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Neo Board Review MAP > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Heart arises from

A

Mesoderm

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2
Q

Heart formation complete by

A

8 weeks

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3
Q

Tube formation

A

First phase of heart formation

Day 15 to 21

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4
Q

Looping

A

Second phase of heart formation
Day 21-28
Determines left/right
Distinct chambers appear

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5
Q

Septation

A

Third phase of heart formation
Day 34–46
Atrial and ventricular septum appear

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6
Q

Fetal circulation

A

Oxygened DV blood enters RA and flows across FO (due to the velocity and angle) into the LA
This oxernnated blood goes to heart (coronary arteries), brain, upper body

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7
Q

Fetal shunts

A

Foramen ovale

Patent ductus arteriosus

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8
Q

Which ventricle provides most of the cardiac output in utero?

A

Right ventricle

= hypertrophied in utero and immediately after birth

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9
Q

What percentage of total blood volume is supplied by each ventricle in utero?

A

RV 70%

LV 30%

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10
Q

What % of total blood volume goes to fetal lungs in the 2nd trimester?

A

10%

3rd trimester - increases to 35%

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11
Q

Which side of the intrauterine heart has higher oxygen saturations?

A

Left side

= Higher oxygenated blood from the umbilical vein shunted across PFO to LA

SVC/IVC blood returns to RA and has low oxygen saturations

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12
Q

Fetal oxygenation in various vessels

A

Uterine artery 98%
Uterine vein 76%
Umbilical vein 68%
Umbilical artery 30%

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13
Q

Fetal compensation for hypoxemic environment

A
  1. Increased fetal EPO
  2. Fetal hemoglobin causes a left shift in oxyhemoglobin curve
  3. Decreased oxygen consumption
    - maternal thermal regulation
    - minimal respiratory effort
    - minimal G.I. digestion/absorption
    - decreased renal tubular reabsorption
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14
Q

In utero, pressures on both sides of the heart are ___?

A

Equal

Due to large communications between atria and great vessels

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15
Q

Fetal regulation of cardiac output

A

Adjustment in fetal HR is the primary mechanism of changing CO in utero

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16
Q

What needs to happen in order for the fetus to transition effectively?

A
  1. Increase in pulmonary blood flow
  2. Distinction between systemic and pulmonary circulations
  3. Switch in ventricular roles
  4. Separation from umbilical and placental circulations
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17
Q

Closure of the PDA after birth is due to:

A

Higher O2 concentration within ductal tissue

Lower amount of E type prostaglandins

  • increased pulmonary blood flow = increased metabolism of PGE in lungs
  • loss of PGE from placenta

Bradykinin from lungs at birth -> vasoconstriction of PDA


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18
Q

Why does umbilical vein constrict?

A

Due to lack of flow once umbilical cord is clamped

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19
Q

Why do umbilical arteries constrict?

A

Because of high oxygen, similar to PDA

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20
Q

When do most structural cardiac anomalies develop by?

A

Eight weeks gestation

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21
Q

What determines growth of the heart and blood vessels in utero?

A

Amount of flow through the vessel or chamber

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22
Q

Right sided obstructive lesion in utero

A

Systemic CO is the same
- more blood across PFO with growth of LV
- usually has VSD with R -> L shunting

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23
Q

Left sided obstructive lesion in utero

A
  • Shift of blood volume from L to R at FO
  • Left sided hypoplasia with growth of RV (now provides all of CO)
  • Often with VSD, which increases L -> R shunting further
  • Intracardiac mixing -> slightly decreased O2 to brain/coronary
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24
Q

Causes of hypoxemia in utero

A

Decreased O2 delivery to placenta

  • maternal hypoxemia
  • decreased uterine blood flow

Placental issue

  • impaired O2 diffusion
  • inadequate placental surface

Umbilical cord issue
- decreased blood flow

To compensate blood flow preferentially goes to heart, brain, and adrenal glands

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25
Q

Fetal compensation for hypoxemia

A

Fetus goes into hibernation mode

  • suppressed respirations
  • bradycardia
  • decrease in CO

O2 uptake does not change significantly

Fetal O2 delivery can be reduced by 50% without significant effect on O2 uptake

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26
Q

What are three determinants of stroke volume?

