absorption
occurs when sound waves encounter a boundary between two different media.
reflection
when waves are reflected off of bone an ____ _____ will be created
acoustic shadow
when us waves encounter a medium with non-homogenous surface
scatter
the consequence of scatter is
speckle
why is gel used in ultrasound
ensures proper contact between transducer and patient, for sound to travel through tissues
frequency (Hz) of the wave is measured in
cycles per second
Ultrasound imaging frequency
1-20 MHz
what frequency is better for deeper structures
lower frequency waves
frequency that provides better resolution for shallow structures
high frequency waves
Ultrasound gets _____ in tissue, signals get ____ in deeper structures, resulting in _____images.
Ultrasound gets attenuated in tissue, signals get weaker in deeper structures, resulting in darker images
_______ may prevent imaging behind solid structures
absorptions
_________may prevent imaging behind solid structures or air
Hard reflections
ultrasound transducer that provides a wide, near field image
Curved Array
when scanning for fetus or abd what type of transducer would you use
Curved array
pie shaped image, quality not as good as curved array.
phased array
what type of transducer would be better for ultrasounding the heart behind ribs
Phased array
transducer that gives the best resolution, used in vascular and superficial soft tissue studies
linear array
runs parallel to the ground separating superior from inferior
transverse plane
oriented perpendicular to ground separating pt left from right
Sagittal/longitudinal plane
separates the pt anterior from posterior
coronal plane
used to image structures that don’t line up with the other planes
Oblique plane
commonly used mode in ultrasound, different shades of gray in a 2 dimensional picture
B mode
captures returning echos along one line of the real time image. Used to quantify motion over time
M mode (motion mode)
frequency shift caused by sound waves interacting with a moving target
Doppler
used to visualize and quantify blood flow information
pulsed wave doppler
shows approx speed and direction of blood flow inside the vessel
color doppler
is used to identify blood flowing toward the transducer
red
is used to identify blood flowing away from the transducer
blue
looks at the strength or amplitude of the returning signal. assigns a color based on the strength or amplitude of the returning signal
power doppler
P on the R side of the cone image indicates what mode
cardiac
P on the L side of the cone image indicates what mode
standard
in cardiac mode the probe should be facing the
L shoulder
the Left ventricle should be on what side of the screen for cardiac mode
Left
in standard mode the probe should be facing the
Left hip
what is the optimal pt positioning for a cardiac ultrasound (Transthoracic echocardiography)
L lat decubitus positon which brings heart forward
steps for Parasternal Long Axis for Echocardiography
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
gold standard for estimating ejection fraction in Echocardiography
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
what are the exceptions that would falsely quantify EF using the eyeball method
Aortic regurgitation
mitral stenosis
fluid is anterior to the descending aorta in the echocardiogram
Pericardial effusion
if the effusion is posterior to the descending aorta
Pleural effusion
diastolic collapse of the Rv with clinical symptoms of hypoperfusion (hypotension, tachycardia, syncope, sob, ect)
Pericardial tamponade
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
Parasternal short axis (PSA view)
“fish mouth and mercedes benz sign view”
to get the mid papillary on the PSA
fan towards apex
papillary muscles in view
Mitral valve view on PSA
fan probe towards base
“fish mouth mitral view)
Aortic valve view on PSA
Fan probe towards base
Mercedes-benz aortic valve
D sign on PSA
R ventricular strain
Apical 4 chamber
Left axilla,
Fan upwards at apex (towards pt head)
Subxiphoid View on Echocardiography
Subxiphoid region
Indicator to Left
overhand grip on probe
probe almost parallel to skin
IVC measurements help with
fluid management
caval index =
preload reserve
electrical path for heart
SA node ->AV node ->HIs purkinje system -> R and L bundle
electricity that moves towards a lead creates ___________ known as a ____
electricity that moves towards a lead creates a positive deflection known as a R wave.
