Cardio 2 (starting at pericarditis) Flashcards
Pericarditis (4)
- Pericardial inflammation
- Viral versus bacterial
- Bacterial causes include pneumococcus, S. aureus, H. influenzae type B
- Cardiac tamponade possibly requiring pericardiocentesis
a. Viral, bacteria, pneumococcal
b. Cardiac tamponade
Pericarditis clinical features (4)
a. Chest pain
b. Respiratory distress, CHF, or tamponade
c. Precordial “knock” or rub (like the sound of shoes walking on snow)
d. The classic signs include exercise intolerance, fatigue, jugular distension, lower extremity edema, hepatomegaly, poor distal pulses, diminished heart tones, and pulsus paradoxus.
Endocarditis overview (3)
a. An infection of the endothelial surface of the heart, with a propensity for the valves
b. Increased risk in children with artificial valves and patches, and patients with central lines
c. 90% of cases are caused by gram positive cocci.
i. Alpha strep, Staph aureus, pneumococcus, group A ß hemolytic streptococci
ii. Bacterial infection in the heart and you get vegetation of bacteria on walls of heart
iii. Can lead to stroke = serious bacterial infection
iv. Big problem for kids
v. Gram positive cocci — strep and staph
Clinical features of endocarditis (5)
a. Fever
b. Tachycardia, CHF, dysrhythmia, cardiogenic shock
c. History of recent cardiac surgery or indwelling vascular catheter
d. Heart murmur
e. Petechiae, septic emboli, or splenomegaly
I. Indwelling catheters, ports are at risk for endocarditis
ii. Drug Abusers
Bacterial endocarditis (4)
- Recurrent fevers
- S. viridans, S. aureus
- Conjunctival hemorrhages
- Classic skin lesions
i. Splinter hemorrhages
ii. Petechiae and purpura*
iii. Osler’s nodes (Lps, pain)
iv. Janeway lesions (proximal palms soles); caused by septic emboli
* Lesions caused by septic emboli and vasculitis
Cardiomyopathies (4)
- Hereditary condition
- Most common genetic cardiovascular disease
- Second most common form of cardiac muscle dysfunction in pediatrics
* 35-40% of all pediatric cardiomyopathies - Most common cause of sudden cardiac death in children and young athletes
a. Kid may not have murmur
b. Hypertrophic cardiomyopathies may not be seen in preschool years
c. Can be seen in later school age and adolescents
Cardiomyopathies outcomes (4)
- Most common outcome – sudden cardiac death
* 36% of all sudden cardiac deaths are due to HCM - Can also cause arrhythmias, atrial fibrillation, endocarditis, heart block, and heart failure
- Atrial fibrillation – 25% of HCM patients
- Heart failure – most common complication of HCM
Cardiomyopathy risk stratification (4 with info)
- Family history
- Sudden death
- Presence of an identified gene
2. Clinical risk factors I. Syncope ii. Non=sustained ventricular tachycardia iii. Resuscitation after cardiac arrest iv. Severe left ventricular hypertrophy v. Abnormal BP responses to exercise
- Onset of symptoms in childhood
- 2 or more = lower survival rates
- Syncope with exercise** any abnormal BP response
- 2 or more have lower survival rates
Pathophysiology of cardiomyopathy (9)
- Idiopathic, non-dilated, asymmetrical hypertrophy of the left ventricle
- Intra-ventricular septum most common
- Can lead to obstruction of left outflow tract – 25%
- Gradient variable
- Left ventricular systolic function generally normal
a. Can cause atypical filling of heart and increased left ventricular end-diastolic pressure - Diastolic dysfunction
- Increased resistance of blood flow
- Reduction in the size of pumping chamber
- Cellular remodeling
a. Not dilated cardiomyopathies = managed medically
b. Cannot get enough blood to coronary arteries, cannot push out and brain gets affected = death
Cardiomyopathy comorbid conditions (11)
Neuromuscular disorders
- Friedrich ataxia
- Infantile myotonic dystrophy
Storage disorders
- Danon disease
- Pompe’s syndrome - cardiomyopathy 2nd to pompe
- Fabry’s syndrome
- Noonan’s syndrome
- Down syndrome
- Beckwith-Wiedemann syndrome - large kids
- LEOPARD syndrome - pulmonic stenosis
- Hunter syndrome
- Hurler syndrome
* Hunter and Hurler = abnormal mucopolysaccharides build up
7 family hx questions to ask with cardiomyopathy
- Has anyone in your family died prematurely, suddenly, or unexpectedly before the age of 35 years old?
- Does anyone in your family under the age of 50 have a heart condition-related disability?
- Do you have any knowledge of any heart conditions that family members may have?
- Is there a family history of seizures, syncope, drowning, and/or motor vehicle accidents?
- Is there a family history of heart defects, intellectual disabilities, or other birth defects?
- Is there a family history of any genetic conditions?
- Is there a family history of death at a young age, due to SIDS?
Cardiomyopathy physical exam (12)
- PE itself is insensitive screening tool
- Hemodynamics alter nature of murmur
- Louder with standing from squating or Valsalva maneuver
- Systolic ejection murmur at RUSB
- Holosystolic murmur at apex
- May hear S3 heart sound
- S4 heart sound often at apex
- Mitral regurgitation
- Palpate pulses
a. Water=hammer pulse - Apical pulse
a. May be sustained
b. Two palpable components - Carotid pulse - Rises fast
- Exertion
a. Decreased peripheral pulses
b. Decrease in systolic blood pressure
Echocardiogram and cardiomyopathy (5)
a. Most sensitive and specific
b. Thickness ≥ 13mm
c. Tissue Doppler Echo – may determine prognosis
d. 3D=E – more accurate
e. False positives and false negatives
electrocardiogram and cardiomyopathy (8)
- Cost-effective vs lack of sensitivity
- False positives
- Screening tool
- P wave peaks
- QRS deviation
- Increased Q, R, S wave amplitude
- ST segment depressions
- T wave flattening or inversion
I. QT prolongation
I. Echocardiogram = most sensitive
ii. Athletes have thicker walls = make sure they have cardiomyopathy
iii. AHA does not endorse doing an ECG - too many echos and expensive
MRI and cardiomyopathy (4)
- When echo cannot detect LVH
- Identify areas of patchy left ventricular wall thickness
- Ability to quantify thickness and left ventricular mass distribution
- May expose delayed enhancement patterns