A

Preload
Afterload
Contractility

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27
Q

Preload

A

Degree of cardiac myocyte stretch at the end of diastole

= Volume in the ventricle at the end of filling = end diastolic volume (EDV)

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28
Q

Afterload

A

Tension/stress that develops in the LV wall during ejection (to push blood out)

Ventricular wall stress = (ventricular P x ventricular radius) / Wall thickness

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29
Q

Contractility

A

Force and velocity of a contraction

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30
Q

Frank Starling principle

A

Increased LV diastolic filling (Inc preload) -> increased stroke volume (pumping ability of the heart)

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31
Q

Qp/Qs < 1

A

Right to left intracardiac shunt (i.e. tricuspid atresia)

  • Lower amount of pulmonary blood flow
  • Qp/Qs < 1
  • Qp/Qs < 0.7 suggests a large shunt



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32
Q

Hypotension vs shock

A

Hypotension: when blood pressure is less than the expected reference range
- tissue perfusion may still be adequate

Shock: when there is decreased tissue perfusion
- usually BP is low but not always

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33
Q

Contributors to shock

A

Low cardiac output
Abnormal vasomotor tone
Low tissue oxygenation

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34
Q

Causes of low cardiac output

A

Low HR
Low SV

High HR can also cause -> decreased ventricular filling time -> decreased preload

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35
Q

Causes of abnormal vasomotor tone

A

Tissue factors
Vascular factors
Neurohormonal factors

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36
Q

Causes of low tissue oxygenation

A

Low O2 delivery to alveoli
Poor lung perfusion
Low O2 caring capacity (low Hb)
Poor O2 release from Hb (left shift in oxyhemoglobin curve)

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37
Q

Hypovolemic shock

A

Most common type of neonatal shock
Occurs when intravascular BV is below a critical level -> poor ventricular filling

Decreased preload -> decreased SV -> decreased CO -> decreased BP -> inadequate tissue perfusion

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38
Q

Cardiogenic shock

A

Myocardial dysfunction leads to

  • Poor ventricular emptying
  • Poor cardiac filling

Decreased contractility -> decreased SV -> decreased CO -> decreased BP -> Inadequate tissue perfusion

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39
Q

Distributive shock

A

Severe vasodilation -> relative decrease in intervascular volume

Decreased SVR -> decreased BP -> inadequate tissue perfusion

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40
Q

Flow restrictive shock

A

Obstruction to cardiac output

Etiologies:
Tension pneumothorax
Cardiac tamponade
Left sided obstructive cardiac defect

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41
Q

Dissociative shock

A

Inadequate oxygen releasing capacity

Etiologies:
Profound anemia
Methemoglobinemia
Excessive carbon monoxide

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42
Q

Compensated neonatal shock

A

Blood flow distributed to brain, heart, adrenal glands expense of non-vital organ perfusion

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43
Q

Uncompensated reversible neonatal shock

A

Bloodflow decreases to all organs

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44
Q

Uncompensated irreversible neonatal shock

A

Irreversible cell damage

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45
Q

How does a neonate compensate for shock via increased blood volume?

A

Renin–angiotensin system increases water reabsorption and decreases urine volume

Autotransfusion = reabsorption of interstitial fluid into vasculature

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46
Q

Stages of uncompensated shock

A

Anaerobic metabolism = major source of energy

Release of chemical mediators (histamine, cytokines) -> decreased tissue perfusion

Capillary endothelium integrity disrupted -> loss of oncotic pressure

Sluggish blood flow -> activation of coagulation cascade -> bleeding

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47
Q

Alpha-2 adrenergic receptors

A

Decreased SVR

Inhibit adenylyl cyclase


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48
Q

Dopamine

A

Endogenous, precursor to epinephrine and norepinephrine
Beta-1 (medium dose) and alpha-1 receptors (high-dose)

Increased HR at medium dose
Increased contractility at medium dose
Increased SVR at high-dose
Increases BP via increased CO and SVR

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49
Q

Dobutamine

A 
Synthetic
Beta-1 and some beta-2

Mild increase in HR
Increases contractility
Decreases SVR
Increases BP by increased CO (increased SV)
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50
Q

Epinephrine - extra effects

A

Increases lactate due to increased glycogenolysis

High Dose epi leads to increased SVR during diastole and improvement in coronary artery perfusion

