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
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
3
Q
How does a fetus receive blood?
A
Fetus receives oxygenated blood from mother via placenta travels back via the umbilical vein
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
5
Q
When does the Ductus arteriosus (DA) and Foramen ovale. (FO) close?
A
A few days after birth.
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
7
Q
What are the causes of congenital disease?
A
Viral infection (German measles), hereditary, Down Syndrome, Teratogens
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
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
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%)
11
Q
What are the categories of congenital heart defects?
A
- Acyanotic Defects
- Cyanotic Defects
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
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
14
Q
What is the apgar score?
A
A quick test performed on a baby at 1 and 5 mins after birth.
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
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
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
18
Q
What determines the direction of a shunt?
A
Pressure rules
• High to Low
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)
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
21
Q
What is the clinical presentation of a Patent Ductus Arteriosus (PDA)?
A
Infant might fatigue quickly, susceptible to pneumonia
22
Q
What are some techniques to treat Patent Ductus Arteriosus (PDA)?
A
- Protoglandins to close the PDA
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.
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
25
What is a Ventral Septal Defects (VSD)?
A hole between the ventricles, which will cause blood to shunt from the left to the right
26
What is Eisenmenger’s syndrome (cyanotic problem)?
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
27
What are the characteristics of Ventral Septal Defects (VSD)?
• 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
28
What are the characteristics of a coarctation of the aorta?
“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
29
What is the presentation of a coarctation of the aorta?
* 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
30
What is triscuspid atresia?
When the triscuspid valve fails to develop
31
What are the characteristics of a triscuspid atresia?
```
• Limited blood flow from RA
to RV, Underdeveloped RV
• Filling of left ventricle and
Survival depends on ASD &
VSD
• Right to left shunt
• Surgery Required
```
32
What is a pulmonary valve atresia?
When the pulmonary valve fails to develop
33
What are the characteristics of a pulmonary valve atresia?
• 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%
34
What are the defects that make up a tetralogy of fallot?
* VSD
* Pulmonary Valve Stenosis
* Overriding Aorta (usually lies over VSD)
* RV Hypertophy (due to PV Stenosis)
35
What are the characteristics of a tetralogy of fallot?
* 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
What is a transposition of the great vessels?
When the Positions of Pulmonary Artery
| and aorta are reversed
37
What are the characteristics of a transposition of the great vessels?
• 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
What is total anomalous pulmonary venous return (TAPVR)?
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
What are the characteristics of a total anomalous pulmonary venous return (TAPVR)?
* 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
What is a Hypoplastic Left Heart Syndrome (HLHS)?
Failure or inadequate development of the left ventricle.
| • Variable aortic & mitral involvement
41
What are the characteristics of a Hypoplastic Left Heart Syndrome (HLHS)?
* Child is dependent upon a PDA for systemic perfusion.
| * Without intervention, HLHS is fatal within the first weeks of life
42
What are the characteristics of the norwood procedure?
• 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
What are the characteristics of a Bi-directional Glenn Shunt Procedure?
* 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
What are the characteristics of the Fontan Procedure?
```
• 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
What are the characteristics of a Pediatric Heart Transplantation?
• ~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
What are some things we'll observe in patients with a congenital defect in regards to PT?
* Labored breathing
* Increased RR
* Diffuse generalized edema
* Decreased urine output
* Eating problems
* Impaired tolerance to activity
* Irritable (Track Using NIPS scale)
47
What are the PT interventions for a patient with a congenital defect?
• 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
What are the normal physical exam findings in athletes?
```
• 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
What are the causes of post exercise syncope?
Exhaustion, Exercise-induced hyponatremia, heat illness, rapid reduction in preload and functional sympatholysis with elevated contractility and HR
50
What are the causes of syncope during exercise?
More concerning; linked to HCOM, arrhythmogenic right ventricular cardiomyopathy.
51
What are the screening recommendations for syncope in an athlete?
• 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
What are the effects of dehydration in an exercising athlete?
```
• 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
What are some acute changes seen post exercise RV remodeling?
• 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
What are some chronic changes seen post exercise RV remodeling?
• 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
What is the etiology of sudden cardiac death?
* 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
What are the common causes of sudden cardiac death in an athlete?
* Youths: HCM (33-50%), Coronary Anomalies (15-20%), Several others each <5%
* Adults: 80% due to undiagnosed CAD, plaque rupture
57
What is the most common mechanism of death in people that die of a sudden cardiac death?
Most common mechanism of death is ventricular tachyarrhythmia.
• Exception Marfan syndrome usually aortic dissection/rupture.
58
What is the etiology of hypertrophic cardiomyopathy?
Strong genetic link to HCOM
• (55% of cases with familial relative)
• More common in Black/African Americans
59
What does hypertrophic cardiomyopathy result in?
A thick, stiff ventricle without any prior adaptations and the heart is less efficient
60
What are the presentations in patients with hypertrophic cardiomyopathy?
```
• 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
What is normal VO2 in athletes?
> 50mL/kg/min
62
What are the most common coronary anomalies?
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
How does a coronary anomaly cause sudden cardiac death?
SCD results from ventricular arrhythmia triggered by ischemia during exercise.
64
What is the mechanism in which a coronary anomaly causes sudden cardiac death?
Coronary blood flow is impaired by the abnormal ostium, compression of the
artery and/or coronary spasm triggered by endothelial dysfunction.
65
What is the characteristic of a coronary anomaly?
Usually asymptomatic, although angina associated with syncope should raise
suspicion
66
What is a Myocardial Bridge?
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
What is a Myocardial Bridge characterized by?
It is characterized by systolic compression of the tunneled segment,
68
What are the characteristics of a myocardial bridge?
• 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
What are the potential complications associated with a myocardial bridge?
Angina, myocardial ischemia, myocardial infarction, left ventricular dysfunction,
myocardial stunning, paroxysmal AV blockade, as well as exercise-induced
ventricular tachycardia and SCD
70
In what condition has a high prevalence of a myocardial bridge been reported?
In heart transplant recipients and in patients with HCOM
71
How is a myocardial bridge usually diagnosed and treated?
* With angiogram
| * Surgical Intervention in some cases
72
What is marfan's syndrome a result of?
From a gene mutation overproduction of transforming
| growth factor beta (TGF-β)
73
What are the cardiovascular disorders that are found in 9/10 patients with marfan's?
```
• Aortic tear or rupture
- Most often in ascending/thoracic aorta
• Mitral valve prolapse
• Aortic regurgitation
• Arrhythmias (atrial & ventricular)
```
74
What are the interventions for marfan's syndrome?
* Close monitoring
* Medications for arrhythmias
* Surgery to correct defects
* Activity modification
75
What is a commotio cordis?
Sudden blunt impact (ball, puck, opponent) to the chest causes sudden death in the
absence of cardiac damage.
76
In what sports is a commotio cordis most common in?
Baseball, ice hockey, lacrosse, football, and martial arts.
77
What does a commotio cordis usually trigger?
A ventricular fibrillation
78
What are the ways to prevent a commotio cordis?
* Shields not demonstrated to be to effective
* Having Defibrillators present at events
* Educate coaches and players to turn away chest from inside pitches
79
What is the most common cause for a sudden cardiac death in an adult?
Undiagnosed heart disease
80
What intensity of exercise do we see the most benefit?
Moderate intensity
81
What are the guidelines of the AHA screening recommendations?
• 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
According to the ECG Screening Athlete “The Seattle Criteria”, what are the normal ECG findings in athletes?
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
What are the PT implications of athletic screening?
• 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
