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Cardiopulmonary > Mid term > Flashcards

Mid term Flashcards

1
Q

What is the secondary regulator of cross bridge cycling and may also control the length of the thin filament with tropomyosin?

A

Caldesmon

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2
Q

What works with tropomyosin and also is a secondary regulator of the crossbridge cycle?

A

Calponin

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3
Q

Tropomyosin works with ________, to INCREASE the activity of myosin ATPase?

A

Calponin

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4
Q

Tropomyosin works with _________, to decrease the rate of contraction?

A

Caldesmon

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5
Q

How much myosin is found in smooth muscle compared to skeletal muscle?

A

about 1/4

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6
Q

Nitriic oxide synthase splits _________ into ________ and _________

A

Arginine; NO; Citrulline

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7
Q

NO is an __________ and acts via the ___________ mechanism

A

Inhibitor; cGMP

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8
Q

Prostacyclin (PGI2) is derived from arachidonic acid via what enzyme?

A

cyclo-oxygenase

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9
Q

This neurotransmitters is hypothesized to be the major vasodilator and works by opening K+ channels, allowing it to leave the cell, thus hyperpolarizing the cell and preventing contraction

A

EDHF (endothelial derived hyperpolarizing factor)

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10
Q

This receptor only binds ET-1

A

ET-A receptor

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11
Q

This receptor binds all 3 endothelins

A

ET-B receptor

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12
Q

Explain the cascade that happens after ET-1 binds the ET-A receptor

A

1) Activation of G proteins
2) Production of PKC and IP3
3) release of Ca from the smooth muscle S.R.
4) Contraction of smooth muscle

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13
Q

What kind of effects are caused by an endothelin binding to an ET-B receptor?

A

trophic effects

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14
Q

neurotransmitters are released from what structures on the neuron when communicating with smooth muscle

A

varicosities

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15
Q

Adenosine causes what?

A

relaxation

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16
Q

Blood vessels arise from coalescence of hemangioblasts which aris from blood islands (large blood vessels develop this way)

A

Vasculogenesis

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17
Q

Vessel formation via branches arising from existing vessels

A

angiogenesis

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18
Q

Early vasulogenesis (week 3) begins where then formation moves where?

A

extraembryonic mesoderm around the yolk sack; lateral plate mesoderm

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19
Q

These cells are what are inside the blood islands and can differentiate into 2 populations of cells?

A

hemangioblasts

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20
Q

What 2 populations can hemangioblasts become?

A 
Endothelial cells (angioblasts)
hematopoietic stem cells
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21
Q

What causes the mesoderm cells to initially start to divide?
-this makes it a mitogen

A

FGF2

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22
Q

VEGF binds to VEGF-R2 (Flk1) to cause hemangioblasts to become what?

A

hemangioblasts (homatopoetic stem cells)

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23
Q

VEGF binds to VEGF-R1 (Flt1) to cause what?

A

hemangioblasts to become the tube (angioblasts)

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24
Q

What signals to express VEGF, which upregulates the VEGF receptor FLK1?

A

HOXB5

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25
Q

What induces loss of contact of endothelial cells with the extracellular matrix, resulting in either the absence of growth or death of endothelial cells? (destroys an area of the wall to allow a branch to bud off)

A

Ang2

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26
Q

What recruits periendothelial cells to come into newly forming vessel and make smooth muscle cells?

A

Ang1

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27
Q

What is used to develop and shape capillary beds appropriately?

A

EPCs (endothelial progenitor cells)

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28
Q

What, besides HOX genes, upregulates VEGF?

A

SHH

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29
Q

What pathway does VEGF work through?

A

Notch pathway

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30
Q

Notch pathway specifies arterial development through expression of what?

A

ephrinB2 ligand

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31
Q

What specific gene controls venous development?

A

EPHB4

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32
Q

What is the master gene for lymphatic vessel differentiation?

A

PROX1

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33
Q

Once the embryo is big enough to actually make thing inside it (end of first month), the fetus takes over production of blood cells where?

A

Aorta-gonad-mesonephros region (AGM)

-where primitive kidneys are forming

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34
Q

What takes over for the AGM to do hematopoiesis? (2-7 months)?

