Cardiology Day Flashcards
heart formation is completed by ? gestation
8 weeks
in fetal circulation, ventricles work in ?
where does RV supply and percentage of blood volume?
where does LV supply and % of blood volume?
work in parallel
RV: 66% blood volume. lower body, placenta
LV: 34% heart brain, upper body.
56% cross PDA
which side heart has higher oxygen saturation in utero.
oxygen in DV and IVC
Left side (65%) - preductal higher, this is due to DV directly shunt cross PFO to LA.
R side (55%): this is due to mixing from IVC
DV 70% oxygen
IVC 45%
SVC 40%
fetal compensation for hypoxic environment
high fetal epo/HCT
high affinity for oxygen by fetal hemoglobin
minimal oxygen consumption (minimal respiratory effort, maternal thermoregulation, minimal GI digestion and absorption, decrease renal tubular reabsorption
fetus can only regular Cardiac output (CO) via what?
increase HR.
CO = SV x HR
hypoxemia vs hypoxia
hypoxemia: decrease amount of o2 in blood (pulse oximeter)
hypoxia: decrease o2 to tissues.
Fetal O2 delivery can be reduced by 50% without significant effect on O2 uptake.
with hypoxia, where does blood shunt in fetal circulation?
how does fetal response to chronic placentla insufficiency.
heart, brain, adrenal gland
DV dilate. shunt blood away from portal circulation –> decrease liver growth, decreased abdominal circumference.
closure of PDA due to (3 reasons)
low amount of PGE (no placenta supply, increase PBF (pulmonary blood flow), increased metabolization of PGE in the lungs)
bradykinin (produced by lung) > constrict PDA
higher oxygen concentration within ductal tissues.
oxygen effect on umbilical artery, PDA and pulmonary vein
oxygen: constrict umbilical artery, PDA,
dilate pulmonary vein.
cardiac output (2 equations)
CO = Systemic blood pressure/ Total peripheral vascular resistance
–>
P = Q (flow) x R
CO = SV x HR
Afterload depend on what?
SVR
ventricular wall thickness and ventricle radius
( ventricular wall stress = ventricular P x ventricular radius / wall thickness)
Frank-Starling: where does curve move?
bad: move down (increase after load)
good: move up (decrease afterload) .
x-axis: preload (LV end-diastolic volume)
y-axis: contractility. (stroke volume)
cardiac filament
actin (thin)
myosin (thick)
increase preload and increase stretch, there’s optimal overlap between thin and thick muscle filaments of sarcomeres
BP formula
BP = CO x SVR
Three types of Shock
Hypovolemic
Cardiogenic
Distributive (sepsis, vasodilator, adrenal insufficiency, anaphylactic)
Compensation Mechanism for Shock
baroreceptors: decrease stimulation of baroreceptros in aortic arch and carotid sinus –> vasoconstriction
Brain chemoreceptors: cellular acidosis -> vasoconstriction, and respiraotry stimulation.
Renin-angiotensin system
humoral response (catecholamines)
autotransfusion: reabosrotpions of interstial fluid
Receptors, their Effects, and mechanism of action
Alpha -1
Alpha-2
Beta-1
Beta-2
Alpha-1
Increase SVR, increase contractility
- signal phospholipase C
Alpha-2
decrease SVR
- inhibit adenylyl cyclase
Beta-1
Increases contractility (mostly ventricles) Increases HR (SA and AV nodes) Increases conduction velocity (higher risk for arrhythmias)
- cAMP
Beta-2
Decreases SVR , Note: also bronchodilation
-cAMP
Dopamine vs. Dobutamine
compound, receptor, dose-dependent, HR, contractile, SVR effect, BP effect
Dopamine:
endogenous
precuorsor to epi and nor-epi
Receptors: beta-1 and alpha-1
low dose: renal, medium: beta-1, high: alpha-1
clinical example: use in “warm shock”
Dobutamine:
synthetic
Receptors: beta-1, some beta-2
not dosing dependent
clinical example: use in cardiogenic shock
Epinephrine:
dose effect
effect on HR, contractility, SVR, BP
low dose: Beta-1 and Beta-2 (similar to dobut)
^ HR, ^ contractility, v SVR, BP: depends -
high dose: alpha-1 and beta-1 (similar to dopa)
decrease HR because ^ vagal tone on SA and AV nodes ( beta receptor in vagal nerve).
