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VF1 - Block 3 > Week 1/2 > Flashcards

Week 1/2 Flashcards

1
Q

Main systems that determine BP

A
  • Heart
  • Vasculature
  • Kidney
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2
Q

Blood Pressure equation

A

BP = CO x TPR

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3
Q

Cardiac Output definition

A

HR x SV

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4
Q

What affects Stroke volume

A
  • Contractility
  • Preload
  • Afterload (TPR)
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5
Q

What affects afterload?

A

TPR

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6
Q

Most important determinant of cardiac role in BP

A

Stroke volume (more than HR)

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7
Q

Most important receptor for BP in vasculature

A

alpha-1

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8
Q

Kidney’s contribution to BP relies on what system?

A

RAAS

Renin

Angiotensin

Aldosterone

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9
Q

What does renin do?

A
  • Converts angiotensinogen (produced by liver) to angiotensin 1
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10
Q

Why is renin secreted? From where?

A
  • The juxtaglomerular cells in the kidney monitor blood flow and sodium content
  • If they sense low blood flow, they secrete renin
  • If they sense low sodium content, they secrete renin
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11
Q

What converts angiotensin 1 to angiotensin 2?

A

angiotensin converting enzyme

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12
Q

What does angiotensin 2 do?

A
  • RAISES BP
  • Causes vasoconstriction through activation of sympathetic nervous system
  • Causes release of aldosterone, which promotes sodium retention to increase blood volume
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13
Q

How does sympathetic NS impact BP?

A
  • Beta-1 receptors increase HR and contractility (SV)
  • alpha-1 receptors cause vasoconstriction
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14
Q

Current guideline for hypertension

A

greater than 130

greater than 80

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15
Q

135/70 BP diagnosis

A
  • Hypertension b/c 135 is greater than 130
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16
Q

Elevated BP

A

Systolic: 120-129

Diastolic: Less than 80

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17
Q

Stage 1 HT

A

Systolic: 130 - 139

Diastolic: 80 - 89

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18
Q

Stage 2 HT

A

Systolic: greater than 140

Diastolic: greater than 90

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19
Q

Essential vs. Secondary hypertension

A
  • Essential = no identifiable cause
  • Secondary = secondary to something else
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20
Q

Drivers of essential hypertension in young people

A
  • high diastolic BP
  • Cardiac Output main contributor
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21
Q

Drivers of essential hypertension in older adults

A
  • high systolic BP
  • TPR main driver
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22
Q

Clues for secondary hypertension

A
  • Younger than 30 or over 50
  • VERY high BP
  • Abrupt onset after years of controlled BP
  • ABDOMINAL BRUIT
  • They’re on more than THREE BP meds and it’s still uncontrolled
  • Excessive hypokalemia (think hyperaldosteronism)
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23
Q

Diseases associated with abdominal bruit

A
  • Renal artery stenosis
  • Fibromuscular dysplasia
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24
Q

What is abdominal bruit?

A
  • turbulent blood flow in renal artery due to occlusion
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25
Q

Illness script fibromuscular dysplasia

A
  • Young woman, super high BP, hear abdominal bruit on exam
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26
Q

Aorta coarctation physical exam findings

A
  • Weak or absent pulse in the lower extremities
  • Upper extremity BP is much greater than lower extremity
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27
Q

Pheochromocytoma

A
  • Pheochromocytoma is a tumor on adrenal glands causing too much NE release
  • Overactivation of B1, alpha1 –> increased BP
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28
Q

Classic symptoms of pheochromocytoma

A
  • Bursts of headaches, palpitations, anxiety, sweating
  • CHECK CHATECHOLAMINE LEVELS
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29
Q

High BP, low K+ levels

A
  • Hyperaldosteronism
  • Aldosterone causes increased sodium retension and increased potassium EXCRETION.
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30
Q

Hyperaldosteronism

A
  • High BP, LOW K+, low renin
    • Renin will also be low b/c the tumor itself is releasing aldosterone
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31
Q

Major drug classes used to treat high BP

A
  • Diuretics
  • Beta blockers
  • Calcium channel blockers
  • RAAS agents
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32
Q

