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Critical Care I > Test 2 ...need to focus > Flashcards

Test 2 ...need to focus Flashcards

1
Q

In tricuspid or mitral regurgitation, what murmur would you expect to hear?

A

Holosystolic

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2
Q

With a VSD, what murmur would you expect to hear?

A

Holosystolic

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3
Q

With a Mitral valve prolapse, what murmur would you expect to hear

A

Late systolic

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4
Q

With pulmonary and aortic stenosis, what murmur would you expect to hear?

A

Ejection (early systolic) with click

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5
Q

what type of murmurs are always pathologic

A

diastolic

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6
Q

In aortic regurgitation, what murmur would you expect to hear?

A

Early diastolic that radiates to the apex

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7
Q

In pulmonary regurgitation what murmur would you expect to hear?

A

Early diastolic that radiates along the left sternal border

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8
Q

In mitral stenosis what murmur would you expect to hear?

A

Mid-diastolic heard at the apex

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9
Q

In tricuspid stenosis, what murmur would you expect to hear?

A

Mid-diastolic heard at the left lower sternal border

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10
Q

• Infants: tachypnea, feeding difficulties (e.g., decreased volume or increased time spent feeding), poor weight gain, excessive perspiration (especially when feeding), and excessive irritability. Wheezing and tachypnea from pulmonary congestion often mistaken for bronchiolitis.
Children: fatigue, exercise intolerance, anorexia, abdominal pain, dyspnea, and cough.
Infants and children:
• Tachycardia, decreased peripheral pulses, delayed capillary refill, and cool extremities. • Abdominal pain is a common presenting complaint and may be overlooked or dismissed. Hepatomegaly, ascites can be present with abdominal distension. • Edema may be present in dependent portions of the body (e.g., lower extremities in an ambulatory child; body wall and sacrum if nonambulatory).

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 410). Wolters Kluwer Health. Kindle Edition.

A

Congestive heart failure

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11
Q

what pH inbalance would you see in Congestive heart failure

A

Metabolic acidosis

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12
Q

Acute HF is used to describe a functional change in the heart that can occur quickly leading to what 4 functional problems

A

congestion
mal-perfusion
tachycardia
hypotension

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13
Q

4 main characteristic signs and symptoms of Heart failure mentioned in Bolick

A

edema
resp distress
growth failure
exercise intolerance

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14
Q

what 2 vitamin deficiencies can cause Heart failure in infants

A

Vit D
Hypocalcemia

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15
Q

where is PMI felt

A

It comes from the RV
felt along L mid clavicular line
at the 4th intercostal space in infants and 5th intercostal space in older patients

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16
Q

Treatment for heart failure

A

Diuretics

ACE Inhibitors - reduce activation of RAA system (perpetuator of HF cycle) and helps prevent remodeling
or
ARBS reduce activation of RAA system (perpetuator of HF cycle) second choice when has dry cough on ACE

B blockers- slow heart rate, prevent arrhythmias, reduce myocardial apoptosis and fibrosis and reduce afterload

aldosterone agonists - similar to ARB but predisposes patients to hyperkalemia

digoxin - increases contractility

inotropes
mechanical support

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17
Q

Diuretics used in HF

A

1st line:
Furosemide (Lasix)

Chlorothiazide (Diuril)

2nd line:

Bumetanide (Bumex)

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18
Q

What diuretic used in HF increases sodium excretion

A

Furosemide (Lasix)

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19
Q

Which can cause ototoxicity

Chlorothiazide (Diuril)

Bumetanide (Bumex)

Furosemide (Lasix)

A

Furosemide (Lasix)

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20
Q

what medication used in HF in used for its antifibrotic effects and promotes remodeling

A

Spironolactone (Aldactone)

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21
Q

Your patient is on Spironolactone (Aldactone) which is an aldosterone antagonist and an ACE (Captopril, Enalapril or Lisinopril). What do you need to monitor more closely

A

This combination may produce hyperkalemia

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22
Q

What side effect can be seen in males for Spironolactone

A

Male Gynecomastia

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23
Q

what ACE inhibitor for HF is preferred in infants and neonates

A

Captopril

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24
Q

What ACE inhibitor for HF can cause angioedema

A

Enalapril

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25
Q

What ACE inhibitor for HF is preferred in adolescents due to daily dosing

A

Lisinopril

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26
Q

What do you need to monitor closely when a pt is on Enalapril

A

Renal function
potassium levels

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27
Q

What is preferred in heart failure and why

ACE or ARBS

A

ACEs because ARBS do not increase bradykinin levels.

ACEs can cause a dry cough

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28
Q

What ARB is used in Heart failure

A

Losartan

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29
Q

What B blocker has been shown to significantly reduce mortality in heart failure

A

Carvedilol

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30
Q

Which B Blocker selectively blocks B-1 receptors with little or no effect on B2 receptors and reduces inappropriate tachycardia

A

Metoprolol succinate

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31
Q

How is Digoxin excreted

A

Kidneys

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32
Q

What inotrope used in HF has a 1-4 hr half life, decreases afterload and increases cardiac output without increasing myocardia oxygen consumption

A

Milrinone

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33
Q

What inotrope is used for short term rescue therapy in HF however can increase arrhythmias and myocardial oxygen consumption

A

Epinephrine

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34
Q

• Inotropic support with β-agonists such as ______ or ______ can improve cardiac output.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 412). Wolters Kluwer Health. Kindle Edition.

A

dopamine
dobutamine

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35
Q

Phosphodiesterase inhibitors (e.g., milrinone) are both an _______ and a _______.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 412). Wolters Kluwer Health. Kindle Edition.

A

inotropic agent

vasodilator

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36
Q

If inotropic support is needed in HF treatment, discontinue chronic _______ therapy.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 412). Wolters Kluwer Health. Kindle Edition.

A

beta-blocker

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37
Q

• _______increases myocardial contractility; maintain normal _______ levels in the setting of heart failure.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 412). Wolters Kluwer Health. Kindle Edition.

A

Calcium
ionized calcium levels

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38
Q

_____ is a potassium-sparing diuretic that has the added benefit of preventing cardiac remodeling in Hf treatment

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 412). Wolters Kluwer Health. Kindle Edition.

A

Aldactone

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39
Q

Timeline to develop post pericardiotomy syndrome

A

within a few weeks to months after surgery

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40
Q

symptoms for post pericardiotomy syndrome

A

2 out of 5 present
fever without other cause
pleuritic chest pain
pericardial effusion
friction rub
new or worsening pleural effusion

as fluid accumulates around the heart, they become short of breath and tachypneic

may hear a pericardial friction rub

Pericardial tamponade occurs when the pericardial effusion is of a size where venous return is impeded and contractility impaired - SS are muffled heart sounds, JVD, hypotension (AKA Becks triad) along with decreased venous return, poor cardiac output -> resp failure, tachycardia, narrowed pulse pressure and poor peripheral perfusion

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41
Q

Treatment for post pericardiotomy syndrome

A

5-7 days of NSAID agents such as Ibuprofen or Ketorolac (this may need to continue for several weeks)

Systemic steroids

Methotrexate for chronic PPS symptoms

Colchicine for joint inflammation

Diuretics when there is edema due to CO

echo guided pericardiocentesis for tamponade - after drained, use isotonic IV fluid for volume replacement

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42
Q

cold shock vs warm shock presentation

A

Cold - features of low cardiac output

  • Tachycardia
  • AMS
  • Poor peripheral perfusion
  • mottled skin
  • prolonged cap refill

Warm- features of high cardiac output

  • vasodilation
  • Tachycardia
  • bounding pulses
  • brisk cap refill
  • flushed
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43
Q 
Medication class that alters the force of energy of muscle contractions 
-Increases CO by increasing contractility
A

Inotropes

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44
Q

Med class that raises blood pressure by increasing vascular constriction

A

Vasopressors

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45
Q

Med class that alters heart rate

A

Chronotropes

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46
Q

med class that affects rate of myocardial relaxation (allows more filling time)

A

Lusitropes

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47
Q

space.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 348). Wolters Kluwer Health. Kindle Edition.

