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Peds Cardiology > 9. Cardiac Intensive Care > Flashcards

9. Cardiac Intensive Care Flashcards

1
Q

When is PVR lowest?

A

Functional residual capacity

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2
Q

What happens to PVR at lung volumes below functional residual capacity?

A

Increases due to reactive vasoconstriction

*Underinflation of lungs, atelectasis and alveolar hypoxia

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3
Q

What happens to PVR at lung volumes above functional residual capacity?

A

Increases due to secondary vasoconstriction from vascular stretch

*Overinflation and increased airway pressure

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4
Q

What can cause an elevated SVC pressure without an elevated LA pressure?

A
  1. Anything that impedes pulmonary blood flow or cases distortion of PA (thombus)
  2. Elevated PVR
  3. Pleural effusion
  4. Atelectasis
  5. Hyperinflation
  6. PV stenosis
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5
Q

What can cause an elevated SVC pressure + elevated LA pressure?

A
  1. Pericardial tamponade
  2. JET
  3. Ventricular dysfunction
  4. Severe AVVR
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6
Q

What can happen to a Glenn patient with elevated SVC pressures?

A

Systemic desaturation due to opening of vestigial veins that drain venous blood to heart

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7
Q

What types of surgeries have a higher incidence of post-operative JET?

A
  1. ToF repair
  2. VSD repair
  3. CAVD repair
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8
Q

Management of JET?

A
  1. Hypothermia
  2. Diminish catecholamines (sedation)
  3. Anti-arrhythmic agents with goal of AV synchrony: Amiodarone, procainamide
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9
Q

What tachydysrhythmia is more common in patients with asplenia?

A

EAT

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10
Q

What anatomy should you think of with DORV, common AV canal, PA, TAPVR?

A

Asplenia

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11
Q

What post-op complication would you consider for all these scenarios:

  1. 2 m/o s/p truncus repair
  2. 6 m/o s/p TGA/VSD repair
  3. 5 m/o s/p CAVD repair
  4. Neoante infracardiac TAPVR repair?
A

Post-op pulmonary HTN

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12
Q

Expected CVP & LA pressure following ToF repair?

A

Elevated CVP
Normal LA pressure

*Restrictive RV physiology

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13
Q

Expected CVP & LA pressure following TAPVR repair?

A

LA pressure > CVP

*LA/LV noncompliant and borderline hypoplasic… higher filling pressure needed

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14
Q

Expected CVP & LA pressure following TGA repair?

A

LA pressure > CVP

*Some degree of LV dysfunction (moreso older patients)

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15
Q

Expected CVP & LA pressure following ALCAPA repair?

A

LA pressure > CVP

*LV dilated with significant dysfunction causing elevated filling pressure

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16
Q

Expected CVP & LA pressure following CoA + VSD repair?

A

LA pressure > CVP

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17
Q

What are the expected changes in CVP and LA pressure in pulmonary HTN?

A

Elevated CVP

Normal or slightly elevated LA pressure

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18
Q

What would AP collaterals, residual VSD following repair, LV dysfunction and coronary ischemia due to filling pressures (LA pressure)?

A

Increase

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19
Q

Describe the 2 phases to HTN following coarct repair

A
  1. Surgical stimulation of sympathetic nerve fibers in tissue of aortic isthmus… release of epi/norepi
  2. After initial 24 hours, increase in renin and elevated diastolic pressure, also assocaited with mesenteric arteritis
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20
Q

What can be done in the pre-operative period to manage initial post-op HTN in patients after CoA repair?

A

Propranolol (neutralizes norepi and epi release following surgery)

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21
Q

Causes of elevated PA pressure after Fontan with an abnormal transpulmonary gradient (>5)?

A
  1. Elevated PVR
  2. PA distortion (thrombus)
  3. Pulmonary issues (pleural effusion, pneumothorax, atelectasis)
  4. Pulmonary venous obstruction
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22
Q

Causes of elevated PA pressure after Fontan with a normal transpulmonary gradient (but normal LA pressures)?