A

Liver

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35
Q

After 7 months, what takes over for the liver in doing hematopoiesis?

A

bone marrow

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36
Q

Abnormally dense collection of capillaries with an incidence of about 10%?

A

hemangioma

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37
Q

Superficial and deep dilated capillaries in the skin?

A

Naevus flammeus (Port wind stain)

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38
Q

What layer of the heart is a functional syncytium of striated cardiac muscle fibers forming 3 major types of cardiac muscle: atrial muscle, ventricular muscles, and specialized excitatory and conductive muscle fibers

A

myocardium

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39
Q

What are the specialized cells that regulate contraction of the heart (sinoatrial node and atrioventricular node)?

A

Nodal cells

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40
Q

What specialized cardiomyocyte produces atrial natriuretic factor?

A

myoendocrine cells

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41
Q

What does atrial natriuretic factor do?

A

stimulates both diuresis and excretion of sodium in urine by increasing the glomerular filtration rate, reduces blood volume

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42
Q

What layer of blood vessels contains vasa vasorum and nervi vasorum?

A

tunica adventitia

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43
Q

What vessels are regarded as the major determinants of systemic blood pressure?

A

arterioles

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44
Q

There are 3 kinds of capillaries, Continuous, Fenestrated, and Sinusoids. Where are fenestrated capillaries found?

A

GI and kidneys

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45
Q

Where are sinusoids (discontinuous capillaries) found?

A

Liver and spleen

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46
Q

How much actin is in smooth muscle compared to skeletal muscle?

A

twice as much

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47
Q

What ligament support the sternocostal joint?

A

Anterior radiate sternocostal ligament

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48
Q

What binds the costovertebral joint?

A

Radiate Ligament

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49
Q

What ligament goes from the crest of the head of the rib and stretches to the intervertebral disk?

A

Intraarticular ligament

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50
Q

What ligament binds a rib to the transverse process of the vertebra above it?

A

Superior costotransverse ligament

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51
Q

What ligament binds the rib to the same number vertebra transverse process?

A

Lateral costotransverse Ligament

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52
Q

Where does the intercostal neurovascular bundle run?

A

bt internal and innermost intercostal muscles

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53
Q

Referring to their relationship to pulmonary segments, arteries are _________ while veins are _________.

A

INTRAsegmental; INTERsegmental

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54
Q

What nerves can be involved in lung cancer?

A
  • Phrenic nerve
  • Vagus nerve
  • Recurrent Laryngeal nerve
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55
Q

What 2 cell types synthesize triacylglycerides?

A

hepatocytes and adipocytes

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56
Q

Dietary TAGs are broken down into what in the intestinal lumen?

A
  • free fatty acids

- 2-monoacylglycerol

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57
Q

Fatty acids need to be tagged with CoA in the intestinal cell in order to undergo reactions. What enzyme facilitates the tagging leading to Fatty acyl CoA?

A

Fatty Acyl CoA synthetase

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58
Q

Fatty acyl CoA combines with what to form Diacylglycerol (DAG)?

A

2-monoacylglycerol

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59
Q

TAGs in the intestinal cells are tagged with what?

A

apolipoproteins and other lipids

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60
Q

The TAGs from intestinal cells are packed into a lipoprotein called what?

A

chylomicron

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61
Q

What are the 2 sources of glycerol in hepatocytes?

A

free glycerol and glucose

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62
Q

Enzyme that is only in hepatocytes and converts glycerol to glycerol 3-P

A

Glycerol kinase

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63
Q

Enzyme that converts dihydroxyacetone phosphate (DHAP) to Glycerol 3-P in hepatocytes after glucose undergoes glycolysis to form the DHAP?

A

glycerol 3-phosphate dehydrogenase

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64
Q

What lipoprotein is made in the liver?

A

Very Low Density Lipoproteins (VLDL)

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65
Q

What enzyme is released from the adipocytes, lines the capillaries, and breaks down TAGs from chylomicrons and VLDLs to form Glycerol and fatty acids to form TAGs within the adipocytes?

A

capillary lipoprotein lipase

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66
Q

What is the source of Glycerol in adipocytes?