A

Cardiac Tamponade

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48
Q

Cardiac arrest ensues with uncorrected cardiac tamponade with what ECG finding

A

Pulseless electrical activity (PEA)

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49
Q

Presentation of Cardiac Tamponade

A

Beck Triad (classic)

  • Hypotension
  • JVD
  • Muffled heart sounds
  • pulsus paradoxus
  • Narrow pulse pressure
  • pericardial rub
  • shock with tachycardia, tachypnea, and depressed mental status
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50
Q

tests for cardiac tamponade

A

echo
chest x ray - globular heart shadow

ECG -
Low -voltage QRS in all leads

Abnormal ST segment

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51
Q

Treatment for cardiac tamponade

A

Medical emergency

needle pericardiocentesis with pigtail to prevent reaccumulating

Fluid resuscitation

Treat underlying disease process (infection)

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52
Q

In trauma patients, hypotension refractory to fluid resuscitation should prompt suspicion of

A

cardiac tamponade

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53
Q

Hypotension with distended neck vein should always include _____ in the differential diagnosis

A

cardiac tamponade

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54
Q

A dilation of the left or both ventricles with impaired contraction/systolic dysfunction in the absence of an abnormal loading condition (e.g., hypertension, valvular disease, or coronary artery disease).

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 351). Wolters Kluwer Health. Kindle Edition.

A

dilated cardiomyopathy

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55
Q

• Hypertrophied, nondilated ventricle in the absence of a hemodynamic disturbance that is capable of producing the existent magnitude of wall thickening (e.g., hypertension, aortic valve stenosis, catecholamine secreting tumors, hyperthyroidism).

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 351). Wolters Kluwer Health. Kindle Edition.

A

Hypertrophic cardiomyopathy.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 351). Wolters Kluwer Health. Kindle Edition.

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56
Q

Restrictive filling and reduced diastolic volume of either or both ventricles with normal to near normal systolic function and wall thickness.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 352). Wolters Kluwer Health. Kindle Edition.

A

• Restrictive cardiomyopathy.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 351). Wolters Kluwer Health. Kindle Edition.

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57
Q

• Ability of the ventricle to pump blood is impaired and cannot maintain adequate cardiac output to meet the body’s demand. • Over time, the ventricles become progressively stiff and do not fill appropriately. • Results in a backup of blood into pulmonary circulation, which causes pulmonary edema, pulmonary hypertension, and atrial enlargement.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 352). Wolters Kluwer Health. Kindle Edition.

A

Dilated cardiomyopathy.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 352). Wolters Kluwer Health. Kindle Edition.

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58
Q

The ventricles become thick and stiff, leading to impaired filling and the inability to meet the cardiac output demands of the body. • Over time, the ventricles become stiffer and can cause obstruction of blood flow out through the aorta.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 352). Wolters Kluwer Health. Kindle Edition.

A

Hypertrophic cardiomyopathy.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 352). Wolters Kluwer Health. Kindle Edition.

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59
Q

Leads to decreased filling compliance of the ventricles, causing severely elevated right atrial (RA) pressures and size. • The severely enlarged atrium can cause atrial arrhythmias (often difficult to control) as well as significant pulmonary hypertension.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 352-353). Wolters Kluwer Health. Kindle Edition.

A

Restrictive Cardiomyopathy

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60
Q

Management of Dilated Cardiomyopathy

A

Oxygen
Inotropic support
continuous tele
Fluid management- Be cautious with fluids

Diuretics - afterload reducers

  • VAD
  • ECMO
  • Transplant
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61
Q

management of Hypertrophic cardiomyopathy

A

No inotropes - can worsen systolic function

B-Blockers - help with chest pain and palpitations

Calcium channel blockers for angina and to improve diastolic function

Avoid dehydration - make sure heart has adequate preload

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62
Q

Management of Restrictive cardiomyopathy

A

No proven therapies currently exist

Anticoagulation is recommended

High risk for sudden embolic events

B Blockers
ACE inhibitors
Diuretics
Pacemakers

VAD
ECMO
Heart transplant - consider early bc pulmonary HTN is contraindication to transplant

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63
Q

Vascular communication between the left pulmonary artery (PA) and the descending aorta

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 358). Wolters Kluwer Health. Kindle Edition.

A

PDA

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64
Q

When does the PDA normally close

A

within the first 12-24 hours of life or by the first week

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65
Q

PDA
what murmur
where do you hear it in neonates vs older children

large PDA

A

Systolic murmur Left sternal border (neonates)

Continuous murmur Left upper sternal border (older children)

loud continuous “Machinery-type” murmur throughout the precordium, bounding pulses

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66
Q

With a large PDA, what do you see with Blood Pressure and pulse

A

Widened pulse pressure with low diastolic pressure

Bounding peripheral pulses

all from over circulation
will have resp distress

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67
Q

large PDA, what will you see on x ray

A

increased pulmonary vascular markings and cardiomegaly from LA and LV enlargement.

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68
Q

In PDA
what will you see on ECG

A

left atrial enlargement and LV hypertrophy with possible biventricular hypertrophy in the presence of PH and obstructive vascular disease.

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69
Q

diagnostic for PDA

A

ECHO

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70
Q

Meds for PDA

A

• Nonsteroidal anti-inflammatory drugs (NSAIDS): Indomethacin or a special intravenous (IV) form of ibuprofen has been used to help close a PDA; especially viable alternative for premature infants. Contraindicated in infants with intraventricular hemorrhage (IVH).

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 359-360). Wolters Kluwer Health. Kindle Edition.

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71
Q

When is surgical intervention required on PDA

A

if open past 3 months of age….Typically closure done in the first 6 months of life

closure via cath is now standard

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72
Q

what is this?

A

PDA

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73
Q

communication in the atrial septum

A

ASD

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74
Q

ASD occurs more frequently in ____

A

females

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75
Q

ASD that is located in the center of the atrial wall near the fossa ovalis and is the most common.

A

Ostium secundum

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76
Q

What type of ASD

located low in the septum at the junction with the AV valves, often associated with abnormal valves

A

Ostium primum

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77
Q

what type of ASD: located at the junction of the SVC and the right atrium, often associated with partial anomalous pulmonary venous drainage of the right pulmonary veins (PAPVR)

A

Sinus Venosus

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78
Q

What shunting occurs in ASDs

A

Left to right

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79
Q

Over time what do you see in an ASD

A

R atrial dilation, R ventricular volume overload and increased PBF

Atrial arrhythmias, CHF, Pulmonary hypertension

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80
Q

clinical presentation in ASD

A

Depends on the size of the defect and the relative compliance of both the ventricles. Even with large ASDs and significant shunts, infants and children are rarely symptomatic

Most patients are asymptomatic but may experience fatigue and dyspnea with large shunts

Auscultation reveals a systolic ejection murmur at the L sternal border (pulmonary blood flow murmur), a wide fixed, split S2, and in large shunts a diastolic murmur from flow across the TV.

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81
Q

ASD diagnostics

A
  • Chest radiograph: cardiomegaly with increased PVM.
  • Electrocardiography: R-axis deviation with right ventricular hypertrophy (RVH) and right bundle branch block (RBBB) pattern.
  • Echocardiogram: sufficient for diagnosis; can miss associated PAPVR.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 362). Wolters Kluwer Health. Kindle Edition.

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82
Q

when do they recommend closure of an ASD

A

3-5 yrs old

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83
Q

most common form of CHD

A

VSD

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84
Q

Communication between the right and left ventricles

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 363). Wolters Kluwer Health. Kindle Edition.

A

VSD

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85
Q

most common type of VSD

A

Perimembranous - doesnt usually close on own

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86
Q

Opening in the upper portion of the ventricular septum

A

Perimembranous VSD

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87
Q

Opening in the septum is just below the pulmonary valve in the ventricular septum

A

Outlet type (subarterial) VSD

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88
Q

opening is just below the AV valves (tricuspid and mitral) in the ventricular septum

A

Inlet type (canal) VSD

Can be associated with Atrioventricular (AVC) defect

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89
Q

an opening in the muscular portion of the lower ventricular septum.

A

Muscular VSD

many of these close spontaneously and do not require surgery

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90
Q

What type of shunting in VSD

A

Left to Right

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91
Q

In Non-restrictive VSD, shunting is determined by the ___

A

Pulmonary vascular resistance (PVR)

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92
Q

Murmur heard in VSD

A

Harsh holosystolic murmur at LSB

may have thrill and/or middiastolic rumble at apex

A systolic regurgitant murmur along the L sternal border is present in all VSDs and may be louder in smaller defects. (loud/harsh)

S1 is normal and the S2 is loud and split. There may be a an S3, thrill at the L sternal border, an active precordium, and a diastolic rumble at the left sternal border in large defects.

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93
Q

Chest XRAy in VSD

A

Enlarged L atrium with prominent main PA

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94
Q

why may you have an infant come in symptomatic at 4-6 weeks of life with VSD

A

As the PVR drops in the in the infant, generally 4-6 weeks of age, VSDs allow shunting from the high-pressure LV to the low-pressure RV across the ventricular septum and into the PA, leading to increased PBF, LA dilation, and LV volume overload.