A
  1. Ventricular dysfunction
  2. Diastolic dysfunction (unfavorable mass/volume changes)
  3. AVVR
  4. Subaortic stenosis
  5. AV dyssynchrony
  6. Pericardial effusion
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23
Q

What can cause giant V waves on a CVP tracing?

A

TR

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24
Q

A-wave on CVP tracing caused by?

A

Atrial contraction

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25
Q

C-wave on CVP tracing caused by?

A

Ventricular contraction against closed tricuspid valve (valve bulges into RA)

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26
Q

V-wave on CVP tracing?

A

Atrial filling

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27
Q

X descent on CVP tracing?

A

Due to tricuspid valve being pulled way from RA during ventricular systole (follows the c-wave)

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28
Q

Y descent on CVP tracing?

A

Blood filling RV

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29
Q

What causes cannon a waves on CVP tracing?

A
  1. RA contracting against an obstructed tricuspid valve- TS, RA masses, RA myxoma, complete heart block, AV dyssynchrony
  2. Resistance to RV filling- Pulmonary HTN or PS
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30
Q

Equation for oxygen excess omega?

A

Oxygen excess omega = Oxygen delivery/Oxygen consumption

or

Oxygen excess omega = SaO2/(SaO2 – SvO2)

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31
Q

Which mediators are decreased in pulmonary HTN?

A
  1. Prostacyclin
  2. Matrix metalloproteinases
  3. NO
  4. Thrombomodulin
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32
Q

Which mediators are increased in pulmonary HTN?

A
  1. TGF-B
  2. Endothelin
  3. Serotonin
  4. Thromboxane A2
  5. Von Willebrand factor
  6. P-selectin
  7. Plasminogen activating inhibitor
  8. Fibrinopeptide A
  9. Tissue plasminogen activator
  10. Angiotensin II
  11. Epinephrine
  12. Insulin-like growth factor
  13. Basic fibroblast growth factor
  14. Platelet-derived growth factor A
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33
Q

What needs to be ruled out prior to initiating management for post-operative pulmonary HTN?

A

Any residual VSD

*Reducing PVR with a significant residual VSD can exacerbate hemodynamic instability

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34
Q

What do class I antiarrhythmics do?

A

Block fast Na channels (local membrane stabilizing activity)

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35
Q

What class antiarrhythmic are quinidine, procainamide, disopyramide?

A

IA

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36
Q

What do the IA antiarrhythmics do?

A

Moderate phase 0 depression/immediate slowing of conduction/prolongation of repolarization/ prolongation of AP and effective refractory period

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37
Q

What class antiarrhythmics are lidocaine, mexiletine, phenytoin?

A

IB

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38
Q

What do the IB antiarrhythmics do?

A

Minimal phase 0 depression/little slowing of conduction/shortening of repolarization/shortening of AP and effective refractory period

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39
Q

What class antiarrhythmics are flacainide, encainide, propafenone?

A

IC

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40
Q

What do the IC antiarrhythmics do?

A

Marked phase 0 depression/marked slowing of conduction/little effect on repolarization/little effect on AP and effective refractory period

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41
Q

What are the class II anti-arrhythmics?

A

B-blockers

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42
Q

Which class of antiarrhythmics prolongs the duration of the cardiac action potential and repolarization, but not conduction (the block K channels)?

A

Class II

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43
Q

Name 3 class III anti-arrhythmics

A
  1. Amiodarone
  2. Sotalol
  3. Bretylium
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44
Q

What class of antiarrhythmics blocks slow Ca channel and increases the effective refractory period of the AV node, slows conduction and rescues automaticity of the sinus/AV nodes?

A

Class IV

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45
Q

What class of antiarrhythmic is verapamil?

A

Class IV

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46
Q

MOA of ASA?

A

Acetylation of cyclo-oxygenase to inhibit production of thromboxane A2, a platelet aggregator

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47
Q

MOA of Heparin?

A

Mucopolysaccharide that increases the rate at which antithrombin III neutralizes thrombin, factor X and also IX, XI, and XII

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48
Q

MOA of Streptokinase?

