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.