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51
Q

Norepinephrine

A

Beta-1 and Alpha-1, some beta-2
Similar to high dose epi
Decreases HR (inc vagal tone on SA and AV nodes)
Increases contractility
Increases SVR
Increases BP because of increased SVR

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52
Q

Milrinone

A

Phosphodiesterase type 3 inhibitor -> increased cAMP similar to Beta stimulation

Decreases SVR more than dobutamine
Increase in contractility

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53
Q

Principles of cardiopulmonary circulation

A

Pulmonary and systemic circulations are separate, balanced, flow in series, and each has its own ventricle

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54
Q

Left to right shunt

A

Oxygenated blood from the left side crosses to the right and returns to lungs

Flow to lungs > flow to body
Qp > Qs
Tachypnea, failure to thrive, congestive heart failure

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55
Q

Right to left shunt

A

Deoxygenated blood crosses to the left, bypasses the lungs, and joins the systemic circulation

Flow to the lungs < flow to the body
Qp < Qs
Cyanosis, acidosis, tachypnea

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56
Q

Factors that increase PVR

A 
…And decrease Qp
Pulmonary vasoconstriction
- hypoxia
- acidosis
Increased interstitial pressure
- atelectasis
- pulmonary edema
- pneumothorax/pleural effusion
- mechanical ventilation
- excess PEEP
Lung hypoplasia
Polycythemia
57
Q

Factors that decrease PVR

A 
Pulmonary vasodilation
- alkalosis
- oxygen
- nitric oxide
- sildenafil
Alveolar expansion
58
Q

Simple mixing cardiac lesions

A

PDA, ASD, VSD
Qp and Qs are not separate and can be unbalanced

There is mixing of pulmonary and systemic venous return with a net left to right shunt

Not ductal dependent

No differential between upper and lower saturations

Present with varying degrees of congestive heart failure

59
Q

Pathophysiology of a neonatal PDA

A 
Falling PVR
Pulmonary overcirculation
Pulmonary hypertension
Diastolic runoff
Increased cardiac work
60
Q

Treatment of simple mixing cardiac lesions

A

Decrease workout breathing with diuretics
Support growth
Support cardiac function (+/- digoxin)
Judicious use of oxygen

Repair:
ASD at 3-5 years of age, earlier if worsening chronic lung disease or ventilator dependence

VSD after six months of age

61
Q

Complex mixing cardiac lesions

A

Complete AV canal, truncus arteriosus, unobstructive TAPVR, single ventricles without outflow obstruction

No separation between Qp and Qs

62
Q

Complete AV canal

A

Primum ASD
Small to large VSD
Lack of separation of the mitral and tricuspid valves

One of the most common cardiac lesions in T21

Repair at 3 to 6 months

63
Q

Truncus arteriosus

A

Single outflow tract
Absence of a pulmonary valve (single S2)
Large truncal (aortic) valve
VSD
Pulmonary arteries arise from ascending aorta
A/W DiGeorge syndrome

Complete mixing of venous return
Can develop pulmonary hypertension

Repair at 1 to 2 weeks

64
Q

Unobstructed TAPVR

A

Pulmonary venous return drains into the right atrium (L -> R shunt) (or another vessel, but not LA)
Some flow crosses the ASD (R -> L shunt)
Complete mixing leads to lower saturations

Right heart enlargement and pulmonary overcirculation occurs as PVR drops

Repair at 2 to 6 months

65
Q

Treatment of complex mixing cardiac lesions

A

Decrease work of breathing with diuretics
Support growth
Support cardiac function (+/- digoxin)
Judicious use of O2 (sat goal 85%)

Surgical repair if CHF cannot be adequately treated and before pulmonary hypertension becomes irreversible

66
Q

Right sided obstructive heart lesion examples

A 
Tetralogy of Fallot
Tricuspid stenosis/atresia
Ebstein’s anomaly
Branch pulmonary stenosis
Supravalvar pulmonary stenosis
Pulmonary stenosis/atresia
67
Q

Tetralogy of Fallot

A 
PROVe
- pulmonary stenosis
- RVH
- overriding aorta
- VSD

Repair at 3–4 months


68
Q

What is a tet spell?