^ contractility, ^ SVR (alpha-1), ^ BP
norepinephrine:
receptor, HR effect, contractility, SVR, BP
Beta-1 and Alpha-1. some Beta-2 (similar to high-dose epi)
DECREASE HR because increase in Vagal tone on SA and AV nodes.
^ contractility, ^ SVR, ^ BP
Milrinone
phosophdesterase type 3 receptor
(PDE 3)
increase cAMP (stop PDE III from breaking down cAMP to AMP. cAMP convert to ATP via adenylyl cyclase)
vasodilation (decrease SVR, decrease coronary artery perfusion)
Hydrocortisone Effect on treating volume-resistant and pressure resistant shock
- block breakdown of catecholamines
- up-regulate cardiovascular adrenergic receptors (sustain response to adrenergic agents)
- hormone replacement if adrenal insufficient
smooth wall, which ventricle
not smooth wall, which ventricle
left ventricle.
R ventricle, (not smooth)
Qp/QS in L to R shunt
Qp/Qs > 1
signs of Qp/Qs > 1
L to R shunt
Tachypnea *Dyspnea *Tachycardia *Diaphoresis *Poor feeding *Poor weight gain *Pulm edema, Cardiomegaly *Rising lactate
Congestive heart failure.
R to L shunt: Qp/Qs ratio
Qp/Qs < 1
Qp / Qs < 1
symptoms
insufficient Qp
R to L shunt.
Hypoxemia * Cyanosis * Tachypnea w/o distress * Dark lung fields on CXR
metabolic acidosis, rising lactate.
signs of pulmonary over circulation
what Qp/Qs
which way is the shunt?
Qp/Qs > 1, L to R shunt
Volume-loaded heart.
What are common cardiac conditions that lead to volume-loaded heart?
L to R shunt, mixing lesions. single ventricle without pulmonary stenosis.
Poiseuille’s law (both for cardiac and pulmonary)
Resistance = (8 u L)/(pi r^4)
if baby has too much pulmonary blood flow, what do you do
PA bands on main pulmonary artery
if baby with mixed heart lesion or single ventricle, but SpO2 is high, what does that mean?
too much blood return from lung to LV.
too much blood to the lung.
Why does active PDA lead to low diastole.
blood is taken away during diastole (likely from PDA),
low diastole pressure
too much blood cross PDA (PDA steal)
diastole is heart filling.
Omh’s law
Resistance = change in pressure / volume of flow
Q = ΔP/R
How to increase PVR
- Pulmonary Vascoconstriction
*Hypoxia
*Acidosis (↑pC02) - Increased interstitial pressure *Atelectasis
*Pulmonary edema *Pneumothorax/Pleural effusion *Mechanical ventilation
*Excess PEEP - Lung hypoplasia
- Polycythemia
How to decrease PVR
- Pulmonary Vasodilation
*Alkalosis (↓pC02)
*Oxygen
*Nitric Oxide - Sildenafil, Bosentan, etc
- Alveolar expansion
Three groups of congenital heart disease
Congestive heart failure
- L to R shunts
- mixing lesions
Cyanotic heart disease
- R side obstruction
- insufficient pulmonary blood flow
- parallel circulation
Hypoperfusion
- L side obstructive lesions
- impaired ventricular function
Congestive Heart Failure:
clinical presentation
pathophysiology
time of symptoms
respiratory distress, tachypnea, tachycardia, poor feeding, poor growth
L to R shunt
Mixing Lesions.
Most common in PCP office in subsequent month.