Qp (quantity of blood to lungs) > Qs (quantity of blood to body)

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95
Q

ECG finding with VSD

A

Large VSDs on ECG will show LA enlargement, L axis deviation, BBB, LV hypertrophy and possible RVH.

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96
Q

what axis deviation is normal in newborns

A

Rightward Axis due to the thickness of the R ventricles

QRS is going down in II and up in aVF for Rightward axis

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97
Q

what Axis deviation

A

Northwest axis deviation (extreme)

QRS is down in both I and aVF

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98
Q

what axis deviation

A

Normal

up in I and aVF

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99
Q

what axis deviation?

A

Left superior axis

up in I

down in aVF

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100
Q

what axis deviation

A

Rightward axis

down in I

up in aVF

normal in infancy

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101
Q

VSD treatment

A

Initial therapy is directed at controlling CHF symptoms through medical management with diuretics, afterload-reducing medications (digoxin), and nutritional support.

If the pt is asymptomatic without evidence of PH, waiting until 4 to 5 years of age is warranted to maximize the potential for spontaneous defect closure.

Spontaneous closure is possible with perimembranous and muscular defects; therefore, surgical repair may be avoided and is only recommended for defects that cannot be medically managed. -half close by age of 2, and 90% by age 6

Surgery is indicated for patients with symptoms of CHF despite maximal medical therapy, growth failure despite supplementation, PH, or LV volume overload.

Typically surgery is done within the 1st year of life.

Most are repaired via an opening in the RA and visualized through the Tricuspid valve; and closed with a synthetic or pericardium patch. Care is taken to avoid the AV conduction tissue in the septum. Transesophageal echo can be utilized to rule out residual VSDs.

Small VSDs can be closed during cardiac catheterization using “clam shell” method.

102
Q

• Defect resulting from nonfusion of the endocardial cushion.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 367). Wolters Kluwer Health. Kindle Edition.

A

Atrioventricular Canal (AVC)

103
Q

What type of AV canal?

ostium primum defect associated with a cleft in the anterior mitral valve (two separate AV valves); no VSD.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 367). Wolters Kluwer Health. Kindle Edition.

A

Partial

104
Q

what type of AV canal?

ostium primum defect with AV valves only partially separated into two valves; has VSD but may be small.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 367). Wolters Kluwer Health. Kindle Edition.

A

Transitional

105
Q

what type oof AV canal?

ostium primum defect with large nonrestrictive VSD and a single AV valve; Three subtypes are recognized (Rastelli types A, B, and C).

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 367). Wolters Kluwer Health. Kindle Edition.

A

Complete

106
Q

Findings for a AV canal defect

A

Systolic regurgitant murmur at the Left lower sternal border

FTT

Resp distress

CHF

107
Q

ECG for AV canal

A

Electrocardiography: left axis deviation, biatrial and biventricular hypertrophy.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 370). Wolters Kluwer Health. Kindle Edition.

108
Q

Main problems in TOF

A

Pulmonary stenosis

Right Ventricular hypertrophy

Overide of Aorta

VSD

109
Q

Boot shaped heart on Xray

A

TOF

110
Q

what shunting is in TOF

A

Pink TET - L to R with CHF and pulmonary overcirculation

or

Too little pulmonary flow

R to L shunt with hypoxia (SaO2 70-80%)

111
Q

TOF ECG findings

A

R axis deviation with RVH

112
Q

TOF murmur

A

Harsh systolic ejection murmur at Upper Sternal border

113
Q

Treatment for TOF

A

Asymptomatic patients: B blocker

Symptomatic/TET spells - infundibular muscle spasms -> R to L shunting through VSD

-Supplemental oxygen, sedation, volume expansion, Knee-chest position

Severe cases - phenyl epinephrine, emergency surgery, ECMO

114
Q

Causes of Pericarditis

A

most often viral origin; bacterial etiology is rare, but S. aureus and Streptococcus pneumoniae are most common

Collagen vascular diseases: rheumatic fever, Kawasaki,

Autoimmune: lupus, scleroderma, Rheumatoid Arthritis

Postpericardiotomy syndrome- common form that follows heart surgery

Dressler syndrome (post ischemia)

Uremic Pericarditis

115
Q

what is happening in Constrictive Pericarditis?

A

Over time it becomes hard for the heart to relax or expand due to perisistent inflammation fibrosis which is caused by the immune cells making the pericardium more stiff

Stroke volume down

HR up

Similar to Tamponade physiology but happens more gradually

116
Q

symptoms of pericarditis

A

Fever

Chest pain that is worse with heavy breathing

improves with sitting up and leaning forward

117
Q

symptoms of Large Pericardial effusions (>100mL of fluid)

A

Decreased Heart sounds

Decreased Cardiac output -> leads to

  • Shortness of breath
  • Low BP
  • Lightheadedness
118
Q

ECG changes in Acute Pericarditis stage 1 (first couple of days to weeks)

then what is the progression for Stage II - IV

A

ST segment elevations

PR segment depressions

then

T waves Flatten

then

T waves invert

eventually return to normal

119
Q

Pericardial Effusion ECG changes

A

Low voltage on QRS or Alternans (QRS complexes have diff heights)

120
Q

Water Bottle Sign on X ray

A

Pericardial Effusion

121
Q
A
122
Q

Bacterial or fungal infection of the endocardial lining of the heart valves

A

Endocarditis

123
Q

Risk Factors for Endocarditis

A
  1. Previous Endocarditis
  2. Prosthetic Valve or Pacemaker
  3. Valvular or Congenital Heart Disease
  4. IV drug use
  5. IV catheter
  6. Immunosuppression
  7. Recent Dental or Surgical Procedure
124
Q

What Bacteria causes Endocarditis

A

Leading: (high fever and hemodynamic instability - Suspect these 2)

  1. Staphylococcus Aureus and MRSA
  2. strep pneumonia
  3. B homlytic Strep

Also:

Less Virulent:

    1. Enterococci
  2. Coagulase-neg Staphylococci

More Virulent:

  1. Staphylococcus aureus
  2. Streptococcus Pneumoniae
  3. B-Hemolytic Streptococci
  4. Aspergillus

Neonates:

  1. S. aureus
  2. Coagulase-neg staphylococci
  3. candida
  4. less frequent - GBS, gram neg rods and S.pneumoniae

Gram negative organisms and fungus - sneaky and can culture neg (HACEK)

  1. Haemophilus
  2. Aggregatibacter
  3. Cardiobacterium
  4. Eikenella
  5. Kingella
    6.
125
Q

Endocarditis symtoms

A
  • Acute vs Subacute/chronic
    • Acute - 2 weeks
    • Subacute- happens over a few months
  • Heart murmur (from blood passing vegetation) - Turbulance
  • Septic Emboli - vegetation breaking off
    • Splinter Hemorrhage (under fingernails)
    • Janeway lesions (hands and feet) - painless
    • Stroke
    • Pulmonary infarts
    • Conjunctival hemorrhage
  • Bacterial Antigen-Antibody Complexes
    • Osler’s Nodes (painful) - Finigers and Toes/feet
    • Roth Spots (eyes)
    • Glomerulonephritis (kidneys)

Neonates

  • fever or hypothermia
  • seizures
  • hemiparesis

Subacute

  • Arthralgias
  • myalgias
  • headache
  • malaise
  • relapsing fever
  • poor appetite
126
Q

Diagnosis for Endocarditis

A

Dukes Major

  • two positive blood cultures for a typical pathogen
  • two or more positive cultures for less common organisms,
  • significant Echo findings.

