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CPR > Cardiology > Flashcards

Cardiology Flashcards

1
Q

3 determinants of arterial pressure

A
  1. Contractile properties of heart
  2. Vasculature properties
  3. Blood volume
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2
Q

Parasympathetic activity to heart causes…

A

Decrease in HR by decreasing spontaneous depolarization at SA node

Decreases contractility

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3
Q

Sympathetic activity to heart causes…

A

Increase HR and contractility

Increases disatolic filling and volume ejected = Increased SV

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4
Q

Baroreceptors

A

Located in aortic arch and carotid sinus

Detect blood pressure and send input to brain for regulation via solitary tract

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5
Q

Brain centers for BP regulation

A

Vasoconstrictor center

Cardiac Accelerator center

Cardiac decelerator center

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6
Q

Renin Angiotensin Aldosterone System

A

Renin converts Angiotensinogen –> Angiotensin I

ACE converts angiotensin I –> Angiotensin II

Angiotensin II = Vasoconstriction –> Increase TPR –> Increase pressure

Angiotensin II = Aldosterone release –> Na reabsorption –> water reabsorption –> Increase Blood volume and pressure

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7
Q

Anti Diuretic Hormone

A

Adds aquaporins to kidney nephron collecting tubule for increased water reabsorption

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8
Q

ANP

A

Atrial natiuretic peptide

Secreted in response to increased ECF

Causes vasodilation and sodium/water excretion —> Decrease BP

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9
Q

Continuous capillaries

A

Skeletal muscle, lungs, skin, fat, CT, nervous system

Endothelial cells overlap to form clefts

Clefts contain tight junctions for strict regulation of solute transport

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10
Q

Fenestrated capillaries

A

Gut mucosa, glomerulus, exocrine glands, ciliary body and choroid plexus

Contain fenestra to allow for more solute/fluid exchange

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11
Q

Discontinuous capillaries

A

Liver, spleen, bone marrow

Large openings to facilitate large transport of solutes and fluid and protein

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12
Q

Arteriolar Vasodilation and Starling

A

Causes increase in hydrostatic capillary pressure due to reduced pre/post capillary resistance

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13
Q

Long term standing/sitting and Starling

A

Increased artial/venous pressure = Increased hydrostatic pressure

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14
Q

Liver failure and starling

A

Reduced protein production = Decreased capillary oncotic pressure –> edema

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15
Q

Malnutrition and Starling

A

Decreased protein intake –> Decreased oncotic pressure –> edema

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16
Q

Late term pregnancy and starling

A

Reduced plasma protein –> decreased oncotic pressure –> edema

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17
Q

Functions of lymphatic system

A

Return filtered blood

Disease Defense

Transport absorbed fat

Return filtered protein

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18
Q

Venous return and how to increase it

A

Amount of blood that returns to right heart per minute

Increase sympathetic activity to veins (contract) = Increase VR

Muscle contraction pushes blood back through veins = Increase VR

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19
Q

Shift VR curve to right

A

Increase blood volume or venous tone

PVP increases –> VR increases

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20
Q

Filling phase of cardiac cycle

A

Begins with opening of mitral valve (Pa>Pv)

Begins with rapid filling, then slowed filling

SA node spontaneously depolarizes, atria excitation increases, P wave, adds some more volume to ventricle

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21
Q

Isovolumetric contraction phase

A

Pressure in ventricle rises

Pv > Patrium so mitral valve closes –> 1st heart sound

Pv < Paorta so aortic valve is closed

Volume remains the same but excitation has reached ventricles, QRS, so ventricle excitation occurs and pressure increases

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22
Q

End of diastole and beginning of systole

A

Closure of mitral valve

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23
Q

Ejection phase

A

Pv > Paorta so aortic valve opens and blood is ejected

Ventricular volume rapidly decreases

Decline in force over time = decreased level of active ventricular cells due to repolarization

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24
Q

Isovolumetric relaxation phase

A

Pv < Paorta so aortic volve closes –> 2nd heart sound

Pv > Patrium so mitral valve still closed

Ventricular cells decrease in activity with constant volume so pressure decreases

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25
Q

Right heart vs left heart cardiac cycle and pressures

A

Cardiac cycle phases are relatively similar

Pressure gradients are dramatically decreased

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26
Q

Tricuspid and mitral valve timing

A

Tricuspid valve closes after and opens before mitral valve

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27
Q

Pulmonary and aortic valve timing

A

Pulmonary valve opens before and closes after aortic valve

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28
Q

Cardiac action potential - Diastole/Rest

A

High permeability to Potassium so resting potential is negative

K-IR channels

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29
Q

Cardiac action potential - Action potential upstroke

A

Voltage Gated sodium channels open and huge influx of Na depolarizes cell

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30
Q

Cardiac action potential - Early repolarization

A

Fast inactivation of Na channels and increase in K permeability due to VGKC

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31
Q

Cardiac action potential - Plateau

A

Voltage Gated Calcium channels open and Ca influx

K permeability decreases - Mg blocks K-IR channels

Plateau of membrane potential due to combating electric forces

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32
Q

Cardiac action potential - Repolarization

A

Inactivation of Ca channels and voltage activation of K rectifier channels

Cell repolarizes

Channels inactivate as cell repolarizes

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33
Q

Purpose of high K permeability

A

Stabilizes resting membrane potential and requires large excitatory stimulus

Reduces risk of arrhythmias

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34
Q

Sympathetic activity and ventricular action potential

A

NE release –> B-adrenergic receptors –> PKA –> enhance activity of Ca, Kr, Ks ion channels

More calcium = stronger contraction

Shortens AP duration and time between beats

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35
Q

Ventricular AP ARP

A

No propagated action potentials can be elicited

Occurs right after rapid depolarization and ends towards end of repolarization

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36
Q

Relative refractory period

A

Larger than normal stimulus can initiate AP

Closer to end of RRP = stronger AP

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37
Q

Supranormal period (SNP)

A

Slightly smaller than normal stimulus elicits normal response

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38
Q

Full recovery time (FRT)

A

Time after which a normal action potential can be elicited with normal stimulus

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39
Q

Long QT syndrome

A

Repolarization of heart is delayed

Usually genetic with delayed rectifier K channels

MUtations cas delayed activation, reduced open probability, and insensitivity to PKA

Arrhythmias occur at higher heart rates b/c can’t shorten AP –> compromised filling

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40
Q

Na/K ATPase level in cardiac vs Skeletal muscle

A

Much more active contributing to higher K gradient

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41
Q

K Permeability in cardiac vs skeletal muscle

A

Much higher in cardiac muscle

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42
Q

Na permeability in cardiac vs skeletal muscle

A

10-50x higher in cardiac

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43
Q

Phase 0 permeability

A

Action potential upstroke

Na influx

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44
Q

Phase 1 permeability

A

Transient increase in K

Inactivation of Na

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45
Q

Phase 2 permeability

A

Increase in Ca (voltage gated)

Decrease in K because of Mg block

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46
Q

Phase 3 permeability

A

Ca channels close

K rectifier channel

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47
Q

Nodal tissue AP vs other parts of heart AP

A
  1. No true resting potential

2. Lower AP amplitude and shorter duration

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48
Q

Nodal AP - Phase 0

A

Upstroke

Voltage activated CALCIUM channels

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49
Q

Nodal AP - phase 3

A

Repolarization

Voltage dependent K rectifier channels

Channels inactivate as cell repolarizes

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50
Q

Nodal AP - Phase 4

A

Pacemaker potential

Early portion - Closure of Krectifier (primarily), Ca, K channels (slight depolarization)

I(f) channels open midway through and allow Na, Ca (less) influx –> further depolarization

Late phase 4 - Voltage T type calcium channels

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51
Q

B adrenergic stimulation on nodal I channels

A

PKA activation of channels

Shifts voltage at which channel activates to more positive –> Phase 4 depolarization begins earlier in repolarization phase

Larger depolarizing current

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52
Q

B adrenergic stimulation on nodal Ca channels

A

Both types of channels increased

Upstroke is larger
Ca influx during phase 4 is larger

Transition from phase 4 to 0 occurs earlier in phase 4

Rate of rise and amplitude increased, duration decreased

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53
Q

Acetylcholine and nodal AP

A

ACh at SA and AV nodes

  1. Ach gate K channels open
  2. Muscarnic receptors activated –> reduces cAMP and negates sympathetic activity
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54
Q

Overall pattern of electrical activation of heart

A

SA node –> Rt atrium before left atrium –> AV node (delay) –> purkinje fiber –> Endocardial ventricle –> Epicardial ventricle

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55
Q

Benefit of electrical pattern of heart activation

A

Delaying ventricle contraction (AV node) relative to atrial = maximize filling

Activating endocardial (surface) cells first and repolarizing last = More efficient contraction