A

Glucose

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67
Q

Adipocytes don’t release their TAGs as lipoproteins. Instead they do what?

A

Store them

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68
Q

What affect does insulin have on adipocytes? 2 things

A
  • stimulation of capillary lipoprotein lipase

- increased activity of GLUT4 glucose transporter

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69
Q

Breakdown of TGs occurs where?

A

adipocytes

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70
Q

What enzyme inside the adipocytes catalyzes the breakdown of TAGs into a free fatty acid and DAG?

A

hormone-sensitive lipase

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71
Q

What hormones stimulate activation of hormone-sensitive lipase?

A
  • Glucagon
  • epinephrine
  • norepiniphrine
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72
Q

What inactivates hormone-sensitive lipase?

A

insulin

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73
Q

Short chain fatty acids released from adipocytes can freely travel through the blood. What happens to longer chain fatty acids?

A

They get carried by albumin

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74
Q

DAGs are broken down into fatty acid and MAGs by what enzyme?

A

lipoprotein lipase

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75
Q

MAGs are broken down into fatty acids and glycerol by what enzyme?

A

monoacylglycerol lipase

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76
Q

Explain the molecular steps involved in activating hormone-sensitive lipase.

A

1) Glucagon and epinephrine activate PKA via cAMP and GPCR cascade
2) phosphorylated PKA activates hormone sensitive lipase

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77
Q

Describe the inactivation of hormone sensitive lipase by insulin.

A
  • insulin activates protein phosphatase 1 (PP1)

- PP1 dephosphorylates hormone senstitive lipase-inactivation

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78
Q

What protein coats lipid droplets in adipocytes and muscle cells and regulates lipolysis by controlling physical access of HSL and can be a target to treat obesity?

A

perilipin

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79
Q

What regulates perilipins?

A

PKA phosphorylates them to make them leave the lipid droplets

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80
Q

Synthetic fat made of sucrose backbone with 6-8 fatty acids

  • no calories
  • no absorbed
  • absorbs vitamins (can cause deficiencies)
  • cramps, bloating, diarrhea
A

Olestra

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81
Q

What enzyme adds a fatty acid to cholesterol to form cholesterol ester?

A

acyl CoA acyl Transferase (ACAT)

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82
Q

What is the purpose of creating cholesterol esters?

A

makes is so hydrophobic that it can’t be part of the membrane anymore so it is packed in the core of the lipoprotein in droplets

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83
Q

Chylomicron properties

A
  • largest
  • least dense
  • high TAG content
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84
Q

apoproteins on chylomicrons

A
  • ApoB-48
  • ApoC-II
  • ApoE
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85
Q

Apoproteins for VLDLs

A
  • ApoB-100
  • ApoC-II
  • ApoE
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86
Q

Apoproteins for IDLs

A
  • ApoB-100

- ApoE

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87
Q

Apoproteins for LDLs

A

ApoB-100

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88
Q

What Apoprotein acts as a cofactor for capillary lipoprotein lipase?

A

ApoC-II

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89
Q

Why are LDLs bad?

A

highest density of cholesterol and can form plaques in blood

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90
Q

Apoproteins for HDL

A
  • ApoA-1
  • ApoC-II
  • ApoE
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91
Q

HDL properties

A
  • Smallest
  • Most dense
  • High protein and phospholipid content
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92
Q

Type 1 hyperlipoproteinemia (familial hyperchylomicronemia) is caused by what and has what effects?

A

Cause: Deficiency in ApoC-II or defective lipoprotein lipase
Effect: increased chylomicrons
increased TAGs

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93
Q

Type II hyperlipoproteinemia (familial hypercholesterolemia) is caused by what and has what effects?

A

Cause: LDL receptor is completely (IIa) or partially (IIb) defective
Effects: increased cholesterol
increased TAG (IIb), normal TAG in IIa
increased LDL
increased VLDL (IIb)

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94
Q

A nascent chylomicron contains what apoproteins?

95
Q

A nascnet chylomicron gets what Apoproteins added by HDLs to form mature chylomicrons?

A
  • ApoC-II

- ApoE

96
Q

What enzyme cleaves ApoE, along with glycerol and fatty acids from IDL to form LDLs?

