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NURS 709 Pathophysiology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What is a lipoprotein?

A

A general term for molecules that are protein and fat

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2
Q

What defines the different type of lipoproteins?

A

They are categorized by density

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3
Q

Which lipoprotein do you want more of?
HLD vs. LDL

A

HDL

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4
Q

What is dyslipidemia?

A

Elevated levels of TC, LDL or triglycerides

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5
Q

How is dyslipidemia measured?

A

It is measured with a fasting lipids profile

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6
Q

What are the goal levels for lipoproteins?

A

LDL<100mg/dl
TC<200mg/dl
HDL>60mg/dl

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7
Q

A severe lipoprotein elevation may cause?

A

xanthomas or acute aterial blockages

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8
Q

What is atherosclerosis?

A

The development of fibrous, fatty lesions in the intima of large and medium-sized arteries (aorta, coronary arteries, cerebral arteries, peripheral arteries)

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9
Q

What is the most common type of coronary heart disease?

A

Atherosclerosis

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10
Q

What are some of the risk factors for atherosclerosis?

A

Family history
Hyperlipidemia
Increasing age
Male Gender
Cigarette Smoking
Obesity/diabetes
Emerging role of inflammation

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11
Q

What are 3 of the biggest contributors to Athlerosclerosis?

A

HTN
LDL
Smoking

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12
Q

What type of calcification occurs in athersclerosis?

A

Distrophic calcification

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13
Q

What do the manifestions of atherosclerosis depend on?

A

the vessel affected and extent of the narrowing

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14
Q

What are the manifestations of atherosclerosis?

A

If occuring in the coronary arteries, exertion can cause chest pain and discomfort

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15
Q

When atherosclerosis occurs in the preripheral arteries it is called?

A

Peripheral Arterial Disease

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16
Q

What is the main symptom of Peripheral Arterial Disease?

A

Intermittent claudication

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17
Q

What is claudication?

A

A dull aching pain often in the calf muscle that occurs due to anerobic metabolism that is most predictable with activity

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18
Q

What are some of the long term manifestations of PAD that are not claudication?

A

Changes in skin->cool, pale
Hair and toenails are abnormal

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19
Q

How is PAD diagnosed?

A

Ultrasound

Signs of chronic hypoxia in the limb

Weak/absense of pedal pulses

Cool skin

Pallor

Hairloss

(Uncle Sam Can Play Hockey)

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20
Q

What is an option for treatment for people with PAD?

A

A stent

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21
Q

What is an aneursym?

A

Atrophy or weakness of the medial layer of vessel wall caused by dilation of the artery

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22
Q

Where are aneursyms commonly found?

A

While they can be located anywhere, they are commonly found in the abdominal aorta or cerebral arteries

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23
Q

What causes an aneursym?

A

Degeneration may be caused by atherosclerosis, connective tissue disorders, increased blood pressure around a stenotic area

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24
Q

What is law of LaPlace?

A

An increasing radius at the weakened spot increases tension inside the wall fo the artery

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25
Q

What is a ‘Triple A’?

A

Abdominal Aortic Aneursym

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26
Q

What demographic is most likely to get a Triple A?

A

Usually men over 50 with a history of smoking

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27
Q

While normally a Triple A is asymptomatic, what is the one tell tale sign?

A

If you see a pulsating mass midline

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28
Q

What is a Aortic dissection?

A

A unique more dangerous aneursym that is common in the ascending aorta that causes a rupture or hemorrage into the vessel wall.

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29
Q

What occurs if someone experiences an aortic dissection?

A

An abrupt and intense pain
BP quickly falls
Most likely fatal

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30
Q

Why does an aortic dissection tear the vessel tissue?

A

The pressure that builds up in the dead end channel from the blood will tear the tissue

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31
Q

What are the units of blood pressure?

A

mmHg

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32
Q

What is the formula for blood pressure?

A

BP=Cardiac output x peripheral vascular resistance

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33
Q

What is the formula for mean arterial pressure?

A

MAP=(Systolic BP + 2Distolic BP)/3

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34
Q

What are the short term regulators of BP?

A

Neural Mechanisms
Humoural Mechanisms

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35
Q

What are the short term neural mechanisms that regulate BP?

A

Baroreceptors
Chemoreceptors

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36
Q

What are the short term humoral mechanisms that regulate BP?

A

RAA System
Vasopressin/ADH

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37
Q

What is the pericardium?

A

The sac around the heart that is filed with fluid

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38
Q

What are the 3 main pericardium problems?

A

Pericarditis
Pericardial effusion
Special Situation: Cardiac Tamponade

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39
Q

What is Pericarditis?

A

Inflammation of the pericardium that may restrict the hearts movement due to:
-Serous exudate filling pericardial cavity
-Fibrous scar tissue making the pericardium stick to the heart

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40
Q

What is pericardial effusion?