A

Infundibular spasm leading to severe obstruction in Qp

Symptoms are cyanosis, tachypnea, irritability, acidosis, cardiac arrest

69
Q

How to treat a tet spell

A

Decrease PVR: O2, iNO, morphine

Increase SVR - knees to chest

70
Q

R-sided obstructive heart lesion pathophysiology

A

Obstruction within the right heart leads to blue blood shunting to the left heart/systemic circulation -> cyanosis
Degree of obstruction determines the signs and symptoms
Severe obstruction requires the PDA to support pulmonary blood flow
- closure of PDA-> severe synosis and cardiogenic shock

Hallmark: R->L flow across PFO and mixing in the LV -> Pre-and post ductal hypoxemia

71
Q

Treatment of right sided obstructive heart lesions

A

Maintain ductal patency with PGE
Decrease oxygen demand
Support cardiac function
Judicious use of oxygen - goal sats 75-85% so that Qp/Qs=1

Surgical repair

  • provide a stable source of pulmonary blood flow and allow PDA to close
  • or if obstruction cannot be relieved, provide an alternative to the PDA
72
Q

Which right sided obstructive lesions require immediate catheter or surgical intervention after birth?

A

None, unless the PDA closes

73
Q

Left-sided obstructive heart lesion examples

A 
HLHS
Shones syndrome
Supravalvar aortic stenosis
Aortic stenosis/atresia
Mitral stenosis/atresia
Obstructed TAPVR
Coarctation of the aorta
Interrupted aortic arch
74
Q

HLHS

A 
Mitral stenosis/atresia
Hypoplastic L ventricle
Aortic stenosis/atresia
Hypo plastic aortic arch
ASD/PDA

Only way for blood to get to coronary arteries is via PDA and retrograde aortic flow

75
Q

Pathophysiology of left sided obstructive lesions

A

Obstruction within the left heart leads to:

  • oxygenated blood to the right heart and pulmonary circulation -> congestive heart failure
  • insufficient systemic flow leading to acidosis and cardiogenic shock

Severe obstructions require ductal support (PDA)
R->L flow across the PDA -> lower post-ductal saturations

76
Q

Left sided obstructive lesions that require immediate intervention after birth

A

HLHS with intact atrial septum and PDA

Obstructed TAPVR and PDA

77
Q

Treatment of left sided obstructive heart lesions

A

Maintain PDA
Support cardiac function
Decrease oxygen demand
Judicious use of oxygen, goal sats 75–85%

Surgical repair aims to

  • relieve the obstruction and get rid of the PDA
  • provide an alternative to the PDA
78
Q

Examples of single ventricles without outflow obstruction

A

Unbalanced AV Canal
Double Inlet left ventricle

Hypoplasia of one of the ventricles
No obstruction to flow to lungs or body

79
Q

Double inlet LV

A

Systemic and pulmonary venous return enter a single ventricle
Complete mixing of blood leads to lower saturations
As PVR drops pulmonary overcirculation develops
Similar physiology to complex mixing lesions

80
Q

Examples of single ventricle lesions with outflow instruction

A

HLHS

Pulmonary atresia

81
Q

d-TGA

A

Parallel circulations
Lack of intracardiac shunt and loss of PDA leads to severe cyanosis, acidosis, shock

Higher post-ductal sats of PDA present = reverse differential

82
Q

L-TGA

A

Congenitally corrected TGA

Increased risk of heart block

83
Q

Cardiac anomalies with Williams

A

Supravalvar AS
Branch PA stenosis


84
Q

Sinus rhythm on EKG

A

P-wave before every QRS
QRS after every P-wave
P-waves upright in leads I and aVF
All P-waves look the same

85
Q

Premature atrial contractions

A

Atrial myocyte initiates a beat between impulses coming from the sinus node
Early P-wave can be buried in T-wave
QRS also arrives early

86
Q

Premature ventricular contractions

A

Early QRS, usually wide or unusual
No P-wave
T wave axis is directly opposite the QRS axis
Compensatory pause afterwards

Reassuring if single morphology, isolated beats, suppresses with sinus tachycardia

87
Q

2nd degree heart block

A

Some atrial activity gets through to the ventricles
Atrial rate is normal
Ventricular rate/rhythm depends on how often the AV conduction occurs