A

Interacts with plasminogen to result in plasmin complex

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49
Q

MOA of TPA?

A

Binds to fibrin

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50
Q

MOA of Warfarin?

A

Interferes with posttranslational modification of vitamin K dependent coagulation factors (II, VII, IX, X and proteins C and S

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51
Q

Name causes of a low CVP

A
  1. Pressure transducer above level of heart
  2. Low intravascular volume
  3. Inadequate preload
  4. Transducer improperly calibrated
  5. Catheter malfunction
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52
Q

Causes of reduced O2 saturation in the RA?

A
  1. Increased O2 extraction
  2. Catheter tip in CS
  3. Anemia
  4. Decreased arterial O2 saturation with normal A-V O2 difference
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53
Q

What does increased O2 delivery do to O2 saturation in the RA?

A

Increases it

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54
Q

Causes of increased O2 saturation in the RA?

A
  1. Atrial level L-R shunt
  2. Anomalous pulmonary vein
  3. LV-RA shunt
  4. Increased O2 delivery
  5. Decreased O2 extraction
  6. Increased dissolved O2 content
  7. Catheter tip position near renal vein
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55
Q

What types of VSD are most likely to result in complete heart block following repair?

A
  1. Canal-type VSD with straddling tricuspid valve

2. Perimembranous VSD (bundle of His courses posterior-inferiorly to defect)

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56
Q

What type of VSDs have the least likely risk for heart block following repair?

A

Muscular/subpulmonary

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57
Q

Following repair of what defect would you expect tachycardia and elevated LA pressures?

A

TAPVR

Left sided strictures are borderline hypoplastic and non-compliant

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58
Q

What is neosynephrine?

A

Pure alpha agonist

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59
Q

When is neosynephrine useful?

A

Decreased pulmonary blood flow in the presence of an unrestrictive VSD or single ventricle (increases SVR and results in increased pulmonary blood flow)

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60
Q

What should be done for an infant with ToF absent PV in respiratory distress?

A

Prone- Can decrease proximal airway obstruction

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61
Q

Why do infants with ToF absent PV have significant respiratory distress?

A
  • Enlarged main and branch PAs compress the proximal airways

- Distal airway disease due to serpiginous pulmonary arterioles encircling the distal bornchioles

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62
Q

Angiotensin II, leukotrienes C4, D4, E4, prostaglandin F2alpha, thromboxane A2, and serotonin all do what to the pulmonary vasculatures?

A

Vasoconstrict

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63
Q

Acetylcholine, bradykinin, prostaglandins E1, E2 and I2, and NO all do what to the pulmonary vasculature?

A

Vasodilate

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64
Q

True or False: Epinephrine, norepinephrine, endothelins, histamine and prostaglandin D2 can have variable effect on the pulmonary circulation?

A

True

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65
Q

What should be done first in a Fontan with elevated PA pressures and tolerable hemodynamics?

A

Echo- Assess for pericardial tamponade and function

  • CXR to assess pulmonary parenchyma
  • If echo/CXR normal, can do cath to rule out thrombosis and stenosis of PAs
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66
Q

Why is milrinone risky in a baby with complete mixing physiology and a BP of 68/22?

A

-Reduced CPP

  • BP shows wide pulse pressure/low diastolic pressure suggesting excessive PBF
  • IV milrinone will cause afterload reduction and lower diastolic even more, which will decrease CPP
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67
Q

What would you consider for an infant with complete mixing physiology and a BP of 68/22?

A
  • IV dopamine
  • pRBCs
  • Volume
  • Decreasing sedation
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68
Q

What are potential findings after a Ross-Konno?

A
  • Residual VSD or RVOT narrowing: LVOT enlarged using a patch
  • Poor LV function: Concentric hypertrophy due to AS, suboptimal myocardial protection during bypass
  • Coronary ischemia: Coronary implantation
  • Neo-AI
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69
Q

True or False: Pulmonary HTN following Ross-Konno is uncommon and unexpected?