A

hepatic lipoprotein lipase

97
Q

Statins block the rate limiting step of cholesterol biosynthesis which is catalyzed by what enzyme?

A

HMG-CoA reductase

98
Q

What space allows cardiac surgeons to access the area posterior to the aorta and pulmonary trunk to clamp or insert the tubes of a bypass machine into these large vessels?

A

Transverse Pericardial sinus

99
Q

What are the two terminating branches of the internal thoracic A.?

A
  • Superior Epigastric A.

- Musculophrenic A.

100
Q

What artery off of the internal thoracic A. runs with the phrenic nerve?

A

Pericardiacophrenic A

101
Q

Name the Paired Lateral Visceral Branches of the Thoracic Aorta

A

Bronchial Arteries

102
Q

Name the unpaired visceral branches off the thoracic aorta

A
  • Mediastinal A.
  • Esophageal A.
  • Pericardial A.
103
Q

Name the paired segmental parietal branches off the thoracic aorta

A
  • Posterior Intercostal A.

- Subcostal A.

104
Q

Lateral mammary arteries can come from what two sources?

A
  • Lateral Thoracic A.

- Lateral cutaneous branches of posterior intercostal A.

105
Q

What cardiac veins empty directly into the right atrium?

A

Anterior cardiac V.

106
Q

The posterior vagal trunk comes mostly from what?

A

Right vagus nerve (anterior vagal trunk from left Vagus nerve)

107
Q

Where does the phrenic nerve run, in relationship to the pericardium?

A

between fibrous pericardium and parietal pleura

108
Q

What are the Atypical intercostal nerves?

A

1 (brachial plexus)
2 (intercostobrachial nerve)
7th-11th (turn into thoracoabdominal nerves)

109
Q

The vagus nerve enters the thorax through what?

A

superior thoracic aperture

110
Q

How does the sympathetic nervous system affect non-sweat gland glandular secretion?

A

Indirectly through vasoconstriction

111
Q

What arteries do not get vasocontricted by the sympathetic nervous system?

A

Coronary Arteries

112
Q

Name the 4 Prevertebral ganglia?

A
  • Celiac ganglion
  • Superior mesenteric ganglion
  • Aorticorenal ganglion
  • Inferior mesenteric ganglion
113
Q

Epinephrine is produced by what cells?

A

Chromaffin cells

114
Q

Explain sympathetic activation of the eyes

A

1) alpha-adrenergic receptors of RADIAL muscles make it contract and dilate pupil letting more light in
2) BETA-2-adrenergic receptors of ciliary muscles of lens relax muscle causing flattening and can see distance better

115
Q

Explain sympathetic activation of the heart

A

1)Beta-1 and 2 adrenergic receptors –>increased heart rate and strength of contraction

116
Q

explain the general rule of thumb referring to receptors on vascular smooth muscle

A
  • alpha receptor cause contraction –>vasoconstriction

- Beta receptors cause relaxation –>vasodilation

117
Q

What areas only have alpha receptors?

A
  • Skin and mucosa
  • Salivary glands
  • brain
118
Q

What receptors cause smooth muscle relaxation and bronchodilation?

119
Q

on the Bronchial glands what receptors decrease secretion?

120
Q

on the bronchial glands, what receptors increase secretion?

121
Q

What receptors decrease motility of the digestive system?

A

Alpha 1 and Beta

122
Q

What receptors cause contraction of sphincters in the digestive system?

123
Q

What receptors cause a decrease in secretion in the digestive system?

124
Q

What receptors in the liver respond to sympathetic activation to increase glycogenolysis (release of glucose)?

A

Alpha 1 and Beta 2

125
Q

What receptors in the adipose tissue respond to sympathetic activation to increase lipolysis?

A

Alpha 1
Beta 1
Beta 3

126
Q

What forms the hard clot between two fibrins?

A

covalent bond between NH2 of glutamine and NH3 of Lysine

127
Q

What enzyme causes the formation of the hard clot?

A

Factor XIIIa-transglutaminase

128
Q

what activates factor XIII (transglutaminase)?

129
Q

Explain the importance of post translational modification of prothrombin?