Types of diuretics

A
  • thiazide diuretics
  • Loop diuretics
  • K+ sparing diuretics
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33
Q

Mechanism of thiazide diuretics

A
  • Block sodium reabsorption in distal tubule
  • Decreased blood volume –> decreased BP
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34
Q

Mechanism of loop diuretics

A
  • Block sodium reabsorption in loop of Henle
  • Shorter duration than Thiazide diuretics, so less used for hypertension
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35
Q

K+ sparing diuretics mechanism of action

A
  • Block effect of aldosterone in kidney
  • Used very specifically for patients with hyperaldosteronism
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36
Q

Prerequisite for using diuretics

A
  • Normal renal function
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37
Q

Side effects of thiazide diuretics

A
  • hyponatremia
  • hypokalemia
  • hyperuricemia –> gout
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38
Q

side effects of K+ sparing diuretics

A
  • HYPERkalemia b/c aldosterone –> K+ excretion
  • Block aldosterone –> block K+ excretion
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39
Q

Do NOT use these types of hypertension drugs on someone with asthma

A

Beta blockers

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40
Q

Types of calcium channel blockers

A
  • dihydropyridines
  • non-dihydropyridines
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41
Q

dihydropyridine mechanism of action

A
  • block smooth muscle contraction
  • Vasodilation
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42
Q

non-dihydropyridine mechanism of action

A
  • block AV node conduction velocity
  • Decrease contractility and HR
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43
Q

RAAS agent types

A
  • ACE inhibitors
  • Angiotensin 2 blockers
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44
Q

ACE inhibitors mechanism of action

A
  • Block conversion of antiogensin 1 to angiotensin 2 by blocking ACE (angiotensin converting enzyme)
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45
Q

Angiotensin 2 blockers mechanism of action

A
  • Block angiotensin 2 from binding its receptor
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46
Q

Side effects of ACE inhibitors

A
  • DRY COUGH due to increased bradykinin
    • Bradykinin is also broken down by ACE. Inhibiting ACE –> increased bradykinin
  • Increased K+ due to decreased aldosterone
  • TERATOGENIC
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47
Q

Side effects of angiotensin 2 blockers

A
  • No cough like ACE inhibitors
  • Still teratogenic, still increased K+
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48
Q

Ideal HT drug for someone who is salt sensitive

A

Thiazide diuretics

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49
Q

Drug commonly prescribed for diabetes patients for HT

A

ACE inhibitors

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50
Q

Hydrochlorothiazide, chlorthalidone

A

thiazide diuretics

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51
Q

Furosemide, Torsemide, Bumetanide

A

loop diuretics

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52
Q

Spironolactone and eplerenone

A

K+ sparing diuretics (aldosterone antagonists)

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53
Q

metoprolol, bisoprolol, carvedilol, and labetalol

A

Beta blockers

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54
Q

Diltiazem, verapamil

A

calcium channel blockers

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55
Q

lisinopril, captopril, enalapril, ramipril

A

ACE inhibitors

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56
Q

losartan, valsartan, olmesartan, candesartan

A

angiotensin 2 receptor inhibitors

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57
Q

HT Medication side effects

A
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58
Q

Overview of BP control mechanisms

A
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59
Q

First line treatment for HT

A

Diuretics

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60
Q

ACE inhibitors

A
  • “pril”
  • Captopril
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61
Q

ARBS

A
  • angiotensin 2 receptor blockers
  • “sartan”
  • Losartan
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62
Q

aldosterone receptor inhibitors (K+ sparing diuretics)

A
  • eplerenone
  • spironolactone
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63
Q

aliskiren

A

Direct renin inhibitor

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64
Q

Propranolol

A
  • Beta blocker
  • Beta1 and beta2
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65
Q

Metoprolol

A
  • B1 blocker
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66
Q

carvedilol and labetalol

A
  • Blocks beta and alpha1 receptors
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67
Q

Beta blocker side effects

A
  • hypotension
  • bradychardia
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68
Q