electricity that moves away from a lead creates a _______ or an _____
electricity that moves away from a lead creates a negative deflection or an S wave
The leads that are placed across the chest are known as the ______-
Precordial leads (V1-V6, V3R, V4R)
Leads I, aVL, V5, V6, V7 cover the
L lateral side of the heart
Leads aVR, V3R and V4R cover the
R side of the heart
Leads II, III and aVF are classically known as the
inferior leads
V1-V4
anterior leads
V1 and V2
give a better idea of how the septum depolarizes
each small box on the EKG is
40 milliseconds in duration
in terms of the amplitude, the ECG is performed at
10millimeters per millivolt, 10 squares high
mathematical way of calculating heart rate on an EKG strip
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
Estimation method for calculating HR
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
NSR is set by the
SA node
Atrial contraction produces what on the EKG
P wave
Ventricular contraction produces what on the EKG
QRS complex
In normal adults, electricity moves downwards and to the left towards the left ventricle.
what does this do to the ekg
On the EKG you will see a R wave in lead I and in aVF
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?
R ventricle
over the first 6 months it starts to shift
If a pt had a right axis deviation, you would see a
lead 1 would have Prominent S wave
In II, III and aV5 they all have prominent S waves so they have the negative deflections
Superior Axis
what does a Superior axis indicate and who is it seen in commonly
Atrioventricular canal
- common in pt with Trisomy 21
Tricuspid Atresia
what represents atrial depolarization (contraction)
P wave
1st half of the P wave represents the
R atrial contraction
2nd half of the P wave represents the
L atrial contraction
Normal values for P wave
No more than 3 squares high and 3 squares wide
Less than 0.3 millivolts or duration less than 120 milliseconds
where is the best place to look at the P wave
leads II and V1 (most prominent deflections on an ECG)
Large peaked P wave is seen in
R atrial enlargement (usually >0.3 millivolts)
a Large notched P wave is seen in
L atrial enlargement
usually greater than 120 milliseconds
what does L atrial enlargement look like in lead V1
slurred terminal portion of the P waves (Biphasic P wave)
what part of the EKG reflects intra-atrial conduction
PR interval
A normal PR interval is less than
200milliseconds
1st degree heart block refers to a PR interval
greater than 200miliseconds
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
2nd degree heart block
second degree heart block that the PR intervals get longer and longer until a QRS is dropped then it starts over
Mobitz type 1 (Wenckebach)
P waves that do not have a QRS complex afterwards. Before the dropped QRS, the PR interval stays the same throughout
Mobitz type 2
which 2nd degree heart block is always pathological
Mobitz type 2
There is no impulses conducted through the AV node to the ventricles
3rd degree heart block
on the EKG strip the atrium and ventricle are beating independent of each other
3rd degree heart block
abnormal conduction through the ventricles can be seen by evaluating the
QRS complex
wide QRS complex is >
120 milliseconds
what has a wide QRS
R bundle branch block because electricity moves slower through the R Purkinje fibers and thus the left ventricle activates first
In R bundle branch block what does EKG show
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
L bundle branch block
V1 has an rS pattern
V6 has the bunny ear pattern with a tall notched R wave
In terms of hypertrophy the QRS deflections reflect the
mass of ventricles
what does R ventricular hypertrophy show on EKG
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
L ventricular hypertrophy
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
the end of the QRS complex to the beginning of the T wave is the
ST segment - isoelectric
changes in the ST segment can reflect
ischema or inflammation
diffuse ST elevations across all of your leads
Pericarditis
what shows ventricular depolarization and can change as the patient ages
T wave
In general the T wave follows the axis of the
QRS
T wave changes along the R precordium is observed in leads
v1-v3
from birth to seven days what do you see on the EKG
positive T waves noted