Contracting from apex to base = ejection efficiency

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56
Q

Nicotinic cholinergic receptors

A

Neuromuscular junction of somatic nerves and skeletal muscle

Autonomic ganglia neurons

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57
Q

Muscarinic cholinergic receptors

A

Postganglionic parasympathetic

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58
Q

M1 receptor location

A

Neuron

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59
Q

M2 receptor location

A

Heart and smooth muscle

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60
Q

M3 receptor location

A

Sweat, salivary, lacrimal, GI, bronchial SM, eye

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61
Q

Cholinergic crisis

A 
Salivation
Lacrimation
Urination
Defecation
Emesis
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62
Q

Muscarinic antagonist clinical signs

A 
Dry mouth
Constipation
Mydriasis
Tachycardia
Decreased lacrimation
Decreased respiratory secretion
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63
Q

Epinephrine adrenergic targets

A

A1
A2
B1
B2

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64
Q

Norepinephrine adrenergic targets

A

A1
A2
B1

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65
Q

Beta 1 receptor action

A

Cardiac stimulation

Lipolysis

Renin release

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66
Q

Beta 2 receptor action

A

Bronchodilation
Vasodilation
Skeletal muscle and liver metabolic response

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67
Q

Alpha 1 receptor action

A

Smooth muscle (vessel) constriction

Increase in TPR and thus increase in BP

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68
Q

Beta 2 receptors and vessels

A

Relaxation of vascular smooth muscles in skeletal muscle vascular beds, splanchnic vessels, coronary vessels

Vasodilation –> Decreased TPR –> Decreased BP

Relaxation of bronchial smooth muscle and dilation of airways

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69
Q

Norepinephrine effects

A

Vasoconstriction –> Increase BP (a1)

Increase cardiac rate and contractility (B1)

Compensatory response decreases HR

Net result = Increased BP

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70
Q

Epinephrine effects

A

Vasoconstriction and increased BP (a1)

Vasodilation in skeletal muscle vascular beds and slight offset of vasoconstriction (b2)

Dose plays a role in effects

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71
Q

Low dose epinephrine

A

BP falls because B2 effects on vascular beds

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72
Q

Increased dose epinephrine

A

More vasoconstriction and increased BP

Beta1 increases pulse pressure

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73
Q

Phentolamine

A

Adrenergic antagonist

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74
Q

Phenoxybenzamine

A

Adrenergic antagonist

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75
Q

Prazosin

A

Adrenergic antagonist

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76
Q

Doxazosin

A

Adrenergic antagonist

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77
Q

Propanolol

A

Beta antagonist

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78
Q

Timolol

A

Beta antagonist

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79
Q

Metoprolol

A

Beta 1 antagonist

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80
Q

Clonidine

A

Alpha 2 adrenergic agonist

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81
Q

Phenylephrine

A

Alpha 1 agonist

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82
Q

Calcium sources in cardiac muscle

A

Extracellular space

Sarcoplasmic reticulum

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83
Q

Method of bringing in Extracellular Ca into cardiac muscle

A

Voltage gated Ca channel (L type)

Na-Ca exchange

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84
Q

L type Ca channel

A

Heart depol –> channel open –> triggers SR Ca release channel

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85
Q

Na-Ca exchanger

A

1 Ca for 3 Na

When membrane is more positive (depolarization) exchanger mediates Ca influx

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86
Q

Ca efflux of cardiac muscle mechanism

A

Ca-ATPase in plasma membrane (PMCA)

Na-Ca exchanger

Cell repolarizes –> Na-Ca exchange = Ca efflux.
–> No Ca entry = no activation of SR Ca release

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87
Q

Contractility

A

Change in force production that occurs independently from change in sarcomere length

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88
Q

Autonomics and contractility

A

Downstream effects of B1 receptor agonists –> more Ca into cell and more Ca release from SR –> More Ca available and more cross bridging

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89
Q

Contractility and heart rate

A

HR can affect contractility independent of autonomics

Increased HR –> Decreased time of disatole for Ca to be removed –> more Ca available at next systole

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90
Q

Contractility and cardiac glycosides

A

Cardiac glycosides enhance contractility

Na/K ATPase inhibited –> increase Na in cell –> Increase Na/Ca exchange activity (Ca influx)

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91
Q

Homeometric regulation

A

Regulation of force through changes in contractility

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92
Q

Stroke Work

A

Energy needed for ejection and energy needed to develop tension in IsoVol Contraction

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93
Q

Most energy required in cardiac cycle during…

A

Isovolumetric contraction

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94
Q

Factors increasing oxygen consuption

A

Increased afterload/contractility

Dilation of ventricular chamber

Increased HR

Increased SV

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95
Q

Heterometric reserve

A

Range of volumes over which an increase in volume leads to increased force

Increase in ventricular volume = thick/thin filament overlap enhancement = enhanced contractile force

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96
Q

Left ventricle Systolic/Diastolic pressure

A

120/5-10

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97
Q

Aorta systolic/diastolic pressure

A

120/80

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98
Q

Right ventricle systolic/diastolic pressure

A

25-30/4-6

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99
Q

Pulmonary artery systolic/diastolic pressure

A

25/10

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100
Q

Stage 1 HTN

A

140-159/90-99

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101
Q

Stage II HTN

A

> 160/ >100

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102
Q

Rationale for treatment of HTN

A

AntiHTN is associated with reduced CV outcomes

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103
Q

First line Diuretics

A

Chlorthalidone

HCTZ

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104
Q

First line ACE inhibitor

A

Benazepril

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105
Q

First line ARB

A

Losartan

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106
Q

First line Ca channel blockers

A

Amlodipine

Diltiazem

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107
Q

First line Beta blocker

A

Metoprolol/Propanolol

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108
Q

Thiazide MoA

A

Block Na/Cl cotransporter in DCT of kidney

Produces negative salt/water balance

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109
Q

Thiazide hemodynamic response

A

Drop in BP due to decreased plasma V and CO

EC volume returns to normal due to Renin-Angiotensin-Aldosterone System

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110
Q

Adverse effects of thiazide type diuretics

A

Hypokalemia

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111
Q

Ace inhibitor MoA

A

Inhibit ACE which converst Angiotensin I –> Angiotensin II

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112
Q

ACE-I hemodynamic response

A

Reduction in systemic vascular resistance and preload

Not much change in pulse rate

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113
Q

ACE-I adverse effects

A

Hypotension

Cough due to increased kinin

Renal insufficiency

Hyperkalemia can occur in patients with renal insufficiency, hypoaldosteronism, K sparing diuretic therapy

Teratogen

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114
Q

ARB MoA

A

Block angiotensin II binding

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115
Q

ARB Hemodynamic response

A

Vasodilation with decreased preload/afterload

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116
Q

ARB adverse effects

A

Teratogen

Les frequent cough

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117
Q

Ca channel blocker MoA

A

Bind to and block VGCC so less calcium for heart contraction and vascular smooth muscle contraction

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118
Q

Ca channel blocker hemodynamic response

A

Vasodilation with decrease in systemic vascular resistance

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119
Q

Ca Channel blocker Adverse effects

A

Constipation

Peripheral edema due to precapillary dilation and post capillary constriction

Negative inotropic action

AV node action may cause bradycardia

Headache

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120
Q

Beta blocker hemodynamic response

A

Decrease HR and contractility and CO

Increase SVR

Decrease in Renin –> less Angiotensin II –> less vasoconstriction

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121
Q

Beta blocker adverse effects

A

Dreams/depression

Aggravation of sever/unstable heart failure

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122
Q

Effect of increase in preload

A

Increase preload –> Increase EDV –> heterometric increase in contractility –> ESV stays the same

Result: Increase SW and subsequently CO

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123
Q

Effect on increase of contractility

A

Increase contractility –> more forceful contraction –> decreased ESV –> increased SV and subsequently CO

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124
Q

How to change flow of blood to organs

A

Relaxing or contracting smooth muscle of arterioles

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125
Q

Methods of altering organ arteriolar tone

A
  1. Direct autonomic control
  2. Local myogenic/metabolic factors
  3. Humoral factors
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126
Q

Direct autonomic control of organ arteriolar tone

A

Sympathetic vasoconstriction

B2 vasodilation

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127
Q

Local myogenic control

A

Blood flow autoregulated within certain level of blood pressure

Increase BP = Increased flow –> Increase resistance (vasoconstriction) = Decrease flow

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128
Q

Local metabolic control

A

Metabolites that induce vasodilation (H, K, Lactate, Adenosine, CO2)

Exercise produces metabolites –> metabolites causes vasodilation so more flow to muscles –> Increased flow eventually washes metabolites out –> vasoconstriction

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129
Q

Humoral factors

A
  1. Catecholamines - Extreme situations
  2. Nitric Oxide
  3. Angiotensin II
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130
Q

