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Acute care > Week 6 > Flashcards

Week 6 Flashcards

1
Q

What is the cardiovascular embryology?

A
  • Mesodermal germ layer gives rise to the cardiovascular system
  • Week 2: heart develops from 2 simple epithelial tubes
  • Week 3-4: Tubes fuse to form single chambered heart.
    • Elongates and bends on itself
    • Endo, myo, and epicardium differentiated
    • Heart beating
  • Week 4: Primitive heart. Atrial segment assumes cranial position
  • Week 5: Endocardial cushions grow towards each other and fuse
  • Week 8: Partitioning into 4 chambered heart complete
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2
Q

What are the small openings between the left and right sides of the heart when the baby is growing in a mother’s womb?

A

• Ductus arteriosus (DA), Foramen ovale. (FO)
• In utero Only 8% flow goes through non-functioning
lung, rest flows through DA
• Shunting protects the developing lungs

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3
Q

How does a fetus receive blood?

A

Fetus receives oxygenated blood from mother via placenta travels back via the umbilical vein

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4
Q

What is the flow of blood like in a fetus?

A

• 50% of Oxygenated blood passes through liver, 50% to
inferior vena cava then to right atrium
• Blood then passes through foramen ovale (FO) to the left atrium and then
to the left ventricle and out the aorta.
• Most oxygenated blood goes to brain

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5
Q

When does the Ductus arteriosus (DA) and Foramen ovale. (FO) close?

A

A few days after birth.

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6
Q

What is a congenital disease?

A

A disease occurring at birth or failure of normal development of cardiovascular system. Usually abnormal opening between adjacent heart chambers

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7
Q

What are the causes of congenital disease?

A

Viral infection (German measles), hereditary, Down Syndrome, Teratogens

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8
Q

What are the intrinsic developmental disorders, disabilities and delays associated with a congenital disease?

A

• Genetic (altered regulation of all organ development)
• Poor perfusion during prenatal period & birth*
• Pediatric Stroke (10% of patients)
- High reoccurrence rate too

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9
Q

What are the extrinsic developmental disorders, disabilities and delays associated with a congenital disease?

A
  • Surgery (Bypass machine)
  • Impaired socialization
  • Environmental Stressors of NNICU
  • Impaired capacity to explore environment
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10
Q

What are the other developmental disorders, disabilities and delays associated with a congenital disease?

A

• Neurodevelopmental disability, affects as many
as 50% of infants undergoing interventions for congenital heart lesion.
• Patients with complex cardiac disease are more likely to have social functioning issues because of their increased risk for severe neurocognitive
impairment
• Children with down syndrome have impaired tolerance to exercise, altered sympathetic response to exercise and are at risk for aneurysm
• An increasing number of patients with CHD are surviving to adulthood (85%)

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11
Q

What are the categories of congenital heart defects?

A
  • Acyanotic Defects

- Cyanotic Defects

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12
Q

What are Cyanotic Defects?

A

Patients who have significant impaired oxygenation and may appear to be blue, and are usually a bit critical and need interventions quite quickly

• Transposition of the Great
Vessels
• Pulmonary Valve Atresia
• Tetralogy of Fallot
• Hypoplastic left heart syndrome
• Shone’s Syndrome
• TAVPR
• Coarctation of the Aorta*, depending on the size, it can be acyanotic and it often goes misdiagnosed
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13
Q

What are Acyanotic Defects?

A

Patient who have a defect, but are still able to maintain normal oxygenation. Can be managed conservatively

  • Atrial Septal Defect (ASD)
  • Patent Ductus Arteriosum (PDA)
  • Ventricular Septal Defect (VSD). Can fluctuate between cyanotic and acyanotic
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14
Q

What is the apgar score?

A

A quick test performed on a baby at 1 and 5 mins after birth.

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15
Q

What are the components/scoring methods of the apgar score?

A 
Appearance
 - Blue or pale all over (0 points)
  - Blue extremities, but pink torso (1 point)
  - Pink all over (2 points)
Pulse
  - None (0)
  - < 100 (1)
  - >/= 100 (2)
Grimace
  - No response (0)
  - Weak grimace when stimulated (1)
  - Cries or pulls away when stimulated (2)
Activity 
  - None (0)
  - Some flexion of arms (1)
  - Arms flexed, legs resist extension (2)
Respirations
  - None (0)
  - Weak, irregular or gasping (1)
  - Strong cry (2)

0-3 critically low
4-6 fairly low
7-10 generally normal
most kids will score around 9

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16
Q

What are left to right shunts (acyanotic)?