70
Q

What are 4 potential causes of elevated LA pressure and tachycardia in a 4 week old after ASO/VSD closure?

A
  • Pericardial tamponade: Elevated RA/LA pressures + Tachycardia
  • JET: Elevated filling pressures due to AV dyssynchrony
  • LV may be unprepared at 4 weeks with higher filling prsesures
  • Myocardial depression from bypass or coronary transfer
71
Q

True or False: AP collaterals can result in elevated LA pressure in a TGA patients?

A

False- May have AP collaterals that result in some LV volume loading, but unlikely to cause an elevated LA pressure

72
Q

JET is more common in infants with corrective surgeries involving what?

A

VSD closure

73
Q

Infants with asplenia or repair of TAPVR have an increased likelihood of what arrhythmia?

74
Q

What factors suggest post-operative re-entrant SVT?

A
  • Sudden onset

- Response to adenosine

75
Q

V-tach in the post-operative period is usually associated with what?

A

Myocardial ischemia

76
Q

What types of CHD have increased association with ischemic bowel syndrome?

A
  • Left-sided obstructive lesions: HLHS, CoA, AS
  • Truncus: Runoff to PAs and truncal regurgitation result in low diastolic pressure and suboptimal perfusion to mesenteric tract
77
Q

True or False: ToF is unlikely to be associated with ischemic bowel syndrome?

A

True

*Especially in absence of excessive pulmonary blood flow from AP collaterals

78
Q

What inotrope increases myocardial oxygen consumption the least?

A

Milrinone

*Doesn’t usually increase HR or BP (which are components of rate pressure index)

79
Q

What is an indirect determinant of myocardial oxygen consumption?

A

Rate pressure index

80
Q

What are 2 components of rate pressure index?

81
Q

What are the 3 assumptions used when calculating Qp:Qs in single ventricle physiology patients?

A
  1. a-v O2 difference between aorta and mixed venous source is 25%
  2. No significant pulmonary venous desaturation (PV sat is 95-100%)
  3. Aortic and PA saturations are equal (aortic by pulse ox)
82
Q

What is the equation for Qp:Qs?

A

Ao-MV saturation/PV-PA saturation

83
Q

After a bidirectional Glenn, what can cause increased SVC pressure with a large transpulmonary gradient?

A
  • Elevated PVR
  • Pulmonary venous obstruction
  • Pulmonary issues: Pleural effusion, pneumothorax, thrombosis within cavopulmonary circuit
84
Q

Poor ventricular compliance could raise SVC pressure, but what other pressure would also be increased?

85
Q

What are the 3 most common risk factors for irreversible pulmonary HTN?

A
  • Increased pulmonary blood flow
  • Increased PA pressure
  • Cyanosis

*Others include pulmonary hypoplasia and pulmonary venous hypertension

86
Q

What are some forms of CHD that have the 3 most common risk factors for pulmonary HTN to persist after surgery (increased pulmonary blood flow, increased PA pressure, cyanosis)?

A
  • Older TGA
  • CAVC
  • Truncus
87
Q

What change in SVR can lead to a hypercyanotic spell in ToF?

A

Decreased SVR

*Leads to increased R-L shunting and cyanosis

88
Q

What are some options for management of a hypercyanotic spell?

A
  1. B-Blocker: Decrease HR/RVOT narrowing
  2. Neosynephrine (alpha agonist): Increase SVR and force more flow to pulmonary circulation
  3. O2: Helps if any issues from pulmonary dsiease
  4. Fluids/pRBCs: Increase flow out narrowed RVOT and improve oxygenation
89
Q

What would happen if isoproterenol was used during a hypercyanotic spell?

A

Could exacerbate cyanosis

  • Vasodilator: Decreased SVR
  • Tachycardia
90
Q

What are etiologies for elevated LA pressures?

A
  1. LA outlet obstruction (mitral stenosis)
  2. LV dysfunction (systolic or diastolic)
  3. Hypoplasia of LV
  4. Pericardial tamponade
  5. AV dyssynchrony
91
Q

What type of RV pathophysiology is seen after ToF repair?