Coronary circulation architecture

A

Coronary vessels arise from sinuses behind aortic valve

High metabolic demand

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131
Q

Coronary exchange vessels

A

Capillary density of the heart is very high

Cardiac fibers are smaller so highly perfused

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132
Q

Cardiac contractility and flow through coronary vessels

A

Flow through coronary vessels decreases during ejection b/c heart is contracted

Flow deficit greatest in subendocardium b/c thats where contractions come from

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133
Q

Control of coronary flow

A

Local metabolic control - Hypoxia and adenosine

Nitric oxide

Net sympathetic activity is vasodilatory

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134
Q

Pulmonary circulation

A

Blood flow through lungs is much higher than metabolic need

Blood shunts away from poorly ventilated areas

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135
Q

Pulmonary edema natural prevention

A

Starling forces favor reabsorption - continuous capillaries

Lymph system drains and removes foreign bodies

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136
Q

Skeletal muscle capillaries

A

Oxidative fibers have more capillary anastamoses

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137
Q

Skeletal muscle starling during exercise

A

Starling forces favor filtration

Vasodilation = increased hydrostatic pressure

Metabolites released into interstitium –> Increased tissue oncotic pressure

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138
Q

HR immediate response to exercise

A

Anticipatory response via sympathetic system

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139
Q

SV immediate response to exercise

A

SV increases as intensity increases

Increased contractility

Increased preload

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140
Q

CO response to exercise

A

HR and SV increase

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141
Q

Blood flow response to exercise

A

Blood distributed to tissues with greatest demand: Heart, lungs, muscles

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142
Q

Blood pressure response to exercise

A

Increased contraction = increased BP (systolic, not diastolic)

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143
Q

Blood response to exercise

A

VO2 difference increases

More oxygen released from Hb

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144
Q

Heart size and rate adaptation to training

A

Increased heart mass, esp left ventricle

Resting heart rate decreases due to increased contractile properties

Range of heart rates increases

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145
Q

SV response to training

A

Increase due to increased preload

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146
Q

CO in response to training

A

CO increases during exercise but stays same at rest

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147
Q

Blood flow response to training

A

Skeletal muscle receives large % during training

Increased capillary growth and blood volume

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148
Q

BP in response to training

A

Systolic and diastolic BP decrease at rest and submaximal exercise

Increased compliance of large vessels

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149
Q

Blood volume in response to training

A

Endurance training increased BV and decreased HCT

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150
Q

Myocarditis definition

A

Inflammatory disease of heart

Inflammatory infiltrates in myocardium

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151
Q

Clinical features of myocarditis

A

Arryhythmias

EKG changes

Heart failure

Fatigue

Dyspnrea

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152
Q

Etiology of myocarditis

A
  1. Infectious - Particularly viral but can be bacterial/fungal/parasitic
  2. Hypersensitivity/autoimmune
  3. Rejection of cardiac transplant
  4. Idiopathic
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153
Q

Gross pathology of myocarditis

A

May appear normal or with dilated ventricles

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154
Q

Microscopic path of myocarditis

A

Necrosis of myocytes, inflammatory infiltrates

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155
Q

Outcome of myocarditis

A

Most recover

Supportive therapy

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156
Q

Cardiomyopathy definition

A

Abnormality or disease of cardiac muscle cells occurring in absence of other known mechanisms of myocardial injury

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157
Q

Primary cardiomyopathy

A

Primary involvement is myocardial and no known etiology

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158
Q

Secondary cardiomyopathy

A

Associated with another cardiac disease such as myocarditis

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159
Q

Dilated cardiomyopathy

A

60% are primary idiopathic

40% are secondary cardiomyopathies: Alcoholism, prev myocarditis, pregnancy, drug/toxin exposure

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160
Q

Physiologic consequences of dilated cardiomyopathy

A

Systolic disorder - Decreased contractility and decreased EF

LV hypertrophy and dilatation, arrhythmias

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161
Q

Hypertrophic cardiomyopathy

A

Hypertrophy of ventricular septum

Gene mutation in gene that encode cardia sarcomeric proteins

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162
Q

Physiologic consequences of hypertrophic cardiomyopathy

A

Diastolic disorder - Decreased LV compliance and decreased LV filling

Sudden death at young age esp in young athletes

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163
Q

Restrictive cardiomyopathy

A

Cardiac wall stiffness (decreased compliance) –> decreased cardiac filling

50% amyloidosis

35% Eosinophilia which causes endocardial fibrosis and stiffening of ventricles

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164
Q

Physiological consequences of restrictive cardiomyopathy

A

Diastolic disorder

Decreased ventricular compliance and decreased cardiac filling

Biatrial dilatation

Normal systolic function

Can result in heart failure and sudden death

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165
Q

Arrhythmogenic cardiomyopathy

A

Fibrosis and fatty replacement of ventricles, esp right

RV dilatation

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166
Q

Physiological consequence of arrythmogenic cardiomyopathy

A

Systolic disorder

Decreased contractility of ventricles and decreased EF, esp right

Arrhythmias

Sudden death at young age

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167
Q

Criteria for diagnosing hypertensive heart disease

A

Cardiac enlargement (LV hypertrophy without dilatation)

Absence of other etiologic factors that would produce LV hypertrophy

History of hypertension

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168
Q

Vascular changes in HTN heart disease

A

Systemic arterioles narrow –> Increased TPR –> Increased afterload –> LV hypertrophy

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169
Q

Mild myocardial hypoxia in HTN heart disease

A

Increased myocyte size = larger diffusion distances from capillaries to individual myocytes –> mild hypoxia

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170
Q

Additional factors of HT heart disease

A

Hypertrophies myocytes dont contract effectively

Interstitial collagen increases –> reduced compliance

Atherosclerosis of coronary arteries decreases myocardial blood supply and exacerbates myocardial hypoxia

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171
Q

Microscopic pathology of HTN heart disease

A

Increased myocyte diameter with increased size nucleus

Nuclei :squared off” or box car shaped

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172
Q

Complications and causes of death in HTN heart disease

A

Congestive heart failure (40%)

Coronary atherosclerosis

Strokes

Nephrosclerosis –> kidney failure

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173
Q

Most common CV anomaly

A

Bicuspid aortic valve

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174
Q

Second most common CV anomaly

A

Ventricular septal defect

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175
Q

Pathogenesis of congenital cardiac abnormalities

A

Sporadic genetic abnormalities

Chromosomal abnormalities

Viral infection during pregnancy (rubella)

Drugs/teratogens

Radiation

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176
Q

Cyanosis

A

Blue discoloration of mucous membranes caused by >2.5gms/dl of deoxyHb in blood

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177
Q

Pulmonary HTN and congenital defects

A

Pulmonary HTN can arise if shunts are present

Left to Right shunts increase blood to lungs and cause hypertrophy of pulmonary arteries

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178
Q

Plexogenic pulmonary HTN

A

Severe form of pulmonary artery hypertrophy

Cannot be corrected by surgery except total lung transplant

Common with VSD

Severe = Eisenmenger syndrom

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179
Q

Eisenmenger Syndrome

A

Reversal of Lt to Rt shunt

Caused by increased pulmonary HTN and shunt reversal

Acyanotic –> cyanotic

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180
Q

Lt to Rt shunts

A

Develop late cyanosis via Eismenger syndrome

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181
Q

Rt to Lt shunts

A

Early cyanosis

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182
Q

Congenital obstructions

A

No cyanosis

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183
Q

Congenital regurgitation

A

No cyanosis

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184
Q

Atrial septal defect

A

Abnormal opening between atria

L –> R

May be asymptomatic until adulthood

RV hypertrophy and dilatation, RA/LA dilatation

Pulmonary HTN infrequent

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185
Q

Types of atrial deptal defects

A
  1. Fossa ovalis (most common)
  2. Primum type - Low on septum and adjacent to AV valves

Sinus venosus type - High on septum, near SVC

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186
Q

Ventricular septal defect

A

Abnormal opening between ventricles

L –> R

Can cause pulmonary HTN if large –> Shunt reversal –> Eismengers

Small VSD’s spontaneously close, no surgery and no pulmHTN

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187
Q

Types of VSD

A

Membranous - Membranous septum, most common, large

Muscular VSD - muscular septum, multiple, small

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188
Q

Atrioventricular septal defect (AVSD)

A

Deficient AV septum associated with mitral and tricuspid valve anomalies

Endocardial cushion defect

Associated with Downs

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189
Q

Types of AVSD

A
  1. Partial - Primum ASD with cleft mitral anterior leaflet

2. Complete AVSD - Primum ASD and Membranous VSD. Large hole in center of heard and a common AV valve

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190
Q

Patent Ductus Arteriosus

A

Persistence of normal fetal structure that connects aorta and pulmonary artery

Pulmonary HTN

May be required for survival in complex cyanotic congenital heart diseases

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191
Q

Tetralogy of Fallot

A
  1. Large and subarotic VSD
  2. Subpulmonary stenosis
  3. Overriding aorta
  4. RV hypertrophy