88
Q

Complete heart block

A

No relationship between P and QRS waves
Ventricular rate remains regular and slow
Atrial rate is faster than ventricular rate but still normal

89
Q

Atrial flutter

A

Very fast atrial rhythm with slow ventricle rhythm
Sawtooth waves

Giving adenosine is diagnostic but not therapeutic

Electrical cardioversion or rapid atrial pacing will break the circuit
Recurrent a flutter - digoxin or propranolol

90
Q

Torsades

A

Polymorphic VT with oscillating pattern of the QRS axis

Treatment with IV magnesium sulfate

91
Q

Causes of prolonged QTc

A 
Hypocalcemia
Hypokalemia
Hypomagnesemia
CNS abnormalities
Myocarditis

Channelopathy
- >75% of LQTS caused by mutations in three genes (KCNQ1, KCNH2, SCN5A)

92
Q

Management of complete heart block

A

Require emergent pacing - neonate with CHF

Require pacemaker:

  • Mobitz II or third degree with symptoms, ventricular dysfunction, low CO
  • CHB with ventricular rate <55
  • CHB + CHD with ventricular rate <70
  • CHB with QRS escape or V dysfunction
93
Q

Most common type of tachyarrhythmia in a newborn

A

Atrio-ventricular re-entry tachycardia (AVRT)

A.k.a. WPW

94
Q

Wolfe-Parkinson-White

A

Accessory pathway permitting conduction across the AV valve

Delta wave present when the atrial impulse enters the ventricles via an accessory pathway

95
Q

Which structural defect is most commonly associated with an accessory pathway?

A

Ebstein’s anomaly

96
Q

EKG findings in Ebstein’s anomaly

A

Very tall P waves

97
Q

What causes increased preload?

A
  • increased circulating blood volume
  • increased venous tone (more BV back to heart)
  • increased ventricular compliance
  • increased atrial contractility
  • decreased intrathoracic pressure (increased venous return)
98
Q

Effect on afterload with ventricular dilation

A

If ventricle is dilated -> increased ventricular wall stress with greater tension on the myocytes -> increased afterload

99
Q

Effect on afterload with ventricular hypertrophy

A

If ventricle is hypertrophied (wall thickened) -> distributed across many cells -> decrease in afterload

100
Q

Qp/Qs > 1

A

Left to right intracardiac shunt (i.e. VSD)

  • Greater pulmonary blood flow
  • Qp/Qs > 1
  • Qp/Qs > 2 suggests a large shunt
101
Q

Etiologies of cardiogenic shock

A 
Cardiomyopathy
Heart failure
Arrhythmias
Perinatal depression (myocardial ischemia)
Acidosis
Sepsis
102
Q

Etiologies of distributive shock

A

Sepsis
Vasodilators
Adrenal insufficiency
Anaphylactic or neurogenic (adults)

103
Q

Alpha-1 adrenergic receptors

A

Increased SVR
Increased contractility

Activate phospholipase C

104
Q

Beta-1 adrenergic receptors

A

Increased contractility
Increased HR

Induce cAMP production

105
Q

Beta-2 adrenergic receptors

A

Decreased SVR
Bronchodilation

Induce cAMP production

106
Q

Low dose epinephrine

A 
Beta-1 and beta-2 (similar to dobutamine)
Increases HR
Increases contractility
Decreases SVR
Can either increase or decrease BP
107
Q

High-dose epinephrine

A 
Alpha-1 and beta-2 (similar to dopamine)
Decreases HR (inc vagal tone on SA and AV nodes)
Increases contractility
Greatly increases SVR
Increases BP due to increased SVR
108
Q

TOF with severe pulmonary stenosis

A

R->L shunt
O2 sats <90%
Leads to cyanosis, may be ductal dependent for Qp, tet spells

109
Q

TOF with mild pulmonary stenosis:

A 
L->R shunt through VSD as PVR drops
O2 sats >90%
Leads to:
- pulmonary overcirculation
- congestive heart failure
- failure to thrive
110
Q

Cause of pre-ductal hypoxemia in left-sided obstructive heart lesions

A

Occurs when there is minimal flow across aortic valve -> retrograde flow in the arch from the PDA