Dukes Minor

  • predisposing conditions such as CHD,
  • fever,
  • embolic vascular phenomena
  • immunologic phenomena,
  • Single blood culture

Definite IE includes satisfaction of two major criteria, one major and three minor criteria, or five minor criteria

Transthoracic echo vs Transesophageal echo

  • Transthoracic is cheaper and less expensive but lower sensitivity
  • Transesophageal is higher sensitivity
127
Q

ECG finding for infective endocarditis

A

Heart Block

Conduction delay with an isolated prolonged PR interval

128
Q

Treatment Endocarditis

A
  1. 6 weeks of IV antibiotics
  2. Follow up with blood cultures every 48-72 hours
  3. NSAIDS and PPI
  4. If autoimmune etiolgoy - corticosteroids
  5. If they have a prostetic valve - typically requires surgical replacement

Empiric

  • 2 broad spectrum antibiotics that covers
    • MRSA (staph)
    • MSSA (staph)
    • Streptococci
    • Enterococci
  • Tailored to type of valve
    • Native Valve or older prosthetic valve
      • Ampicillin-Sulbactam
      • Gentamicin
      • Cant tolerate Beta Lactams?
        • Vancomycin
        • Gentamicin
        • Ciprofloxacin
    • Newer Prostetic Valve (less than 12 months)
      • Vancomycin
      • Gentamicin
      • Rifampin

Blood Cutures show MSSA Native Valve Endocarditis

  • Nafcillin or Oxacillin
  • Allergic to PCN?
    • Cephalosporin

Blood Cultures show MRSA Native Valve Endocarditis

  • Vancomycin

Blood Cultures show Staph aureus prostethic valve endocarditis

  • Vancomycin
  • Gentamicin
  • Rifampin

Streptococcal Endocarditis

  • PCN G or Ceftriaxone for 4 weeks
  • Add Gentamicin to either to shorten treatment to 2 weeks
  • If allergic to B lactams or have a resistant…Vancomycin monotherapy

Enterococcal Endocarditis

  • Gentamicin plus either PCN, Ampicillin or Vancomycin for 6 weeks
  • If vancomycin resistant enterococcus -> Teicoplanin or Daptomycin

HACEK Endocarditis

  • Native Valve: Ceftriaxone for 4 weeks
  • Prostetic valve: Ceftriaxone for 6 weeks
129
Q

For individuals at high risk for endocarditis what is the recommendations prior to dental procedures

A

Oral Amoxicillin 1 hr before the procedure

or

IV/IM Ampicillin 1 hr before the procedure

if Allergic to PCN

Azithromycin, Clarithromycin, Cephalexin or Clindamycin orally 1 hr prior

130
Q

Postinfectious complecation of Group A Beta-Hemolytic Streptococcus (GAS) Pharyngitis

A

Rheumatic Fever

(from Strep Pyogenes “Strep Throat”)

131
Q

Symptoms of Rheumatic fever

A
  • Sudden-onset sore throat
  • fever
  • difficulty swallowing
  • scarlatina rash (Erythema Marginatum)
  • nausea
  • vomiting
  • abdominal pain
  • enlarged anterior lymph nodes
  • tonsillopharyngeal erythema.
  • Migratory arthritis
  • pancarditis
  • PANDAS

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 438-439). Wolters Kluwer Health. Kindle Edition.

132
Q
A
133
Q

Major diagnostic criteria of Acute Rheumatic fever

A

Jones Criteria

Polyarthritis

Carditis

Subcutanious nodules

Erythema Marginatum

Syndenham Chorea

+ previous Strep infection - Streptococcal antibody test (antistreptolysin O titer) is the most reliable lab evidence of prior infection.

Minor criteria

  • Fever
  • Raised ESR//CRP
  • Arthralgia
  • Prolonged PR interval
  • Previous RF

ECHO may be obtained to assess for valvular abnormalities (mitral valve thickening, chordae tendineae lengthening, aortic valve insufficiency, or mitral valve insufficiency)

134
Q

treatment for Rheumatic fever

A

Rest

anti-inflammatory meds NSAIDs (naproxen/ Ibuproprofen) ASA or corticosteroid if no improvement

antibiotics to wipe out any strep hanging around

either Single dose of: Benzathine PCN (benzylpenicillin) - 1st choice or

course of oral PCN VK or amoxicillin

if they have a PCN allergy use a first generation cephalosporin (cephalexin)

clindamycin or a macrolide (Azithromycin or Clarithromycin)

to eradicate beta-hemolytic streptococcus, ASA for inflammation, and bed rest. Long-term PCN prophylaxis (preferably IM) is required

135
Q

Heart complications associated with Rhumatic Fever - Chronic Rheumatic heart disease

A
  • Regurgitation and Stenosis
    • Mitral
    • Aortic
136
Q

Systolic ejection murmur

LLSB or between LLSB and Apex

Grades I-II/VI

Vibratory , musical quality

Intensity decreases in upright position

Usually heard ages 3-6 yrs old

A

Stills murmur

137
Q

describe a Still’s Murmur

A

Systolic ejection murmur

LLSB or between LLSB and Apex

Grades I-II/VI

Vibratory , musical quality

Intensity decreases in upright position

Usually heard ages 3-6 yrs old

138
Q

nutritional requirements in HF patients

A

120-160 Kcal/kg/day to thrive

increase of 50-100% protein may be needed

omega 3 fatty acid supplements

may be at risk for Vit D deficiency → due to prolonged use of diuretics, limited mobility

Magnesium deficiency → patients on diuretic therapy

Zinc and selenium protect cell membrane from free radial injury and are cardioprotective against CAD and cardiac dysfunction

139
Q

What will labs show on Post pericardiotomy syndrome

A

CBC (leukocytosis, eosinophila), procalcitonin (marker to evaluate presence of bacterial infection), blood cultures, and wound culutres if drainage is present, elevated inflammatory markers (CRP/ESR)

Troponin 1, CKMB, BNP, and lactate levels provide insight into myocardial injury and systemic perfusion

140
Q

HR for SVT

other requirements?

A

Rates in infants can be 300, adolescents even 220

Rate above 220 infant

children over 180

abnormal P waves

no beat to beat variability

narrow QRS complex tachycardia

141
Q

electrical pathway of the heart

A

SA node

AV node

Bundle of HIS

Purkinje Fibers

142
Q

Treatment for SVT

A

w/ poor perfusion synchronized cardioversion starting with 0.5-1 J/Kg and can be increased to 2J/kg

NEVER delay cardioversion while awaiting IV placement in unstable pt

IV access- 0.1mg/kg/dose adenosine (blocks AV conduction thereby terminating most SVT in which the AV node forms part of the reentry circuit)

Caution to use adenosine in astmatic pt as it can induce bronchospasm

Stable pt- vagal maneuvers

Bag of ice on forehead up to 10 seconds

Valsalva maneuver in older pt

Chronic mgmt- digoxin, propranolol, or nadolol

Other tx- antiarrhythmics flecainide, propafenone, sotalol, amiodarone

If other tx fails radiofrequency catheter ablation

143
Q
A
144
Q

what does Atrial Flutter look like

A

Regular rhthym

Atrial 250-350 bpm

AV conduction ratio usually 2:1, can be 3:1 or 4:1

P waves that give off a saw tooth appearance

145
Q

Treatment for Atrial Flutter

A

Medication

cardioversion

Definitive treatment -> Catheter ablation

rate control-slow ventricular rate digoxin, propranolol, CCB

pts receiving digoxin should avoid cardioversion unless arrhythmia is life threatening (associated with malignant ventricular arrhythmias) rapid atrial esophageal pacing may be effective

rhythm control- antiarrhythmic meds to suppress dysrhythmias

electrophysiology study and catheter ablation are a class 1 indication for recurrent or persistent AF pts over 15kg

146
Q

Atrial Fibrillation - what does this look like

A

Atrial Heart rate > 500 BPM

No P waves

No AV conduction ratio

Irregularly irregular rhythm

QRS complexes have no pattern

Ventricular rate of 120-80 bpm

147
Q

Holiday Heart Syndrome

A

Atrial Fibrillation occurs after Binge Drinking

148
Q

Treatment in Atrial Fibrillation

A

Treatment- B blockers and CCB

Digoxin, propranolol, verapamil can be used to slow the ventricular rate and reduce patient symptoms

Antiarrhythmic meds reduce risk of recurrence – sotalol and amiodarone

anticoagulant therapy -at risk for clots due to pooling blood

Cardioversion

149
Q

Bundle of Kent

A

Accessory pathway that acts as a shortcut from Atria to ventricles

WPW syndrome

150
Q

what inherited mutation associated with WPW

A

Autosomal dominant mutation of the PRKAG2 gene

151
Q

drugs that promote QT that can lead to toursade

A

antiarrhythmics - blocks sodium and k channels - quinidine, disopyramide, procainamide, lidocaine, mexiletine, flecainide, and propafenone

phenothiazines

tricyclics

ampicillin

organophosphate insecticides

152
Q

Bazett’s Formula

A

To get QTc

Qt (ms)

divided by

The square root of RR(s) divided by 1s

Long QT is >440 ms males

>460 ms in females

153
Q

Treatment Toursades

A

Mag Sulfate (25-50mg/kg max 2g)

Electrical pacing

Mgmt- BB (propranolol 2-4mg/kg/day), atenolol (0.5mg/kg/day), surgical therapy (cardiac pacemaker, ICD, left cardiac sympathetic denervation surgery)