Name L to R shunt lesions
ASD, VSD, PDA
complete AV canal
PAPVR (partial anomalous pulmonary venous return, part of pulmonary V drains to SVC)
are L to R shunt duct dependent
No
Sat normal in the absence of lung disease
not caught on pulm oximetry screening.
what happens to blood flow across PDA in pulmonary HTN
blood flow cross PDA in systole AND diastole: continuous murmur, bounding pulses, wide pulse pressure (low diastolic pressure due to PDA steal)
How can the velocity of flow across PDA (assed in Echo) help determine PA pressure.
pressure gradient = 4x velocity ^2
Velocity: velocity of flow across the PDA
PA pressure calculation:
BP - pressure gradient = systolic PAp
PA pressure SHOULD BE 1/4 of Systemic pressure
Device PDA closure criteria
700 g and bigger
> 3 DOL
ductus > 3mm long
smallest diameter of ductus </= 4mm
ductal dependent - contradicting
CoA or LPA stenosis contradicting.
risk PDA device closure
throbmosis,
heart injury
device migration.
and many more
Mixing Lesions: examples
why are they different than L to R lesions
why are they different from Cyanotic heart disease
*Truncus Arteriosus,
* unobstructed TAPVR
* Single ventricle without outflow obstructions:
- double inlet LV
-Tricuspid atresia + VSD
- Unbalanced AV canal
Some blue blood enters the systemic circulation, resulting in a drop in 02 sat (to a variable extent)
*Not a cyanotic heart lesion: while the 02sat may be low due to the mixing, the patient has excessive pulmonary blood flow
Not duct dependent
O2 sat 85-100%
often but not always fail CCHD
Truncus Arteriosus is associated with what syndrome
DiGeorge Syndrome
(another cardiac lesion in DiGeorge is interrupted aortic arch, ToF, and VSD)
PA exposed to systemic pressure
Management of L-R shunt and Mixing lesions
Diuretics, HFNC
Fortify calories, NG tube.
judicious use of oxygen sat goal < 85%
Drive up PVR
^ SVR (vasodilators)
normal hematocrit
early surgery if. Qp/Qs cannot be balanced. BEFORE pulmonary HTN become irreversible.
Symptoms of Cyanotic Heart Disease
hypoxemia
either both pre- and post- low. or pre-ductal < post ductal.
poor response to 100% O2 (especially PaO2)
central cyanosis
failed CCHD
NO respiratory distress
How to distinguish the cyanosis in:
Cyanotic heart disease
Lung disease w/o PPHN
PPHN
Cyanotic Heart Disease:
no respiratory distress. low sat pre- and post. (equal) (pulmonary atresia, intact septum) or reverse differential.
when at 100% oxygen, small increase in SpO2 and PaO2
50% with murmur
Lung Disease (no PPHN): low sat pre and post. respond well to 100% O2 (SpO2 and pO2 increase)
PPHN: pre-ductal and post ductal difference (post ductal very low).
respond well to 100% O2 (SpO2 and pO2 increase)
Cyanotic hear disease has two categories. What are they?
Obstruction along pathway to pulmonary circulation
Tricuspid stenosis or atresia
Neonatal Ebsteins
TOF
Pulm valve stenosis
Pulmonary atresia w/ VSD
Pulmonary atresia w/ intact ventricular septum
Supravalvar pulmonary stenosis
Branch pulmonary stenosis
Circulation in parallel.
1st line when suspecting cyanotic heart disease due to obstruction along pathway to pulmonary circulation
once pre- and post ductal sats are low, poorly responsive to oxygen.
start PGE
call cardiology
also evaluate for PPHN and lung disease
Management of cyanotic heart disease due to obstruction along pulmonary circulation
Maintain ductal patency (to provide a stable source of pulmonary blood flow)
Decrease oxygen demand if sats< 70%
*mechanical ventilation
* sedation/paralysis
*maintain normal temperature
* Normalize hematocrit
Support cardiac function
* correct acidosis
Judicious use of oxygen
(hypoxemia is expected; providing oxygen may lead to excessive pulmonary blood flow, acidosis and congestive heart failure)
Circulation in Parallel
D-Transposition of the great arteries
some w/ VSD, some w/ ASD, some with nothing
? mixing inside the heart determines treatment.
Do D-Transposition always have pre- and post- duct split?
