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