from 1 week to adolescence what happens to the T waves
the t waves flip over and are negative
After your teenage years, what happens to T waves
they flip over and become positive in the r precordium
after one week old, positive T waves seen in V1 reflect
RVH
the beginning of the QRS complex to the End of the T wave
QT interval
when measuring QT interval what leads do you use
Lead II and V5
Pt with prolonged QT interval is at risk for
ventricular arrhythmia and sudden death
Bazett’s formula
Divide QT interval by the sq root of the preceding RR complex (ms between QRS complexes right before the QT interval of interest)
In general the number to keep in your head for Bazett’s formula is less than
QTc = 450 ms
Anatomic presence of an accessory conduction pathway that allows for reentrant SVT
Wolff-Parkinson White (WPW)
what population is at higher risk for WPW
males
Symptoms of WPW
palpitations presyncope/syncope sudden cardiac death Dizziness Chest Pain
characteristic ECG findings associated with WPW
short PR interval
delta wave which is a slurring of the P wave into the QRS
widening of the QRS complex
Associated congenital heart disease lesions in WPW
Ebstein anomaly (abnormal development of tricuspid valve)
Hypertrophic cardiomyopathy
L-transposition of great arteries (congenitally corrected transposition of great arteries, ventricular inversion)
diagnostics of WPW
ECG
Echocardiogram
Holter exercise stress ECG
Treatment WPW
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
meds contraindicated in WPW
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
genetics Long QT
Can be inherited in both autosomal dominant and receptive fashions
Symptoms Long QT
syncope/presyncope
Palpitations
Sudden cardiac arrest
Lightheadedness
Normal QTc
males: <440ms, females <460ms
For assessing QTC what leads do you use on EKG
II or V5
How do you calculate QTC
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.
2 other arrhythmias seen in long QT
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.
How do you treat Torsades de point in long QT
magnesium sulfate
PALS algorithm
diagnostic tools for long QT
ECG
Stress Testing
Holter monitor
Genetic testing
Probability tool used in long QT
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%)
what are the 3 types of long QT and what are their frequencies
LQTS1 -most common
LQTS2
LQTS3- least common type
Associated gene mutation for
LQTS1
Mutation in KCNQ1
Associated gene mutation for
LQTS2
Mutation in KCNH2
Associated gene mutation for
LQTS2
Mutation in SCN5A
LQTS1 due to loss of function in ?
Due to loss of function in the potassium ion gene
what is the key EKG feature for LQTS1
Early peaking T wave that comes soon after QRS complex
Most common trigger to lethal cardiac events in LQTS1
Exercise is the most common trigger to lethal cardiac event with swimming being the most common “SWIM”
LQTS2 due to loss of function in ?
Due to loss of function in the potassium ion gene
what is the key EKG feature for LQTS2
T wake is not as early peaking and has a saddleback-shaped appearance
Most common trigger to lethal cardiac events in LQTS2
Emotional stress is the most common trigger to lethal cardiac event “STARTLE”
LQTS3 due to increased function of ?
Gain of function in the Sodium ion gene
what is the key EKG feature for LQTS3
The T wave has a late peaking appearance to it
Most common trigger to lethal cardiac events in LQTS3
Periods of high vagal tone such as sleep and repose (state of tranquility) are the most common trigger to lethal cardiac event “SLEEP”
Treatment in LQT
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
atriums empty into the ventricles with contraction and blood flow through mitral and tricuspid valves
what is this?
Active or passive?
Diastole
Active
Atrial kick?
important piece of diastole
atrial contribution to ventricular filling
what valves are open during systole
Aortic and pulmonary
what valves are closed during systole
Mitral and tricuspid
full ventricles contract and pump blood to the lungs and body
Systole
allows blood to flow from pulmonary vasculature to the body while in utero
PDA (patent ductus arteriosus)
The heart grows …..
as blood flows
Blood follows the path of
least resistance
pressure leads to _____
Hypertrophy. If you have high BP, your heart is pumping against a high resistance so your ventricle will muscularize.
