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Cardiac ROTATION > Concepts/Hemodynamics > Flashcards

Concepts/Hemodynamics Flashcards

1
Q

Cardiac output definition

A

amount of blood ejected by the LV in 1 minute.

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2
Q

CO may be determined by what test

A

cardiac catheterization

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3
Q

CO formula

A

SV X HR

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4
Q

Normal CO =

A

4-8 L/min

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5
Q

3 factors affecting cardiac output

A

Changes in HR
Changes in contractility
Changes in venous return

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6
Q

How does excessive High HR affects cardiac output?

A

excessively high HR, ↓diastolic filling time thus ↓ CO

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7
Q

Changes in contractility affect CO how?

A

↑ Sympathetic activity causes ↑ myocardial contractility (positive inotropy) and thus more blood is ejected (↑ SV); this ↑ CO

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8
Q

What change in preload affect CO?

A

↑ preload, ↑ force of contraction thus ↑ CO

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9
Q

Changes in resistance increase or decrease will affect

A

SV and CO

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10
Q

High afterload effect on SV and CO

A

= ↓ SV and ↓ CO

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11
Q

Changes in venous return

A

↓ blood volume, ↓ venous return, ↓ preload = ↓ SV and ↓ CO

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12
Q

Venous constriction effect on venous return, SV, and CO

A

= ↑ venous return to the heart, ↑ preload,

↑ SV, ↑CO

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13
Q

Cardiac index is the

A

CO corrected for differences in body size.

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14
Q

CI is based on

A

It is based on body surface area (BSA)

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15
Q

CI formula is

A

CI = CO/BSA

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16
Q

Normal CI =

A

2.5 - 4L/min

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17
Q

2 things that increase CI

A

Exercise

Mild tachydysrhythmias

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18
Q

2 things that my decrease CI

A

Decrease myocardiac contractility, MI, CHF, cardiomyopathy and electrolyte imbalance

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19
Q

Increase afterload ______CI

A

decrease

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20
Q

Things that can increase afterload

A

Valvular stenosis and pulmonary HTN

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21
Q

Changes in preload that can decrease CI

A

Hypovolemia

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22
Q

How does tachy and irregular rhythm decrease CI

A

↓ diastolic filling time and causes loss of atrial kick.

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23
Q

What is Stroke Volume (SV)?

A

SV is the amount of blood ejected by the ventricle with each contraction; the difference between end-diastolic volume and end-systolic volume

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24
Q

SV formula

A

EDV-ESV

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25
Q

What is ejection fraction?

A

The percent of how much blood is pushed out of the left ventricle during contraction verses how much was there prior to contraction

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26
Q

Normal EF is

A

greater than 50 % but usually 60-75%

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27
Q

Preload is the___? What is it determined by ?

A

stretch on the myofibrils at the end of diastole; determined by the pressure in the ventricle at the end of diastole.

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28
Q

The pressure or volume in the ventricles at the end of diastole.

A

Preload

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29
Q

↑ preload is accomplished by

A

↑ volume return to the ventricles

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30
Q

Evaluation of preload: What evaluated RV preload?

A

RV preload = CVP or RAP (Right Atrial Pressure)

Note as preload ↑, myocardial oxygen demand/consumption ↑

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31
Q

What evaluates LV preload?

A

o LV preload = PAOP or LAP (Left Atrial Pressure)

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32
Q

Mitral valve stenosis on preload

A

Increase

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33
Q

Mitral insufficiency on preload

A

Increase

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34
Q

Aortic insufficiency on preload

A

Increase

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35
Q

Increase blood volume on preload

A

Increase

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36
Q

Decrease blood volume on preload

A

Decrease

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37
Q

Vasodilators on preload

A

Decrease

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38
Q

Vasoconstrictors on preload

A

Increase

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39
Q

Afterload is the pressure

A

against which the ventricle must pump to open the

semilunar valve.

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40
Q

Vascular resistance:
o RV afterload =
o LV afterload =

A

oPVR (Pulmonary Vascular Resistance)
oSVR (Systemic Vascular Resistance)
o Ventricular diameter
o Mass and viscosity of blood

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41
Q

Mass and viscosity of blood affect

A

Vascular resistance

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42
Q

As afterload increase, what happens to myocardial oxygen demand/consumption

A

Increase

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43
Q

Aortic valvular stenosis effect on afterload

A

Increase

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44
Q

Aortic valvular stenosis effect on afterload

A

Peripheral arterial vasonstriction

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45
Q

Hypertension effect on afterload

A

Increase

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46
Q

How does polycythemia affect afterload?