A

Shunts where the left side heart (systemic circuit, which is oxygenated) shunts some blood into the right side

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17
Q

What are right to left shunts (cyanotic)?

A

When the right side (pulmonary circuit low or dexoygenated blood) shunts into the left side, the systemic circuit

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18
Q

What determines the direction of a shunt?

A

Pressure rules

• High to Low

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19
Q

What is a Patent Ductus Arteriosus (PDA)?

A

When the ductus arteriosus which normally closes at birth within hours, remains open and and creates a left to right shunt. (Aorta to Pulmonary Artery)

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20
Q

What are the characteristics of a Patent Ductus Arteriosus (PDA)?

A
  • Creates high pressure in pulm. art.
  • May require surgical intervention
  • Fairly asymptomatic
  • May create pulmonary arterial hypertension, because we are putting more volume in the higher pressure, which may load the right heart
  • Can potentially lead to HF if its in a large enough vessel or is never addressed
  • Babies have no significant findings at birth, until they are older
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21
Q

What is the clinical presentation of a Patent Ductus Arteriosus (PDA)?

A

Infant might fatigue quickly, susceptible to pneumonia

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22
Q

What are some techniques to treat Patent Ductus Arteriosus (PDA)?

A
  • Protoglandins to close the PDA
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23
Q

What are Atrial Septal Defects (ASD)?

A

A defect that creates a blood flow between the atria, and most often causes a left to right shunt.

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24
Q

What are the characteristics of an Atrial Septal Defects (ASD)?

A
  • Can cause volume overload: right heart and pulmonary vasculature damage
  • May result in R heart failure
  • Shortened life span
  • Usually repaired at 4- 6 years
  • Usually identified quickly
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25
Q

What is a Ventral Septal Defects (VSD)?

A

A hole between the ventricles, which will cause blood to shunt from the left to the right

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26
Q

What is Eisenmenger’s syndrome (cyanotic problem)?

A

The condition where during a ventral septa defect, If pressures in right ventricle become too high, blood can shunt right to left if the defect is large enough

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27
Q

What are the characteristics of Ventral Septal Defects (VSD)?

A

• Large defects can result in increased pressure in pulm artery,
- Can become permanent even with repair to VSD
• Can cause overloading of the right side and result in ventricular issue in the R heart
• Can reduce CO of the left side, because instead of pumping all the volume through the aorta, it pumps it to the right side, so we lose some output
• Mostly identified at birth

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28
Q

What are the characteristics of a coarctation of the aorta?

A

“Pinching” or aorta
• Usually distal to subclavian artery
• May be due to abnormal involution of Ductus Arteriosus
• Severity dependent on degree of pinching and location

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29
Q

What is the presentation of a coarctation of the aorta?

A
  • BP may be normal or elevated in arms, lower in legs
  • May not be detected until later in childhood
  • Kidneys see low BP and release substances to increase BP
  • Present in 15-20% of CHD cases
  • ABI and Pulse Differential may be affected
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30
Q

What is triscuspid atresia?

A

When the triscuspid valve fails to develop

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31
Q

What are the characteristics of a triscuspid atresia?

A 
• Limited blood flow from RA
to RV, Underdeveloped RV
• Filling of left ventricle and
Survival depends on ASD &amp;
VSD
• Right to left shunt
• Surgery Required
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32
Q

What is a pulmonary valve atresia?

A

When the pulmonary valve fails to develop

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33
Q

What are the characteristics of a pulmonary valve atresia?

A

• No exit from the right ventricle
• Blood regurgitates into the left atrium via the foramen ovale
• The lungs get perfused retrograde flow via a wide PDA
• Considered a Critical Congenital Heart Defect, requires intervention soon after birth, drugs to keep PDA
patent
• This cardiac abnormality is very rare and accounts for only 1-3%

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34
Q

What are the defects that make up a tetralogy of fallot?

A
  • VSD
  • Pulmonary Valve Stenosis
  • Overriding Aorta (usually lies over VSD)
  • RV Hypertophy (due to PV Stenosis)
35
Q

What are the characteristics of a tetralogy of fallot?

A
  • Blueness appears soon after birth, in infancy or childhood
  • Infants might have sudden episodes of cyanosis, unconsciousness and possible seizures (Tet Spells)
  • Early surgery indicated
36
Q

What is a transposition of the great vessels?

