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Cardiac Study Guide

The fetal cardiac cycle differs from the adult cycle in that blood bypasses the lungs and liver through various channels. In the fetal cycle, blood flows from the umbilical vein to the inferior vena cava, right atrium, foramen ovale to the left atrium, and left ventricle through the ductus arteriosus to the systemic circulation. Congestive heart failure is the inability of the heart to pump enough blood to meet the body's metabolic demands, leading to edema, decreased cardiac output, poor growth, cardiomegaly, and tachycardia. Treatment aims to improve cardiac output and remove excess fluid. In infants, the right side of the heart is larger

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Lindsay Birnbrich
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60 views3 pages

Cardiac Study Guide

The fetal cardiac cycle differs from the adult cycle in that blood bypasses the lungs and liver through various channels. In the fetal cycle, blood flows from the umbilical vein to the inferior vena cava, right atrium, foramen ovale to the left atrium, and left ventricle through the ductus arteriosus to the systemic circulation. Congestive heart failure is the inability of the heart to pump enough blood to meet the body's metabolic demands, leading to edema, decreased cardiac output, poor growth, cardiomegaly, and tachycardia. Treatment aims to improve cardiac output and remove excess fluid. In infants, the right side of the heart is larger

Uploaded by

Lindsay Birnbrich
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as DOCX, PDF, TXT or read online on Scribd
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Cardiac Study Guide

1. Compare adult/normal cardiac cycle to the fetal cardiac cycle.

- O2 is not needed in the lungs except a small amount to allow growth

- The ductus venosus, the foramen ovale, and the ductus arteriosus allow the blood to bypass
the fetal liver and lungs

Fetal blood flows through ductus venosus (channel between umbilical vein & inferior vena
cava) to RA. Foramen ovale (between atria)-RA to LA. To LV via ductus arteriosus (channel
b/t pulm artery & desc aorta to systemic circ. Some blood through ductus arteriosus from head &
upper extremities to superior vena cava to RA to RV to pulm. artery.

2. What is Congestive Heart Failure – Inability of the heart to pump enough amt. of blood into
the body’s circulation @ normal pressure to keep up w/ the body’s metabolic demands

 Know Signs & Sx of CHF


- Wt. gain d/t edema
- ↓ CO
- FTT; poor feeding → ⊘ grow & meet developmental milestones
- Cardiomegaly
- Tachycardia @ rest

 Treatment of CHF

***GOAL: Treat & improve CO & remove excess fluid***

- Digoxin; ↑ CO

2. What’s the structural anatomical differences in a newborn/infant’s heart vs adults?

R side of the heart is lager than the L side d/t most of the work it has been doing in utero

- ventricle wall thickness affects BP; specifically the L vent d/t blood from the L vent
goes to the aorta which supplies the rest of the body

***Infant heart cannot increase vol or pressures easily, therefore change in HR is how they
compensate***

3. Congenital heart defects: what does it d/t the pum./systemic curculation


***Murmur = first sign of a cardiac defect***
Types:
- Increased/Decreased Pulmonary blood flow
- Obstructed systemic blood flow
- Mixed defects; mix of O2 & unoxygenated blood

Cyanotic vs acyantoic Which are which?

Acyanotic Cyanotic
- ↑ pulm. blood flow - ↓ pulm. blood flow

- Obstruction to blood - Mixed blood flow


flow from ventricles

5. Know the pathophysiology of the 4 types of defects:

 Increased pulm blood flow: shift from high pressure of the heart to low pressure (L→R)
- ASD/VSD
- PDA
 Decreased pulm blood flow: obstruction of pulmonary BF & an anatomic defect b/w the
R→ L side of the heart; deoxygenated blood enter the systemic circulation
- TOF
- Tricuspid atresia
 Mixed defects: aorta is connected to the R vent instead of the L; Pulmart is connected to
the L vent. instead of the R
- Hyperplasitic L heart syndrome
- Transposition of the great arteries
- Truncus arterious
 Obstructive system blood flow: pressure that occurs before the defect in vent is ↑;
pressure after defect ↓→ ↓ CO
- P. stenosis/A. stenosis
- Coracation of the aorta; narrowing in the aorta somewhere

6. Digoxin:

 Normal digoxin blood level: 0.8-2 ng/L


 What is digitalization- like a loading dose; gets the body into therapeutic range
 What is dig toxicity: Bradycardia; dysrthymias, N/V, blurred vision (halo), anorexia
 What other physiologic processes promotes dig toxicity- Hypokalemia

**NEED to KNOW: HR; 80-130 up to 2 y.o. (apical), Electrolyte levels; liver & kidney function
7. What is Rheumatic Fever?

 Cause: Group A Beta Hemolytic Streptococcus GABHS


 Diagnoses: labs- hx URI, Pos throat cx; ASO that shows recent strep. infect, ↑ CRP, ESR
 Diag: EKG, Echocardiogram
 Jones Criteria:
- Major: Nontender SQ nodules, Rash, Involuntary muscle movements (chorea)
- minor: Fever, Joint pain
 Treatment: PNC + ASA
 Prevention: prophylaxis for endocarditis

8. What is Kawasaki Disease:

**Concern: Cardiac Aneurysms or coronary artery dilation; echocardio is done in q stage

 Diagnosis: HARD to dx; based on symptoms: CRASH & Burn


 Treatment: IGIV (immunioglobulins) + ASA

9. Infective Endocarditis

 Definition: inflammation of the lining, valves, or great vessels of the heart d/t bacterial
infection
 Diagnosis: Common clinical Sx is recurrent fevers
 Treatment: IV ATB (antibiotics)

***BEST way to treat is to PREVENT it!***

10. How do you know which size BP cuff to use?

11. Why is an infant’s BP lower at first?

Ventricle wall thickness affects BP; specifically the L vent however @ birth the R side of the
heart is lager than the L side

- Since the L vent is thinner & smaller it isn’t able to pump as hard the R side = Not
pumping as hard → Not as much pressure behind it; the size & thinness of the wall
reflects the lower BP

***BP increases w/ age d/t the lungs & the L side of the heart begin to help out the R side; the
more a muscle is worked the stronger & larger it grows → More muscle = more power behind
the blood being ejected***

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