A

Glutamic acid gets and an extra COO-, causing a double negative charge which attracts calcium released by exposed collagen

130
Q

What is required to modify Glutamate to gamma-carboxy-glutamate in prothrombin?

131
Q

What form of vitamin K is required to modify prothrombin and what enzyme does this?

A

reduced; epoxide reductase

132
Q

What drugs inhibit epoxide reductase?

A

anti clotting drugs

  • Warfarin (Coumadin
  • Dicoumerol
133
Q

What clotting factors besides prothrombin require vitamin K?

A

X, IX, VII

134
Q

What do you add to blood to find the time for a PTT test?

135
Q

What is added to blood to find the time for a PT test?

A

Tissue factor (Tissue thromboplastin)

136
Q

What is the PTT testing and what is the normal time?

A

factor XII–>fibrin clot (intrinsic and common pathways)

-35 seconds

137
Q

What is the PT testing and what is the normal time?

A

Factor VII to fibrin clot (extrinsic and common pathways)

-12 seconds

138
Q

Factor XIII deficiency is known as what?

A

hemophilia

139
Q

What causes the plateau (phase 2) in the slow cardiac action potential?

A

influx of calcium

140
Q

What channels cause the unstable prepotential of a slow cardiac action potential?

A

“funny” sodium channels

141
Q

What node has a greater density of “funny” sodium channels

142
Q

Normal time range for PR interval

A

.12-.2 seconds

143
Q

Normal QRS duration

A

up to .1 seconds

144
Q

normal QT interval duration

A

Up to .43 seconds (must be corrected for heart rate)

145
Q

Normal R-R interval (heart rate)

A

.6 to 1 sec (heart rate: 60-100bpm)

146
Q

On an ECG how much time is 1 little square?

A

.04 seconds

147
Q

What are the four components of hemostasis?

A

1) Vascular spasm
2) formation of platelet plug
3) formation of blood clot
4) repair of damage

148
Q

What stimulates platelet production?

A

thrombopoietin (TPO)

149
Q

what terminal of TPO is like EPO?

A

amine terminal

150
Q

What organs make TPO?

A

Liver and Kidney

151
Q

What controls throbopoietin secretion?

A

it binds to MPL receptor on platelets which interalize it and destroy it

152
Q

What are contained in platelet vesicles?

A
  • ATP and ADP
  • thromboxane Ax
  • fibrin stabilizing factor (clot stability)
  • Platelet-derived growth factor (repair)
  • Serotonin (5-HT)
153
Q

What are the primary causes of vascular spasm?

A

1) Myogenic-direct response to injury
- no neurons or reflexes involved
2) Platelet factors-Serotonin
- Thromboxane A2

154
Q

What contributes to the vascular spasm but on it’s own cannot initiate it?

A

Neural reflex initiated by the mechanical injury and pain

-neither necessary or sufficient for spasm to occur

155
Q

What plasma protein binds collagen to the collagen receptor on the platelet?

A

Von Willebrand Factor

156
Q

What does the platelet do upon activiation?

A
  • Swells

- Extends podocytes

157
Q

What causes platelet vesicles to be released?

A

contraction by actin and myosin after activation and swelling

158
Q

What triggers glycoproteins on the platelet membrane to become sticky?

A

Thromboxane A2 and ADP released from vesicles

159
Q

Explain getting rid of a clot

A

1) Tissue plasminogen activator is released by damaged tissue
2) this is inhibited by tPA inhibitor that is in blood
3) Once healed, endothelial cell expresses thrombomodulin which binds to thrombin and become an anticoagulant
4) This activates protein C
5) This inactivates the tPA inhibitor
6) tPA can now activate plasmin to lyse fibrin

160
Q

What chemicals LIMIT clotting

A

1) Fibin
- Binds thrombin and prevents it from working
2) Prostacyclin
- made at time of injury by endothelial cells
- vasodilation
- limit platelet aggregation
3) Antithrombin III
- when thrombin binds to it, works as an anticoagulant
4) Heparin
- derived from mast cells
- increases antithrombin efficacy

161
Q

What are the the 2 functions of activated protein C?