A

When the Positions of Pulmonary Artery

and aorta are reversed

37
Q

What are the characteristics of a transposition of the great vessels?

A

• Deoxygenated blood from RV goes into systemic circuit
• O2 from blood goes back into lung
• Child only survives if AS, VSD or PDA present
• Surgery Option
- Arterial Switch

38
Q

What is total anomalous pulmonary venous return (TAPVR)?

A

When the pulmonary veins don’t connect to the left atrium, and instead they go to the right side of the heart, via an abnormal (anomalous)
connection

39
Q

What are the characteristics of a total anomalous pulmonary venous return (TAPVR)?

A
  • Usually child possesses an ASD, which is only way for oxygenated blood to get to Left side
  • Child will require surgery soon after birth, considered a critical congenital heart defect.
  • Can be supracardiac, cardiac or infracardiac
40
Q

What is a Hypoplastic Left Heart Syndrome (HLHS)?

A

Failure or inadequate development of the left ventricle.

• Variable aortic & mitral involvement

41
Q

What are the characteristics of a Hypoplastic Left Heart Syndrome (HLHS)?

A
  • Child is dependent upon a PDA for systemic perfusion.

* Without intervention, HLHS is fatal within the first weeks of life

42
Q

What are the characteristics of the norwood procedure?

A

• Done within the first 2 weeks of a life
• Surgeons create a “new” aorta and connect
it to the right ventricle
- Constructed utilizing the pulmonary root, ascending aorta, and homograft tissue.
• A Bialock-Tussing Shunt is then placed from either the aorta or the right ventricle
to the pulmonary arteries.
• Thus the heart becomes a “single ventricle” structure capable of pumping mixed blood to lungs and periphery.
• Arterial oxygen saturation following procedure 70-75%
• Mixed venous oxygen saturation is usually forty-five to fifty-five percent.

43
Q

What are the characteristics of a Bi-directional Glenn Shunt Procedure?

A
  • This usually is performed when an infant is 4 to 6 months of age.
  • Creates a direct connection between the pulmonary artery and the superior vena cava.
  • Directly returns venous blood to lungs, from UE.
  • Right Ventricle still pumps mixed blood but this procedure reduces it’s work.
44
Q

What are the characteristics of the Fontan Procedure?

A 
• Done at 18months to 3yrs of age.
• Doctors now connect the
pulmonary artery to the inferior
vena cava.
• Now venous blood completely bypasses the right ventricle
• Once this procedure is complete, oxygen-rich and oxygen-poor blood no longer mix in the heart and the
infant’s skin will be cyanotic.
• Kids may still require heart
transplantation
45
Q

What are the characteristics of a Pediatric Heart Transplantation?

A

• ~10% of CHD cases uncorrectable.
- Most common hypoplastic left heart syndrome (HLHS), changing though since surgical procedures and technology improving.
• Survival in excess of 20 years after pediatric heart transplantation (HTx) has been
achieved in some cases
- 70% of their recipients survive at least 5 years.
• HTx can provide excellent quality of life for pediatric patients, and progress has been
made prolonging graft survival, however it will not last a normal lifespan.
• If this occurs later in life the only effective therapy is re-transplantation (re-HTx).
- Re-HTx currently accounts for 5.6% of pediatric HTx in North America, and
- Nearly 10% of HTx in pediatric patients >11 years of age

46
Q

What are some things we’ll observe in patients with a congenital defect in regards to PT?

A
  • Labored breathing
  • Increased RR
  • Diffuse generalized edema
  • Decreased urine output
  • Eating problems
  • Impaired tolerance to activity
  • Irritable (Track Using NIPS scale)
47
Q

What are the PT interventions for a patient with a congenital defect?

A

• Post Op: prevent complications
- Inactvity, pulmonary complications, etc
- FAMILY EDUCATION!!!!!!!!!!!
• Early mobilization
• Ambulation: if appropriate team effort
• Positioning: Prone> side-lying> supine for ventilation/perfusion matching.
• Some activity and exercise restrictions may be present
• Acceptable Pulse oximetry cutoffs may be lower depending on case
- Communicate with RN, MD, RRT etc
• Some patients may need guidance away from competitive sports

48
Q

What are the normal physical exam findings in athletes?

