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Patho 2 (Path 311) > Mod 1 Congenital Heart Diseases (CHD) > Flashcards

Mod 1 Congenital Heart Diseases (CHD) Flashcards

Mod 1 Cont'd

1
Q

How early can congenital heart diseases develop?

A

Prior to 8 weeks.
- family Hx and Genetics play a factor

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2
Q

What are causative associations of congenital heart disease?

A
  • Drugs/alcohol abuse
  • Maternal diabetes, infection, exposure to solvents
  • previous miscarriages
  • Genetics (chromosomal defects i.e downs)
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3
Q

What is the difference between acyanotic disease and cyanotic heart disease?

A
  • Acyanotic disease shunts oxygenated blood from the left side of the heart to the right
    (L->R)
  • Cyanotic heart disease shunts deoxygenated blood from the right to the left (R->L)
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4
Q

What are hallmarks of Acyanotic heart disease?

A
  • L->R
  • Increased pulmonary blood flow
  • Increases workload on right ventricle
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5
Q

What are hallmarks of Cyanotic heart disease

A
  • All congenital that start w/”T” are cyanotic
  • Decreased pulmonary blood flow
  • Requires a PDA for survival (ductal depedent)
  • hypoxemia & central cyanosis
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6
Q

Why are cyanotic heart diseases a problem?

A
  • Decreased oxygenated blood is shunted from the right to the left side resulting in severe hypoxemia and central cyanosis.
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7
Q

What are the 5 cyanotic heart defects we focus on?

A
  1. Truncus arteriosus
  2. Transposition of Great Arteries
  3. Tricuspid Atresia
  4. Tetralogy of Fallot
  5. Total Anomalous Pulmonary venous Return
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8
Q

What is the “snowball” effect of high pressures in the pulmonary vasculature?

A

Lead to R -> L Shunt

  • PDA/PFO are kept open by high pressures in pulmonary vasculature
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9
Q

What is the order of structures in the Ascending Aorta?

A

Think ABCS
1. Aorta
2. Brachiocephalic
3. Left Common Carotid
4. Left Subclavian

  • Note The right subclavian and right common carotid artery branches of the brachiocephalic artery
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10
Q

What is Hypoplastic Left Heart Syndrome (HLHS)?

A

A heart condition where the left ventricle is underdeveloped and there is severe narrowing in the ascending aorta.

  • Mitral valve and aorta may also be missing.
  • A Ductus arteriosus is necessary for systemic blood flow.
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11
Q

Pathophysiology: What are the latent implications of Hypoplastic Left Heart Syndrome (HLHS)?

A

A Severe condition where there is restricted blood flow to systemic circulation

  • All blood flow comes (R -> L) via PDA/FO
  • PDA dependent to have ANY systemic circulation through the RV and a ASD is necessary for pulmonary blood flow to get in into the RA.
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12
Q

Clinical Manifestations of Hypoplastic Left Heart Syndrome (HLHS)

A
  • Poor feeder w/SOB and is weak
  • Typically pale w/Poor perfusion
  • peripheral pulses are poor to absent.
  • A loud murmur (midsystolic gallop), hepatomegaly, and cardiomegaly will also be present.
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13
Q

Management of Hypoplastic Left Heart Syndrome (HLHS)

A

Prostaglandin (PGE1) to maintain an open ductus

  • No handling or suctioning at all
  • Intubate and ventilate, high at lowest PO2’s (Keep SpO2s @75-80) to keep PVR
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14
Q

What are the oxygen goals for babes with Hypoplastic Left Heart Syndrome (HLHS) when ventialted??

A

High CO2’s w/pH of 7.20

  • Target lower end of PO2 to keep PVR high
  • my need subatmospheric O2 w/CO2 or NO2 mixtures to get 17-20% (don’t worry about this last point)
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15
Q

Why are O2 targets low for Hypoplastic Left Heart Syndrome (HLHS)?

A

To maintain a balanced pulmonary and systemic circulations and optimize oxygen delivery to the body. Think of it as permissive hypoventilation.

  • High CO2s (or low O2’s) -> vasoconstriction increases (or keeps) PVR to shunt blood where it needs to go.
  • Left heart is underdeveloped, meaning the right side has to work harder. Elevated pulmonary pressures can make it difficult for blood to flow through the lungs and receive oxygen.
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16
Q

What is Ventricular Septal Defect (VSD)?

A

When there is a opening between the right and left ventricles via the septum.

  • Pressure are the same on both sides.
  • So the size of the septal defect is important in this defect
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17
Q

Pathophysiology of Ventricular Septal Defect (VSD)?

  • snowball effect?
A

Increase in pulmonary blood flow. Acyanotic => (L->R) Shunt.

  • Small VSD is asymptomatic
  • Large VSD = increased pulmonary blood flow + CHF
  • Increased pulmonary blood flow causes increased PVR and hypertrophy of the pulmonary arteries and L atrium.
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18
Q

Management of Ventricular Septal Defect (VSD)?

A

Most heal spontaneously.

  • Large VSD cause CHF which may require O2 and/or Vasodilators (to decrease load), and surgical repair.
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19
Q

Clinical Manifestations of Ventricular Septal Defect (VSD)?

A

Depends on size, but, a large VSD would cause CHF.

CHF includes:
- tachypnea
- tachycardia
- feeding difficulties, - diaphoresis
- failure to thrive
- cardiomegaly

20
Q

What is a Atrial Septal Defect (ASD)?

A

Opening between the right and left atria via septum.

  • ASD and PFO are not the same thing.
21
Q

Pathophysiology of Atrial Septal Defect (ASD)?

A

Increase in pulmonary blood flow.