Most common cyanotic congenital disease

Usually NO pulmHTN because lung vessels protected by subpulmonary stenosis

Good results with surgical repair

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192
Q

Types of Tetralogy of Fallot

A

Types based on pulmonary stenosis severity

  1. Pink: Mild stenosis, no cyanosis
  2. Classic: Moderate-severe stenosis, Cyanosis
  3. PA-VSD - Complete absence of pulmonary valve and main pulmonary artery, with cyanosis
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193
Q

Transposition of Great Arteries

A

Pulmonary artery comes off LV and aorta comes off RV

Two separate circulations, not compatible with life unless shunt present

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194
Q

Types of TGA

A
  1. TGA + no VSD = 65%, rare pulmHTN

2. TGA + VSD = 35%. Severe pulmHTN

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195
Q

How to treat TGA

A

Give PGE so DA remains

Create shunt

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196
Q

Truncus arteriosus

A

One common trunk the gets blood from RV and LV

Early cyanosis because deoxygenated blood can travel through aorta

Severe PulmonaryHTN

DiGeorge Syndrome

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197
Q

First heart sound: Occurs during what part of cardiac cycle and why

A

Isovolumetric contraction

Closure of mitral/tricuspid valves

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198
Q

Second heart sound: Occurs during what part of cardiac cycle and why

A

Isovolumetric relaxation

Closure of aortic/pulmonic valves

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199
Q

Third heart sound: Occurs during what part of cardiac cycle and why

A

Early ventricular filling

Normal in children, abnormal in adults

Rapid ventricular filling or dilated ventricle

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200
Q

Fourth heart sound: Occurs during what part of cardiac cycle and why

A

Atrial contraction

Blood hitting stiffened ventricle

Ventricular hypertrophy/ischemic ventricle

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201
Q

Pulmonary stenosis

A

Pulmonary valve obstruction

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202
Q

Types of pulmonary stenosis

A

Based on severity of obstruction

  1. Isolated PV stenosis: RV hypertrophy, tricuspid regurg, RA/PA dilatation
  2. PV atresia with intact ventricular septum: PDA required for survival. Hypoplastic RV and tricuspid valve
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203
Q

Congenital Aortic stenosis

A

Aortic valve obstruction

204
Q

Types of congenital aortic stenosis

A

Severity based on level of obstruction

  1. Isolated AV stenosis: LV hypertrophy, mitral regurgitation, LA dilatation
  2. AV atresia with intact ventricular septum: PDA required for survival
205
Q

Coarctation of aorta

A

Ridge like indentation or narrowing of distal aortic arch

50% have congenitally bicuspid AV

Hypertension in arms, hypotension in legs

Shunting around narrowing through enlarged collateral arteries

206
Q

Types of coarctation of aorta

A

With (infants) and without (adults) PDA

207
Q

Ebstein anomaly

A

Tricuspid valve malformation - septal and posterior leaflets point downwards and allow blood to flow back into RA

Torrential tricuspic regurgitation

Massive RA/RV dilatation

208
Q

Congenital heart disease patients and endocarditis

A

Increased risk

209
Q

Survival of children with Congenital HD

A

85% survive to adulthood

210
Q

Fetal Circulation Overall

A

Oxygenated blood from placenta returns via umbilical vein –> into IVC vis Ductus venosus –> LA via foramen ovale –> systemic circulation –> RA –> RV –> pulmonary artery –> through ductus arteriosus –> umbilical artery

211
Q

Pathophysiology and consequences of PDA

A

Pediatric congestive heart failure

Pulmonary vascular occlusive disease

Excessive blood return to left heart

Endarteritis risk

212
Q

Pediatric Congestive Heart failure

A

Pulmonary edema and decreased efficiency of gas exchange = tachypnea

CO increases because more work needed to push out blood

Inability to eat well b/c feeding requires work and energy –> impaired weight gain

213
Q

Pulmonary vascular occlusive disease

A

Pulmonary arterioles respond to increased pressure and flow by constricting

Arterioles can lose ability to relax and are fixed at high pressure –> increase in pulmonary pressure and subsequent Rt to Lt shunting (Eisenmenger syndrome)

214
Q

Excessive blood return to left heart

A

LV dilatation and increased ED-pressure

215
Q

Endarteritis risk

A

1%/yr risk of PDA infection due to turbulent flow

216
Q

Type of murmur in VSD

A

Holosystolic murmur

LV pressure is higher than RV for entire systole

217
Q

Most common mumur heard in AVSD

A

Systolic ejection murmur at PV

Excessive flow across PV

218
Q

Pathyphys of AVSD

A

Left to right shunting at atrial and ventricular level

High flow to pulmonary arteries and increased blood return to left heart

219
Q

Pathophys changes seen in pulmonary artery stenosis - neonates and older

A

Neonates - Hyperplasia which produces more efficient work, can handle pressure load

Neonates/older children - hypertrophy

220
Q

Pathophysiology of aortic stenosis - neonates

A

LV in utero deals with low afterload so it doesn’t work as hard as RV

Aortic stenosis can cause LV to work hard and after birth, LV may not be able to handle increased pressure load

Diastolic LV dysfunction –> Increased LV EDP –> Increased LA pressure –> Increased pulmonary venous presurre –> Increased PA/RV pressure

221
Q

Pathophysiology of aortic stenosis - Older children

A

Rarely symptomatic, diagnosed after being evaluated for murmur

Able to maintain LV systolic performance through hypertrophy

222
Q

Intervention for PDA

A

Indomethacin to close PDA

Catheter based closure of PDA

223
Q

ASD intervention

A

Surgical closure but need to asses pulmonary arterial resistance first

224
Q

VSD interventions

A

Medication - diuretics, ACE-I to reduce pulm overcirculation

Surgical closure

225
Q

AVSD intervention

A

Medication to reduce pulmonary overcirculation

Surgical closure

226
Q

Pulmonary stenosis intervention

A

Neonates - need intervention

Catheter balloon based vavluloplasty

227
Q

Aortic stenosis intervention

A

Catheter based balloon valvuloplasty

228
Q

Intervention for coarctation of aorta

A

Neonates/young children - surgical reconstruction

Catheter based balloon angioplasty

229
Q

Intervention for ToF

A

BTT shunt - surgical PDA

Complete repair

230
Q

TGA intervention

A

Balloon atrial septostomy to create large atrial communication and maximize mixing

231
Q

Total anomalous pulmonary venous return (TAPVR)

A

Problem with connection of pulmonary venous confluence to primitive LA –> veins have nowhere to drain

Pop off vessel develops which can go

  1. Superiorly to innominate vein
  2. Inferiorly through diaphragm to IVC/hepatic veins
  3. Infracardiac to coronary sinus

Oxygenated pulmonary venous blood goes back to RA

Infants will be cyanotic but not in distress (if vein isnt obstructed)

232
Q

TAPVR intervention

A

Surgical

Emergency if vein is obstructed

233
Q

Tricuspid atresia

A

Failure of tricupsid valve formation, no right ventricle - single ventricle

234
Q

Intervention for single ventricle

A

Ultimate goal is to separate systemic and pulmonary circulation

Stage 1 surgery: BTT shunt for pulmonary flow, cut atrial septum

Stage 2: Glenn procedure. SVC detached from RA and sewn to right PA (bypass right heart completely)

Stage 3: Fontan procedure. IVC detached from RA and connected to pulmonary arteries

All systemic blood flows to pulmonary arteries, bypassing right heart

235
Q

Hypovolemic shock classification

A

Results from decreased preload

Hemorrhage or fluid loss

236
Q

Cardiogenic shock classification

A

Pump failure

Decreased systolic function and CO

237
Q

Distributive shock classification

A

Vasodilatory shock
Severe decrease in SVR and increase in CO

Septic, anaphylaxis, neurogenic shock

238
Q

Hypovolemic shock: CVP, CO, SVR

A

CVP - Decreased

CO - Decreased

SVR - Increased (sympathetic reflex)

239
Q

Cardiogenic shock: CVP, CO, SVR

A

CVP - Increased (can’t pump out preload)

CO - Decreased

SVR - Increased

240
Q

Distributive shock: CVP, CO, SVR

A

CVR - Same or decreased

CO - Increased

SVR - Huge decrease (vasodilation)

241
Q

Truncus arteriosus adult structure

A

Aorta and pulmonary trunk

242
Q

Bulbus cordis adult structure

A

Smooth L/R ventricle

243
Q

Ventricle adult structures

A

Trabeculated L/R ventricle

244
Q

Sinus venosus adult structure

A

Coronary sinus and smooth RA

245
Q

Ductus arteriosus adult structure

A

Ligamentum arteriosum

246
Q

P wave signifies

A

SA conduction and atrial depolarization

247
Q

P-R interval

A

AV node

248
Q

QRS signifies

A

Ventricular depolarization

249
Q

ST interval

A

Isoelectric segment

250
Q

T wave signifies

A

Ventricular repolarization

251
Q

Long P-R =?