A

Increase

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47
Q

Drug that ↓ afterload

A

Hydralazine

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48
Q

Drugs that ↑ afterload:

A

LED
Levophed
Epinephrine
Dopamine

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49
Q

What is the intrinsic rate of a transplanted heart? i.e. non-innervated = no vagus nerve innervation.

A

120-130 BPM

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50
Q

What does Frank Starling’s Law mean?

A

Starling‟s Law states that the greater the stretch of the cardiac muscle, the more forceful the heart‟s contraction and beat.

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51
Q

Frank Starling’s Law limitation, When the muscle is overstretched, the force of contraction may

A

decrease below normal levels, causing circulatory failure.a rubber band breaking when stretched too far, rendering it useless.

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52
Q

Nicotinic receptors are located on

A

Located on the motor endplate

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53
Q

o All neuromuscular blocking agents work here.

A

Nicotinic receptors.

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54
Q

Pulsus paradoxus what is it? How do you treat it? What is in an indication of?

A

Pulsus paradoxus is an exaggeration of normal physiologic response to inspiration.

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55
Q

Pulsus paradoxus normal BP vs BP with inspiration

A

The normal ↓ BP during inspiration 10 mm Hg or less; therefore a BP ↓ > 10 mm HG during inspiration is pulsus paradoxus.

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56
Q

What are three things that PULSUS PARADOXUS INDICATES? Cardiac wise

A

Pericardial effusion
Constrictive pericarditis
Cardiac tamponade
Advance cardiogenic shock

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57
Q

What are three things that PULSUS PARADOXUS INDICATES? other than cardiac

A

Severe lug disease
advanced heart shock
hemorrhagic shock

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58
Q

Main treatment of cardiac tamponade

A

The main cause is cardiac tamponade and the treatment would be pericardiocentesis.

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59
Q

There is a patient having a laminectomy (bloody surgery). The orthopedic physician wants the patient to be hypotensive in order to decrease blood loss. An
ABG is drawn after the case has been going on for 4 hours. The patient is in metabolic acidosis. Why? and what solution (2 possible) ? if the physician ignore and wants pt hypotensive?

A

The increase blood loss leads to ↓ oxygen carrying capacity
Patient is hypotensive, ↓ peripheral perfusion
This ↓ in O2 capacity and ↓ perfusion causes the body to stop aerobic metabolism and switch to anaerobic metabolism
The byproduct of anaerobic metabolism is LACTIC ACID>.
Return the patient to a normotensive state by giving IVF and blood in order to correct the acidosis.
2. If # 1 does not work, then give NaHCO3
- You must stop the case, because if the patient stays acidotic and hypotensive they will expire.

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60
Q

Parasympathetic Nervous System

Cholinergic: dominant when?

A

Calm situations

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61
Q

Sympathetic Nervous System

Cholinergic: dominant when?

A

Crisis situations

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62
Q

Promotes activities that restore the body’s energy and resources

A

Cholinergic

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63
Q

Promotes activities that prepare the body

for crisis situations

A

Sympathetic nervous system

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64
Q

Eyes with parasympathetic

A

Constrict

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65
Q

Eyes with Sympathetic

A

Dilate

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66
Q

Parasympathetic on heart

A

↓ Rate, ↓ contractility

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67
Q

Sympathetic on Heart

A

Heart: ↑ Rate, ↑ contractility

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68
Q

Parasympathetic on lungs

A

bronchoconstriction

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69
Q

Sympathetic on lungs

A

Bronchodilation

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70
Q

ParaSympathetic on liver

A

Glycogenesis

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71
Q

Sympathetic on Liver

A

Glycogenolysis, Lipolysis

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72
Q

Parasympathetic on GI

A

↑ secretion ↑Salivary flow, ↑ Motility,

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73
Q

Sympathetic on GI

A

↓Salivary flow, ↓ Motility, ↓secretion

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74
Q

Bladder and parasympathetic

A

Bladder contracted

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75
Q

Sphincter and parasympathetic

A

Sphincter open

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76
Q

Bladder and sympathetic

A

Bladder relaxed

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77
Q

Sphincter and sympathetic

A

Sphincter closed.