No.
if mixing occurs (VSD and ASD), pre- and post- will be the same. (both low).
the earlier, the more severe cyanosis, the more likely the defect have D-TGA.
What’s difference between CXR on cyanotic heart disease due to pulm obstruction vs. D-TGA.
normal pulmonary vascular marking on CXR for D-TGA.
Decrease pulmonary marking for pulm. obstruction cyanotic heart lesion.
Management of Parallel Circulation
give PGE
if SpO2 low at birth, may give O2 during transition to promote drop in PVR
(drop in PVR, increase PBF, more return to LA, and more L to R shunt on ASD)
–> acute severe drop in pre- and post-ductal sats if the rise in LAp close PFO.
Echo for intracardiac mixing ability
if SpO2 low (<70%), ASD small, move to balloon atrial septostomy.
if cyanotic heart disease, what to do first
start PGE
r/o respiratory cause and PPHN.
Hypoperfusion’s presentation
decrease systemic perfusion of upper or lower body or both.
Poor pulses, hypotension, tachycardia, tachypnea, pallor, cool extremities, high lactate.
Name lesions associated with
Hypoperfusion lesions cardiac conditions.
what syndrome
Left-sided obstructive lesions:
obstructive TAPVR,
mitral valse stenosis/atresia,
supra-valvar aortic stenosis,
aortic stenosis/atresia,
interrupted aortic arch
coarctation of aorta
HLHS
Shones Syndrome
(4 LV outflow tract abnormalities: coarctation, subaortic obstruction- blockage below the valve, parachute mitral valve, mitral valve stenosis/regurgitation)
Hallmark of Many L sided Obstructive lesions
High Sat pre-duct
Low sat post-duct
Right-to-Left flow across the ductus leads to lower post-ductal saturations.
(But at atrial and ventricular level, shunt is still L to R)
just like PPHN
two cardiac lesions need IMMEDIATE intervention
(PGE won’t help much)
Obstructive TAPVR
HLHS w/ intact Atrial Septum.
Both are completely obstructed pulmonary venous return.
Examples of Inadequate systemic blood flow without obstruction (poor function or steal):
Arrhythmias,
Myocarditis,
Cardiomyopathies,
Systemic Infections
Metabolic Disorders
Steal away from the systemic circulation: ex Vein of Galen
Treatment of Lesions Causing Hypoperfusion
keep duct patent.
decrease oxygen demand
support cardiac Fx. (correct acidosis, inotropic supoort, volume resus)
judicious use o oxygen
HLHS repair
stage 1 norwood w/ RMBTT shunt
Stage I norwood w/ Sano
Example of single ventricle w/o obstruction
Do they need PGE
unbalanced AV canal
double inlet LV
does NOT need PGE
(similar physiology like mixed lesions: Truncus, TAPVR w/o obstruction, CAVC)
might need to partially obstruct pulm blood flow. but go home w/o surgery
Neonatal Long QT syndrome:
describe what it’s like
which leads to calcualte.
bradycardia
+/- irregular rhythm (can cause heart block)
can has 2:1 block in LQTS
QTc : 490.
look for lead II, V5
tiny box 0.04, big box 0.2
3 genes cause long QT syndreom.
KCNQ1 (LQT1), KCNH2 (LQT2), SCN5A (LQT3)
(this was ON the board!)
what electrolytes abnormalities cause long QT
hypoCalcemia, Hypo K, Hypo-Mg.
2nd degree or heart block: two types
Morbitz I or Wenckebach:
benign, block within AV node, seen w/ medication or high vagal states
Morbitz II: may progress to CHB w/o adequate escape rhythm. evaluate for LQTS, Myocarditis.
< ___ bpm what fetal HR is associated with fetal hydrops and perinatal death?