A

Restrictive

*RV is noncompliant and has significant diastolic dysfunction

92
Q

What is the relationship between pericardial volume and pressure?

A

Curvilinear

*Pericardial pressure doesn’t increase with volume until a certain volume threshold is reached, then the pressure rapidly increases with further increase in volume

93
Q

What causes HTN after a CoA repair?

A

Excess catecholamines

94
Q

What is often used to treat HTN after CoA repair?

A

B-blockers: Esmolol

-Vasodilators like nitroprusside or hydralazine can also be used

95
Q

What should be considered as a cause for desaturation in a child with Glenn physiology?

A

Decompressing venous collaterals

*Any increase in PVR can open these

96
Q

How does a low paCO2 result in desaturation in a Glenn patient?

A
  • Low PaCO2 will reduce cerebral blood flow

- This then indirectly reduces pulmonary flow which reduces saturation

97
Q

What pharmacologic agents have an efficacy for JET?

A
  1. Amiodarone
  2. Procainamide
  3. Digoxin

*Adenosine may help diagnose, but won’t treat

98
Q

What non-pharmacologic interventions help with JET?

A
  1. Hypothermia

2. Sedation

99
Q

If you plot lung volumes on the X axis and PVR on the Y axis, what shape is the curve?

100
Q

True or False: An infant with moderate TR can have a dilated RA without significantly elevated RA pressure?

A

True

*Relatively compliant RA

101
Q

What happens to the atrial pressures in restrictive cardiomyopathy?

102
Q

True or False: A large pericardial effusion will have low RA pressures?

A

False- Elevated

103
Q

In chronic dilated cardiomyopathy, what happens to the atrial pressures?

104
Q

What needs done after TAPVR repair with an elevated PASP and normal LA pressure?

A

Echo or cath to rule out any residual PV obstruction

*Pulmonary HTN occurs often, but gradient needs evaluated

105
Q

What must be done prior to starting therapy for pulmonary HTN (iNO, milrinone, sildenafil, etc) after TAPVR repair?

A

Ensure there is no residual PV obstruction

106
Q

What can be used in the setting of catecholamine-resistant shock after CPB?

A
  • Vasopressin
  • Steroids
  • Thyroxine
  • ECMO
107
Q

What is commonly seen on ECG following ToF and Truncus repair?

A

RBBB

-Significant incisions into RV muscle

108
Q

What is commonly seen on ECG following subaortic muscle resection?

109
Q

Q waves in I and aVL?

110
Q

True or False: It is normal to see Q waves on ECG following ASO?

111
Q

What is the equation for transpulmonary gradient?

A

PA pressure - LA pressure

112
Q

What does it tell you if a simultaneous PA wedge and ventricular end-diastolic pressure have no gradient?

A

No stenosis of AV valve or pulmonary venous anatomy

113
Q

True or False: If the transpulmonary gradient is elevated, the PVR is likely elevated?

114
Q

Improvement in diastolic function or lusitropy will have what effect on stroke volume?

A

Increase it

115
Q

Abnormal diastolic function and very dilated atria with intact systolic function should make you think of what?

A

Restrictive cardiomyopathy

*Atrial pressures are elevated and affect the PA pressures often resulting in pulmonary HTN

116
Q

What are some morbidities associated with restrictive cardiomyopathy?

A
  • CVA
  • Atrial tachydysrhythmias
  • Sudden death
117
Q

What are vasoconstrictors that are part of the group of mediators that compromise the neurohumoral response in heart failure?

A
  1. Angiotensin II
  2. Arginine vasopressin
  3. Endothelin
  • Vasoconstrictors that result in cardiac stimulation and fluid retention
  • Norepinephrine also stimulates the heart as part of this response
118
Q

What 2 effects do BNP have?

A
  1. Vasodilation

2. Natriuresis

119
Q

ECG with diminished voltages, T-wave flattening and T-wave inversions following cardiovascular collapse should make you think of what?