A

Conduction problem through AV node/bundle branches/Purkinje

252
Q

Wide QRS = ?

A

Bundle branch or purkinje problem

253
Q

Unipolar leads

A 
V1
V2
V3
V4
V5
V6
aVF
aVL
aVR
254
Q

Bipolar leads

A

Vector combination of aVF/aVR/aVL

255
Q

Lead I looks at what part of heart

A

High lateral

256
Q

Lead II/III look at what part of heart

A

Inferior

257
Q

aVF looks at what part of heart

A

Inferior

258
Q

V1 lead looks at what part of heart

A

Septal

259
Q

V2/V3/V4 looks at what part of heart

A

Anterior

260
Q

V5/V6 looks at what part of heart

A

Lateral

261
Q

Arteriosclerosis encompasses ?

A

Atherosclerosis

Arteriolosclerosis

Monckeberg medial calcific sclerosis

262
Q

Atherosclerosis definition

A

Atheromatous plaque formation within large/medium sized arteries and elastic arteries

263
Q

Pathogenesis of atherosclerosis

A
  1. Endothelial cell dysfunction
  2. Smooth muscle proliferation and migration into intima
  3. Macrophage proliferation and migration into intima
  4. Hyperlipidemia
264
Q

Endothelial cell dysfunction

A

May stimulate smooth muscle proliferation with synthesis of collagen, elastic fibers, proteoglycans

Can induce macrophage proliferation

265
Q

Smooth muscle proliferation

A

Synthesize ECM and accumulate lipids

266
Q

Macrophage proliferation

A

Increased phagocytosis and accumulation of lipids within macrophages (foam cells)

Inflammatory cell recruitment

Oxidation of LDL

267
Q

Hyperlipidemia

A

Promotes endothelial and smooth muscle cell injury

Increase penetration of lipids into plaque, increase formation of lipid laden foam cells in plaque

268
Q

Complications of atheroma formation

A

Narrowing of lumen

Calcification and ulceration of plaque

Hemorrhage into plaque

Weakening of vessel wall with formation of aneurysms

269
Q

Arteriolosclerosis

A

Disease of arterioles

  1. Hyaline arteriolosclerosis (hyaline accumulation)
  2. Hyperplastic arteriolosclerosis - Lumen narrowing by proliferating fibroblasts and smooth muscle cells in onionskin pattern

Elderly patients or young HTN/diabetic patients

270
Q

Monckberg Medial Calcific Sclerosis

A

Disease of medium to small sized arteries

Calcification of media

> 50yrs old

Calcification of tunica media without inflammation

271
Q

Hemostasis sequence of events

A

Vascular injury –> Responsive vasoconstriction –> subendothelial tissue exposure leads to platelet aggregation –> TF exposure begins coagulation cascade –> –> fibrin accumulation and permanent hemostatic plug

272
Q

Platelet aggregation

A

vWF = platelet aggregation

Platelet receptors for ADP/thrombin –> Activate COX-1 and fibrinogen binding protein

273
Q

Intrinsic pathway of coagulation cascade

A

Factor VIII, IX, XI, XII –> Factor V

274
Q

Extrinsic pathway of coagulation cascade

A

TF + Factor VII –> Factor X

275
Q

Antithrombin

A

Blocks Factor IX, X, XI, Thrombin

276
Q

Protein C

A

Activated protein C (with protein S cofactor) blocks V and VIII

277
Q

TPA

A

Activates plasminogen –> plasmin –> fibrinolysis

278
Q

PT monitoring

A

Prothrombin time

Assesses extrinsic pathway

279
Q

aPTT

A

Activated partial thromboplastic time

Assesses intrinsic pathway

280
Q

LMWH vs UFH

A

Both are efficacious and safe but LMWH needs no monitoring

281
Q

Enoxaparin

A

Prototype LMWH

282
Q

Fondaparinux

A

Pentasaccharide analog

283
Q

Heparin MoA

A

Binds to antithrombin and causes conformational change –> mediates binding to Factor X to prevent clotting

284
Q

UFH vs LMWH vs Fondaparinux MoA

A

UFH can mediate both antithrombin-Factor X binding AND antithrombin-thrombin binding

LMWH and Fondaparinux can only block Factor X, not long enough to mediate thrombin-antithrombin connection

285
Q

Heparin pharmacodynamics

A

UFH can bind to no coagulation proteins and needs to be monitored

LMWH and fondaparinux do not bind to other proteins

286
Q

Heparain monitoring

A

aPTT

287
Q

Reversal of UFH

A

Protamine sulfate

Binds heparin so no anticoagulant activity

288
Q

Heparin Induced thrombocytopenia

A

Heparin molecules cross react with patient IgG and can cause a thrombotic response and thrombocytopenia

289
Q

Highest risk of HIT when using?

A

Unfractioned Heparin

After major surgery

290
Q

HIT diagnosis

A

Decreased platelets >50% or thrombosis 5-10 days after heparin treatment

291
Q

Treatment of HIT

A

Stop Heparin and use alternate anticoagulant

Argatroban - Direct thrombin inhibitor

292
Q

Warfarin

A

Oral anticoagulant

Vitamin K antagonist - Prevents synthesis of clotting factors that require Vit K: II, VII, IX, X, protein C/S

Monitor with PT

293
Q

Rifampin and Warfarin

A

Decrease Warfarin activity

294
Q

Antimicrobials and Warfarin

A

Increase Warfarin activity via enzymes and by decreased Vit K absorption in gut

295
Q

Alcohol and Warfarin

A

Acute use - Increased activity

Chronic use - Decreased activity

296
Q

Metronidazole and Warfarin

A

Increased activity

297
Q

Amiodarone and Warfarin

A

Large increase in activity

298
Q

Dabigatran

A

Direct thrombin inhibitor

No monitoring required but can use aPTT

Use for stroke prevention or systemic embolism

299
Q

Idarucizumab

A

Antidote for Dabigatran

Use if life threatening bleeding/uncontrolled hemorrhage

300
Q

Rivaroxaban (Xarelto)

A

Factor Xa inhibitor

Reduce stroke and systemic embolism risk

DVT/PE phrophylaxis

CYP450

301
Q

Apixaban (Eliquis)

A

Factor Xa inhibitor

Reduce stroke and systemic embolism risk

CYP3A4

302
Q

Edoxaban

A

Latest factor Xa inhibitor

Stroke and systemic embolism prevention

PE/DVT treatment in patients who have been treated with parenteral anti-coagulant for 5-10 days

303
Q

Bivalirudin

A

Parenteral direct thrombin inhibitor

Used in percutaneous coronary interventions after acute infarction and stent placement

304
Q

Argotroban

A

Used in PCI and HIT management

305
Q

Clopidogrel

A

Block platelet ADP receptor that activates fibronogen binding protein

Decrease platelet aggregation and clotting

306
Q

Abiciximab

A

GpIIa/IIIa receptor antibody

Inhibits platelet aggregation

307
Q

TPA

A

Tissue plasminogen activator = Clot breakdown

Ischemic symptoms ST elevation MI <12hr

PCI while stenting

Acute ischemic stroke within 3-4.5hrs of symptom onset

Use in PE management with associated shock

308
Q

Physiological roles of cholesterol

A

Lipid component of membranes

Precursor o steroid hormones and Vit D

Source of bile acids which help in lipid digestion and absorption

309
Q

Most abundant saturated fatty acid

A

Palmitic acid

310
Q

Trans fatty acids

A

Lower HDL and raise LDL

Decrease membrane fluidity

311
Q

Monounsaturated Fatty acids

A

Oleic Acid (18:1)

Mediterranean Diet

Lower LDL and Raise HDL

312
Q

Polyunsaturated fatty acids

A

Omega 3 and omega 6

Lower LDL and raise HDL

313
Q

Cholesterol biosynthesis

A

Fatty acid beta oxidation in mitochondria –> acetyl coA –> Citrate and exits mitochondria into cytoplasm –> Lyase splits citrate to Acetyl CoA –> Acetoacetyl CoA –> HMG CoA –> Mevalonate –> –> cholesterol

314
Q

Rate limiting step of cholesterol biosynthesis

A

HMG CoA reductase

Rxn occurs in SER

315
Q

HMG CoA reductase

A

Rate determining step of cholesterol biosynthesis

Cholesterol activates proteolytic degradation

Amount of enzyme controlled by induction/repression

Require NADPH

316
Q

Stage 2 cholesterol biosynthesis

A

Mevalonate –> 5 carbon chain –> Combine to make 30 C chain Squalene

Require NADPH

317
Q

Stage 3 cholesterol biosynthesis

A

Cyclization

Use NADPH

318
Q

Stage 4 cholesterol biosynthesis

A

19 steps

Use NADPH and Oxygen

Cholesterol formation

319
Q

Normal/high free cholesterol and HMG CoA reductase

A

SCAP-SREBP complex remains in ER membrane

No involvement with promoter region so no transcription/translation of HMG CoA reductase