< 55 bpm
L-TGA has what cardiac arrhythmia
What other cardiac lesion is associated with this arrhythmia?
complete heart block
(complete AV canal, single ventricle lesion) > both are left atrial isomerism
conditions associated with complete heart block
L-TGA
complete AV canal,
single ventricle lesion,
left atrial isomerism
maternal lupus (damage is irreversible, dilated cardiomuyopathy)
what needs pacemaker in neonatal period
- Mobitz II or CHB with symptoms, ventricular dysfunction or low cardiac output
- CHB withV-escape rate < 55 bpm
*CHB + structural heart disease withV-escape rate < 70 bpm
*CHB with wide QRS escape or complex ventricular ectopy
Three Types of SVT
- Re-entrant tachycardias between Atria and Ventricles: WPW, AVNRT(AV node re-entrant tachycardia -> common SVT in adolescents)
- Re-entrant tachycardias within the atria: Atrial flutter
- Automatic tachycardias
what congenital heart disease is associated with an accessory pathway and what arrhythmia can it lead to?
Ebstein’s anomaly
WPW -> SVT
Describe the other Kind of SVT: Atrial Flutter
adenosine does not work!
re-entrant tachycardias within the atria.
P wave (sawtooth),
Atrial rate: 300-600
Ventricular rate: 180-200
Flutter is super fast
adenosine block AV not but doesn’t block circuit –> sawtooth, –> back to flutter
Tx: electrical cardioversion or rapid atrial pacing. beta blocker
Rx to suppress recurrent A-flutter: digoxin, propanolol
automatic SVT:
examples and EKG characteristics
Automatic tachycardias: sinus tachycardia, ectopic atrial tachycardia (EAT), multifocal atrial tachycardia (MAT), junctional ectopic tachycardia (JET)
HR increase and decreases gradually
HR varies during tachycardia
The rhythm doesn’t break with adenosine or cardioversion.
Giant P wave, RBBB
Ebstein
Delta wave in WPW is because of what? how is this related to the formation of SVT (WPW)
conduction down the accessory pathway
impulse begin in atria, circuit develop which involves the AV node and an accessory pathway
1:1 conduction
Normal QRS Axis:
what does QRS looks like in lead I and lead aVF
0-100*
(100 degree)
QRS mostly UP in lead I
QRS definitely UP in lead aVF
QRS Axis:
- two important lead (where they point to)
- what does upward and downward QRS mean
- where is 0 degree
Lead I (3 O’clock) & Lead aVF (6 O’clock)
upward: move toward the positive pole of the lead.
downward: away from the positive pole of the lead.
Lead I is 0 degree (3 O’clock) (goes clockwise)
heart drives from what part of the primitive cell layer
mesoderm
% of total blood volume in fetal pulmonary circulation
7-15% in 2nd trimester.
35% in 3rd trimester.
decrease to 20% at 38 week gestation. (due to pulm vessel sensitive to low O2)
oxygen saturation in fetal circulation:
DV, IVC, SVC, RA, LA, RV, LV
DV: 70%,
IVC and SVC: 45% and 40%.
RA, RV = 55%
LA, LV = 65% (higher as DV directly shunt cross PFO to LA)
pre-ductal sat higher than lower ductal sat.
fetal response to hypoxemia
suppressed respiration, bradycardia, decrease in CO
SV depends on what
preload, afterload and contractility
why is MCA diastolic blood velocity go up during anemia ?
Increased diastolic blood velocity of middle
cerebral artery
Marker of compensatory redistribution of blood
to the brain during hypoxemia/severe anemia
what does absent and reverse ductus venous flow during atrial systole indicates what?
decrease fetal cardiac contractility
umbilical vein pulsation.
hypotension vs. shock
hypotension: less than normal
inadequate tissue perfusion -> shock
Type of Neonatal shock
Hypovolemic,
Cardiogenic
Distributive
Flow restrictive
Dissociative
how is renin-angiotensin system work in shock
low BP
renin secreted by kidney.
angiotensinegen secreted by liver
renin convert angiotensinogen to aniotensin I
Angiotensin I goes to angiotensin II (by angiotensin converting enzyme in lung capillary)
angiotensin II: 1) vasoconstriction. 2) adrenal gland > aldosterone.