Volume leads to _____
Dilation
If you have a volume loaded heart
umbilical vein is carrying ______ blood from ___ to ____
umbilical vein is carrying oxygenated blood from mom to baby
PO2 of umbilical vein is
30-35mmgHg
in fetal circulation how many umbilical veins are there
1
in fetal circulation how many umbilical arteries are there
2
in fetal circulation from the umbilical vein….track the circulation
Mom to umbilical vein -> 50% travels to provide hepatic blood flow/ 50% to the IVC where it joins in with cyanotic 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 ->L atrium -> the 5% of venous blood returning from the lungs from the pulmonary v. joins here -> L ventricle -> systemically
Umbilical arteries carry ______ ______ from ____ to the _____
deoxygenated blood from the heart to the placenta (two arteries)
What are the two places fetal circulation bypasses the lungs
PFO and PDA
what ventricle works harder in utero
L ventricle
R ventricle gets very little blood flow
65 % of the descending aorta output returns to the
placenta
Descending aorta takes blood
deoxygenated blood sent to fetus and placenta through the umbilical arteries (65%)
first few breaths in a newborn. what happens?
Oxygen content in the newborn raises dramatically -oxygen is a potent pulmonary vasodilator
vessels in the pulmonary 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.
CVP (central venous pressure) is the pressure in the
R atrium
If pt had pulmonary htn or L atrial HTN from some obstruction the pulmonary wedge pressure would be
elevated
Pulmonary wedge pressure
reflection of left heart’s cardiac output
normal pressure in R atrium (CVP)
6-10 (normal 2-6)
M=3
normal pressure in RV
25/3
normal pressure in Pulmonary Artery
25/10
M=16
If the pulmonary A is 10 there is
Pulmonary stenosis or obstruction there
Lv pressure
100/8
M=16
aortic pressure
100/60
M=83
LA pressure
M=8
RV should be ___ of the pressure in the LV
1/4
Pulmonary HTN - mean pulmonary artery pressure is greater than
25
Pulmonary Capillary Wedge pressure
6-12
If you have pulmonary HTN does your wedge pressure accurately detect the L sided heart pressure
no - the resistance in your lungs is high
left ventricular end diastolic pressure (LVEDP)
3-12
If your LVEDP is high, what happens
blood does not want to travel into the LV - see in diastolic cardiomyopathy
LVEDP is a measure of
diastolic function
RV 80/9
Pulmonary A mean pressure is 30
what is this?
Pulmonary HTN
Superior vena cava Saturations should be
75%
R atrium saturations
75%
Pulmonary artery saturations
75%
L Atrium saturations
100%
L ventricle saturations
100%
Pulmonary veins saturations
100%
Aorta saturations
100%
what is the defect?
Where is it shunting?
superior vena cava 70%
R atrium 79%
R ventricle 78%
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
What is the defect?
where is the shunting?
Superior vena cava 70%
R atrium 70%
R ventricle 85%
VSD
red blood shunting across and bump up the sats
Cardiac output components
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
filling pressure in the ventricles at the end of diastole
Preload
measure of cardiac pump performance, the degree of muscle fiber shortening
Contractility
resistance the ventricle has to overcome to eject blood
afterload
volume of blood pumped from one ventricle of the heart with each beat
stroke volume
Corrects Cardiac output for body surface area
Cardiac index
resistance the pump must overcome to eject
PVR and SVR
Qp
quantity of pulmonary blood flow
Qs
quantity of systemic blood flow
normal Qp:Qs ratio
1:1
Qp:Qs is <1.5:1
small shunt
Qp:Qs is 1.5-2:1
moderate shunt
> 2:1 for Qp:Qs
Large shunt
What happens when PVR goes down
what causes PVR to decrease
Pulmonary vasodilation
causes of PVR decrease?
- normal ventilation
- Oxygen
- Nitric Oxide
- Hypocarbia
- Sildenafil
- AcetylcholinePGE
- Milrinone
- Calm
What causes PVR to increase
Sympathetic stim Stress Agitation Hyperinflation Hypercarbia Acidosis Viscosity
(vasoconstriction)
What causes SVR to go up or down
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
infants myocardium resembles 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.
determines cardiac rate and rhythm
impulse conduction
cardiac rate is determined by the cell with the fastest intrinsic rate. All slower cells have their rates suppressed.
overdrive suppression
What CNS mediated reflexes control cardiac rate and contractility resulting in homeostasis of the aforementioned parameters.