A

Serous exudate filling pericardial cavity-aka an accumulation of fluid in the pericardial cavity

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41
Q

What is Constrictive pericarditis?

A

Fibrous scar tissue making the pericardium stick to the heart

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42
Q

What are the two different categories of pericarditis?

A

Acute-often viral or after trauma
Chronic-exudate may remain for months or years

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43
Q

What is generally seen in the capillaries during acute pericarditis?

A

Increased capillary permeability allows exhudate into pericardial cavity

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44
Q

What are the symptoms of acute pericarditis?

A

Sharp chest pain, EKG changes, a friction like sound (like sandpaper) when auscitating the heart sounds

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45
Q

What is generally the cause of chronic pericarditis?

A

Often due to autoimmune disorders and it generally less severe although it still requires monitoring

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46
Q

What are the causes that can result in a pericardial effusion?

A

Usually the result of a d/t infection or inflammation

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47
Q

What are the negative effects on the heart from a pericardial effusion?

A

It can compress the heart, which increases intracardiac pressures and reduces venous return to the heart.

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48
Q

How is a pericardial effusion treated?

A

With a pericardiocentesis->Literally place a needle in between the viseral and paretal layer and drain the fluid

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49
Q

What occurs to the left ventricle during a paricardial effusion?

A

Because the heart cannot expand, the left ventricle can’t accept enough blood.
This leads to decreased cardiac output, which results in a drop in blood pressure which can lead to shock.

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50
Q

What occurs to the right ventricle during a pericardial effusion?

A

The right ventricle can’t accept enough blood leading to increased systemic venous pressure and jugualar vein distension

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51
Q

What is a cardiac tamponade?

A

Significantly more severe than a pericardial effusion->

it is a severe compression of the heart due to a large acute pericardial effusion. This is normally caused by bleeding into the pericardial sac

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52
Q

What are the symptoms of a cardiac tamponade?

A

Jugular vein distension
Drop in systolic BP
Circulatory shock (can lead to)
Weak pulse pressure
Muffled heart sounds

Whatever Jackie Doesn’t Care Maybe

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53
Q

Balance between ______________ ______________ supply and demand must be maintained.

A

myocardial oxygen

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54
Q

What is myocardial oxygen demand influenced by?

A

Heart Rate
Contractility
Muscle Mass
Ventricular wall tension

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55
Q

Ventricular wall tension is influenced by?

A

Afterload

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56
Q

What is myocardial oxygen supply influenced by?

A

coronary blood flow
O2 carrying capacity
Vascular resistance

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57
Q

What is the difference between an ischemia and an infarction?

A

Ischemia: effect of reduced perfusion
Infarction: Effect of absent/acute lack of perfusion

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58
Q

The left main coronary arteries subdivide into?

A

The circumflex coronary artery (Above)
The left anterior descending coronary artery

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59
Q

What is the leading cause of death in the US?

A

Coronary Artery Disease

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60
Q

What is coronary artery disease?

A

Heart disease due to impaired coronary blood flow usually due to atherosclerosis

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61
Q

What are the 3 established risk factors for coronary artery disease and what are the 3 risk factors that are starting to be recognized as major risk factors?

A

Hypertension, hyperlipidemia, smoking

Diabetes, Chronic Kidney disease and obesity

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62
Q

Coronary artery disease subdivides into acute and chronic syndromes/diseases. What are the two categories of acute coronary syndromes?

A

Unstable Angina, Non-STEMI

ST-segment elevation MI (STEMI)

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63
Q

What are the diagnosis factors for Coronary artery disease?

A

Severity of chest pain
Timing of chest Pain
Cardiac Enzymes blood markers
EKG Changes in the ST segment
Direct imaging of coronary arteries

(Sally Takes Cold Evening Drives)

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64
Q

What is troponin?

A

An enzyme only found in cardiac myocytes

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65
Q

If troponin is in circulating blood, what does that mean?

A

It means cardiac myocytes have died in some sort of infarction, **seen in both STEMI and nonSTEMI

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66
Q

What causes the pain during a myocardial ischema?

A

The O2 shortage forces the myocardium to use anaerobic metabolism and this is what causes the pain

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67
Q

What physiological compensation normally occurs right before chest pain?

A

There is a mild increase in HR and BP due to SNS compensation

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68
Q

What are the Sequelae and complications of a myocardial ischema?

A

Angina
Conduction abnormalities/dysrhymias
Myocardial infarction

Unlikely:
Heart failure
Sudden death

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69
Q

What is a predictable first warning sign of coronary artery disease?

A

A stable angina

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70
Q

What is predictable with stable angina and what does this indicate?