320
Q

Low free cholesterol and HMG CoA Reductase

A

SCAP-SREBP complex unstable and dissociates and goes to golgi to get cleaved –> SREBP binds to promoter region and induce HMG CoA reductase transcription/translation

321
Q

Fates of cholesterol

A

Membrane structure

Precursor for steroid hormones and Vit D

Esterification for storage/elimination

Precursor to bile salts

322
Q

LCAT esterification

A

For HDL transport to liver

323
Q

ACAT esterification

A

Esterifies cholesterol making it hydrophobic

Clumps together in cytoplasm/vacuoles

Cell storage

324
Q

Esterified cholesterol in liver

A

Can be made into bile acids

7-a-hydroxylase

Requires NADPH, Vit C

325
Q

7 alpha hydroxylase regulation

A

Enzyme induction by cholesterol binding to liver LXR receptor –> –> enzyme production

Enzyme repression by bile acids

326
Q

How to increase cellular cholesterol

A

Increase uptake

Increase biosynthesis

Cholesterol esterase

327
Q

How to decrease cholesterol in cel

A

Esterification

Cholesterol metabolism to bile acids/steroids

Cholesterol release for transport to liver

328
Q

Release of cholesterol from cell

A

Golgi directed trafficking to plasma membrane –> pumped to exterior surface by CERP –> Transfer to HDL

329
Q

Statins

A

Compettive inhibitors of HMG CoA reductase

Act at low concentrations

Decreased cholesterol synthesis:
Liver = decreased VLDL output and decreased LDL production
Tissues = LDL induction and increased LDL uptake

Increase HDL

Need to monitor liver enzymes and CK for myopathies

330
Q

Bile acid sequestering Resins

A

Reduced recycling lowers bile salt concentration –> Lowers feedback repression of 7a hydroxylase –> Increased cholesterol conversion to bile acids –> Lower cholesterol –> More LDL receptors –> Increased LDL uptake –> Lower plasma cholesterol

331
Q

Nicotinic acid

A

Decrease release by adipose tissues of fatty acids to lower availability to making TAGs and cholesterol for VLDL

332
Q

Fibrates

A

Lower curculating TG’s

Improve HDL

333
Q

Ezetimibe

A

Lowers intestinal absorption of dietary cholesterol

Binds to NPC1L1 protein on epithelial cells

334
Q

Aneurysm definition

A

Abnormal localize dilatation of a tubular structure

335
Q

Aneurysm etiology

A

Atherosclerosis

Congenital

Infection

Structural abnormalities

Vasculitis

336
Q

Atherosclerotic aneurysm - Which vessel and complications?

A

Usually involve abdominal aorta

Complications:
1. Rupture with massive hemorrhage –> sudden death

  1. Compression of adjacent structures
  2. Occlusion of arterial branches
  3. Embolism from mural thrombus with ischemia or infarction of distal extremities
337
Q

Syphylitic aneurysms - vessel involved and complications

A

Usually ascending aorta

Can extend proximally to produce aortic valve annular dilatation and regurg

Clinical symptoms due to compression of adjacent structures

Lymphocytic/plasma cell infiltration

338
Q

Dissecting aneurysms

A

Dissection of blood along a plane of cleavage through media of aortic wall, hematoma formation

HTN, bicuspid aortic valve, medial degeneration, aortic weakness, Marfans/EDS

339
Q

Mechanism of dissecting aneurysm

A

Weakened media allows intima to buckle into lumen

Pressure wave of blood impacts on bulging intima to produce tear

Blood dissects through intima tear into media, BP promotes dissection along weakened media

340
Q

Clinical features of dissecting aneurysm

A

Chest pain

Occlusion of arterial branches of aorta

Aortic valve regurg

Rupture with hemorrhage –> death

341
Q

Vasculitis

A

Inflammation of vessel causing medial injury

Autoimmune

342
Q

Giant cell arteritis

A

Chronic inflammatory disease of large sized arteries

Granulomatous, giant cells

Often cranial vessels

343
Q

Clinical signs of giant cell arteritis

A

Headache

Tenderness of artery

Visual disturbances

344
Q

Diagnostic testing for giant cell arteritis

A

ESR elevated

Temporal artery biopsy

345
Q

Polyarteritis nodosa

A

Fibrinoid necrosis and acute inflammation of medium sized muscular arteries

346
Q

Clinical signs and diagnosis of polyarteritis nodosa

A

Young adult-middle age

Symptoms vary by organs affected

Biopsy of affected organ for diagnosis

347
Q

Granulomatosis with polyangitis

A

Granulomatous vasculitis of small arteries, arterioles, capillaries

348
Q

GPA histo triad

A

Acute necrotizing granulomas of nose, sinuses, upper airways

Granulomatous arteritis or capillaritis of lung

Glomerulonephritis

349
Q

Clinical signs of GPA

A

Middle aged

Male > Female

Infiltrate/mass in lung

Sinusitis

Renal abnormalities

Nasopharyngeal ulceration

350
Q

Diagnostic studies for GPA

A

Nasal/sinus biopsy

Lung biopsy

Renal biopsy

ANCA (anti neutrophil cytoplasmic antibodies)

351
Q

Cause of increase in CHD?

A

Longer life span

Smoking

Diet

Activity

352
Q

Framingham study factors

A

Elevated cholesterol

HTN

Smoking

353
Q

Seven countries study

A

Link between diet and heart disease

LDL as risk factor

354
Q

Two main functional consequences of valvular disease

A

Stenosis - Failure of valve to open completely

Regurgitation - Failure of valve to close completely

355
Q

Functional regurgitation

A

Regurgitation cause by dilatation of valvular annulus in setting of ventricular dilatation

356
Q

Murmur

A

Abnormal heart sounds, caused by abnormal blood flow

357
Q

Causes of aortic stenosis

A

Degenerative fibrocalcific aortic valve disease

Congenitally bicuspid aortic valve with degeneration

Postinflammatory valve disease

358
Q

Causes of aortic regurgitation

A

Diseases that dilate aorta

Bicuspid aortic valve

Postinflammatory valve disease

Infective endocarditis

359
Q

Causes of mitral stenosis

A

Postinflammatory valve disease (99%)

Radiation valulopathy

Rare diseases

360
Q

Causes of mitral regurgitation

A

Myxomatous mitral valve degen (floppy), with mitral prolapse

Postinflammatory

Infective endocarditis

Papillary muscle rupture (MI)

Annular dilatation (ischemic heart disease with secondary LV dilatation)

Annular calcification

361
Q

Degenerative fibrocalcific aortic valve disease

A

Age related - eldery

Dystrophic calcification on sinus side of aortic valve

Mitral valve normal or shows annular calcification

362
Q

Physiological consequences of Senile aortic valve disease

A

Stenosis, with or without regurg

Increased pressure gradient across valve, LV hypertrophy without dilatation due to pressure overload

CHF or sudden cardiac death

363
Q

Congenital bicuspid aortic valve

A

1-2% of population, silent until adulthood

Two unequal sided cusps

Dystrophic calcification on sinus side of valve at accelerated rate

Congenital ascending aortopathy - prone to developing aneurysms and dissections

Stenosis and LV hypertrophy

364
Q

Mitral valve prolapse

A

Redundant leaflet tissue balloons back into LA during systole

Myxomatous degeneration of leaflet tissue

365
Q

Mitral valve prolapse complications

A

Infective endocarditis

Mitral regurg

Stroke or systemic infarct from thrombi on leaflets

366
Q

Physiological consequences of mitral valve prolapse

A

Regurgitation

LV hypertrophy and dilatation due to volume overload

LA dilatation

Increased risk for atrial and ventricular arrhythmias

367
Q

Mitral annular calcification

A

Elderly women

No inflammation, valve leaflets mildly affected

Mitral regurgitation

Calcified particles may break loose and embolize

368
Q

Rheumatic fever

A

Systemic autoimmune disease following Strep infection

Autoimmune rxn after bacterial antibodies cross react with normal tissue

Fever, migratory polyarthritis

Disease reactivated by new strep infections

Heart failure occurs after decades

369
Q

Acute rheumatic heart disease - pancarditis

A

Myocarditis - Aschoff bodies

Pericarditis - fibrinous

Endocarditis - small non infectious vegetations

370
Q

Aschoff body

A

Pathognomonic of rheumatic heart disease

Giant cells (Aschoff giant cells)

