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CCRN-NIC > Cardiac > Flashcards

Cardiac Flashcards

1
Q

Cardiac Output equation

A

CO = SV x HR

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2
Q

Where does blood flow through the DA in fetal circulation?

A

Blood passes from the pulmonary artery to the aorta through the DA, bypassing the lungs

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3
Q

What does prostaglandin do?

A

causes vasodilation by direct effect on the smooth muscle in the DA
also dilates the pulmonary and systemic vascular beds so the infant should be monitored closely for hypotension

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4
Q

How long does PGE take to work?

A

usually works within minutes to hours of starting the medication

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5
Q

Why is PGE administered as a continuous drip?

A

PGE has a short half life

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6
Q

What other fluids/medications can be run with PGE

A

Not many medications are compatible, check with pharmacist. Avoid any medications with variable rates (no boluses, only continuous drips)
Only D5W and D10W

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7
Q

Main side effect of PGE to watch out for?

A

Apnea/Respiratory depression
Usually seen in the first few hours of infusion, especially when
PPV should be readily available

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8
Q

Less common side effects of PGE?

A

Fever, irritability, jitteriness, seizure-like activity
Hypocalcemia and hypoglycemia
Diarrhea (because it stimulates intestinal smooth muscle)
Inhibits platelet aggregation, monitor for bleeding
May affect bones if given for long period of time (cortical hyperostosis - tenderness and pain in bones)

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9
Q

Name the left-sided obstructive cardiac anomalies (4)

A

Coarctation of the aorta
Interupted aortic arch
Aortic valve stenosis
Hypoplastic left heart syndrome

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10
Q

Name the Cyanotic CHD anomalies that are NOT ductal dependent (5)

A 
Tetralogy of Fallot
Tricuspid Atresia 
Truncus Arteriosus
Total anomalous pulomary venous connection
Ebstein anomaly
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11
Q

Name the Cyanotic CHD anomalies that ARE ductal dependent (4)

A

Pulmonary Atresia with intact Ventricular Septum
Pulmonary Atresia and Ventricular Septal Defect
Transposition of the Great Arteries
Transposition of the Great Vessels

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12
Q

Definition of Coarctation of the Aorta (COA)

A

Coarctation = narrowing
COA is the narrowing of the descending aorta
The narrowing is often located just distal to the origin of the left subclavian artery and adjacent to the DA
This area is called the aortic isthmus (the portion of the aorta beyond the left subclavian artery and before the DA)
The severity of COA depends on how narrow and where exactly the narrowing is located

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13
Q

Which syndrome is associated with COA?

A

Turners Syndrome

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14
Q

Types of COA (3)

A

Isolated COA - no PDA it has closed off, narrowing causes obstructed flow from L vent, leading to increased pressure and pulmonary venous congestion occurs

COA with VSD - elevated L vent pressure, shunting of blood from L to R causing pulmonary overload

Preductal COA - dependent on the PDA for distal aorta and lower body blood flow (needs PGE)

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15
Q

S/S of COA

A
  • S/S of congestive heart failure d/t high afterload
  • decreased of absent pulses in the lower extremities
  • cool to touch lower extrems
  • higher BPs in upper extrems vs lower extrems is the most consistant factor in critical COA and presents 97% of the time ***
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16
Q

Prognosis and correction of COA

A

CHF management
PGE
Balloon dilation, stent placement, or surgical resection of abnormal segment and reanastomosis, or subclavian patch across the area of obstruction
Prognosis is based on the severity of the coarc and of the method of correction

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17
Q

Most common complication of COA

A

hypertension

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18
Q

What is Interuppted Aortic Arch? (IAA)

A

Complete discontinuity of the proximal and distal portions of the aortic arch.
A VSD is almost always present to allow oxygenated blood to flow from L to R into the pulmoary artery through the PDA to the aorta distal to the interruption

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19
Q

Which anomalies can be found with a CCHD screening?