Verapamil and Diltiazem

A
  • calcium channel blockers
  • non-dihydropyridines
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69
Q

side effects/contraindications with calcium channel blockers

A
  • Main side effect: constipation due to inhibition of GI smooth muscle contraction. Also causes peripheral edema.
  • Contraindicated in reduced ejection fraction heart failure or w/ other drugs that also ¯ cardiac contractility/rate/AV conduction.
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70
Q

Nifedipine

A
  • calcium channel blocker
  • dihydropyridine
  • Only acts on vasculature to vasodilate (no impact on cardiac conduction)
  • If BP falls rapidly, then cardiac rate will increase (baroreceptor reflex, leading to ↑ SNS activity to heart and reflex tachycardia).
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71
Q

Drug most responsible for drug-induced hyponatremia

A
  • Thiazide diuretics
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72
Q

Diuretic side effects

A
  • hyponatremia
  • hypokalemia
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73
Q

Step 2 Drugs

A
  • Sympatholytics that do NOT involve beta-blockade
    • Clonidine
    • Reserpine
    • Prazosin
  • Direct acting vasodilaters
    • hydralazine
  • Nitrovasodilaters
    • nitroglycerin
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74
Q

Prazosin

A
  • Selective alpha1 blocker
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75
Q

Unique side effect of prazosin

A
  • “First dose faint effect”
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76
Q

minoxidil

A
  • Mechanism not completely understood:
    • Opens K+ATP channels causing hyperpolarization of VSMC resulting in vasodilation.
    • Possible NO donor.
  • Therapeutic use:
    • Hypertension
    • Androgenic alopecia (Rogaine®)
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77
Q

Vasa vasorum

A
  • Large arteries
  • Large veins
  • Found in tunica adventitia
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78
Q

Large arteries vs. large veins

A
  • Arteries = Very thick tunica media (elastin)
  • Veins = much thinner media
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79
Q

Inner elastic lamina

A
  • Medium arteries
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80
Q

Valves are characteristic of…

A
  • Medium veins
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81
Q

veins

A
  • Valves
  • Irregular-shaped lumen
  • thinner tunica media than arteries
  • thick tunica adventitia (connective tissue)
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82
Q

3 types of capillaries

A
  1. Continuous
  2. Discontinuous
  3. Fenestrated
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83
Q

Where are continuous capillaries found?

A
  • Skeletal muscle
  • lung
  • CNS
  • connective tissue
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84
Q

where are discontinuous capillaries found?

A
  • Intestinal tract
  • endocrine glands
  • kidney
  • pancreas
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85
Q

where are fenestrated capillaries found?

A
  • liver
  • spleen
  • bone marrow
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86
Q

pericyte

A
  • stem cells that can form new endothelial cells
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87
Q

AV valve histology

A
  • Made of collagen
  • Stains blue on trichrome stain
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88
Q

Goal of primary hemostasis

A
  • Formation of the platelet plug
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89
Q

Goal of secondary hemostasis

A
  • Formation of the fibrin clot/hemostatic plug
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90
Q

fibrinolysis

A
  • The process of removing a clot
91
Q

First response of vasculature to injury

A

Vasoconstriction

92
Q

Glycoprotein 1b

A
  • Found on platelet surface
  • Adheres to Von Willebrand Factor on exposed endothelium
  • Allows platelets to adhere to damaged vessel wall and then begin aggregating
93
Q

Glycoprotein 2b/3a

A
  • Found on platelet surface
  • Exposed during platelet activation
  • Allows platelets to bind to each other (aggregate)
94
Q

What clotting factor does VWF carry?

A

Factor VIII

95
Q

Where is VWF found?

A
  • Endothelium
  • platelet granules
  • Plasma
96
Q

What does VWF do?

A
  1. Promotes adherance of platelets to endothelial lining
    1. Binds collagen and then GP1b binds VWF to adhere to collagen
  2. Promotes aggregation
    1. GP2b/3a on activated platelets bind VWF. VWF provides bridge for platelets to aggregate.
97
Q

What is Tissue Factor? Where is it found?