Histiocytes

Lymphocytes

Plasma cells

Surrounds a focus of

371
Q

Chronic rheumatic heart disease

A

Deforming fibrosis of valves

Mitral valve almost always involved

Isolated mitral valve - 75%

Combined mitral/aortic valve - 25%

Tricuspid valve uncommon, PV rare

372
Q

Pathology of rheumatic mitral valve disease

A

Diffuse fibrosis of mitral valve, calcification

Commissural and chordal fusion

373
Q

Physiological consequences of rehumatic mitral valve disease

A

Usually stenosis but sometimes regurg or both

Severely dilated RA, no LV changes

Atrial arrhythmias

increased risk for left atrial thrombus and embolism

374
Q

Infective endocarditis definition

A

Colonization or invasion of heart valves by microorganism

375
Q

Predisposing factors of infective endocarditis

A

Preexisting valve disease

Congenital heart disease

Immunodeficiency

Any endocardial injury

376
Q

Most commonly affected valves in infective endocarditis

A

Normal people - left sided valves

IV drug users - Right sided valves

377
Q

Complications of infective endocarditis

A

Valve dysfunction - Regurgitation to due leaflet perforations or chordal rupture

Annular or myocardial abscess
Systemic/pulmonary emboli

Glomerulonephritis

378
Q

Non bacterial thrombotic endocarditis

A

Formation of small vegetations on the endocardial surface due to an underlying hypercoagulable state - ABSENCE OF MICROBE INFECTION

  1. Usually debilitated patients
  2. Cancer patients esp mucinous carcinomas that produce circulating mucin –> can cause formation of small thrombi
379
Q

Main causes of aortic stenosis

A

Bicuspid aortic valve

Aortic sclerosis

380
Q

Bicuspid aortic valve

A

More susceptible to calcification

Often collagen disorder and dilation of ascending aorta

Symptoms only occur with stenosis

381
Q

Aortic Sclerosis

A

Thickening/calcification of leaflets

Similar pathophys to atherosclerosis

382
Q

Physical Findings of Aortic sclerosis but not severe stenosis

A

Systolic ejection murmur heard early in systole

Low grade murmur

383
Q

Physical findings of aortic sclerosis w/ more severe stenosis

A

Systolic ejection murmur heard later in systole

Higher grade murmur

May lose S2

Decrescendo murmur @AV due to aortic insufficiency

Carotid pulses have delayed upstroke and decreased amplitude

384
Q

Symptoms of severe aortic stenosis

A
  1. Angina
  2. Syncope
  3. Dyspnea on exertion
385
Q

Chest XR findings for Aortic stenosis

A

Subtle findings

Prominent LV

Calcification of AV

386
Q

EKG findings in aortic stenosis

A

LV hypertrophy so increased QRS amplitude

387
Q

Echocardiography for aortic stenosis

A

Identify # of leaflets

Identify calcification of valves

Measure pressure gradient and vavlular area

Measures velocity of blood through valve: Increased stenosis = increased velocity

> 4m/s is severe stenosis

388
Q

Valve pressure gradient and area in aortic stenosis

A

> 40mm Hg
<1cm squared area

Consistent with severe aortic stenosis

389
Q

Cardiac catheterization

A

Performed when echo indicates severe aortic stenosis and valve replacement is planned

Measures pressure gradient and valvular area

390
Q

Length of time to death with aortic stenosis symptoms

A

Angina - 5 yrs

Syncope - 3 years

Dyspnea on exertion - 2 years

391
Q

Aortic stenosis therapy

A

No treatment, valve replacement needed

392
Q

Mechanical valve replacement

A

Durable and long lasting but are susceptible to thrombosis

Pt on anticoagulants for life

393
Q

Bioprosthetic valve replacement

A

Use synthetic material or animal

No need for anticoagulants but not as durable as mechanical valve

394
Q

VTE prophylaxis

A
  1. Early ambulation
  2. Sequential compression devices
  3. Anticoagulation
395
Q

2 most common symptoms of chest pain

A

Dyspnea

Chest pain

396
Q

Acute cor pulmonale

A

Large PE

RV failure caused by primary disorder of respiratory system

Symptoms: Shock, collapse, syncope

Exam: Hypotension, distended neck veins

CXR: Normal

ABG’s: Decrease pO2, decreased CO2

EKG: S1Q3T3

397
Q

Acute unexplained dyspnea

A

Medium sized PE

SOB without syncope and no chest pain

Elevated RR

Normal ECG, CXR

Differential: CHF, hyperventilation

398
Q

Pulmonary infarction

A

Occlusion of small vessel with no collateral circulation –> infarction

Acute pleuritic pain
Dyspnea +/- hemoptysis

Tachypnea
Crackles/wheezes/rub in lungs

CXR: Consolidation in lung periphery, possible effusion

Ddx: Pneumonia

399
Q

Wells Criteria

A

Probability score based on symptoms/history

400
Q

D dimer

A

Sensitive test for PE
Not specific

D dimer = clotting is occurring

401
Q

Chest CT for PE

A

Sensitive and specific

402
Q

Ventilation Perfusion scan

A

Substitute for Chest CT

Pregnant women/women of child bearing age

Pts with normal/near normal CXR

Abnormal renal function so risk with contrast

403
Q

Prophylactic PE treatment

A

Anticoagulation - decrease further clotting and allowing fibrinolytic system to activate

IVC interruption

404
Q

Definitive PE treatment

A

Thrombolytic therapy - bleeding risk

Pulmonary embolectomy

405
Q

Left main coronary artery branches

A

Left anterior descending

Circumflex (lateral)

406
Q

Right main coronary artery

A

Descends as posterior descending artery

407
Q

Most common sites for grade 4 atherosclerotic lesions

A

Proximal 1/3 of LAD and LCX and most of RCA

408
Q

Angina Pectoris definition

A

Ischemic heart pain

Can be Stable, Unstable, Variant

409
Q

Stable angina

A

Poor blood flow through atherosclerotic lesions

Exacerbated with exercise

Resolves with nitroglycerin

410
Q

Unstable angina

A

Highly occluded artery - thrombus and possible embolus

Pain at rest and gets worse over time

411
Q

Prinzmetal angina

A

Variant

Due to vasospasm

412
Q

Acute myocardial Infarction

A

Ischemic necrosis of portion of myocardium

413
Q

Transmural infarction

A

Entire or nearly entire ventricular wall thickness

414
Q

Subendocardial infarction

A

Less than 1/3 of inner wall

415
Q

Complications of myocardial infarction

A

Sudden death

Cardiogenic shock

Transmural infarct –> ventricular aneurysms or mural thrombi (embolization)

Cardiac rupture

416
Q

Sudden cardiac death

A

Death when not expected, usually due to coronary artery disease

417
Q

End stage ischemic heart disease

A

Progressive CHF due to ischemic heart disease

Most common indication for heart transplant

418
Q

Determinants of myocardial oxygen demand

A

Heart rate

Afterload

Preload

Contractility

419
Q

Myocardial oxygen supply

A

Coronary blood flow

Coronary perfusion pressure (aortic diastolic pressure)

420
Q

Organic nitrates

A

Nitroglycerin & Isosorbide dinitrate

MoA: Prodrug for Nitric oxide –> venous decrease in vascular resistance –> decrease preload –> Reduce myocardial oxygen demand

421
Q

Nitroglycerin

A

Used for treatment and prophylaxis

Sublingual to bypass liver

Side effects - Tolerance, headache, syncope, interaction with PDE5 inhibitors

422
Q

Isosorbide dinitrate

A

Slow acting so only use for prophylaxis

Headache, tolerance, PDE5 inhibitor interaction

423
Q

Beta blocker MoA

A

Decrease heart rate, contractility, BP during exercise

Contraindications - bradyarrythmias, HF, AV block, asthma

424
Q

Ca Channel blocker MoA

A

Block L type calcium channels –> vasodilation, decreased contractility, decreased AV conduction

Decrease demand and increase supply (coronary artery vasodilation)

AE: Hypotension, constipation, HF, AV block, edema

425
Q

Ranolazine

A

Inhibits inward Na channels

Unknown angina mechanism

Use when other drugs don’t work

Long QT

426
Q

Atrial flutter ECG characteristics

A

Rapid atrial activity (~300bpm)

Reentrant circuit around Tricuspid valve

Saw toothed pattern

427
Q

Atrial fibrillation ECG characteristics

A

Chaos

Multiple reentry circuits

Numerous atrial depolarizations and only some become QRS

Irregularly irregular

428
Q

Class I anti arrhythmia drugs

A

Sodium channel blockers

429
Q

Class II anti arrhythmia

A

Beta blocker

430
Q

Class III anti arrhythmia

A

K channel block

431
Q

Class IV anti arrhytmia

A

Calcium channel blocker

432
Q

Lidocaine

A

Na channel blocker

Greatest affinity for inactivated channels

Decreases automaticity

Decrease phase 4 slope

433
Q

Lidocaine uses

A

V tach

V fib

434
Q

Lidocaine adverse effects

A

CNS stimulation

435
Q

Amiodarone

A

Class III

Block Na, K, Ca channels

Alpha/Beta blocker

436
Q

Amiodarone effect on: AP duration
Refractory period
Conduction velocity
PR, QRS, QT intervals