A

Myocarditis

120
Q

ALCAPA ECG?

A

Q waves in I and aVL

121
Q

What is the main clue to EAT?

A

Abnormal P-wave axis

*But could be in sinus region mimicking sinus tachycardia

122
Q

What are 3 properties of milrinone?

A
  1. Afterload reduction
  2. Inotropy
  3. Lusitropy
123
Q

What is an explanation for desaturation and cyanosis after surgical ASD closure?

A

IVC baffle: Inadvertent closure of ASD by sewing patch to Eustachian valve

*In an IVC-confluent secundum ASD, the posterior rim of the septum primum is often absent and the defect may be contiguous with the IVC

124
Q

What is seen during cath if during ASD closure, a patch is sewn to the Eustachian valve accidentally?

A

Catheter from femoral vein will enter LA, but not SVC or right heart

125
Q

What echo finding is most specific for cardiac tamponade?

A

Diastolic collapse of RA/RV

*RA/RV are compliant, so increased intrapericardial pressure leads to collapse when the intracavitary pressures are only slightly higher than those in the pericardium

126
Q

What causes RA collapse in diastole during tamponade?

A
  • At end-diastole (atrial relaxation), the RA volume is minimal, but pericardial pressure maximal
  • This causes the RA to buckle
127
Q

When does RV collapse occur in tamponade physiology?

A

Early diastole

*When RV volume is still low

128
Q

True or False: RV collapse is more specific than RA collapse in tamponade physiology?

129
Q

What circumstances might you not see RV collapse in tamponade physiology?

A
  • RV is hypertrophied

- RV diastolic pressure greatly elevated

130
Q

LA collapse occurs in what % of patients with hemodynamic compromise due to tamponade?

131
Q

When can LV collapse be seen in tamponade physiology?

A

Cases of regional cardiac tamponade

*Overall less common since LV wall more muscular

132
Q

What is IVC plethora and what does it reflect?

A
  • Dilation and <50% reduction in diameter during inspiration

- Marked elevation in CVP

133
Q

What change in the IVC can be seen in patients with cardiac tamponade?

A

IVC plethora- Dilation and <50% reduction in diameter during inspiration

134
Q

Qp:Qs equation?

A

SaO2-SvO2 – SpvO2-SpaO2

135
Q

For Qp:Qs calculation in complete mixing physiology, what assumptions are made?

A
  • SaO2 = SpaO2

- SpvO2 = 100%

136
Q

What would expect in a patient with complete mixing physiology and low SVR?

A

Cyanosis

-Poor pulmonary blood flow

137
Q

How do you manage cyanosis in a patient with complete mixing physiology?

A
  • Increase afterload (alpha-agonist)

- Lower PVR (iNO)

138
Q

How do you manage inappropriately high saturations in a patient with complete mixing physiology?

A

-Decrease afterload

139
Q

What are the most common infusion reactions to IVIG?

A
  • Fever
  • Chills
  • Rash
  • Hypotension
140
Q

What can worsen hypotension after IVIG is given for myocarditis?

A

The use of other afterload reducing heart failure medications

141
Q

Hypotension following IVIG infusion can develop in what time-frame?

A

1-6 hours from onset of infusion

142
Q

Why are antiplatelets/anticoagulation used in severe heart failure?

A

Can get embolic events from apical or LA thrombus

143
Q

Describe persistent pulmonary HTN of the newborn?

A
  • Elevated PVR due to lung disease (prematurity, meconium aspiration, etc)
  • Leads to R-L shunting via PDA due to elevated PVR and persistent fetal circulation
144
Q

What measures help with PPHN?

A
  • Mechanical ventilation
  • Antibiotics
  • iNO
  • ECMO
145
Q

What should ventricular dysfunction and ventricular ectopy in a neonate post-ASO make you think of?