A
  • Found on damaged endothelium
  • Starts off the clotting cascade (external pathway)
98
Q

Factor VIII

A
  • Cofactor
  • Complexes with Factor IXa to activate Factor X –> Xa
99
Q

Tenase

A
  • Factor ten cleaving complex
  • Factor VIIIa + Factor IXa activate Factor X (to Xa)
100
Q

Prothrombinase

A
  • Factor Va + Factor Xa
  • Together they activate prothrombin –> thrombin
101
Q

Factor Va

A
  • Cofactor
  • Complexes with Factor Xa (protease) to activate prothrombin
102
Q

Tissue Factor Pathway Inhibitor

A
  • Inhibits Tissue Factor/7a complex at the very beginning of the extrinsic pathway
  • Also inhibits Xa
  • The main extrinsic pathway regulator
103
Q

Protein C/Protein S

A
  • Degrades 8a and 5a
  • Inhibits coagulation pathway
104
Q

Antithrombin

A
  • anticoagulant
  • inhibits thrombin plus some others
105
Q

plasmin

A
  • Breaks down the clot
106
Q

Stages of clotting

A
  • Primary hemostasis
    • Formation of the platelet plug
  • Secondary hemostasis
    • Formation of the fibrin clot
  • Termination/attenuation
    • Inhibitors of coagulation
  • Fibrinolysis
    • Plasmin system
107
Q

Clotting cascade

A
108
Q

Factor V Leiden

A
  • The most common mutation causing thrombosis
  • Factor 5 becomes resistant to inactivation by Protein C
109
Q

Prothrombin gene mutation

A
  • Causes increased production of prothrombin –> increased clotting
110
Q

Antithrombin deficiency

A
  • Causes thrombosis
111
Q

How does heparin work?

A
  • Works with antithrombin to inactivate thrombin
  • If antithrombin is deficient, heparin does not really work
112
Q

Protein C/S deficiency

A
  • These are anticoagulants
  • They inhibit Factor V and Factor VIII activation
  • lack of them –> thrombosis
113
Q

Common risk factors for VTE

A
114
Q

Which tests for thrombosis can be used any time and which cannot?

A
  • Any time: genetic tests
  • Not any time: Protein C, S, and antithrombin levels are affected by acute clots and anticoagulation medication, so you need to test them at the right time to get accurate readings.
115
Q

How long to treat with anticoagulants?

A
  • Transient risk factors: 3 months
  • Persistent risk factors (inflammatory bowel, cancer): indefinitely
116
Q

Virchow’s triad that leads to thrombosis

A
  1. Vascular injury
  2. Hypercoagulability
  3. Circulatory stasis
117
Q

What does thrombin feed back to activate?

A
  • 11
  • 5
  • 8
118
Q

tPA

A
  • tissue plasminogen activator
  • The enzyme that converts plasminogen to plasmin
119
Q

Main antiplatelet drugs

A
  • ADP Receptor Antagonists
  • NSAIDS
  • Glycoprotein Antagonists
120
Q

Clopidegrol/Plavix

A
  • Antagonist for ADP receptor on platelets –> blocks platelet activation
  • Used for prevention of acute MI
121
Q

Aspirin

A
  • Antiplatelet drug –> antithrombotic
  • Inhibits production of thromboxane = inhibits platelet aggregation
122
Q

Abciximab

A
  • Antiplatelet drug = antithrombotic
  • Antibody that binds glycoprotein 2a/3b (“ab”) –> fibrin cannot crosslink
123
Q

Eptifibatide

A
  • Antiplatelet drug = antithrombotic
  • Mimics structure of fibrin = competitively inhibits glycoprotein 2a/3b
  • Derived from snake venom
124
Q

Tirofiban

A
  • Antiplatelet drug = antithrombotic
  • Antagonizes glycoprotein 2b/3a
  • Used up to 18 hours after acute MI
125
Q