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78
Q

Parasympathetic on adrenal gland

A

No effect

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79
Q

Sympathetic on adrenal gland

A

Secretes epinephrine and norepinephrine

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80
Q

First Degree A-V Block definition

A

o A delay in passage of impulse from the atria to the ventricles.

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81
Q

First Degree A-V Block Treatment is

A

usually unnecessary when it is asymptomatic

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82
Q

Second Degree A-V Block definition

A

Some impulses are conducted and others are not.

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83
Q

Second degree AV block Divided into 2 categories:

A

Type I Wenckebach

Type II Mobitz

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84
Q

Type I Wenckebach usually occurs at? due to ?

A

Usually occurs at the level of the AV node and is often due to increased parasympathetic tone or to drug effect (digitalis, propranolol, verapamil). It is

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85
Q

Type I Wenckeback characteristics

A

characterized by a progressive prolongation of the PR interval until an impulse is completely blocked.

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86
Q

Treatment of 2nd degree AVB type I ? What is priority?

A

o Treatment is rarely needed unless severe S/S are present. Priority given to identifying cause.

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87
Q

Type II Mobitz 2nd Deg AVB.This form of AV block occurs

A

below the level of the AV node either at the

bundle of HIS or bundle branches.

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88
Q

The hallmark of Type II Mobitz 2nd Deg AVB. block is that the

A

PR interval does not lengthen before a dropped beat

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89
Q

Type II Mobitz 2nd Deg AVB usually associated with

A

It is usually associated with an organic lesion in the conductive pathway and thus associated with a poorer prognosis and a complete heart block may develop.

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90
Q

Treatment (Bradycardia algorithm) of type II Mobitz 2nd deg AVB

A

Atropine 1 mg rapid IVP: for symptomatic bradycardia
Transcutaneous / Transvenous pacemaker
Catecholamine infusions: Dopamine, Epi, Levophed
Permanent pacemaker.

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91
Q

Third Degree A-V Block indicates

A

Complete absence of conduction between the atria and the ventricles.

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92
Q

Treatment of Third Degree A-V Block

A

Atropine 1 mg rapid IVP: for symptomatic bradycardia
Transcutaneous / Transvenous pacemaker
Catecholamine infusions: Dopamine, Epi, Levophed
Permanent pacemaker

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93
Q

Third degree AV block at the AV node may be caused by

A

increased parasympathetic tone associated with inferior infarction, toxic drug effects (digitalis, propranolol) or damage to the AV node

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94
Q

o Third degree AV block at the infranodal level is usually associated with

A

Infranodal conduction disease. May also be due to coronary atherosclerosis, which is usually associated with an extensive anterior MI.

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95
Q

Your patient is in congestive heart failure (CHF). What would you do? What are the signs and symptoms, and treatment?

A

CHF is a state in which there is impaired cardiac function such that the ventricle is unable to maintain a CO sufficient to meet the metabolic needs of the body.

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96
Q

Structures that tend to fail in a patient with CHF?

A

The LV, RV, or both fail.

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97
Q

Left side heart failure: Explain what happens to CO, LV pressure and volume and LV issue?
Is the LA able to empty in the LV? What happens to LA pressure? How does that affect the lungs?

A

Left sided heart failure
↓ CO, ↑ LV pressure and volume. -LV can‟t pump blood returning from the lungs…
o LA unable to empty into LV thus ↑ LA pressures.
o LA pressure reflected back to lungs producing pulmonary congestion.

98
Q

When pulmonary congestion occurs what happens to pulmonary pressure?

A
  1. Pulmonary pressure causes fluid to leak = pulmonary edema.
  2. Oxygenation of blood as O2/CO2 exchange is impeded.
99
Q

o Pressure to lungs : Increase pressure in the right side effects.

A

↑ pressure to the right side of heart.
o Right heart can‟t pump to lungs due to ↑ pressure in the pulmonary vasculature.
o Venous return impeded as right side of heart fails
o As Pressure builds, body organs become congested with venous blood.

100
Q

o Right-sided heart failure may occur first in the case of

A

RV infarcts.