111
Q

Cardiac anomalies with Alagille

A

Branch PA stenosis
Pulmonic stenosis
TOF

112
Q

Cardiac anomalies with DiGeorge

A

VSD
Truncus arteriosus
TOF
Interrupted aortic arch

113
Q

Cardiac anomalies with Holt Oram

A

ASD

VSD

114
Q

Cardiac anomalies with Marfans

A

Aortic root dilation

Aortic valve prolapse

115
Q

Cardiac anomalies with Noonans

A

Pulmonary stenosis

TOF

116
Q

Cardiac anomalies with T21

A

ASD
VSD
Common AV canal

117
Q

Cardiac anomalies with Turners

A

Bicuspid aortic valve
Aortic stenosis
Coarctation
Interrupted aortic arch

118
Q

Causes of PACs

A 
Very common, usually benign
Increased vagal tone
Central line
Electrolyte abnormalities
Hypoxemia
Thyroid problems
Cardiomyopathy
Drugs (digoxin, caffeine, beta-agonist)
119
Q

Causes of PVCs

A 
Immature myocardium
Electrolyte problems
Metabolic disease
Cardiomyopathy
Intracardiac tumors
120
Q

2nd degree heart block - Wenckebach

A

Progressive PR prolongation -> dropped sinus beat -> short recovery PR

121
Q

2nd degree heart block -  Mobitz II

A

Normal PRs with a dropped sinus beat
Pathologic, can cause symptoms
May progress to complete heart block
Eval for LQTS, Myocarditis

122
Q

WPW and SVT

A
  • impulse begins in the atria
  • Circuit develops which involves the AV node and accessory pathway
  • abrupt onset and termination
  • fast (190-300) and regular
  • always 1:1 conduction
123
Q

Treatment of WPW

A

Vagal maneuvers or adenosine
If not effective cardioversion or rapid atrial pacing

Recurrent WPW SVT - Propranolol or digoxin

124
Q

Examples of automatic SVTs

A

Sinus tachycardia
Ectopic atrial tachycardia (EAT)
Multifocal atrial tachycardia
Junctional ectopic tachycardia

125
Q

Consider an automatic tachycardia if…

A

Heart rate increases and decreases gradually
Heart rate varies during the tachycardia
Rhythm doesn’t break with adenosine or cardioversion

126
Q

Treatment of automatic SVT

A

Vagal man. or adenosine only briefly inhibit conduction to ventricle
Electrical cardioversion does not stop tachycardia

RX: flecainide, amiodarone, sotalol
Want to slow atrial activity or decrease ratio of conduction across AV node

127
Q

Northwest left axis deviation on EKG

A

190 to -100
Negative QRS in leads I and aVF
Coarctation

128
Q

Right axis deviation on EKG

A

100 - 190
Negative QRS in lead I, positive QRS in lead aVF
Normal newborn axis
Right ventricular hypertrophy (TOF, coarct)

129
Q

Left axis deviation on EKG

A 
-100 to 0
Positive QRS in lead I, negative QRS in lead aVF
AV canal
Primum ASD
Tricuspid atresia

Also called superior axis deviation

130
Q

Normal axis on EKG

A

0-100

Positive QRS in lead I and aVF

131
Q

Which electrolyte abnormality causes Short QT?

A

Hypercalcemia

132
Q

Which electrolyte abnormality causes prolonged QT?

A

Hypocalcemia

133
Q

What electrolyte abnormality causes long PR, wide QRS, and peaked T waves?

A

Hyperkalemia

If worsens can have absent P-wave and sinusoidal asystole

134
Q

What electrolyte abnormality causes depressed ST, biphasic T-wave, and prominent U wave?

A

Hypokalemia

135
Q

How does a neonate compensate for shock via vasoconstriction?

A
  1. Decreased stimulation of baroreceptors in aortic arch and carotid sinus
  2. Chemoreceptors respond to cellular acidosis
  3. Catecholamine release
136
Q

What cardiovascular structure develops from the 3rd pharyngeal arch?

A

Carotid arteries

137
Q

What cardiovascular structure develops from the right 4th pharyngeal arch?

A

Subclavian artery

138
Q

What cardiovascular structure develops from the left 4th pharyngeal arch?

A

Aortic arch

139
Q

What cardiovascular structure develops from the left 6th pharyngeal arch?

A

PDA

Neo Board Review MAP (18 decks)

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