Summary of antiplatelet drugs

A
126
Q

Antithrombotics that target Xa

A
  • RivaroXaban
  • ApiXaban
  • Fondaparinux
127
Q

Antithrombotics that inhibit thrombin

A
  • Argatroban
  • Bivalirudin
  • DaBigatran
128
Q

Anticoagulant drugs

A
  • Antithrombotics
129
Q

Heparin

A
  • anticoagulant
  • Helps antithrombin work
  • Inhibits thrombin and Factor Xa
  • Side effect: Heparin-induced Thrombocytopoenia (HIT)
  • Must be given via IV
130
Q

Low molecular weight heparins

A
  • Anticoagulant
  • “parin” =
  • Enoxaparin (Lovenox®)
  • Dalteparin (Fragmin®)
  • Much smaller than heparin
  • Easier absorption and administration
  • Given SubQ instead of IV
131
Q

Argatroban

A
  • Anticoagulant
  • Directly inhibits thrombin
  • Derived from leeches
132
Q

Dabigatran/Pradaxa

A
  • Anticoagulant
  • Oral direct thrombin inhibitor
  • No blood testing or monitoring like warfarin
133
Q

Warfarin/Coumadin

A
  • Anticoagulant
  • Inhibits vitamin K epoxide reductase –> less reduced vitamin K in your system –> cannot form clotting factors 2, 7, 9, 10
134
Q

Concerns/side effects of warfarin

A
  • Must limit dietary intake of vitamin K (leafy greens)
  • Lots of drug interactions
  • Need frequent blood testing
  • Genetic polymorphisms of CYP2C9
135
Q

Direct Xa inhibitors

A
  • Anticoagulants
    •Rivaroxaban (Xarelto®)*
  • •Apixaban (Eliquis®)*

•Edoxaban (Savaysa®)*

136
Q

Thrombolytic drugs/clot busters

A

Plasmin-dependent

  • Tissue Plasminogen Activator
    • Recombinant-tPA
  • Streptokinase
    • Enzyme secreted by bacteria
  • Urokinase
    • Urinary-type PA

Direct fibrinolytic

  • Originally purified from venom of Agkistrodon contortrix (Copperhead snake)
    • Alfimeprase
    • Fibrolase
137
Q

Pulmonary hypertension critera

A
  • Pulmonary Artery pressure greater than 20 mmHg
138
Q

Main symptoms of pulmonary hypertension

A

shortness of breath, lightheadedness

139
Q

Pathology of pulmonary hypertension

A
  • Heart problems
  • Lung disease
140
Q

Pathology of pulmonary arterial hypertension

A
  • Problem with the pulmonary vasculature itself
141
Q

CTEPH

A
  • Chronic thrombembolic pulmonary hypertension
  • A category of pulmonary hypertension
  • Due to incomplete resolution of acute thrombosis –> clot in the lungs = blockage of vasculature
142
Q

What are the 5 groups of pulmonary hypertension?

A
  1. Pulmonary arterial hypertension
  2. Pulmonary hypertension due to cardiac disease
  3. PH due to lung disease
  4. CTEPH
  5. Multifactorial mechanisms
143
Q

Signs of pulmonary hypertension

A
  • Edema in the lower extremities
    • Due to right heart failure/back pressure from the pulmonary vasculature
  • Enlarged liver (right side organ problems) –> ascites
144
Q

What is the pathologic change characteristic of pulmonary arterial hypertension?

A
  • plexiform lesions
145
Q

Diagnostic criteria for pulmonary arterial hypertension

A
  • mean pulmonary arterial pressure greater than 20 mmHg AND
  • left wedge pressure less than 15 mmHg
  • pulmonary vascular resistance greater than 3 wood units
146
Q

What is the result of heart looping?

A
  • Atria located more posteriorly, ventricles located more anteriorly
147
Q

truncus arteriosus becomes

A
  • aorta and pulmonary artery
148
Q

bulbus cordis becomes

A
  • ventricular outlets
149
Q

primitive ventricle becomes

A

inlet of the ventricles

150
Q

primitive atrium becomes

A

right and left atria

151
Q

sinus venosus becomes

A

part of the right atrium

152
Q

Foramen ovale is formed by a hole between what?