101
Q

Top causes of Left sided heart failure; be able to say at least first 4

A
  1. Acute LV MI
  2. Cardiomyopathy
  3. Atherosclerotic heart disease
  4. ↑ circulating volume
  5. Aortic stenosis/insufficiency
  6. Cardiac tamponade
  7. Mitral stenosis/ insufficiency
  8. Tachy/Bradycardia
102
Q

Top causes of Right sided heart failure: be able to say at least first 4

A
  1. Left-sided heart failure
  2. Atherosclerotic heart disease
  3. Acute RV MI
  4. Tachy/Bradycardia
  5. Pulmonary embolism
  6. Fluid overload
  7. Excess sodium intake
  8. Mitral stenosis
  9. Atrial or ventricular septal defect
  10. Pulmonary outflow stenosis
  11. COPD
  12. Pulmonary hypertension
  13. Cor Pulmonale
103
Q

Cor pulmonale is HF due to

A

Lung pathology

104
Q

General symptoms /Clinical Manifestations of HF

A

Chest discomfort, SOB, orthopnea, paroxysmal nocturnal dyspnea, weight gain, ↓ urination, edema

105
Q

Right sided HF signs and symptoms

A 
Right Depend E JAH
Dependent edema
JVD
Ascites
Hepatomegaly
106
Q

Left sided HF signs and symptom s

A 
Orthopnea
Cyanosis
Hypoxia
Dyspnea
More systemic signs
107
Q

Cough with Frothy sputum is sign of what kind of HF

A

LEFT

108
Q

Treatment of HF

A

Cardiac glycosides and AMRINONE

109
Q

Amrinone mechanism of action

- cardiac contractility

A

↑ cardiac contractility without ↑ rate by ↑ cellular levels of cyclic AMP

110
Q

Amrinone and vascular smooth

A

Relaxes vascular smooth muscle producing peripheral vasodilation (↓ preload and ↓ afterload

111
Q

Amrinone bolus and infusion

A

Initial bolus 0.75-1.5 mcg/kg over 2-3 min followed by infusion 5-10 mcg/kg/min.

112
Q

Vasodilators action in patient with HF

A

improve LV function by lowering systemic vascular resistance: ↓ afterload
o Nitroglycerin
o Nitroprusside

113
Q

What is a quick fix for hyperkalemia?

A

Glucose, insulin and NaHCO3:

114
Q

Action of Glucose insulin and bicardbonate in HYPERKalemia

A

temporarily drive K+ into cell

115
Q

Why give NaCO3, how does it drive K+ into the cell?

A

Because the cells are trying to compensate for the acidic environment by exchanging K+ out of the cell and H+ into the cell

116
Q

Ca++ Chloride or Ca++ gluconate IV to stimulate

A

cardiac contractility: contraindicated in patients on digoxin

117
Q

After giving insulin , glucose and. NaHCo3

A

Follow up with Kayexalate and sorbitol or HD for permanent removal

118
Q

Calcium is contraindicated in what kind of patients

A

DIGOXIN

119
Q

What is angina and how do you treat it?

o Angina-

A

a state of transient myocardial ischemia without cell death

120
Q

Ischemia- Local and temporary deficiency of blood supplies due to

A

obstruction of circulation to a part. Ischemia leads to anaerobic metabolism and accumulation of lactic acid, causing chest pain

121
Q

Epinephrine is used to

A

used to ↑ CO by ↑ HR, resulting in an ↑ in cerebral and coronary blood flow and an ↑ in SVR

122
Q

First-line drug for any pulseless rhythm

A

Epinephrine

123
Q

Epinephrine dose

A

1 mg IV push Q 3-5 minutes.

124
Q

Epinephrine CO, PAOP, SVR, MAP, HR, CVP and PVR

A

↑ CO, ↑PAOP, ↑SVR, ↑MAP, ↑HR, ↑CVP, ↑PVR

125
Q

Epinephrine dose infusion

A

1 - 4 mcg/min

126
Q

A natural catecholamine that is the immediate precursor of norepinephrine

A

Dopamine

127
Q

When is dopamine used?

A

It is used to ↑ low BP refractory to fluid therapy, to treat heart failure, increase renal perfusion, and correct hemodynamic imbalance in shock syndrome.

128
Q

Dopamine Onset and duration

A

5 minutes, duration 10 minutes.

129
Q

Low dose dopamine

A

Low dose (renal perfusion) + 1-3 mcg/kg/min

130
Q

Dopamine Medium dose

A

(↑ contractility) = 3-10 mcg/kg/min. (Vasoconstriction) > 10 mcg/kg/min.