A

AP duration - Prolonged

Refractory period - Prolonged

Conduction velocity - Slowed

Intervals - prolonged

437
Q

Amiodarone uses

A

V tach

V fib

Atrial fib when structural disease present

438
Q

Amiodarone toxicities

A

Cutaneous

Eye - Corneal deposits, optic neuritis

Lung - fibrosis

Cardiac - VT/VF

Liver - hepatitis

Thyroid - Hypo/hyper

439
Q

Amiodarone drug interactions - pharmacokinetic

A

Warfarin b/c inhibits CYP450

Digoxin - P-gp inhibition

440
Q

Beta blocker effect on:

SA/AV automaticity
AV nodal conduction
AV nodal refractory period

Net effect

A

Automaticity in SA/AV - Decreased

Nodal conduction - Slowed

Nodal refractory period - Prolonged

Net effect - Cardiac slowing

441
Q

A fib drug indication

A

Metoprolol

442
Q

Beta blockers and arrhythmias

A

A fib with RVR

A flutter

PSVT

Tachycardias

443
Q

Beta blocker AE

A

CV - aggravation of severe CHF, slow AV conduction

Pulmonary - Bronchospasm in severe asthmatics

444
Q

Beta blocker drug interactions

A

Drugs that impair Av conduction (Digoxin, Ca channel blocker)

445
Q

Calcium channel blockers

A

Blocks activated/inactivated CA channel

Slow AV conduction

446
Q

Indications for Ca channel blockers

A

SVT - slows ventricular rate

A fib - slow ventricular rate

447
Q

a wave

A

atrial contraction

448
Q

c wave

A

RV contraction

TV bulging into RA

449
Q

v wave

A

Increased RA pressure due to fill against closed TV

450
Q

Fixed splitting

A

Heard in ASD

Increased flow through RV so pulmonary valve closure is delayed

451
Q

Aortic area - systolic murmur

A

Aortic stenosis

Aortic valve sclerosis

Flow murmur

452
Q

Pulmonic area - systolic ejection murmur

A

Pulmonic stenosis

Flow murmur

453
Q

Tricuspid area - holosystolic murmur

A

Tricuspid regurgitation

VSD

454
Q

Tricuspid area - diastolic murmur

A

Tricuspid stenosis

ASD

455
Q

Mitral area - holosystolic murmur

A

Mitral regurgitation

456
Q

Mitral area - systolic murmur

A

Mitral valve prolapse

457
Q

Mitral area - diastolic murmur

A

Mitral stenosis

458
Q

ACCF/AHA Stage A

A

At risk for HF but no symptoms or structural disease

459
Q

ACCF/AHA Stage B

A

Structural disease but without signs/symptoms of HF

460
Q

ACCF/AHA Stage C

A

Structural heart disease with prior/current symptoms of HF

461
Q

ACCF/AHA Stage D

A

Refractory HF

Require special intervantion

462
Q

NYHA I

A

No limitation of physical activity

463
Q

NYHA II

A

Slight limitation of physical activity

Comfortable at rest but normal physical activity = HF symptoms

464
Q

NYHA III

A

Marked limitation of physical activity

Comfortable at rest but less than ordinary activity = HF symptoms

465
Q

NYHA IV

A

Unable to carry on any physical activity without HF symptoms

HF symptoms at rest

466
Q

Leading causes of HF

A

Ischemic heart disease

Cardiomyopathy

467
Q

Alcoholic cardiomyopathy

A

Dilated cardiomyopathy

468
Q

Cocaine cardiomyopathy

A

Long term use

Dilated cardiomyopathy without CAD, vasculitis, or MI

469
Q

Heart failure pathogenesis

A

Index event (MI etc) that decreases pumping capacity of heart –> compensatory mechanisms activated, restore CV functions so patient asymptomatic –> Long term compensatory mechanisms lead to secondary end organ damage within ventricle –> LV remodeling and cardiac decompensation

470
Q

Compensatory mechanism long term effects - Sympathetic system

A

Renin release

Can lead to:

Desensitization of Beta receptors

Myocyte hypertrophy, necrosis, apoptosis, fibrosis

Vasoconstriction in kidneys

471
Q

Compensatory mechanism long term effects - RAS

A

Can lead to:

Increase salt/water retention –> increased preload

472
Q

Aldosterone actions in compensatory response

A

Increase Na absorption and K excretion

Stimulation of collagen synthesis –> fibrosis (remodeling)

473
Q

ADH actions

A

Thirst stimulation

Water reabsorption

Vasoconstriction with increased SVR

474
Q

Long term effects of Salt/water retention

A

Caused by RAS, sympathetic, and ADH release

Pulmonary congestion and peripheral edema

475
Q

Long term effects of vasoconstriction

A

Caused by sympathetic and RAS

Increased cardiac afterload –> more energy needed from LV and further dysfunction

476
Q

Long term effects from sympathetic stimulation

A

Increased energy expenditure of heart –> can cause arrhythmias

477
Q

Short term effect of cardiac remodeling due to RAS/Sympathetic

A

Adaptive remodeling

Increased sarcomere number with increased CO

478
Q

Long term effect of cardiac remodeling due to RAS/sympathetic

A

Maladaptive

Accelerated cell death, arrhythmias, pathologic remodeling

479
Q

Platelets COX enzyme and PG activity

A

COX-1

Thromboxane

Vasoconstriction, platelet aggregation

Thrombosis

480
Q

Gastric mucosa COX enzyme and action

A

COX 1

Gastric protection (less acid)

481
Q

Joints COX enzyme and action

A

COX 2

Pain

Inflammation

482
Q

Endothelial cells COX enzyme and action

A

COX 2 mainly (slight COX1)

Vasodilation

Decreased platelet aggrefation

483
Q

Celecoxib

A

Selective COX-2 inhibitor

484
Q

Aspirin

A

Covalently modifies COX-1/2

Irreversible binding

485
Q

NSAIDs

A

Reversible block of COX enzymes

486
Q

How to limit Acetaminophen toxicity

A

N-acetylcysteine

Detoxifies NAPQI

487
Q

NSAIDs and pregos

A

NO!!!

488
Q

ACEH

A

Acid cholesterol ester hydrolase

Hydrolysis of cholesterol esters to form FFA and free cholesterol

489
Q

What increases LDL receptor formation?

A

Low INTRACELLULAR cholesterol concentration

SREBP mechanism induces transcription/translation of LDL

490
Q

VLDL: Source, ApoProteins, function

A

Source: Liver

ApoProteins: CII, E, B100

Function: FFA to adipose/muscle
CE –> LDL

491
Q

IDL: Source, apoProteins, function

A

Blood

E, B100

CE –> Liver via ApoE R

492
Q

LDL: Source, ApoProteins, Function

A

Blood

B100

CE –> peripheral cells via B100

493
Q

HDL: Source, apoP, function

A

Liver

A1, CII, E

Supply CII and E to VLDL

Reverse cholesterol transport

494
Q

LPL: Site of action, activator, function

A

Capillary walls

ApoCII

Excise FFA from TG in VLDL for use by adipose and muscle

495
Q

ACAT: Site of action, activator, function

A

Inside cells

Free cholesterol

Esterify cholesterol for storage

496
Q

LCAT: Site of action, activator, function

A

Blood

ApoA1

Esterifies free cholesterol and adds to HDL for transport to liver

497
Q

CERP: Site of action, activator, function

A

Plasma membrane

ApoA1

Flips Cholesterol and Lecithin to outer layer of membrane for LCAT action

498
Q

MTP: Site of action, activator, function

A

Intestine/liver/smooth ER

Loads TAG onto B100

499
Q

ApoA1: Site of action, function

A

Blood/plasma membrane

Activates LCAT/CERP. Binds ApoA1 receptor on cells for cholesterol extraction

500
Q

ApoB100: Site of action, function

A

Liver, cells

Ligand for LDL receptor, export/packaging of VLDL from liver into blood

501
Q

ApoCII: Site of action, function

A

Capillary walls

Activate LPL

502
Q

ApoE: Site of action, function

A

Liver

Return of IDL/LDL to liver after LPL activity

503
Q

Adenosine

A

Antiarrhythmic

Slow HR by decreasing K conductance

Bronchoconstriction

504
Q

Isoproterenol

A

B1 B2 direct agonist

Bronchodilator

Treat for heart block/arrest, shock

AE: HR increase, BP decrease

505
Q

Dobutamine

A

B1 direct agonist

Heart failure, cardiogenic shock

AE: Tachycardia, arrhythmias

CPR (3 decks)

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