154
Q

causes of V fib

A

hypoxia, hyperkalemia, digoxin, or quinidine toxicity, MI, myocarditis, or complications from cardiothoracic surgery CHD

155
Q

wide complex tachycardia defined as a series of 3 or more PVCs with a HR between 120 and 200 bpm

A

Ventricular Tachycardia

156
Q

treatment in unstable Ventricular tachycardia

A

Synchronized cardioversion

0.5-1J/kg

Pulseless VT -> defibrilation of 2-4 J/kg

Stable -

antiarrhythmics such as amiodarone, sotalol or lidocaine

157
Q

what congenital defects have R - L shunting

A

Tetralogy

Transposition

Tricuspid atresia

158
Q

what congenital defects have L to R shunting

A

Patent ductus arteriosus

VSD

ASD

159
Q

what CHD have mixing of blood (mixed shunting)

A

Truncus

TAPVR

HLH

160
Q

supravalvar stenosis is associated with what 2 syndromes

A

Williams syndrome and Alagille syndrome

161
Q

Pulmonary valve doesnt close all the way so in diastole blood leaks back

A

Pulmonary Regurgitation

162
Q

Pulmonary valve doesnt open all the way in systole making it harder to pump to the lungs

A

Pulmonary stenosis

163
Q

What two other conditions/syndromes are associated with pulmonary stenosis

A

Tetrology of Fallot

Noonan’s Syndrome

164
Q

when pulmonary stenosis develops over time due to mechanical stress….there is Fibrosis and Calcification of the valve which causes what sound

A

Ejection click

with Turbulence - Crescendo-Decrescendo murmur Between S1 and S2

165
Q

What happens as a result of Pulmonary stenosis?

A

Concentric R ventricular Hypertrophy

(R ventricle is working harder to push blood past the stenosis…Sarcomeres in the cardic muscle are added in parallel)

Blood backs up -> R sided heart failure

Microangliopathic Hemolytic anemia (RBC are damaged having to fit through the valve…get broken into schistocytes and expelled in urine)

Hemoglobinuria

Symptoms

  • Blood Backs up
    • Distended Neck Veins
    • Swelling in ankles and feet
    • hepatosplenomegaly
  • ​Cyanosis
  • Shortness of Breath
  • Fatigue
166
Q

Treatment for Pulmonary stenosis

A

Balloon Valvuloplasty

possible PGE

167
Q

Aortic valve doesnt open all of the way during systole making it harder for blood to be pumped to the body

A

Aortic stenosis

168
Q

What causes Aortic stenosis

A

Stress over time in adulthood

Bicuspid Aortic Valve - wears down faster

Chronic Rheumatic fever (commisural fusion)

169
Q

what do you hear in aortic stenosis

A

Ejection Click

crescendo-decrescendo murmur between S1 and S2

170
Q

What does aortic stenosis cause

A

Concentric Left Ventricular Hypertrophy

(Sarcomeres added in parallel)

Heart Failure - exercise induced symptoms (angina, ect)

Microangiopathic Hemolytic Anemia

Hemoglobinuria

171
Q

treatment in Aortic stenosis

A

Initial medical management for a neonate who presents in a low CO state consists od CV resuscitation, inotropic and ventilatory support and initiation of PGE to restore systemic perfusion.

Possible biventricular repair if large enough

For infants catheter balloon valvuloplasty or surgical valvotomy is often initial treatment of choice.

172
Q

What syndrome are individuals predisposed to Bicuspid Aortic Valve

A

Turner Syndrome (mosaicism)

173
Q

What bp gradient is significant in coarctation

A

>20mmHG

174
Q

3 sign on x ray

A

coarctaion

sonmetimes seen in older children

175
Q

whos more at risk for coarctation

what should they be worked up for?

A

Females

80% are associated with bicuspid aortic valve

work up for Turner’s syndrome

176
Q

4 extremetity blood pressures…what warrants further eval?

A

SBP > 15 mmHg than lower extremety

177
Q

treatment coarctation

A

Initial stabilization includes an infusion of PGE, to restore ductal patency and distal perfusion

Continuous infusion of nipride or B-Blockers like esmolol are often required in the immediate post-op period. Then transition to oral therapy with ACE-I such as captopril or enalapril or B-Blocker like propranolol or atenolol prior to discharge.

Done by left thoracotomy

178
Q

all four pulmonary veins drain aberrantly into the systemic venous system or the RA.

A

TAPVR

179
Q

4 categories of TAPVR

A

Supracardiac- most common form, in which the pulmonary veins drain into the SVC via the left vertical vein to the innominate vein.

Infracardiac- 2nd, th pulmonary veins drain into the portal vein, ductus venosus, hepatic vein, or inferior vena cava below the diaphragm. (Most likely to become obstructed).

Intracardiac- pulmonary venous hypertension with resultant pulmonary edema, PH, LCOS and severe hypoxemia.

Or mixed

180
Q

Most common form of TAPVR

the pulmonary veins drain into the SVC via the left vertical vein to the innominate vein.

A

Supracardiac

181
Q

which type of TAPVR

2nd, th pulmonary veins drain into the portal vein, ductus venosus, hepatic vein, or inferior vena cava below the diaphragm. (Most likely to become obstructed).

A

Infracardiac

182
Q

which type of TAPVR

pulmonary venous hypertension with resultant pulmonary edema, PH, LCOS and severe hypoxemia.

A

Intracardiac

183
Q

What does the pt look like with obstructed TAPVR

A

creates pulmonary venous hypertension with resultant pulmonary edema, PH, LCOS, and severe hypoxemia.

There is an increased RV impulse, a widely split and fixed S2 which can be increased, a systolic ejection murmur, and a diastolic rumble if there is excessive flow across the TV.

If there is PV obstruction present with marked cyanosis, LCOS, and respiratory distress in the neonatal period.

A heart murmur is often absent, but there may be a GALLOP!!!

184
Q

What does the pt look like with unobstructed TAPVR

A
185
Q

snowman sign on x ray

A

TAPVR

186
Q
A
187
Q

ECG on TAPVR

A

R axis deviation and RVH

188
Q

Treatment for TAPVR

A

Absolutely no nitric oxide!! Giving NO will. Increase PBF to the lungs and is contraindicated in preoperative obstructed pulmonary veins.

These babies need emergent care and surgical repair.

189
Q

Characterized by the aorta arising from the anatomic RV and the PA arising from the anatomical left ventricle. There might be a VSD

A

Transposition of Great Arteries

190
Q

diabetic mothers are at higher risk for developing the defect

A

Transposition of Great Arteries

191
Q

2 parallel circuits

Right ventricle attaches to aorta

Left ventricle to pulmonary artery

A

Transposition of Great Arteries

192
Q

The urgency of repair TGA depends on what

A

The amound of mixing between the 2 sides (mostly at the ASD)

193
Q

“egg on a string” with a large. Globular heart or be normal, on X ray

A

Transposition of Great Arteries

194
Q

Treatment for TGA

A

PGE may be needed to maintain ductal flow but can be trialed off once open atrial communication is confirmed. If desats occur, the infusion should be resumed, and ductal flow is necessary to increase pulmonary venous return to the LA, increasing the pressure gradient between the LA and RA, thereby aiding in atrial mixing.

Trickiest part is moving the coronary arteries to go with the aorta

195
Q

An inflammation of the blood vessels that can lead to necrosis and arterial aneurysms, more specifically coronary artery aneurysms.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1350). Wolters Kluwer Health. Kindle Edition.

A

Kawasaki disease

196
Q

age and gender most affected by Kawasaki

A

• Affects 9.1 to 32.5 per 100,000 children annually, with a small male predominance. • Most commonly affects patients under the age of 4 years, with a peak incidence between 18

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1350). Wolters Kluwer Health. Kindle Edition.

197
Q

diagnostic criteria for Kawasaki disease

A
  • Specific criteria, in addition to fever for 5 days, must be met for the diagnosis of classic (4–5 criteria) or atypical or incomplete Kawasaki (2 criteria).
  • Bilateral painless bulbar conjunctival injection: without exudate.
  • Changes in lips and oral cavity: injected oral mucosa, dry/cracked lips, strawberry tongue.
  • Polymorphous exanthema.
  • Cervical lymphadenopathy (≥1.5 cm): typically unilateral.
  • Changes in extremities (e.g., palms of hands and/or soles of feet).

Acute: erythema and edema; convalescent: peeling/desquamation.