131
Q

Dopamine side effects at high doses

A

May induce myocardial ischemia. Nausea and vomiting especially at high doses

132
Q

Relative Contraindications to the use of dopamine

A

o The presence of ↑ vascular resistance, pulmonary congestion, or ↑ preload is a relative contraindication to the use of dopamine

133
Q

Dopamine precautions at high doses

A

o Renal ischemia at high doses.

o Tissue sloughing if IV infiltrates

134
Q

High dose of dopamine (works like Levophed)

A

> 20 mcg/kg/min

135
Q

Dobutamine (Dobutrex)

A

Synthetic sympathomimetic catecholamine with inotropic, chronotropic and vasodilator effects.

136
Q

What receptors does dobutamine stimulates?

A

It stimulates β1 and α1 receptors.

137
Q

When to use dobutamine?

A

Useful in treating heart failure (especially with ↑ SVR and PVR), to increase contractility with no significant increase in heart rate.

138
Q

Dopamine vs dobutamine

A

It is similar to dopamine but does not cause a significant rise in BP.

139
Q

Dobutamine actions on CO, PAOP, SVR, MAP, HR, CVP and PVR

A

↑ CO, ↓ PAOP, ↓ SVR, ↑ MAP, ↑ HR (slowly), ↓ CVP, ↓P

140
Q

Dobutamine infusion rate

A

Infuse at 2-10 mcg/kg/min. May go up to 40 mcg/kg/min. with MD approval.

141
Q

This medication May induce myocardial ischemia.

A

Dobutamine

142
Q

SE of Dobutamine

A

HA, nausea, tremor and ↓ K+

143
Q

Atropine is an _____how does it work?

A

An anticholinergic parasympathetic. (Muscarinic receptors) It ↑ CO and ↑ HR by blocking cardiac vagal stimulation in the heart.

144
Q

Atropine used in

A

Used in bradycardia and bradydysrhythmias, blocking cardiac vagal reflexes (also to ↓ secretions and broncodilitation)

145
Q

Atropine dose

A

IV: give 1 mg q 3-5 minutes, not to exceed 3 mg.

Give rapid IVP as pushing slowly may cause paradoxical bradycardia lasting 2 minutes.

146
Q

Morphine is a

A

Narcotic analgesis

147
Q

3 main action of morphine

A

It relieves pulmonary congestion, lowers myocardial O2 consumption, and reduces anxiety.

148
Q

Analgesia of choice in pain associated with MI.

A

Morphine

149
Q

Morphine on veins and preload

A

Dilates veins and ↓ preload.

150
Q

SE of Morphine

A

Side effects include respiratory depression, hypotension, ↑ ICP, N/V.

151
Q

Antidote of morphine

A

Narcan.

152
Q

Nipride (Nitroprusside). What is it and what is the action on CO, LV and BP

A

A venous and arterial dilator used to ↑ CO by ↓ LV afterload, to ↓ blood pressure in hypertensive crisis, and to ↓ pulmonary hypertension

153
Q

Nitroprusside actions on CO, PAOP, SVR, MAP, HR, CVP and PVR

A

↑ CO, ↓ PAOP, ↓ SVR, ↓ MAP, ↑ HR, ↓ CVP, ↓ PVR Infuse

154
Q

Nitroprusside dosing

A

0.5 – 10 mcg/kg/min.

155
Q

How long is nitroprusside solution stable for

A

24 hours

156
Q

What should you check for nitroprusside? when?

A

Check thiocyanate level if infusion continues longer than 72 hour or if rate ≥ 4 mcg/kg/min.

157
Q

Signs of Nitroprusside toxicity

A

Almond breath Antidote: Amyl nitrate inhaled, NA thiosulfate IV.

158
Q

Nitroglycerin (Tridil) What is it and what is it used for?

A

A venous vasodilator used to ↓ preload and afterload in LV failure. It is also used for myocardial ischemia and as a dilator for coronary vasculature.

159
Q

NTG dosing

A

There is no optimum fixed dose. Titrate to response. Most patients respond to 50 – 200 mcg/min.

160
Q

NTG precautions.

A

Precautions: When piggybacking, do so close to the insertion site as tubing can absorb 40% -80% of drug.