A

HLPHS, TOF, TGV, TVPVR, pulmonary artesia, critical aortic stenosis, and truncus arteriosus

20
Q

PDA S/S

A

Presents at 4-7 DOL with inability to wean from vent or has a need for increased vent support or FiO2
Apneic/bradycardic
increased pulmonary vasculature and cardiomegaly
bounding peripheral pulses
widening pulse pressure (>20mmHG)
low diastolic blood pressure
unexplained metabolic acidosis
continuous murmur in the upper left sternal border
most likely will develop pulmonary edema

21
Q

Why do preemies have more of an increased risk of PDA than term babies?

A

Premiees have more circulating prostaglandins and are not as sensitive to oxygen as term babies would be in the case of closing the PDA

22
Q

What inhibits the PDA from closing?

A

PGE

23
Q

Gold standard for PDA diagnosis

A

echocardiogram

BNP levels of 70-100 can also be used to help dx

24
Q

PDA treatement

A 
fluid restriction
diuretics
ventilation therapy
NSAIDS
surgical management (ligation)
prevent anemia - transfusions
25
Q

Kidneys make PGE through the _______ ____ pathway

A

arachidonic acid

26
Q

DX of COA

A

CXR will show enlarged heart and pulmonary vascular markings
ECHO is the gold standard, but cannot rule out COA in the presence of a PDA
MRI is used to locate exactly where the narrowing occurs

27
Q

CO of a newborn

A

120-200ml/kg/min

28
Q

Preload

A

volume of blood in ventricles before the heart contracts

The more the heart stretches the more the output will be
ex. delayed cord clamping

29
Q

Afterload

A

resistance of blood leaving the ventricle

dependent on systemic and pulmonary vascular resistance

30
Q

Shock 3 types

A

Hypovolemic
Distributive
Cardiogenic

31
Q

SVT causes

A

Cardiac defects
Wolff-Parkinson White syndrome
Myocarditis

32
Q

Medications for SVT (4)

A

adenosine
propranolol
procainamide
amiodarone

33
Q

Cardioversion joules/kg for SVT

A

0.5-1 J/kg

34
Q

Adenosine dosage

A

0.1mg/kg

35
Q

Which arrhythmia is common to babies of mothers with lupus

A

Complete heart block (3rd degree AV block)

36
Q

Complete heart block (3rd degree AV block) is defined as

A

complete blockage of impulse between atria and ventricles

37
Q

Treatment of Complete heart block (3rd degree AV block)

A 
Temporary or permanent pacing 
Isoproterenol drip (used to stabilize infant before surgery)
38
Q

Why is atropine given to heart block patients?

A

Atropine - given to increase pace maker sites to make the escape rhythm faster

39
Q

Atrial flutter

A

Sawtooth appearance on EKG

40
Q

Atrial flutter causes

A 
Damage to the sinus node
CDH
Cardiac Cath
Digoxin toxicity
Cardiac surgery
41
Q

Atrial flutter Tx

A

Digoxin
Propranolol
if unstable, cardiovert at 1-2J/kg

42
Q

Hyperkalemia EKG effects

A

tall tented T waves
disappearance of the P wave
Widening of the QRS

appears like Vtach but is not

43
Q

Hyperkalemia Tx (5)

A

Diuretic (depletes K+ through urine)
IV calcium (will see narrowing of QRS on EKG)
Glucose/insulin infusion (push K+ into cells)
Sodium Bicarb (to correct acidosis which can cause the K+ to be elevated)
Albuterol (pushes K+ into cells)
Kayexalate (removes K+)

Cardioversion does not
work (the problem isnt electrical its electrolytical)

44
Q

Cyanotic Cardiac Defects (5)

A 
TOF (Tetralogy of Fallot)
TGA or TGV - Transposition of the greater arteries or vessels
Truncus arteriosus
Tricuspid atresia
Hypoplastic left heart syndrome (HLHS)
45
Q

Acyanotic Cardiac Defects (7)

A 
PDA
ASD
VSD
AVC (AV canal)
Pulmonic stenosis (PS)
Aortic Stenosis (AS)
Coarctation of the aorta
46
Q

Tetralogy of Fallot definition

A

Most common defect
Combination of 4 defects:
PS, VSD, overriding aorta, and R ventricular hypertrophy

Depends on the level of pulmonary stenosis (pink tet vs blue tet)

CCRN-NIC (3 decks)

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