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
humeral control of the heart affecting cardiac rate and contractility include what
adrenal gland secretion of adrenaline and norepinephrine.
drugs that are inotropic effecting cardiac rate and contractility
adrenocortical steroids
thyroid hormones
glucagon
the difference between the pressures at the arterial and venous ends
what is this estimated at
capillary hydrostatic pressure
estimated at 32 and 15 mmHg
what hydrostatic pressure is usually 0
tissue hydrostatic pressure
The oncotic pressure averages ____ in the capillary and less than ___ in the tissue
25mmHg
5mmHg
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 ___
out into the tissue
pull it back
lymphatic flow and the volume in a 24 hour period approximates the total body plasma volume.
what is increased when the plasma proteins are low, capillary permeability is high or there is an increase in hydrostatic pressure across the capillary
Lymphatic flow
what happens when the total lymphatic flow exceeds the capability of the lymphatic system, when there are lymphatic obstructions or high CVPs
Edema
the resistance to flow is determined only by the radius and length of the vessel and the viscosity of the blood
Poiseuille’s law
term used to describe the distensibility of blood vessels
Capacitance
a term to denote the ability of the distal vascular bed to accept flow
Capacity
reflexes that involve humeral modulation of vascular tone
RAAS (vasoconstrictive)
arginine vasopressin hypothalamic osmoreceptor system
Vasodilator effects by ANP and BNP
R ventricular impulse is located
under the xiphoid sternum
if the r ventricular impulse is more prominent than the ________ after —- hours of age, it is abnormal and requires evaluation
left apical impulse after 12 hours of age
A2 is always loudest where?
at the Lower left sternal border
All high frequency murmurs occur at the _____ in systole
apex
A qR pattern in V1 denotes
r ventricular hypertrophy
when qR pattern is absent in V6, it is highly associated with
hypoplastic L heart
in utero when does the heart develop
3rd week and is complete by day 45
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)
Situs solitus
when the atria and main stem bronchi develop opposite
Situs inversus
The absence of lateralization of the atria nd the thoracic organs
Situs ambiguous
When there are 2 r or 2 left atrial chambers
Atrial isomerism
when the atria connects to the ventricles in the way they should. RA connects to RV and LA connects to LV
concordant
When the RA connects to the LV and the RA to the LV
discordant
The atria connect to only one ventricle
univentricular
AV is straddling and committed to whichever ventricle is receiving more than 50% of output
ambiguous
when the RV connects with the PA and the LV with the aorta
concordant ventriculoarterial connections
When the aorta arises from the RV and the PA from the LV
transposition of the great arteries
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.
Double outlet
If the connection consists of only one great vessel or a common arterial trunk
Single outlet
fetal blood flow
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
when the placenta is removed form the circulation what begins to rise?
systemic vascular resistance
pulmonary pressures begin to decrease
at what age does pulmonary vascular resistance decrease to normal levels after birth
6-8 weeks
when does the foramen ovale finally close
within 3 months
fibrin fuses septal wall together
it may not close
normally the ductus closes in
4-10 days
ductus venosus usually closes within
3-7 days then becomes ligamentum venosum
3 important parts to a patient history when evaluating cardiac
1) Gestational and perinatal history
2) Postnatal and present history
3) Family History
Relevant maternal history
Healthy while pregnant?
Receive prenatal care?
Routine Ultrasound? did they show anything of concern?