A
  • septum secundum
153
Q

The flap that closes over the foramen ovale after birth is what structure?

A
  • septum primum
154
Q

The foramen ovale shunts blood from where to where?

A
  • right atrium to left atrium
  • Oxygenated blood comes in to right atrium from umbilical vein. Oxygenated blood goes to left atrium to aorta and out to the body. Bypasses pulmonary artery for the most part.
155
Q

AVSD (atrio-ventricular septum defect) is a result of what embryological problem?

A
  • Septation of the AV canals
156
Q

Septation of the AV canal forms what?

A
  • tricuspid valve
  • mitral valve
157
Q

Muscular ventricular septum defects result from…

A
  • Problems with ventricular septation
158
Q

What fuses during ventricular septation?

A
  • Muscular interventricular septum and the endocardial cushion
159
Q

d-transposition of the great arteries results from what developmental problem?

A
  • Bulbus cordis and truncus arteriosus fail to twist/spiral
  • Makes RV continuous with the pulmonary artery and the LV continuous with the aorta
160
Q

Normal fetal circulation

A
  • Oxygenated blood from umbilical vein travels up through the fetus
  • Some of it bypasses the liver via the ductus venosus to travel up to right atrium
  • Right atrium receives oxygenated blood from inferior vena cava and deoxygenated blood from superior vena cava. They mix in r. atrium.
  • Mostly oxygenated blood is shunted from r. atrium to l. atrium through the foramen ovale
  • Some mixed blood makes it to the r. ventricle and is pumped out the pulmonary artery.
  • A small amount of pulmonary artery blood goes to the lungs. Most of it is shunted to the descending aorta via the ductus arteriosus.
161
Q

What closes the foramen ovale?

A
  • PVR falls right when baby takes first breath
  • Leads to more blood going to lungs and then returning to left atrium
  • left atrial pressure rises –> closes the flap
162
Q

Blue babies have what diagnosis?

A
  • d-transposition of the great arteries
163
Q

Classic presentation of blue babies

A
  • Tachypneic (breathing rapidly) but not struggling
  • Low oxygen saturation
  • Usually they look fine until the ductus arteriosus closes
164
Q

What is the hyperoxia test? What is the purpose?

A
  • Give baby oxygen for 10 minutes and watch the oxygen saturation
  • If baby is cyanotic due to heart problems, the oxygen saturation will not change. If due to lung problems, the oxygen saturation should go up.
165
Q

What is the role of prostaglandin E1?

A
  • Maintains ductus arteriosus opened
166
Q

Pathophysiology of d-transposition of the great arteries

A
  • aorta comes off right ventricle
  • Pulmonary artery comes off left ventricle
  • Result: deoxygenated blood returns to right atrium and gets sent back to body. Oxygenated blood circulates between left side of the heart and the lungs. There are 2 separate circuits that do not mix.
167
Q

Treatment of d-transposition of the great arteries

A
  • Prostaglandin E1 immediately
  • Balloon atrial septostomy
  • Long term: arterial switch operation
168
Q

Cause of tetralogy of fallot

A
  • anterior deviation of the coronal septum
169
Q

4 things seen with tetralogy of fallot

A
  1. Ventricular septal defect
  2. pulmonary artery stenosis
  3. right atrial hypertrophy
  4. overriding aorta
170
Q

cause of truncus arteriosus

A
  • the bulbus cordus and truncus arteriosus do not divide (remember, they divide and then they twist during fetal development)
  • This is a defect in the septation of the embryonic truncus
171
Q

Result of truncus arteriosus

A
  • a common trunk from which the aorta, pulmonary artery, and coronary arteries are derived
  • Also see a VSD
172
Q

pathophysiology of tetralogy of fallot

A
  • Increased resistance due to subpulmonic stenosis causes deoxygenated blood (from systemic veins) to shunt right to left (from RV to aorta) causing systemic hypoxemia (cyanosis)
  • Amount of shunting depends on degree of RV outflow tract obstruction as well as changes in systemic and pulmonary vascular resistances
173
Q

what’s the treatment for tetralogy of fallot?