Size dependent
- (mostly asymptomatic). (L->R) Shunt.
- Can cause volume overloading of the R heart -> exercise intolerance (CHF,SOB)

22
Q

Atrial Septal Defect (ASD)

  • what are different types of septal defects that can be causal agents?
A
  • Ostium secundum is NOT a foramen ovale either
  • Sinus venosus : (chamber upstream of R atrium that houses the cardiac pacemaker and becomes incorporated into the R atrium during development)
  • Ostium primum: (defect in the atrial septum at the level of the tricuspid and mitral valves)
  • Ostium secundum: (hole in the center of the atrial septum)
23
Q

Management of Atrial Septal Defect (ASD)

A

Surgical repair on bypass if severe

24
Q

To do list

A

Add Croup, and pre and post ductal issues

25
Q

What is Intraventricular Hemorrhage (IVH)?

A

TLDR: Bleeding of vessels in the brain bc of immature vasculature = can’t regulate cerebral blood flow = compression of brain parenchyma.

  • Blood fills the ventricles bc of poor cerebral blood flow management -> compression of brain parenchyma
  • not laymen defintion Intracranial hemorrhage arising in the germinal matrix and periventricular regions of the brain in preterm infants.
26
Q

Risk factors of Intraventricular Hemorrhage (IVH)

A

Prematurity, birth asphyxia, hypoxia, hypercapnia, acidosis, RDS, pneumothorax, changes in hemodynamic status, rapid blood volume expansion, PDA.

27
Q

Pathophysiology of Intraventricular Hemorrhage (IVH)

A

Bleeding starts in the germinal matrix (a highly vascular network that matures and gets smaller w/gestational age)

28
Q

Why is Intraventricular Hemorrhage (IVH) especially problematic in preemies?

A

Preemies can’t tolerate flucations in hemodynamics bc the fragile blood vessels wouldn’t be able to handle them.

29
Q

How many ventricles are affected by Intraventricular Hemorrhage (IVH)?

A

4 Cerebral ventricles.
- Lateral Ventricles (1&2)
- 3rd ventricle
- 4th ventricle

30
Q

Clinical Manifestations of Intraventricular Hemorrhage (IVH)?

A

subtle to catastrophic
Asymptomatic to bulging fontanels, sudden drop in hematocrit, apnea, hypotension, hypotonia, bradycardia, acidosis, seizures, and loss of consciousness.

  • Best way to identify and monitor IVH is w/ultrasound or CT scan
31
Q

Management of Intraventricular Hemorrhage (IVH)

A

Give supportive treatments that avoid risk factors, So…
- Maintain CPP
- Suppress seizures
- manage resp. status
- Shunts & punctures to drain excess fluid

32
Q

What is Tricuspid Atresia?

A

The tricuspid valve doesn’t exist, so blood can’t go from the RA to the RV. (R->L) Shunt.

Needs 1 for survival:
- Atrial septal defect
- Ventricular septal defect
- Ductus Arteriosus

33
Q

Clinical manifestations of Tricuspid Atresia?

A
  • Cyanosis & SOB
  • weak feeder/weak in general
  • blue baby
  • may or may not have a murmur.
  • Probably CHF when the above close.
34
Q

Management of Tricuspid Atresia

A
  • Prostaglandin E1 to keep the ductus open
  • Immediate catheterization to improve atrial flow by enlarging the PFO
  • Surgical connection of PA to RA with septal defect closure
35
Q

What is Tetralogy of Fallot (TOF)

A

Cyanotic heart with 4 defects:

  1. Overriding aorta, aortic valve is too wide and is open to both ventricles (RV and LV).
  2. Pulmonary artery stenosis
  3. R ventricular hypertrophy
  4. VSD (hole in wall between RV and LV)
36
Q

What needs to be present for a babe w/Tetralogy of Fallot (TOF)

A

A patent ductus arteriosus (PDA) to allow pulmonary blood flow if pulmonary stenosis is severe.

37
Q

Is Tetralogy of Fallot (TOF) acanoytic or cyanotic?

A

Cyanotic (but can be both bc of pressure gradients)

  • Decreased pulmonary blood flow
  • severe if pressure gradients cause it to be a (R->L) shunt.
38
Q

Pathophysiology of Tetralogy of Fallot (TOF)?

A
  • PDA must be present.
  • Causes an outflow obstruction to the right ventricle causing increased right ventricular pressures, decreased pulmonary blood flow, shunting through the VSD.
39
Q

Clinical manifestations of Tetralogy of Fallot (TOF)?

A
  • Severe cyanosis at birth & tachypneic
  • SpO2s in the 60s & SOB
  • failure to thrive
  • clubbing
  • syncope (loses conscious freq)
  • TET Spells
40
Q

What are TET spells?

A

Any Stress/activity that affects blood flow w/in heart by increasing (R->L) shunts.

  • leads to hyperpnea, decreased heard sounds, and fainting.
41
Q

How do you correct TET spells?

A

Knees to chest & O2.
- older kids can squat

42
Q

What does squatting do for older kids w/a potential heart defect?

A

Increases PVR and decreases severity of (R->L) shunt across VSD.

43
Q

Pathophysiology of TET spells?

A
  1. Tet spells decrease SVR
  2. lead to (R->L) shunt
  3. Lead to decreased blood flow to lungs
44
Q

CxR of
Tetralogy of Fallot (TOF) would have what sign?

A

Boot

45
Q

What is the difference between ASD and Ostium secundum

A

ASD’s are PFO’s that failed to close. Ostium Secondum (and others) are defects like secondary holes/failure of tissue to form properly

46
Q

Reference this as you review aka download image

A

Patho 2 (Path 311) (15 decks)

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