Relevant Maternal Infections to Cardiac History
TORCH
Toxoplasmosis Other Rubella Cytomegalovirus Herpes
Maternal medications relevent to Cardiac history
Did she take any meds
Phenytoin
Lithium
Retinoic acid
warfarin
Postnatal and present history
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)
In infants for cardiac history feeding is actually a ____ test
exercise - if they are able to feed and grow, it is not usually a cardiac issue
family history for cardiac
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
physical exam cardiac
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
when S2 sounds are widely split
what does it mean
Abnormal splitting can be reflective of volume overload or electrical delay in a bundle branch block
S2 narrowly split means
Pulmonary HTN
aortic stenosis
S2 is entirely stenosis can mean
severe aortic stenosis
severe pulmonary HTN
Abnormal heart sounds are categorized into
systolic murmurs diastolic murmurs continuous murmurs Gallops Clicks
murmur barely audible
Grade I/VI
murmur soft but easily audible
Grade II/VI
murmur moderately loud but no thrill
Grade III/VI
murmur loud and accompanied by a thrill
Grade IV/VI
murmur audible with stethoscope barely on chest
Grade V/VI
murmur audible with stethoscope off the chest
Grade VI/VI
3 categories of murmurs
Ejection
Late Systolic
Holosystolic
murmur usually reflective of pulmonary stenosis or aortic stenosis
Ejection
murmur usually reflective of Mitral valve prolapse
Late systolic murmur
Murmur usually reflective of Tricuspid regurgitation, mitral regurgitation, VSD
Holosystolic murmur
Midsystolic murmur described
Ejection systolic
Crescendo/decrescendo murmur…starts soft, gets loud then soft again
murmur heard throughout systole between S1 and S2
Holosystolic murmur
murmur that is short and heard right at the beginning
early systolic murmur
murmur that is accompanied by a mitral click
Late systolic murmur
Diastolic murmurs are always ________
pathologic
systolic may be benign or pathologic
Early pitched diastolic murmur
higher pitched Aortic regurgitation (radiates to apex) pulmonary regurgitation (radiates along left sternal border)
Mid diastolic murmur
lower pitched
use bell of stethoscope
mitral stenosis (apex)
tricuspid stenosis (left lower sternal border)
Continuous murmurs are reflective of
PDA
AV fistula
Shunt murmur post surgery
Venous hum
aortic valve stenosis murmur would be best appreciated in the
aortic valve area - in the Right upper sternal border
Pulmonary murmurs are best appreciated in the
Left upper sternal border
Mitral murmurs are usually heard along the
apex
VSD , tricuspid regurgitation or Stills murmur are best heard at the
left lower sternal border
Gallops are broken down to
S3
S4
S3 is usually heard at the
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
is S3 normal?
it can be normal in children and young adults and it can also be reflective of pt with dilated ventricles and decreased compliance
S4 is heard where and is it bad?
heard at apex and always pathologic associated with decreased ventricular compliance associated with myocardial ischemia and ventricular hypertrophy
3 types of clicks
Ejection click
mid-systolic click
Diastolic opening snap
Ejection click is appreciated where and reflective of what
apex
aortic stenosis or if bicuspid aortic valve
Mid systolic clicks are appreciated where and reflective of what
apex
mitral valve prolapse
diastolic opening snap are appreciated where and reflective of what
Apex or Left lower sternal border
mitral stenosis
Pericardial friction rub
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
what is the most common congenital heart defect
VSD
As far as coronary defects or obstructions, which side would be worse
L side
where do the coronary arteries branch off of
Aorta
Circumflex artery branches off of
L coronary artery
3 categories of CHD circulation problems
Too much pulmonary blood flow
too little pulmonary blood flow
Too little systemic blood flow
Too much pulmonary blood flow, you have what symptoms
Tachypnea increased wob murmur diaphoresis fatigue poor feeding FTT cardiomegaly hepatomegaly pulmonary edema
example would be VSD
In too much pulmonary blood flow what is the relationship with Qp and Qs
Qp>Qs
Qs is always 1 all the time
Too little pulmonary blood flow, what is the relationship with Qp and Qs
Qp
what symptoms for too little pulmonary blood flow
cyanosis clubbing murmur Polycythemia Fatigue
cyanosis in extremities
Acrocyanosis. in infants normal finding from immature circulation
Too little systemic blood flow Qp vs Qs
example
Qp> Qs
quantity of blood to lungs >quantity of blood to body
classic example is aorta coarctation
symptoms for systemic blood flow
tachypnea increased wob cool extremities pallor murmur diaphoresis fatigue poor feeding FTT cardiomegaly hepatomegaly
in aortic coarctation before the narrowing the pressures are
high
in aortic coarctation after the narrowing (distal) the pressures are
lower
screening tool/assessment for coarctation
how would you perform
what would signify reason for concern
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
If the 4 extremity blood pressures are positive then what do you do?
