Cardio exam 5 Flashcards
4 determinants of cardiac fxn
contractility
preload
afterload
HR
Relationship b/t PCWP and PADP
PADP 1-4mmHg greater than PCWP
higher in pulmonary disease
Test to determine b/t systolic and diastolic HF
echo
Hypertrophy type and cause
concentric from pressure overload
eccentric from volume overload
Division b/t nonprogressive and progressive shock pressure
45mmHg systolic
Tx for anaphylatic/neurogenic shock
sympathomimetics
Impact of increased preload on pressure cycle of heart
increased LVEDV
slight increase in afterload
Impact of contractility on pressure cycle of heart
increased max LV pressure and stroke volume
no change in LVEDP
decreased LV end systolic volume
Chronic HF treatment focus
neurohormonal modulation
Side effects of diuretics with HF
overdiuresis electrolyte imbalances (K+ and Mg2+)
1st line tx for systolic HF
ACE-I’s
3 drugs decreasing mortality with systolic HF
beta blockers
ACE-I’s
spironolactone
Ejection fraction eqn
EDV-ESV/EDV
CO and TPR relationship
CO=arterial BP/TPR
Exercise and neurohormonal control
skeletal m. vasodilation causes decreased TPR
sympathetics cause increased HR, contractility and venoconstriction
increases arterial BP, increasing flow to muscle
Intrapleural pressure and RA pressure relation with CO
breathing decreases intrapleural pressure, increasing RA pressure
cardiac output increases with more negative intrapleural pressure (due to increased RA pressure)
Sympathetics role in shock
maintains normal BP/cardiac compensation
except in brain and heart (local mediators)
overwhelmed in shock and cannot compensate enough
Cellular effects of progressive shock
lysosomal enzyme release
decrease in high energy phosphates (irreversible)
acidosis
Cause of neurogenic shock
rapid loss of vasomotor tone
drops VR and CO
Cause of anaphlyatic shock
Ab-Ag response via mass histamine release
causes massive vasodilation
Difference b/t severe sepsis and septic shock
severe sepsis can be corrected by fluids
Most common cause of septic shock with burn victims
Pseudomonas
Bugs with early onset neonatal sepsis
Group B strep
E. coli
H. flu
Listeria
Bugs with late onset neonatal sepsis
S. epidermidis
N. meningitidis
H. flu
High and low pathogenic gram + bugs with sepsis
S. aureus/S. pneuno high
S. epidermidis/E. faecalis low
Virulence factors for sepsis
gram (-) have LPS
gram (+) have peptidoglycan/teichoic acid/superantigens
Peptidoglycan virulence with sepsis
activates defense pathways
Superantigen virulence with sepsis
activates T cells nonspecifically (without Ag) by binding outside of HCM II and T cell receptor
examples: TSS1 and SPE
LPS virulence with sepsis
cleaves C3 to C3b, causing C5 to be cleaved into C5a which attracts neutrophils
also lipid A is toxic, causing cytokines/coagulation
Sepsis bug with increased risk with Sickle Cell
salmonella
Pyogenic IL’s
IL1
IL6
TNF-alpha
Chemoattractant molecules
IL8
C5a
Breakdown of dorsal mesentery of heart
transverse pericardial sinus
Endocardial cushion origin
in bulbus/truncus is neural crest
b/t A and V not neural crest
Tetralogy of Fallot
Pulmonary obstruction
RVH
Overriding aorta
VSD
Aortic arches and what they become
I-maxillary a. II-hyoid/stapedial a. III-internal and common carotid IV-R subclavian and aortic arch VI-R pulmonary a. and L pulmonary a./ducts arteriosus
Veins obliterated with great venous shift
R umbilical
L cardinal/vitelline
What does supracardinal v. become
azygos system
What is Eisenmerger syndrome?
R to L shunt caused by a L to R shunt
irreversible pulmonary HTN
Secundum ASD
asymptomatic till 30’s
RV volume overload/R axis deviation
RVH and failure eventually
Sinus venosus ASD
R pulmonary v. connected to R atrium
Assc of endocardial cushion defect
Trisomy 21
Patent ductus arteriosus meds
NSAIDs close it
PGE2 keeps it open
Assc with coarctation of aorta (8)
bicuspid aortic valve Turner's syndrome Berry aneuryms ascending aortic aneurym bacterial endocarditis PDA VSD
Mitral valve abnormalities presenting as mitral stenosis
doulbe orifice MV
parachute MV
accessory MV
What is Ebstein’s anomaly?
part of triscupid valve in apical RV
causes tricuspid regurg
What is a Blalok-Taussig shunt and use?
subclavian v. to pulmonary artery connection
for tetralogy of fallot
Goals of Tetralogy of Fallot surgery
remove pulmonary obstruction
closure of VSD/shunts
competent pulmonic valve
Necessity for life with tricuspid atresia
patent ductus arteriosus
ASD
What is a Fontan repair?
vena cava to pulmonary artery connection
to bypass R side of heart
Conditions you see paradoxical emobli
R to L shunts
5 R to L shunts
TOF transposition of great arteries patent truncus arteriosus tricuspid atresia TAPVC
Pressures in TOF
R side greater than L side
What sx do you see with R to L shunts?
cyanosis
What is always present in total anomalous pulmonary venous connection?
ASD or patent foramen ovale
L to R shunts (4)
ASD
VSD
PDA
AV defect
VSD assc’s
Tetralogy of Fallot
Trisomy 21
AV septal defect and assc
malformation of tricuspid and mitral valves
Down syndrome
What are Quilty lesions seen with?
Cardiac transplant
overlies myocardium
mostly T cells
Problem with long term cardiac transplant
stenosing intimal proliferation of coronary arteries
silent MI’s
Post op problems with cardiac transplant
infection/malignancy
EBV assc with B cell lymphoma
What are heart failure cells?
hemosiderin deposition in macrophages
due to congested capillaries leaking into alveolar spaces
Impact of placenta removal from fetal circulation
increased resistance in umbilical vein
flow stops in umbilical vein and arterty
Impact of first breath on neonatal circulation
decreased resistance of lungs
closure of foramen ovale
ductus arteriosus close with oxygen exposure
Timeframe of closure/stopped flow in fetal circulation loops
umbilical v./ductus venosus-days
foramen ovale-minutes
ductus arteriosus/umbilical a.-hours
Pathologies increasing cardiac output
Beri beri
AV shunts
hyperthyroidism
anemia
Pathologies decreasing cardiac output
MI
shock
severe valve disease
1st degree heart block
fixed PR interval greater than 200ms
2nd degree type 1 heart block
lengthening PR interval with a dropped QRS
2nd degree type 2 heart block
fixed PR interval with more P than QRS
R bundle branch block
lead V1 has slurred S and wide QRS
lead I has wide QRS
both deflected up
L bundle branch block
lead V1 is downwardly deflected and wide QRS
lead I has wide QRS
LVH on EKG
V1/V2 down + V5/V6 up is over 35mm
deep S wave on V1
RVH on EKG
R axis deviation
R/S over 1 on V1
deep S wave on V6
R atrial abnormality
V1 P wave over 1.5mm OR
II P wave over 2.5mm
L atrial abnormality
V1 P wave over 1mm deep and wide OR
II P wave longer than 120ms
