Cardio exam 5 Flashcards by Grant Oakley

4 determinants of cardiac fxn

contractility
preload
afterload
HR

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Relationship b/t PCWP and PADP

PADP 1-4mmHg greater than PCWP

higher in pulmonary disease

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Test to determine b/t systolic and diastolic HF

echo

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Hypertrophy type and cause

concentric from pressure overload

eccentric from volume overload

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Division b/t nonprogressive and progressive shock pressure

45mmHg systolic

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Tx for anaphylatic/neurogenic shock

sympathomimetics

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Impact of increased preload on pressure cycle of heart

increased LVEDV

slight increase in afterload

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Impact of contractility on pressure cycle of heart

increased max LV pressure and stroke volume
no change in LVEDP
decreased LV end systolic volume

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Chronic HF treatment focus

neurohormonal modulation

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Side effects of diuretics with HF

overdiuresis
electrolyte imbalances (K+ and Mg2+)

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1st line tx for systolic HF

ACE-I’s

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3 drugs decreasing mortality with systolic HF

beta blockers
ACE-I’s
spironolactone

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Ejection fraction eqn

EDV-ESV/EDV

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CO and TPR relationship

CO=arterial BP/TPR

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Exercise and neurohormonal control

skeletal m. vasodilation causes decreased TPR
sympathetics cause increased HR, contractility and venoconstriction
increases arterial BP, increasing flow to muscle

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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)

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Sympathetics role in shock

maintains normal BP/cardiac compensation
except in brain and heart (local mediators)
overwhelmed in shock and cannot compensate enough

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Cellular effects of progressive shock

lysosomal enzyme release
decrease in high energy phosphates (irreversible)
acidosis

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Cause of neurogenic shock

rapid loss of vasomotor tone

drops VR and CO

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Cause of anaphlyatic shock

Ab-Ag response via mass histamine release

causes massive vasodilation

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Difference b/t severe sepsis and septic shock

severe sepsis can be corrected by fluids

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Most common cause of septic shock with burn victims

Pseudomonas

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Bugs with early onset neonatal sepsis

Group B strep
E. coli
H. flu
Listeria

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Bugs with late onset neonatal sepsis

S. epidermidis
N. meningitidis
H. flu

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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

Cardio exam 5 Flashcards

(76 cards)