161
Q

Nitroglycerin solution stable for ? how about tolerance

A

Solution stable only 24 hours

Patients develop tolerance over 1-2 days.

162
Q

Patient has hyponatremia, why?

A

Hyponatremia is when an excess of water relative to the amount of sodium in the body produces a dilutional effect on sodium concentrations.

163
Q

What is hyponatremia?

A

Sodium < 136

164
Q

SIADH is a

A

condition characterized by impaired renal excretion of water, resulting in oliguria, high urine specific gravity, water intoxication and hyponatremia.

165
Q

Other causes of hyponatremia include:

A

Sodium depletion
Diuretics
 Diarrhea
 Nasogastric suction
 Abnormal losses via diaphoresis
 Salt-losing renal diseases: interstitial nephritis
 Hyperglycemia (glucose induced diuresis)

166
Q

Other causes of hyponatremia include:

A
  • Sodium depletion
  • Diuretics
  • Diarrhea
  • Nasogastric suction
  • Abnormal losses via diaphoresis
  • Salt-losing renal diseases: interstitial nephritis
  • Hyperglycemia (glucose induced diuresis)
167
Q

Kidneys when there is excess sodium?

A

o Kidneys may retain larger amounts of water in excess of sodium

168
Q

Normal ICP

A

0-15 mmHg

169
Q

CPP (Cerebral perfusion pressure)

A

CPP = MAP – ICP

170
Q

What does CPP represents?

A

This represents the pressure gradient driving cerebral blood flow (CBF) and hence oxygen and metabolite delivery

171
Q

CPP normal pressure

A

o Normal 70-100 mmHg

172
Q

Trace the path of blood through the heart

A 
Inferior, Superior (Common) Vena cava
↓
Right Atrium
↓
Tricuspid Valve
↓
Right Ventricle
↓
Pulmonic Valve
↓
Pulmonic Artery
↓
Lungs
↓
Pulmonary Vein
↓
Left Atrium
↓
Mitral (Bicuspid) Valve
↓
Left Ventricle
↓
Aortic (Semilunar) Valve
↓
Aorta
↓
Systemic Circulation
173
Q

Describe the relationship between CO2 and a head injury.

A

A PaCO2 of 30-35 mmHg (moderate hyperventilation) causes vasoconstriction (arterial) and thus decreases cerebral blood volume. Decreasing the cerebral blood volume will decrease the intracranial pressure. CO2 is a potent vasodilator.

174
Q

If you continue to hyperventilate the patient in 12 hours will they still be vasoconstricted?

A

Yes

175
Q

OxyHemoglobin Dissociation Curve

This curve describes the relationship between

A

available oxygen and amount of oxygen carried by hemoglobin.

176
Q

Horizontal axis and vertical axis of the oxyhemoglobin dissociation curve.

A

The horizontal axis is Pa02, or the amount of oxygen available. The vertical axis is SaO2, or the amount of hemoglobin saturated with oxygen.

177
Q

Once the PaO2 reaches 60 mm Hg the OxyHgb dissociation curve is

A

almost flat, indicating there is little change in saturation above this point.
o So, PaO2 of 60 or more is usually considered adequate.

178
Q

OxyHgb dissociation curve at less than 60 mmHg

A

less than 60 mm Hg the curve is very steep, and small changes in the PaO2 greatly reduce the SaO2. The term “affinity” is used to describe oxygen’s attraction to hemoglobin binding sites.

179
Q

OxyHgb dissociation curve at less than 60 mmHg

A

less than 60 mm Hg the curve is very steep, and small changes in the PaO2 greatly reduce the SaO2.

180
Q

The term “affinity” is used to describe

A

oxygen’s attraction to hemoglobin binding sites.

181
Q

Oxyhgb Affinity changes with

A
  • variation in pH,
  • temperature,
  • CO2 and,
  • 2,3,-DPG
  • a metabolic by-product which competes with O2 for binding site
182
Q

Traditionally the curve starts with:

A
  • pH at 7.4,
  • temperature at 37 Centigrade, and
  • PaCO2 at 40.
  • Changes from these values are called “shifts”.
183
Q

A left shift will on oxyhgb

A

increase oxygen’s affinity for hemoglobin.

o In a left shift condition (alkalosis, hypothermia, etc.) oxygen will have a higher affinity for hemoglobin.