Alpha-1 receptor’s cardiac effect
signal pathway / mechanism
increase SVR
increase contractility (positive inotropes)
smooth muscle contraction
signal phospholipase C
Alpha-2 receptor’s cardiac effect
signal pathway / mechanism
decrease SVR
smooth muscle relaxation
inhibit adenylyl cyclase
Beta-1 receptor’s cardiac effect
signal pathway / mechanism
increase contractility (in ventricles)
increase HR (SA and AV nodes)
increase conduction velocity (higher risk for arrhythmias)
smooth muscle relaxation
induce cAMP production
Beta-2 receptor’s cardiac effect
signal pathway / mechanism
decrease SVR
bronchodilation
smooth muscle relaxation
induce cAMP production
Epi’s effect on coronary artery perfusion (CAP)
High dose Epi improve coronary artery perfusion (CAP)
high dose epi > increase SVR during diastole > improve coronary artery perfusion.
LV myocardium perfused during diastole
CAP = Ao diastolic P - LV end diastolic P
If inc SVR -> Ao diastolic P increases > inc CAP
If dec SVR -> Ao diastolic P decreases > dec CAP
Epi’s effect on lactate
increase lactate
epinephrine increases glycogenolysis
Cyanotic heart disease due to R obstruction management and timing with surgery (temporary)
PGE
then within 1 week:
Balloon dilation. RVOT stent, PDA stent, BTTshunt
L-TGA is associated with what other neonatal heart condition
neonatal heart block
In left-sided obstructive lesions, what is the pre- and post-ductal sat normally like.
What does pre-ductal hypoxemia mean?
normally: lower pos-ductal sat (because R to L shunting at ductus level)
pre-ductal hypoxemia means minimal flow across the aortic valve and retrograde flow in the arch.
signs and symptoms of hypoperfusion
poor pulses, hypotension, tachycardia, tachypnea, pallor, cool extremities, high lactate
single ventricle with outflow obstruction:
examples
management
HLHS w/ LVOT (aortic stenosis)
Pulmonary atresia w/ intact ventricular septum
need PGE
need intervention to substitute for ductus before going home (BTT shunt, ductal stent)
Name 3 groups of neonatal congenital heart disease.
For each group, please give the following:
Clinical Presentation
Pathophysiology
Saturation
Ductal depend/PGE or not
Treatment
CHF:
- Respiratory distress, poor growth, symptoms later, pass CCHD.
- L - R shunt, Mixing lesions
- SpO2 normal and pre-post same
- no PGE
- decrease pulm overcirculation, reduce/support respiratory effort, O2 contraindicated.
Cyanotic Heart disease:
- Hypoxemia, central cyanosis, without respiratory distress (until acidotic). Most common symptomatic form of CHD in neonates, fail CCHD
- impaired flow to lung (R side obstructive lesions), parallel circulations
- SpO2 low, pre-post same. or post> pre in DTGA.
- Yes PGE
- PGE, balance Qp/Q2, careful with O2, urgent ballon atrial septostomy in D-TGA
Hypoperfusion:
- Decreased perfusion, poor pulses, hypotension, tachycardia, pallor, acidosis. Second most common symptomatic form of CHD in neonates. can be missed on CCHD.
- L side obstructive lesions. poor ventricular function.
- normal or low. Pre-post same or pre > post.
- Yes PGE
- PGE, balance Qp/Qs, oxygen typically contraindicated, support venticular fx. might need urgent procedure.