A
  • Surgical
  • Patch the hole between right and left ventricles
  • Relieve RV outflow obstruction either by resecting the muscle bundles leading to the PA or by cutting away the PA valve itself
174
Q

cause of total anomalous pulmonary venous return

A
  • the pulmonary veins do not make it back properly to the left atrium. They drain abnormally.
  • Result: complete mixture lesion
175
Q

cause and result of tricuspid atresia

A
  • the tricuspid valve never forms
  • result: you only have a single ventricle b/c you do not develop a right ventricle
  • Complete mixture lesion
    • Blood from RA goes into foramen ovale and mixes with left side of heart
176
Q

gray babies diagnosis

A
  • coarctation of the aorta
177
Q

signs of gray baby

A
  • tachypneic WITH grunting/struggling
  • High oxygen saturation
  • Pulse is nearly absent, particularly in lower extremities
178
Q

what happens to the flow of blood with coarctation of the aorta?

A
  • The flow is obstructed –> increased afterload
  • Diminished function of the left ventricle
179
Q

Why does the coarcted baby get worse when the ductus arteriosus closes?

A
  • the ductus arteriosus is very close to the coarctation usually
  • That opening provides more space for blood flow. The narrowing is worse after the ductus closes.
180
Q

5 T’s of cyanotic congenital heart disease

A
  1. d-transposition of the great arteries
  2. tetralogy of fallot
  3. truncus arteriosus
  4. total anomalous pulmonary venous return
  5. tricuspid atresia
181
Q

3 left to right shunt lesions

A
  1. ventricular septal defect
  2. atrial septal defect
  3. patent ductus arteriosus
182
Q

what determines amount of left to right shunting in a large VSD?

A
  • systemic vascular resistance
  • pulmonary vascular resistance
183
Q

What is the pathophysiology of a large VSD?

A
  • Babies present around 6-8 weeks of age with heart failure (dilated pulmonary artery, dilated left atrium, dilated left ventricle)
  • Pulmonary vascular resistance is still high until about 6-8 weeks of age. While pulmonary resistance is high, blood continues going out the aorta, which is normal.
  • Once pulmonary resistance drops, the blood shunts to right ventricle and goes through aorta.
184
Q

why is the left side of heart and pulmonary artery dilated with a large VSD?

A
  • The shunt happens in systole, so the blood does not stay in the right ventricle basically at all.
  • It gets pumped from left ventricle straight back to pulmonary arteyr, so the PA, LA, and LV are getting more flow as a result of the hole
185
Q

What does the size of the shunt depend on for ASDs?

A
  • size of the hole
  • filling properties (compliance) of the ventricles
186
Q

ASD’s present with…

A

These are usually asymptomatic in children. Picked up by an astute clinician.

187
Q

Why is ASD a left to right shunt lesion?

A
  • The diastolic pressure in the LV is always higher than the diastolic pressure in the right ventricle
  • RV is more compliant than LV
  • Pushes blood from LA to RA
188
Q

Size of the shunt in a patent ductus arteriosus depends on what

A
  • pulmonary vascular resistance
  • arterial vascular resistance
189
Q

pathophysiology of a patent ductus arteriosus

A
  • Systemic vascular resistance is higher than pulmonary vascular resistance in a baby
  • Blood shunts from the aorta to the pulmonary artery
190
Q

Cardiac impact of patent ductus arteriosus

A
  • Dilated left atrium and left ventricle b/c you get more blood flow through the pulmonary artery –> more blood from to LA and LV
191
Q

How does a large PDA present?

A
  • Congestive heart failure around 6-8 weeks for same reason as VSD heart failure
192
Q

cause of Eisenmenger syndrome

A
  • Results from chronic left to right shunt due to unrepaired congenital heart disease
193
Q

Eisenmenger syndrome results

A
  • severe cyanosis due to extremely high pulmonary vascular resistance –> left to right shunting reverses to right to left shunting over time.
  • very high PVR causes the right to left shunting –> deoxygenated blood going through aorta –> cyanosis
194
Q

Kawasaki Syndrome

A
  • Acquired heart disease
195
Q

cause of kawasaki syndrome

A
  • unknown, but genetic predisposition
  • current theory: autoimmune disorder
196
Q

How is a kawasaki syndrome diagnosis made?