echo
refer to cardiology
most severe form of coarctation
interrupted aortic arch
in transposition of the great arteries what other defect is essential for mixing to prevent heart failure
ASD
Transposition babies are sometimes put on what to keep the ductus open
PGE
patho for ASD
left to right shunting (atrial) 🡪 R atrial dilation, R ventricle volume overload
presentation for ASD
fatigue + dyspnea, systolic ejection murmur at left sternal border (large → diastolic murmur)
Plan of Care ASD
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
Patho for VSD
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)
presentation for VSD
systolic regurgitant murmur along the left sternal border (louder the murmur, smaller the defect)
plan of care VSD
Surgical closure if S/S of HF, growth failure, PH, or LV volume overload
Spontaneous closure possible for perimembranous/muscular defects – medically managed
patho coarctation of aorta
narrowing of the aorta (location determines severity of illness)
presentation coarctation of aorta
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
plan of care coarctation of aorta
emergent infusion of PGE (restore ductal patency) and surgical repair of coarctation – in older children, able to perform elective non-emergent repair
interrupted aortic arch patho
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
presentation interrupted aortic arch
cardiovascular decompensation at time of ductal closure, requires CT/MRI or echo to diagnose
interrupted aortic arch plan of care
emergent PGE infusion to maintain ductal patency until surgical intervention can be made
aortic stenosis patho
thickened, rigid valve causing outflow obstruction from the L ventricle
aortic stenosis presentation
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
plan of care aortic stenosis
Echocardiogram + doppler to measure pressures in the aorta + left ventricle, repair with valvuloplasty, valve replacement, or resection of membrane causing obstruction
do you have normal or decreased spo2 in ASD and VSD
normal
boot shaped heart on xray is consistent with
Tetralogy of fallot
4 components of Tetralogy of Fallot
Pulmonary stenosis
VSD
Aortic override
RV is hypertrophied (thickened) - it is seeing high pressure because its pumping against the high pressure from pulmonary stenosis
snowman sign on xray
Total anomalous Pulmonary venous return
Total anomalous Pulmonary venous return
pulmonary veins miss the left side of the heart so the oxygenated blood is going back to the right side of the heart. if they have a restricted ASD they have very little systemic circulation.
Highest risk TAPVR
infradiaphragmatic TAPVR
How do you keep the ductus arteriosus patent
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, but your in the EC, you can intubate, you may buy them time
if you have too little systemic blood flow
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
what genetic syndromes are highly associated with congenital cardiac defects
Trisomy 21, 18, 13
22q11 deletion
williams syndrome
Alagille syndrome
Noonan syndrome
in utero that is associated with congenital cardiac defects
Maternal diabetes Antiepileptic drugs (ie) Depakote) psychiatric medications thyroid dysfunction maternal autoimmune disease alcohol abuse smoking HTN infectious illness (less likely to be structural, more likely for myopathies)
3 types of Cardiomyopathy
Dilated - most common
Hypertrophic
Restrictive
Pressure overload lesions
aortic stenosis
pulmonary stenosis
coarctation of aorta
hypoplastic left heart
increased RV outflow tract obstruction -> increased RV pressure -> increased preload ->increased RA pressure -> R to L shunting ->cyanosis
Pulmonary stenosis
to separate aortic stenosis from hypoplastic left heart syndrome
get an ECG