Alagille:
gene mutation
cardiac lesion
other symptoms
JAG1
Branch PA stenosis, PS, TOF
Prominent forehead, butterfly hemivertebrae, anterior chamber abnormalities of the eye
DiGeorge:
gene mutation
cardiac lesion
other symptoms
22q11 deletion
VSD, Truncus, Tetralogyof Fallot, IAA
Hypoplasia of thymus and parathyroid, cleft palate
Holt Oram:
gene mutation
cardiac lesion
other symptoms
TBX 5 mutation
“Heart - hand syndrome” AD
ASD, VSD
upper limb anomalies
Marfans:
gene mutation
cardiac lesion
other symptoms
FBN1 mutation
Aortic root dilation, valve prolapse
Long limbs, scoliosis,pectus
Noonans:
gene mutation
cardiac lesion
other symptoms
PTPN mutations
PV stenosis, Tetralogyof Fallot
Widely spaced eyes, ptosis, low set ears, webbed neck, pectus, cryptorchidism
Downs:
gene mutation
cardiac lesion
other symptoms
Trisomy 21
ASD, VSD, CAVC
Bilateral epicanthal folds, tongue protrusion, low nasal bridge, hypotonia, brushfield spots
Turners:
gene mutation
cardiac lesion
other symptoms
XO
Bicuspid AoV, AS, CoA, IAA
Webbed neck, lymphedema
Williams:
gene mutation
cardiac lesion
other symptoms
7q11 deletion
Supravalvar AS, Branch PA stenosis
Elfin facies, stellate pattern of iris, short anteverted nose, long philtrum, prominent lips
P waves are upright in what leads
lead I and aVF
PAC is caused by what
atrial myocyte initiate a beat between impulses coming from sinus node
hence if HR ^, PAC goes away
Three different patterns of PAC
How to tell if it’s a PAC?
Normally conducted PAC (early P wave, reached AVB node, AV node is ready to conduct)
Aberrant PAC (early P wave, reach AV node a little too early)
Blocked PAC (early P wave reaches the AV node so earlier that it’s blocked)
To tell if it’s a PAC:
look for a P wave before the early beat or look at the T wave immediately before an unusual complex/pause: if it’s altered, likely PAC.
Causes of PAC
- Increased vagal tone / sinus bradycardia
- Mechanical stimulation (central line tip in the atrium)
- Electrolyte abnormalities (glucose, potassium )
- Hypoxemia
- Hyperthyroidism/Hypothyroidism
- Myocarditis/Cardiomyopathy/Atrial tumors
- Drugs: Digoxin, caffeine, α or β-agonists,
What does PVC look like
- early QRS (wide and unusual)
- no proceeding P wave
- T wave following wide QRS is directly opposite the QRS axis
- followed by compensatory pause
PVC causes
- Immature myocardium
- Electrolyte disturbance
- Metabolic disease
- Cardiomyopathy
- Intracardiac tumors
which lead is used to calculate QTc
Lead II and V5
two types of neonatal tachycardias
- SVT (supraventricular) (tachycardia arising from or above the bundle of His)
- Ventricular Tachycardia (VT)
treatment for WPW-type SVT
break A-V circuit:
- vagal maneuver or adenosine. (block AV node)
- cardioversion or rapid atrial pacing (is unstable)
SVT is well tolerated unless unrecognized for > 24h.
treatment to prevent WPW-type SVT recurrence:
Propanolol or digoxin
Procainamide, flecainide, sotalol
why is diagnosing atrial flutter tricky?
- When flutter is conducting 1:1 it is difficult to differentiate from other narrow complex SVTs (Hint: Flutter is typically very fast)
- A-flutter + antidromic WPW wide complex tachycardia (resembles VT)
- A-flutter with 2:1 or 3:1 conduction resembles complete heart block (Hint: the atrial rate is normal in CHB and very fast in Flutter)
EKG Left axis devision:
what quadrants of QRS
what cardiac disease
what does lead I and aVF looks like
-100* - 0*
AV canal,
primum ASD
Tricuspid atresia
lead I: UP, aVF: DOWN
EKG showed “Northwest”/LAD (left axis deviation)
what quadrants of QRS
what cardiac disease
what does lead I and aVF looks like
190 - - 100*
coarctation.
QRS down in lead I and aVF
EKG Right Axis Deviation/Normal newborn Axis
what quadrants of QRS
what cardiac disease
what does lead I and aVF looks like
100* - 190*
RV hypertrophy: ToF, Coarctation. or normal newborn.
lead I: DOWN, aVF: mostly UP.
When deoxygenated hemoglobin is below ? g/dL, can infant appear cyanotic?
i.e. if infant has hemoglobin of 12g/dL, below what ? SpO2, will infant become cyanotic?
Central cyanosis occurs when deoxygenated hemoglobin < 3g/dL
In this case, 12 g/dL = 100%.
(12-3)/12 x 100% = 75%