• Other findings. • Cardiovascular: heart murmur, congestive heart failure, pericardial effusion, ECG changes (e.g., arrhythmias, abnormal Q waves, prolonged PR or QT intervals, ST segment changes), and enlarged cardiac silhouette on chest radiograph, myocardial infarction, and arterial aneurysms throughout the body, including the coronaries. •

Gastrointestinal: abdominal pain, diarrhea, nausea and/or vomiting, hepatitis. •

Musculoskeletal: arthritis. • Pulmonary: upper respiratory tract symptoms, pulmonary infiltrate. • Genitourinary: sterile pyuria. •

Joint: arthralgias, arthritis. •

Skin: perineal rash; transverse furrows of fingernails (Beau lines). •

Laboratory abnormalities. • Leukocytosis; increased neutrophils, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), platelets, serum transaminases, and γ-glutamyl transferase; hypoalbuminemia, anemia. • Sudden-onset high fever: typically the first presenting sign.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 1350-1351). Wolters Kluwer Health. Kindle Edition.

Mnemonic CRASH and BURN

C= conjuntivitis

R= Rash

A= Adenopathy (Cervical)

S= Strawberry tongue (Oral Changes)

H= Hands and Feet (extremity changes)

BURN= fever >5 days

Mnemonic

A, Rash: Maculopapular, diffuse erythroderma, or erythema multiforme-like.

B, Conjunctivitis: Bulbar conjunctival injection without exudate; bilateral.

C, Oral changes: Erythema and cracking of lips (cheilitis); strawberry tongue; erythema of oral and pharyngeal mucosa.

D and E, Palmar and plantar erythema: Usually accompanied by swelling; resolves with subsequent periungual desquamation in the subacute phase.

F, Cervical adenopathy: Usually unilateral, node ≥1.5 cm in diameter.

G, Coronary artery aneurysms:

H, Peripheral artery aneurysms:

198
Q

3 phases of Kawasaki

A

Acute - weeks 1-2

Subacute: week 2-4

Convalescent - week 3 - 8

199
Q

pertinent labs in Kawasaki

A

• Inflammatory markers: elevated CRP and ESR. • CBC: leukocytosis, neutrophilia, eosinophilia, anemia, and thrombocytosis. • Metabolic panel: hypoalbuminemia, hypokalemia, elevated transaminases and GGT, elevated pancreatic enzymes. • Coagulation factors: elevated fibrinogen.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 1351-1352). Wolters Kluwer Health. Kindle Edition.

200
Q

Treatment for Kawasaki

A

Prompt diagnosis is key. •

IV immunoglobulin (IVIG) 2 g/kg. •

Aspirin (ASA) 80 to 100 mg/kg/day divided every 6 hours and weaned with defervescence. •

Long-term therapy: Treatment is tailored to the risk level identified and includes: •

Risk level I: no coronary involvement. ASA for 6 to 8 weeks with counseling follow-up every 5 years. •

Risk level II: coronary artery dilation with resolution by 8 weeks. ASA for 6 to 8 weeks with counseling follow-up every 3 years. •

Risk level III: coronary aneurysm measuring 3 to 6 mm. ASA until resolution of aneurysm and limited activity for 8 weeks if <10 years of age. Stress test every 2 years and prior to admission into sports for those >10 years of age. Annual echocardiography and angiography if abnormal stress test is observed. •

Risk level IV: nonobstructive coronary aneurysm measuring >6 mm and/or multiple complex aneurysms. Long-term ASA in addition to anticoagulation therapy. Annual stress test, biannual echocardiography and ECG in addition to a cardiac catheterization on a biannual or annual basis. No high-impact sports. Counseling. •

Risk level V: obstructed coronary aneurysms. All recommendations included in risk level IV in addition to β-adrenergic blocking agents.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 1352-1353). Wolters Kluwer Health. Kindle Edition.

DO NOT DELAY TREATMENT OF KD TO OBTAIN ECHOCARDIOGRAM CONFIRMING KAWASAKI DISEASE!

The mainstay initial treatment for both complete and incomplete KD is a single high dose of IVIG together with acetyl- salicylic acid (ASA), which is supported by clinical trial evidence. The efficacy of IVIG administered in the acute phase of KD is well established to reduce the prevalence of coronary artery abnormalities

ASA has been used in treatment of KD for many years. Although ASA has important anti-inflammatory activity (at high doses) and antiplatelet activity (at low doses), it does not appear to lower the frequency of development of cor- onary abnormalities.177 During the acute phase of illness,

Give High-dose IVIG (2 g/kg given as a single intravenous infusion) within 10 days of illness onset but as soon as possible after diagnosis,

Only give past the 10th day in presence of fever, and significant elevation of inflammatory markers, or coronary artery abnormalities

ASA is administered every 6 hours, with a total daily dose of 80 to 100 mg·kg. ASA is reasonable until the patient is afebrile

Corticosteroids have only been shown to benefit in very high risk cases

IVIG RESISTANCE

IVIG second course 2g/kg

Methylpred 20-30 mg/kg IV x 3 days

Infliximab may be given instead of second course IVIG

201
Q

Treatment in syncopy

A

Neurocardiogenic:

90% of patients will have improved symptoms with increased fluid and salt intake. Goal for teen girls is 3L daily and goal for teen boys is 3.5L daily, along with 8 gm extra sodium

Abortive techniques: lying down with presyncope, compression stockings to prevent venous pooling, counter-pressure maneuvers like squatting and leg crossing, and avoiding stimuli that cause syncope

2nd line treatment includes midodrine, fludrocortisone, SSRIs, and beta blockers

Admit if central cyanosis, abnormal ECG, pathologic cardiac murmur, history of CHD repair, loss of consciousness >5min, neurological deficit, severe dehydration, severe anemia, adrenal crisis, severe hypoglycemia

202
Q

what lesions need PGE

A

Used for cyanotic lesions such as Pulmonary stenosis, Aortic Stensosis, Coarc, TOF, TGA, TAPVR

203
Q

meaning of spleen and liver enlargement

A

Liver -> systemic venous congestion

Spleen -> consider infective endocarditis

204
Q

Wide pulse pressure may be seen in

A

PDA, truncus arteriosus, AC malformations, aortic insufficiency

205
Q

Narrow pulse pressure seen in

A

pericardial tamponade, aortic stenosis, HF

206
Q

excellent data as to systemic and pulmonary venous anatomy, proximal pulmonary pulmonary artery anatomy, relationships of great arteries and arch abnormalities

A

Chest CT angiogram

207
Q

what can cause vocal cord paralysis

A

Important cause of laryngeal dysfunction

May be unilateral or bilateral

Mostly caused by damage to recurrent laryngeal nerve then by central lesion → Left recurrent laryngeal nerve passes around the aortic arch and is more susceptible to damage then right laryngeal nerve

Causes

Peripheral nerve damage (neck traction during delivery of infant or thoracic surgery), mediastinal lesions

Central causes → arnold-chiari malformation, hydrocephalus, intracranial hemorrhages

208
Q

manifestations of vocal cord paralysis

A

bipasic stridor

alterations in voice and cry, including weak cry in infants

Hoarseness

Aphonia

At risk for aspiration → manifested by cough/choking with drinking, coarse airway sounds audibly and by auscultation

209
Q

treatment in vocal cord paralysis

A

patients with traumatic injury to recurrent larygneal nerve often have spontaneous improvement over time, usually within 3-6 months

if paralyzed vocal cord not recovered in 1 year of injury → likely permanently damanged

Gelform injection of a paralyzed vocal cord can responsition the cord and improved phonation and airway protection

patient who have severe airway obstruction and aspiration may need tracheostomy tube placement

210
Q

Neonatal infections

  • Common organisms
  • empiric treatment
A

Common organisms: GBS, E. coli, Listeria monocytogenes, S. aureus, Enterococcus species, HSV, CMV, Varicella-zoster virus, RSV, Candida species

ampicillin, gentamicin or cefotaxime, when HSV is suspected acyclovir

211
Q

Treatment for

Acute Bacterial Sinusitis

A

Amoxicillin or

Augmentin

212
Q

Treatment for

Acute pharyngitis

strep +

A

Amoxicillin or penicillin

213
Q

Treatment for Adenovirus

A

supportive care

immunocompromise receive

Cidofovir

214
Q

Treatment for Acute otitis media

A
215
Q

Pneumonia

Common causes by ages

A

Neonates < 30 days

  • Bacteria
    • E.coli
    • Group B Streptococcus
    • Listeria Monocytogenes
  • Other Causes
    • Bacteria
      • Group D strep
      • H. Influenzae
      • Strep pneumoniae
      • Ureaplasma urealyticum
      • Bordetella pertussis
    • Viruses
      • Herpes simplex virus
      • Cytomegalovirus