A
  • First criteria: High and persistent fever for greater than 5 days
  • Then they must have 4 of 5 additional features:
    • Polymorphous rash
    • Conjunctivata erythema (redness of the eyes)
    • strawberry tongue
    • swelling in hands and feet
    • isolated cervical lymph node
197
Q

what is the major problem with kawasaki syndrome?

A
  • coronary artery aneurysms
198
Q

Treatment for kawasaki syndrome (acute and chronic)

A
  • Acute: IGG infusions, aspirin
  • Chronic: aspirin
199
Q

normal aortic pressure range

A

80 - 120 mmHg

200
Q

normal pulmonary artery pressure range

A

10 - 25 mmHg

201
Q

Pressure in the large veins (vena cava, etc)

A

4 mmHg

202
Q

What drives flow in the cardiovascular system?

A
  • Pressure drop between the outlet and inlet sides of the heart
  • i.e. aortic (arterial) pressure is greater than venous pressure
203
Q

typical flow (cardiac output) through cardiovascular system

A

5 L/min

204
Q

rate pressure product

A
  • RPP = HR x Systolic BP
  • Mirrors Power = CO x mean pressure difference
  • A change in RPP reflects a change in myocardial oxygen demand
205
Q

Myocardial oxygen demand is determined by… and is important because…

A
  • Determined by cardiac power (Power = CO x mean pressure difference)
  • Myocardial oxygen demand determines coronary artery flow demand
206
Q

Normal value for End Diastolic Volume

A

120 mL

207
Q

Normal value for End systolic Volume

A

40 mL

208
Q

Normal value for end aortic diastolic pressure

A

80 mmHg

209
Q

Normal value for peak systolic aortic pressure

A

120 mmHg

210
Q

Normal value for end diastolic left ventricular pressure

A

5 mmHg

211
Q

How to calculate ejection fraction

A
  • The amount of blood ejected from the heart over the total amount of volume in the heart
  • Ejection Fraction = Stroke volume/EDV
212
Q

Pulse pressure

A
  • The difference between systolic and diastolic BP
  • Normal = 120 - 80 = 40
213
Q

Normal ejection fraction

A

55 - 70%

214
Q

3 Fetal shunts

A
  1. Ductus venosus
  2. foramen ovale
  3. ductus arteriosus
215
Q

ductus venosus

A
  • Shunts oxygenated blood from umbilical vein (oxygenated) to inferior vena cava during fetal development to bypass the liver
216
Q

foramen ovale

A
  • shunts blood from right atrium to left atrium during fetal development, bypassing the lungs
217
Q

ductus arteriosus

A
  • fetal shunt
  • Deoxygenated blood from SVC returns to RA and some of it still goes to RV (despite foramen ovale), which is then pumped to pulmonary artery
  • most of the blood pumped to pulmonary artery is shunted through ductus arteriosus to the descending aorta
218
Q

blue babies vs. gray babies

A
  • Blue babies = cyanotic
    • d-transposition of the great arteries
    • tetralogy of fallot
    • Total anomalous venous return
    • tricuspid atresia
  • Gray babies = congestive heart failure
    • coarctation of the aorta
    • aortic stenosis
    • mitral stenosis
    • hypoplastic left heart syndrome
219
Q

5 T’s of congenital heart disease

A
  • d-transposition of the great arteries
  • tetralogy of fallot
  • truncus arteriosus
  • total anomalous pulmonary venous return
  • tricuspid atresia
220
Q

The most common cause of cyanotic congenital heart disease in the neonatal period

A

d-transposition of the great arteries

221
Q

Most common cyanotic congenital heart disease after infancy (post neonatal)

A

tetralogy of fallot

222
Q

dry cough side effect of what drug class?

A

ACE inhibitors

223
Q

most common mutation causing thrombosis

A

Factor V Leiden

VF1 - Block 3 (7 decks)

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