A 
• Reversible!!!! Left Ventricular
Hypertrophy
  - LV wall thickness (LVWT) and LV cavity size, permits enhanced filling.
  - Increased CO maintained at high HR
• Bradycardia, because SV is so high
• Increased VO2max
• Sinus Arrhythmia
• Transient Split S2
   - Related to changes 
  - Changes with inspiration and expiration
  - Less common in adults
49
Q

What are the causes of post exercise syncope?

A

Exhaustion, Exercise-induced hyponatremia, heat illness, rapid reduction in preload and functional sympatholysis with elevated contractility and HR

50
Q

What are the causes of syncope during exercise?

A

More concerning; linked to HCOM, arrhythmogenic right ventricular cardiomyopathy.

51
Q

What are the screening recommendations for syncope in an athlete?

A

• Until diagnosis or pathologic causes excluded,
exercise is generally restricted.
• R/O post vs during; ask bystanders
• Screen for defects (Marfan’s, HCOM etc)

52
Q

What are the effects of dehydration in an exercising athlete?

A 
• Performance suffers, earlier fatigue
• Can reduce exercise SV and CO,
• Especially in the heat but can
happen even without hyperthermia
• Less able to tolerate hyperthermia
• Eventually MAP may drop
• When coupled with heat illness can potentially trigger arrhythmias
• Rehydration Strategy (NATA)
53
Q

What are some acute changes seen post exercise RV remodeling?

A

• Elevations of proBNP and increased cardiac troponin T levels in 60% of subjects(esp in marathons) ,
- 40% exceeding the threshold usually used to
diagnose MI.
- Non elite runners post marathon (avg 41y/o)
- Biomarkers findings correlated with impaired
left ventricular diastolic function, increased
pulmonary artery pressures, and RV dysfunction
• Similar findings in ultramarathon runners
• Acute effects all reversed in the days after events

54
Q

What are some chronic changes seen post exercise RV remodeling?

A

• Accumulation of coronary artery calcium (CAC) with myocardial fibrosis; and
• RV fibrosis secondary to episodic volume/pressure overload.
• Increased prevalence of atrial
fibrillation
• Study did not support an adverse impact of endurance athletics on either CAC or cardiovascular events

55
Q

What is the etiology of sudden cardiac death?

A
  • SCD is the leading cause of non traumatic mortality in athletes
  • Low overall prevalence ; ~100 to 150/year; OR 2.3 to 4.4/100,000 per year
  • Black/African American 5.6/100,000 per year
  • Athletes aren’t at a greater risk for SCD than general population*
  • SCD can occur in any sports, most often in US: football and basketball.
  • Male to female ratio of ~9:1 at all levels of competition
56
Q

What are the common causes of sudden cardiac death in an athlete?

A
  • Youths: HCM (33-50%), Coronary Anomalies (15-20%), Several others each <5%
  • Adults: 80% due to undiagnosed CAD, plaque rupture
57
Q

What is the most common mechanism of death in people that die of a sudden cardiac death?

A

Most common mechanism of death is ventricular tachyarrhythmia.
• Exception Marfan syndrome usually aortic dissection/rupture.

58
Q

What is the etiology of hypertrophic cardiomyopathy?

A

Strong genetic link to HCOM
• (55% of cases with familial relative)
• More common in Black/African Americans

59
Q

What does hypertrophic cardiomyopathy result in?

A

A thick, stiff ventricle without any prior adaptations and the heart is less efficient

60
Q

What are the presentations in patients with hypertrophic cardiomyopathy?

A 
• Ejection murmur changes with position
  - Softens during sitting/squatting
  - Amplifies during standing/Valsalva 
• Persistent Split S2
  - No change with breath holds
• S4 Gallop possible too
• Syncope or Dyspnea during exercise
• Persistent hypertrophy despite detraining
61
Q

What is normal VO2 in athletes?

A

> 50mL/kg/min

62
Q

What are the most common coronary anomalies?

A

The most common anomalies are left coronary artery origins in the right sinus of Valsalva and right coronary artery origins in the left sinus of Valsalva.

63
Q

How does a coronary anomaly cause sudden cardiac death?

A

SCD results from ventricular arrhythmia triggered by ischemia during exercise.

64
Q

What is the mechanism in which a coronary anomaly causes sudden cardiac death?

A

Coronary blood flow is impaired by the abnormal ostium, compression of the
artery and/or coronary spasm triggered by endothelial dysfunction.