1-3 months

  • Bacteria
    • S. pneumoniae
    • Chlamydia Trachomatis
    • B.pertussis
  • Viruses
    • RSV
    • Influenza
    • Parainfluenza
    • Adenovirus
  • Other causes
    • Bacteria
      • H.Influenzae
      • Moraxella catarrhalis
      • Staph aureus
      • U. urealyticum
    • Virus
      • Cytomegalovirus
      • Metapneumovirus

3 mos - 5 years

  • Bacteria
    • Mycoplasma pneumoniae
    • C.Trachomatis
    • S.pneumoniae
  • Virus
    • RSV
    • Influenza
    • Parainfluenza
    • Adenovirus
    • Rhinovirus
  • Other
    • Bacteria
      • H.Influenzae
      • M.catarrhalis
      • S. aureaus
      • Neisseria meningitis
      • mycobacterium tuburculosis
      • Varicella-zoster

5 years to adolescents

  • Bacteria
    • M.pneumoniae
    • C.Trachomatis
    • S.pneumoniae
  • Other
    • Bacteria
      • H.influenzae
      • Legionella Species
      • M. tuberculosis
      • S.aureus
    • Virus
      • Adenovirus
      • Ebstein-Barr virus
      • Influenza virus
      • Parainfluenza
      • Rhinovirus
      • RSV
      • Varicella-zoster
216
Q

Treatment for Pneumonia by age

A

Birth - 1 month: Parenteral Ampicillin and gentamicin. Can consider cefotaxime in addition to or in lieu of gentamicin

1 month to 3 months well appearing: Amoxicillin (high dose)

Alternative agents: Sulfamethoxazole/trimethoprim, amoxicillin-clavaulanic acid, or macrolide. Can also use parenteral ceftriaxone for first dose then change to oral amox

1 month to 3 months ill appearing: Parenteral cefotaxime or cefuroxime

consider addition of macrolide if concerns for pertussis or chlamydia

4 months to 5 years: Amox (high dose)

Alt: Sulfamethoxazole/trimethoprim, Augmentin or macrolide

>5 years to adolescence: Macrolide alone if low suspicion of Strep pneumoniae

Add: If persist or conern for S. pneumonia - Add B-lactam antibiotic such as amox or cephalosporin

217
Q

synagis qualifications

A

Synagis is indicated for the prevention of serious lower respiratory tract disease caused by RSV in children at high risk of RSV disease

  • Infants born before 29 weeks, 0 days gestation who are younger than 12 months at the start of RSV season
  • For infants born during the RSV season, fewer than 5 monthly doses will be needed
  • If born greater than 29 weeks, 0 days may qualify for if
    • Congenital heart disease
      • Acyanotic heart disease who are receiving medication to conrol congestive heart failure and will require cardiac surgical procedures and infants with moderate to severe pulmonary hypertension
      • Cyantoic heart disease- cardiac specialist decides
      • Recommendations apply to infants in the first year of life who are born within 12 months of onset of the RSV season
      • After surgical procedures that involve cardiopulmonary bypass, for children who are receiving prophylaxis and who continue to require prophylaxis after a surgical procedure, a post operative dose of palivizumab (15mg/kg) should be considered after cardiac bypass or at the conclusion of extra corporeal membrane oxygenation for kids <24 months
      • Children <2yo undergo cardiac transplantation during the RSV season may be considered for palivizumab
      • DO NOT give it to
        • Hemodynamically insignificant heart disease
          • Secundum atrial septal defect,
          • Small ventricular septal defect
          • Pulmonic stenosis
          • uncomplicated aortic stenosis
          • Mild coarctation of the aorta
          • Patent ductus arteriosus
          • Infants with lesions adequately corrected by surgery, unless they continue to require medication for CHF
          • Infants with mild cardiomyopathy who are not receiving medical therapy for condition
          • Children in the second year of life
    • Chronic lung disease
      • Gestation age <32 weeks, 0 days and requirement of >21% Oxygen for at least the first 28 days of birth- during first year of life, during RSV season
      • Only recommended in second year of life if meat CLD requirement and continue to require medical support (chronic corticosteroid therapy, diuretic therapy, or supplemental oxygen) during the 6th months prior to the second RSV season
    • Or another condition
      • Infants with neuromsk disease or congenital anomaly that ipparis the ability to clear secretions from the upper airway because of ineffective cough are known to be at risk for a prolonged hospitalization and should be considered during the first year of life
      • If <24mo and severely immunocompromised (chemo/ transplant/ etc) during the RSV season
      • Down syndrome only if they meet other qualifications (HD, CLD, premature)
      • Cystic fibrosis only if
        • CLD and/ or nutritional compromise in first year of life
        • Second year of life if severe lung disease or weight for length less than the 10th percentile
  • Typically NOT recommended in the second year of life
  • Unless CLD who continues to require medical interventions 6 months prior to the RSV season
  • If any infant/ child is hospitalized with RSV while receiving vaccine, the vaccine monthly should be discontinued bc the likelihood of a second infection is very low
  • Those in neonate area who qualify should receive the first dose 48-72 hours before discharge to home or promptly after discharge
  • Hospital prevention is based off of adherence to infection-control practices

RSV Seasonality

  • 5 monthly doses at 15mg/kg will provide more than 6 months of serum palivizumab concentrations above the desired level
  • Not recommended to give more than 5 doses
  • Typically November- march (coverage till april)
  • If october -february (coverage till march)
  • If initiated in december- april (covers may)
  • If born in january receive last dose in march
    *
218
Q
A
219
Q

Croup

What causes it

How do you treat it

A

Parainfluenza 1,2,3,4

RSV

Dex 0.6mg/kg x 1 dose

Racemic epi (peak effect 10-30 min fades 60-90 min)

Rebound effect may occur- monitor for 3 hours after rac epi

may repeat racemic epi every 20 min for 1-2 hrs max

220
Q

Meningitis common organisms by age

A

Neonates <3 mth

  • GBS
  • E.Coli
  • Listeria monocytogenes
  • Other gram neg bacilli
  • HSV can cause severe encephalitis
  • Less common
    • Listeria monocytogenes
    • Enterococcus faecalis
    • Neisseria Meningitis
    • Strep pneumoniae
    • other streptococci
    • Citrobacter species
    • Salmonella
    • Pseudomonas aeruginosa
    • Haemophilus influenzae
    • Staphylococcus aureus

1-3 months

  • S.pneumoniae
  • Gram-neg bacilli
  • GBS
  • Less common
    • N. miningitidis

> 3 months

  • S. pneumoniae
  • Neisseria meningitidis
  • less common
    • Gram neg bacilli
    • Group B strep

3 months- 9 years

  • Streptococcus pneumoniae & Neisseria meningitidis are the most common causes of acute bacterial meningitis.
  • Group B streptococcus is responsible for a small percentage.

10 years – 18 years

  • N. meningitis is responsible for the majority of bacterial meningitis.
  • H. influenzae should be considered for those unvaccinated from Hib vaccine and those from underdeveloped countries.

Enteroviruses are the most common cause of viral meningoencephalitis.

Arboviruses, transmitted commonly via vectors such as mosquitoes and ticks are responsible for some cases of meningoencephalitis in summer months.

  • West Nile, La Crosse, Powassan and St. Louis are the most common.
221
Q

Kernig and Brudzinski sign

A

meningitis

222
Q

meds for Meningitis

A

Newborns (0-28 days)

  • Cefotaxime plus ampicillin with/without gentamicin
  • Alternative - ampicillin plus gentamicin

Infants and toddler (1 month to 4 yrs)

  • Ceftriaxone or cefotaxime plus vancomycin

Children and adolescents 5-13 plus adults

  • ceftriaxone or cefotaxime plus vancomycin
  • Alt Cefepime plus vancomycin

Children > 1 month

Empirical board spectrum antimicrobial coverage with vancomycin and either cefotaxime or ceftriaxone should be started.

Acyclovir should be initiated for all infants and children with suspected HSV encephalitis.

Duration of treatment (N. 388)

N. meningitidis is 5-7 days

H. Influenzae is 7-10 days

S. pneumoniae is 10-14 days

Gram-negative bacilli should be treated for a minimum of 21 days or 14 days beyond the first negative CSF culture, whichever is longer.

Lipincot:

Recent neurosurgery or ventricular shunt: coagulase-negative staphylococci (Staphylococcus epidermidis), methicillin-susceptible and methicillin-resistant Staph. aureus (i.e., MSSA, MRSA), aerobic gram-negative bacilli (Pseudomonas aeruginosa), Propionibacterium acnes.