A

Coronary ischemia

146
Q

How is echo helpful in assessing for coronary ischemia post-ASO

A
  • Rule out other issues like tamponade
  • Assess for ventricular dysfunction
  • Assess for new valvular regurgitation (due to papillary muscle ischemia)

*Coronary origins very hard to see after reimplantation

147
Q

What would you expect on ECG for a neonate with coronary ischemia following ASO?

A

Regional ischemic pattern (ST-T changes)

148
Q

How is definitive diagnosis of coronary ischemia following ASO made?

A

Cath or CTA

149
Q

What is the recommended management of infracardiac TAPVR?

A

Surgery

*Septostomy not recommended b/c only palliative and delays surgery

150
Q

How might TAPVR present?

151
Q

What should you always confirm on Echo prior to cannulating an infant to ECMO if able?

A

Pulmonary veins

*Veins become very hard to see once on ECMO

152
Q

What is the role of PGE in TAPVR?

A

Can be harmful- increases PBF and reduces PVR which can exacerbate pulmonary venous congestion

153
Q

Transient AV block following cardiac surgery is seen in what % of patients?

154
Q

What proportion of patients will have return of AV conduction and in what time frame following transient AV block after surgery?

A
  • Half

- Around 3 days

155
Q

The incidence of permanent complete AV block is highest with repair of what?

A
  • Lesions near AV node
  • Membranous and inlet VSDs
  • L-TGA
  • AVCD
  • ToF
156
Q

If sinus rhythm doesn’t return after how many days will it most likely not return following post-operative AV block?

A

7 days

*Recommend pacemaker implantation for post-op AV block that persists for at least 7 days following surgery

157
Q

What is a rare complication of surgical closure of a PDA what would result in left lung oligemia?

A

Ligation of the LPA

  • CT chest would show a poorly vascularized left lung, residual PDA and ligated LPA
  • Angio would have minimal flow to left lung
158
Q

What should raise your suspicion of inadvertent ligation of the LPA during surgical closure of the PDA?

A

Asymmetric pulmonary blood flow

159
Q

What physiological changes happen with sternal closure?

A
  • Decreased SV
  • Decreased CO
  • Decreased mean BP
  • Decreased cerebral oxygenation
  • Increased intrathoracic pressure
  • Decreased total lung compliance
160
Q

What does an open chest help with?

A
  • Decompression of the heart

- Minimizes tamponade physiology

161
Q

How fast and how long do you atrial overdrive pace to convert atrial flutter?

A

70% atrial cycle length
3-4 seconds

*If you don’t have pacing wires, can use esophageal pacing

162
Q

Why is a burst rate of 70% the atrial cycle length used to convert atrial flutter?

A

To avoid risk of deterioration into atrial fibrillation

163
Q

What is the initial maximal dose of iNO to achieve therapeutic pulmonary vasodilatory effect?

A

20ppm

*Higher doses associated with increased risk of side effects and no improvement in outcomes

164
Q

What are side effects of iNO?

A
  • Systemic hypotension
  • Methemoglobinemia
  • Rebound pulmonary HTN upon weaning
  • Elevated nitrous oxide
165
Q

How does systemic HTN and decreased stroke volume change pressure-volume loops?

A

-Taller and narrower

  • Systemic HTN (increased aortic pressure) will increase afterload… this increases LV pressure required to open aortic valve
  • Aortic valve closes at a higher end-systolic pressure which (without change in inotropic state) yields reduced stroke volume (decreased width of pressure-volume loop)
  • End-systolic pressure-volume relationship (contractility slope) remains unchanged
166
Q

What medication can be used in the case of systemic HTN and decreased stroke volume to improve hemodynamics?

A

Sodium nitroprusside

167
Q

What are agents that increase SVR/afterload and decrease stroke volume?

A
  • Phenylephrine
  • Vasopressin
  • Epinephrine
168
Q

What effects does sodium nitroprusside have?

A

Decrease afterload
Improve stroke volume
Improve cardiac output

169
Q

What effect do B-blockers have?

A
  • Slow HR
  • Improved diastolic ventricular filling
  • Improved coronary artery flow
170
Q

Equation for EF?

Peds Cardiology (20 decks)

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