A
  • Inactivation of tPA inhibitor

- Inactivation of factors VIIIa and Va

162
Q

Explain the Leiden mutation

A

On factor V which prevents it from being inactivated by Protein C- causes blood clots

163
Q

What does the Primary heart field become?

A

Atria, Left ventricle, and part of the right ventricle

164
Q

What are formed by the secondary heart field?

A

Remainder of the right ventricle and the outflow tract (Conus cordis and truncus arteriosus)

165
Q

What is the master gene for left sided ness and can lead to heart defects

166
Q

describe the pathway leading to PITX2 expression

A

5HT(serotonin)–>FGF8–>Nodal and Lefty2–>PITX2

167
Q

What goes into the early primitive atrium?

A

Common cardinal vein (via posterior and anterior cardinal veins) taking blood from embryo back to the heart

168
Q

In the embryo where are red blood cells being made?

169
Q

What drains the red blood cells from the yolk sack to the embryological atrium?

A

Vitelline vein

170
Q

What brings oxygenated blood to the fetus?

A

umbilical vien

171
Q

What are the 5 embryological dilations in order of blood flow?

A
  • Sinus venosus
  • Primitive atrium
  • primitive ventricle
  • bulbus cordis
  • Truncus Arteriosus
172
Q

What does the Sinus venosus become in adult?

A
  • Smooth part of right atrium (sinus venarum)
  • Coronary Sinus
  • Oblique vein of left atrium
173
Q

What does the primitive atrium become in an adult?

A

Trabeculated part of right and Left atria (auricles)

174
Q

What does the primitive ventricle become in an adult?

A

Trabeculated part of right and left ventricles

175
Q

What does bulbus cordis become in an adult?

A
  • Smooth part of right ventricle (Conus Cordis)

- Smooth part of left ventricle (Aortic Vestibule)

176
Q

What does truncus arteriosus become in an adult?

A
  • Aorta

- Pulmonary Trunk

177
Q

What specificies the venus end of the endocardial tube?

A

retinoic acid

178
Q

Low concentrations of retinoic acid specify what in the endocardial tube development?

A

Anterior structures and outflow track

179
Q

In growth and development of the heart, what parts of the endocardial tube grow fastest?

A
  • Ventricles

- Truncus Arteriosus and bulbus cordis (outflow tract)

180
Q

Cardiac looping is dependent on what?

A

Laterality pathway and proper expression of transcription factor PITX2

181
Q

These types of ventricular septal defects require surgical correction?

A

membranous

182
Q

What type of ventricular septal defects are most common?

A

Muscular (These spontaneously close)

183
Q

If the ventricles aren’t separated and oxygenated and deoxygenated blood mix, where does blood tend to flow?

A

Lungs because there is less resistance which in turn increases arterial wall thickness thus increasing resistance making the right ventricle pump harder and hypertrophy

184
Q

What causes foreman ovale to close?

A

At birth, lungs open, right atrial pressure drops which causes blood to push other way on the septum and it fuses and closes.

185
Q

What do the vitelline veins contribute to in an adult?

A
  • hepatic sinusoids
  • inferior vena cava
  • GI veins
186
Q

What is the vein that is used to shunt blood from the left anterior cardinal vein to the right anterior cardinal vein to push all systemic blood to the right side of the developing heart?

A

brachiocephalic vein

187
Q

What are the adult remnants of the left horn of sinus venosum?

A
  • Oblique vein of left atrium
  • Coronary sinus
  • smooth part of right atrium
188
Q

What plays a role in partitioning the aorta and pulmonary trunk?

A

Neural crest cells

189
Q

Name the defect: Pulmonary stenosis, ventricular septal defect, overriding aorta, right ventricular hypertrophy

A

Tetrology of fallot

190
Q

Aortic arch IV makes what on the left and right respectively?

A

Aortic Arch; Right subclavian

191
Q

Aortic arch VI gives rise to what?

A
  • pulmonary arteries

- ductus arteriosus

192
Q

What keeps the ductus arteriosus open in utero?

A

prostaglandin E2

193
Q

What common medication can cause early closure of ductus arteriosus?

194
Q

Defect causing pulmonary veins to drain into the right atrium instead of left?

A

Total Anomalous Pulmonary Venous Return (TAPVR)

195
Q

How can a child survive with TAPVR?