65
Q

What is the characteristic of a coronary anomaly?

A

Usually asymptomatic, although angina associated with syncope should raise
suspicion

66
Q

What is a Myocardial Bridge?

A

When an epicardial coronary artery(LAD, LCx, right coronary vessels), which are supposed to lay on top of the myocardium is tunneled
within the myocardium

67
Q

What is a Myocardial Bridge characterized by?

A

It is characterized by systolic compression of the tunneled segment,

68
Q

What are the characteristics of a myocardial bridge?

A

• Most patients remain asymptomatic
- May present with atypical or angina-like chest pain with no consistent association between symptom severity and the length or depth of the tunneled segment or the degree of systolic compression.
• Resting ECGs are frequently normal
• Stress testing may induce nonspecific signs of ischemia, conduction disturbances, or
arrhythmias.

69
Q

What are the potential complications associated with a myocardial bridge?

A

Angina, myocardial ischemia, myocardial infarction, left ventricular dysfunction,
myocardial stunning, paroxysmal AV blockade, as well as exercise-induced
ventricular tachycardia and SCD

70
Q

In what condition has a high prevalence of a myocardial bridge been reported?

A

In heart transplant recipients and in patients with HCOM

71
Q

How is a myocardial bridge usually diagnosed and treated?

A
  • With angiogram

* Surgical Intervention in some cases

72
Q

What is marfan’s syndrome a result of?

A

From a gene mutation overproduction of transforming

growth factor beta (TGF-β)

73
Q

What are the cardiovascular disorders that are found in 9/10 patients with marfan’s?

A 
• Aortic tear or rupture
  - Most often in ascending/thoracic aorta
• Mitral valve prolapse
• Aortic regurgitation
• Arrhythmias (atrial &amp; ventricular)
74
Q

What are the interventions for marfan’s syndrome?

A
  • Close monitoring
  • Medications for arrhythmias
  • Surgery to correct defects
  • Activity modification
75
Q

What is a commotio cordis?

A

Sudden blunt impact (ball, puck, opponent) to the chest causes sudden death in the
absence of cardiac damage.

76
Q

In what sports is a commotio cordis most common in?

A

Baseball, ice hockey, lacrosse, football, and martial arts.

77
Q

What does a commotio cordis usually trigger?

A

A ventricular fibrillation

78
Q

What are the ways to prevent a commotio cordis?

A
  • Shields not demonstrated to be to effective
  • Having Defibrillators present at events
  • Educate coaches and players to turn away chest from inside pitches
79
Q

What is the most common cause for a sudden cardiac death in an adult?

A

Undiagnosed heart disease

80
Q

What intensity of exercise do we see the most benefit?

A

Moderate intensity

81
Q

What are the guidelines of the AHA screening recommendations?

A

• Indicated for any athlete 12-25
• Yes to any of the 14 question warrants further examination before participation in sports.
• AHA does not support the
usage of mass ECG screenings
- Cost, logistics, low incidence and type 1 errors with ECG

82
Q

According to the ECG Screening Athlete “The Seattle Criteria”, what are the normal ECG findings in athletes?

A

Results from adaptation of the cardiac autonomic
nervous system to conditioning.
1. Sinus bradycardia (>= 30 bpm)
2. Sinus arrhythmia
3. Ectopic atrial rhythm
4. Junctional escape rhythm
5. 1° AV block (PR interval > 200 ms)
6. Mobitz Type I (Wenckebach) 2° AV block
7. Incomplete RBBB
8. Isolated QRS voltage criteria for LVH
9. Early repolarisation
10. Convex (‘domed’) ST segment elevation combined
with T-wave inversion in leads V1–V4 in black/African
athletes
• Reduced the false-positive rate from 17% to 4.2%

83
Q

What are the PT implications of athletic screening?

A

• Recreational Athletes likely at low risk, increased with uncontrolled risk factors
• Risk of adverse event during exercise including SCD decreases with increased
frequency and volume of exercise
• For someone who has never exercised before, recommend gradually increasing activity starting with low <3METs (walking)
• Take Vitals, check for arrhythmias, report undiagnosed findings to PCP
• Utilize PARQ or ACSM Pre-Activity Screen
• Consider SubMax ETT or Response to low-mod exercise: walking, stairs etc
• Effectively educate staff on CPR, have access to defibrillators
• Climate control in clinic/facility, access to water and electrolytes

Acute care (9 decks)

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