  • vancomycin + cefepime; vancomycin + ceftazidime; or vancomycin + meropenem.

Basilar skull fracture: Streptococcus pneumoniae, Neisseria meningitidis, Strep. pyogenes. •

  • Management: vancomycin + 3rd-generation cephalosporin.
223
Q

otitis media common organisms

A
  • strep pneumoniae
  • nontypable Haemophilus influenzae
  • moraxella catarrhalis
  • Group A strep - less frequent
224
Q

treatment for Otitis media

A
  • The recommended first-line therapy for most children meeting criteria for antibiotic therapy is amoxicillin (80-90 mg/kg/day in two divided doses)
  • Some children with mild illness or uncertain diagnosis may be observed if appropriate follow-up within 48-72 hours can be arranged with initiation of antibiotic therapy if symptoms do not self-resolve.
  • The failure of initial therapy with amoxicillin at 3 days suggests infection with β-lactamase-producing H. influenza, M. catarrhalis, or resistant Strep. pneumoniae.
  • Recommended next-step treatments include high-dose amoxicillin-clavulanate (amoxicillin 80-90 mg/kg/day), cefdinir, or ceftriaxone (50 mg/kg IM in daily doses for 3 days).
  • IM ceftriaxone is especially appropriate for children with vomiting that precludes oral treatment.
225
Q

MSSA treatment

A

Treatment options: *

Cefazolin, oxacillin, or nafcillin IV or cephalexin PO

Alternative options: Clindamycin or vancomycin IV; clindamycin PO

226
Q

MRSA treatment

A

Treatment options:*

Vancomycin

Clindamycin - Some may become resistant; should be considered in refractory hypotension with concern for toxic shock.

Bactrim

Linezolid

Daptomycin - Not for treatment of pneumonia or children <1 yrs.

227
Q

ABX for appendicitis

A

Piperacillin/Tazobactam (Zosyn)

228
Q

Clostridium difficile treatment

A

Discontinue inciting abx

Metronidazole is currently the drug of choice for the initial treatment of children and adolescents with mild to moderate disease

Oral vancomycin or vancomycin administered by enema with or without intravenous metronidazole is indicated as initial therapy for patients with severe disease and for patients who do not respond to oral metronidazole.

Severe or fatal disease is more likely to occur in neutropenic children with leukemia, in children with intestinal stasis (eg, Hirschsprung disease), and in patients with inflammatory bowel disease.

Antiperistaltic medications should be avoided because they may obscure symptoms and precipitate complications, such as toxic megacolon.

229
Q

organisms for Fever of unknown orgin (temp >100.9 most days for at least 3 weeks or after a week of intense eval without diagnosis)

A

Most common infecious causes: EBV, Bartonella henselae, UTI and osteomyelitis

Salmonellosis

Tuberculosis

Rickettsia diseases

Syphilis

Lyme disease

Cat-Scratch disease

Atypical prolonged common viral disease

EBV

CMV

Viral hepatitis

Coccidioidomycosis

Histoplasmosis

Malaria

Toxoplasmosis

230
Q

TB organisms

A

Caused by an acid-fast bacilli of the mycobacterium tuberculosis complex

Most common cause is M. Tuberculosis

Also caused by M. bovis, africanum, bovis BCG, caprae, mungi, orygis, canetti, microti

231
Q

TB treatment

A

Steroids as adjunctive therapy for TB meningitis reduce death and tuberculomas

  • Dexamethasone 0.3-0.4 mg/kg/day for first 2 weeks then tapered for 2 weeks
  • Prednisolone 2mg/kg/day for 2 weeks then tapered for 2 weeks

Used liquid and fixed dose formulation for best adherence

Child may always have “abnormal” CXR

Drug related hepatitis is concern with isoniazid and rifampin therapy

  • Peripheral neuritis is rare but can occur with INH therapy, can be prevented with concomitant administration of pyridoxine
  • Rifampin will change color or urine to deep organ red during initial part of therapy

Severe cases of TBM or military TB- do monthly liver function test

  • Contact clinician with signs of hepatoxicity- vomiting, abdominal pain, jaundice
232
Q

malaria organism

A

P. falciparum

  • P. falciparum accounts for the majority of severe malaria and death
    • The vast majority of of persons returning to the US infected with P. falciparum acquired the infection in sub-saharian Africa during the previous 1-2 months.
  • P. vivax, P. ovale, P. malariae, P. knowlesi

*A traveler returning from an endemic area with fever has malaria until proven otherwise*

233
Q

treatment of malaria

A

Atovaquone-proguanil and artemether-lumefantrine are first-line treatments for chloroquine resistant malaria, which is present throughout the world with the exception of Central and South America and some countries in the Middle East.

For severe malaria, IV quinidine or artesunate are recommended.

  • Special attention should be given to blood glucose and cardiac rhythm with IV quinidine, given possible hypoglycemia and long QT syndrome.

Exchange transfusion may be considered when parasitemia reaches greater than 5-10%.

Consultation with subspeciality services is based on severity of presentation and patient’s response to therapy

  • Specialists from ID, neurology, GI, nutrition, critical care and rehabilitation medicine may be valuable.
234
Q

Pertussis (Whooping cough) organism

A

Caused by Bordetella pertussis, a gram negative pleomorphic bacillus

235
Q

Treatment of pertussis

A

Macrolide antibiotics (azithromycin, clarithromycin, or erythromycin)

erythromycin not recommended for neonates due to development of pyloric stenosis

Treatment during the catarrhal phase eradicates nasopharyngeal carriage of organisms within 3-4 days and may lessen symptoms

Treatment during the paroxysmal stage does not alter the course of the illness but decreases potential for spreading the disease to others.

Hospitalize young infants or any age group with moderate to severe resp distress, dehydration, or evidence of encephalopathy

Prevention: DTaP

236
Q

Rocky Mountain spotted fever organism

A

Infection with Riskettsia rickettsii, an obligate intracellular gram (-) coccobacillus, results in vasculitis

from ticks or blood transfusion (Rare)

237
Q

organism for Lyme disease

A

After inoculation of Borrelia burgdorferi spirochetes into the skin by the black-legged tisk, the organism disseminates to numerous organs → immune respone

238
Q

treatment for lyme

A

Treatment

Doxcycline for 10 days (10 days or less are safe and have not been proven to cause dental staining in children less than 8 years old), Amoxicillin for 14 days, or Cefuroxime for 14 days

Alternative therapy includes azithromycin for 14 days

Arthiritis is treated using the same oral regimen as for early localized disease but for 28 days. For persistent or recurrent arthritis, the doxy course should be repeated or IV ceftriaxone for 14-28 days

Mycoarditis is treated with IV cetriaxone for 14-21 days

CNS disease is treated with IV ceftriaxone for 14 days

239
Q

Treatment for Rocky Mountain spotted fever

A

Treatment: may take several weeks to resolve

**Treatment should not await serologic confirmation in the appropriate epidemiologic and clinical setting**

Doxcycline is favored for all ages of children for 7-10 days and continue until fever has ceased for 72 hours and clinical disease has resolved.

Fluoroquinolones may be effective

Chloramphenicol was the previous standard but it no longer recommended

240
Q

Viral Meningitis Treatment

A

Usually self limiting

However if HSV suspected to be the cause -Acyclovir IV

241
Q

Bronchilitis Pathogens

A

RSV

Adenovirus

influenza

parainfluenza

Human metapneumovirus (hMPV)

242
Q

How do you close a PDA

A

Endomethacin

243
Q

Common heart defects in Down syndrome

A

AV septal defect

VSD

PDA
TOF

244
Q

Which meningitis has

increased protein and low glucose in CSF

A

Bacterial

245
Q

which type of meningitis

has WBC <100 on CSF

A

Viral

246
Q

acidosis and hypercarbia _____ pulmonary vascular resistance which can cause worsening hypoxia.

A

increase

247
Q

Suspicious for meningitis

CSF contains RBC in a non-bloody tap

what does this mean

A

Suspicious for HSV meningitis. Start Acyclovir

248
Q

what syndrome commonly has TOF

A

DiGeorge

249
Q

what syndrome goes with cardiomyopathy

A

Noonans

250
Q

Viral causes of myocarditis

A

specifically

Coxsackie Viruses A and B

Parvovirus B19 and Human Herpesvirus type 6

not as common, Adenovirus

EBV

Hepatitis C

influenza

parainfluenza

HIV

CMV

unusual for herpes to be isolated and most commonly parvovirus or coxsackie viruses are isolated.

Critical Care I (27 decks)

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