184
Q

With a left shift, SaO2 will increase at a

A

given PaO2, but more of it will stay on the hemoglobin and ride back through the lungs without being used. This can result in tissue hypoxia even when there is sufficient oxygen in the blood.

185
Q

A right shift and affinity

A

decreases oxygen’s affinity for hemoglobin.

186
Q

o In a right shift (acidosis, fever, etc.) oxygen has a ____What does it means?

A

lower affinity for hemoglobin. Blood will release oxygen more readily.This means more O2 will be released to the cells, but it also means less oxygen will be carried from the lungs in the first place.

187
Q

Temperature- Increasing the temperature does what?

A

denatures the bond between oxygen and hemoglobin, which increases the amount of oxygen and hemoglobin and decreases the concentration of oxyhemoglobin. The dissociation curve shifts to the right.

188
Q

pH- A decrease in pH (increase in acidity) by addition of carbon dioxide or other acids causes a

A

Bohr Shift.

189
Q

A Bohr shift is characterized by

A

causing more oxygen to be given up as oxygen pressure increases and it is more pronounced in animals of smaller size due to the increase in sensitivity to acid

190
Q

The ejection fraction is a

A

measurement of the heart’s efficiency and can be used to estimate the function of the left ventricle, which pumps blood to the rest of the body.

191
Q

The left ventricle pumps only a fraction of the blood it contains. The ejection fraction is the

A

amount of blood pumped divided by the amount of blood the ventricle contains.

192
Q

A normal ejection fraction is more than

A

55% of the blood volume.

193
Q

If the heart becomes enlarged, even if the amount of blood being pumped by the left ventricle remains the same, the relative

A

fraction of blood being ejected decreases.

194
Q

A healthy heart with a total blood volume of

A

100 mL that pumps 60 mL to the aorta has an ejection fraction of 60%.

195
Q

Define PEEP.

A

Positive end expiratory pressure (PEEP) is a mode of therapy used with mechanical ventilation. At the end of exhalation the patient‟s airway pressure is maintained above atmospheric pressure. The purpose is to prevent alveolar collapse at end expiration.

196
Q

Benefits of PEEP

A

o Improve functional residual capacity (FRC)

o Enhance oxygen transport (allows for > PaO2 without requiring ↑ FI

197
Q

What are the complications of PEEP?

A

Complications
o Impaired venous return, resulting in ↓ C.O.
o ↓ venous return, ↓C.O. ↓O2 delivery even though ↑ PaO2
o Barotrauma- rupture of lung tissue. PEEP levels >15 cm H2O are considered dangerous (tension pneumo).

198
Q

Blood goes from

A

High pressure (Arteries) to Low pressure (Venous)

199
Q

Pulse ox reads Hgb saturation in the

A

arteries.

200
Q

Anterior Cerebral Artery supplies what lobes?

A

o Supplies frontal and Parietal Lobes

o Supplies leg area of precentral gyrus

201
Q

Middle Cerebral Artery (MCA)

A

Supplies most of the basal ganglia and parts of internal capsule.

202
Q

Supplies almost all cortical surface of brain.

A

MCA

203
Q

Internal Carotid Artery

A

o Supplies portions of basal ganglia

o Supplies part of internal capsule.

204
Q

o Supplies Circle of Willis

A

Internal Carotid Artery

205
Q

Supplies anterior portion of the circle of willis

A

Anterior Communicating Artery

206
Q

o Supplies medial occipital lobes and medial temporal lobes

o Supplies thalamus

A

Posterior Cerebral Artery

207
Q

Which branch of the circle of willis Supplies Thalamus

A

Posterior Cerebral Artery

208
Q

Which branch of the circle of willis Supplies Thalamus

A

Posterior Cerebral Artery

209
Q

o Supplies medial occipital lobes and medial temporal lobes

A

Posterior Cerebral Artery

210
Q

Supplies upper surface of Cerebellum and midbrain

A

Superior Cerabellar Artery

211
Q

Basilar artery

A

• AICA Anterior Inferior Cerabellar Artery
Undersurface of Cerebellum and pons
•PICA Posterior Inferior Cerabellar Artery
o Undersurface of Cerebellum and Midbrain