A

They must have an atrial septal defect to get oxygenated blood to the left side of the heart
-or surgery

196
Q

Why is a double aortic arch a problem?

A

it can compress esophagus and trachea

197
Q

Baby is cyanotic, blood flow issues below diaphragm

-heart is ok and blood getting to head, neck and upper limb

A

Coarctation of aorta

198
Q

Heart outside of body

A

Ectobis cordis

199
Q

How do you modify the ionotropy of cardiac muscle?

A

Altering the amount of Ca++ available to bind to troponin

200
Q

What is a cardiac glycoside which increases the contractility of the heart without increasing the energy demands by blocking the Na+/K+ ATPase pump?

201
Q

What leads look at the inferior portion of the heart?

A
  • II
  • III
  • aVF
202
Q

What leads look at the septal portion of the heart?

203
Q

What leads look at the anterior portion of the heart?

204
Q

What leads look at the lateral portions of the heart?

A
  • I
  • aVL
  • V4
  • V5
  • V6
205
Q

What lead usually shows an inverted P wave for a normal functioning atrium?

206
Q

What leads normally show an upright P wave?

A

1, 2, V4-V6, aVF

207
Q

What is represented by a prolonged P-R interval? Greater than .2 sec?

A

First degree AV block

208
Q

What is represented by a shortened (less than .12 sec) PR interval?

A

Pre excitation syndromes

209
Q

What is the most common Pre-excitation syndromes (causes shortened PR interval?

A

Wolf-Parkinson- White syndrome (WPW)

210
Q

What is the normal QRS complex duration?

A

.05-.11 sec

211
Q

What leads normally have narrow/small Q waves? (1-2 mm)

A

1, aVL, aVF, V5, and V6

212
Q

What is wrong when there is an absence of the small Q waves in the leads where you should see them?

A
  • bundle branch block

- ventricular hypertrophy

213
Q

The T wave is normally upright in what leads?

A

1, 2, V3-V6

214
Q

The T wave is normally inverted in what leads?

215
Q

In the standard leads, the T wave should not be greater than ________.

216
Q

in the precordial leads, the T wave should not be greater than ________.

217
Q

What pathology should you be thinking if you see an irregular Q wave?

A

Necrosis or infarction

218
Q

What is the name of the bundle that originates at the SA node and distributes depolarization to the left atrium?

A

Bachmann’s bundle

219
Q

What are the two locations of baroreceptors in the arterial system?

A

Carotid sinus

Aortic arch

220
Q

If a patient has sinus bradycardia and is also hemodynamically compromised what drug is used for initial treatment?

221
Q

What do you treat Supraventricular tachycardia with? SVT?

222
Q

A chest tube is normally placed in what intercostal space?

A

5th or 6th

223
Q

Velocity=?

A

Q/A; flow or cardiac output/cross sectional area

224
Q

Q=?

A

DP/Resistance; Pressure gradient/resistance

225
Q

CO=?

A

1) (arterial pressure - venous pressure)/ TPR;

2) SVxHR

226
Q

Poiseuille’s law states that Resistance R=?

A 
(8hL)/(pr^4)
h=viscosity
L=length of vessel
p=pi
r=radius of vessel
227
Q

Reynold’s number predicts when turbulence will occur. What is this equation?

A 
Nr=rdv/h
r=density
d=diameter
v=velocity
h=viscosity
228
Q

When the reynolds number reaches this number, turbulence occurs?

229
Q

Compliance = ?

A

change in volume/change in pressure

230
Q

Pulse Pressure=?

A

systolic-diastolic pressure

231
Q

Mean pressure=

A

Diastolic + 1/3 X pulse pressure

232
Q

BP=

233
Q

Renin is released into the bloodstream from the kidneys in response to what?

A

Drop in blood pressure

234
Q

List off the affects that Angiotensin II has?

A

1) increases aldosterone secretion from adrenal cortex
2) acts directly on kidneys to increase Na+ and water retention
- Same effect as aldosterone (up blood volume, preload, stroke volume, and therefore BP
3) increase thirst
4) increase ADH secretion
5) cause global vasoconstriction

Cardiopulmonary (2 decks)

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