212
Q

Olfactory Nerve

A

o Sensory

o Smell

213
Q

II. Optic Nerve

A

o Sensory

o Vision

214
Q

III. Ocular Motor Nerve

A

o Motor
•Most EOM movement, raise eyelids
o Parasympathetic:
• Pupilary constriction, Lens shape

215
Q

IV. Trochlear Nerve: Sensory or Motor

A

Motor

• Down and inward movement of the eye

216
Q

V. Trigeminal Nerve

A

o Motor
• Muscles of mastication
o Sensory
• Sensation of face and scalp, cornea, mucous membranes of mouth and nose

217
Q

VI.Abducens Nerve

A

o Motor

• Lateral eye movement

218
Q

VII. Facial Nerve

A

o Motor
 Facial muscles, close eye, labial speech
o Sensory
 Taste (sweet, salty, sour, bitter) on anterior two-thirds of tongue
o Parasympathetic
 Saliva and tear secretion

219
Q

VIII. Acoustic nerve

A

o Sensory

 Hearing and Equilibrium

220
Q

Glossopharyngeal

A

o Motor
 Pharynx (phonation and swallowing)
o Sensory
 Taste on posterior one-third of tongue, pharynx (gag reflex)

221
Q

Parasympathetic of glossopharyngeal

A

• Parotid gland, carotid reflex

222
Q

Vagus Nerve Motor and Sensory

A

o Motor
• Pharynx and Larynx (talking and swallowing)
o Sensory
• General sensation from carotid body, carotid sinus, pharynx, viscera
o Parasympathetic
 Carotid reflex

223
Q

VI. Spinal Nerve

A

Motor

 Movement of trapezius and sternomastoid muscle

224
Q

VII. Hypoglossal

A

o Motor

 Movement of tongue

225
Q

The Patient is vented and has an ABG reading with a PaO2 of 130 on FiO2 50%. Some thing is wrong, PaO2 should be higher than 130.What may be causing the ↓ oxygenation?

A

o Right mainstem intubation
o Atelectasis
o ↓ CO

226
Q

Signs and Symptoms of ↑ ICP.

What are early interventions that you can perform as a nurse to ↓ ICPs prior to any MD orders?

A

o ↓ Stimulation
 ↓ sympathetic stimulation, ↓ HR, ↓ BP = ↓ ICP
 Reverse Trendelenburg
 Proper neck alignment
A flexed head will increase ICP by constricting venous drainage.

227
Q

NeuroTransmitters Excitation is the

A

response of the subsynaptic membrane to the neurotransmitter substance that lowers the membrane potential to form an excitatory postsynaptic potential. Sodium ions rush into the neuron, whereas potassium ions leave the cell trough the postsynaptic membrane.

228
Q

Inhibition acts on a cell so that it is

A

more difficult for it to fire.

229
Q

The membrane potential is raised to form the

A

inhibitory postsynaptic potential.

230
Q

The inhibitory neurotransmitters

A

increase permeability to only potassium and chloride ions in the synaptic membrane.

231
Q

Acetylcholine

o Usually excitatory, it is found in the

A

motor cortex, skeletal muscle, preganglionic autonomic nerves, postganglionic parasympathetic nerves, and postganglionic sympathetic nerves to sweat glands.

232
Q

Acetylcholine

Usually excitatory, it is found in the

A

motor cortex, skeletal muscle, preganglionic autonomic nerves, postganglionic parasympathetic nerves, and postganglionic sympathetic nerves to sweat glands.

233
Q

Muscarinic receptors

A

 Are located in all of the postganglionic parasympathetic endings and the postganglionic sympathetic endings to sweat glands.

234
Q

o Chief neurotransmitter of the parasympathetic nervous system

A

ACH

235
Q

Norepinephrine

A

o Usually excitatory, and found in the postganglionic sympathetic nerves.

236
Q

o Chief neurotransmitter of the sympathetic nervous system

A

NE

237
Q

Dopamine

______Effectst

A

o Inhibitory

238
Q

o Affects control of behavior and fine movement

A

Dopamine

239
Q

o Adrenergic receptors

A

 Norepinephrine stimulates alpha > beta.

 Epinephrine stimulates alpha and beta equally

240
Q

Can be synthesized to NE to EPI

o Dopaminergic receptors

A

Dopamine

241
Q

Can be synthesized to NE to EPI

A

Dopamine; Dopaminergic receptors

242
Q

19

A

19

Cardiac ROTATION (2 decks)

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