A

A stable angina is predictable onset with activity (can be with significatn emotional distress as well) and subsides with rest indicating that the myocardium is experiencing ischemia

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71
Q

For a stable Angina, an ECG may show?

A

ST-segment depression

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72
Q

What are the other types of Myocardial Ischemia?

A

Variant or Vasospastic
Silent ishemia

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73
Q

What is occuring during a Vasospastic ischemia?

A

The coronary arteries are physically tightening unpredictably often at night

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74
Q

People who have ischemia but are experiencing no pain are likely to have what kind of ischemia?

A

Silent

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75
Q

What are the 3 Acute coronary syndromes?

A

Unstable angina
Non-ST segment elevation MI
ST segment elevation MI

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76
Q

What type of angina is considered the precursor or harbinger of a myocardial infarction?

A

Unstable Angina

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77
Q

An unstable angina occurs when?

A

A significant portion of a coronary artery is blocked and pain may happen without any exertion

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78
Q

What is different in regards to pain from an unstable angina and a stable angina?

A

Anginal pain is more severe, lasts longer and is less predictable

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79
Q

What acute coronary syndrome does NOT have elevated cardiac enzymes?

A

Unstable Angina

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80
Q

What do we see on a EKG if a patient has an unstable angina?

A

No ST elevation, ST segment may be depressed or the T wave is inverted

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81
Q

What is a myocardial infarction?

A

A sudden blockage of one or more coronary arteries that stops blood flow to a section of the myocardium and the myocardium begins to die

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82
Q

Where is the most common place to have a myocardial infarction?

A

The tissues of the left ventricle

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83
Q

What are the manifestations of a MI?

A

Patient will be sweating, nausous, experiencing chest pain that doesn’t go away and will be very anxious.

Ischemia chest pain does not go away with rest
Diaphoresis
Nausea/Vomiting
Anxiety

*Women often have different symptoms

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84
Q

What are the manifestions that are more likely to be seen in women who are experiencing an MI?

A

Fatigue
Insomnia
Back pain
Shortness of breath
Pain on right side of jaw

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85
Q

At the tissue level, what are the effects of an MI?

A

reduced myocardial contractility
(not participating in systole)

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86
Q

What are the overall effects of an MI?

A

Abnormal ventricular wall motion
Reduced contractility and compliance
Reduced stroke vol->Reduced EF->decreased CO
dysrythmias

If you have an MI, the cells that die wont be able to act normally, resulting in reduce function

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87
Q

What is the difference between a myocardial infarction and cardiac arrest?

A

A myocardial infarction is blocked blood flow causing tissue death while a cardiac arrest is a severe dysrythmia

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88
Q

An MI in the __________ ___________ coronary artery usually results in death.

A

Left main

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89
Q

The diagnosing blood marker of an MI is?

A

Cardiac enzymes (troponin) in circulating blood

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90
Q

A NSTEMI has?

A

Symptoms of an MI but NO elevation of EKG, but has cardiac enzymes in the blood

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91
Q

A STEMI has?

A

Raising of the ST segment
Cardiac enzymes in the blood

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92
Q

Which is more severe?
A STEMI or a NSTEMI

A

A STEMI

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93
Q

What are 3 severe complications of an MI?

A

Papillary muscle rupture
Cardiac Rupture
Cardiogenic shock

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94
Q

What valve is normally effected by papillary muscle rupture?

A

The mitral valve

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95
Q

What is a cardiac rupture?

A

The necrotic area of the ventricle wall ruptures after a MI leading to massive bleeding into the pericardium (leading to a cardiac tamponde)

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96
Q

What is considered cardiac shock?

A

When an MI affects >40% of the left ventricle and causes a severe drop in systemic and cardiac circulation

Most likely not survivable

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97
Q

What is the milder complication of an MI?

A

Heart failure

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98
Q

What is preload?

A

Volume that fills the heart at the moment of diastole from the pulmonary vein and vena cava

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99
Q

True/False

Coronary artery disease is more likely to result in chronic ischemia (causing a stable angina) than acute coronary syndrome.

A

True

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100
Q

A Cardiac tamponade will directly impact which function of the heart?

Afterload or Preload?

A

Preload

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101
Q

What is Valvular heart disease?

A

Damage or changes to any of the four heart valves that creates abnormal blood flow and increases cardiac work

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102
Q

Normal valves allow ________________ and ___________________ blood flow.

A

unidirectional and unimpeded

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103
Q

VHD:
What is regurgitation?

A

valve doesn’t close properly and allows backflow creating volume work

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104
Q

VHD:
What is stenosis?

A

the valve opening is restricted, preventing forwards flow, creating pressure worke

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105
Q

What is a murmur?

A

An audible turbulent blood flow across a heart valve

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106
Q

What are two of the most common causes of Valve disease?

A

infective endocarditis or rheumatic fever

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107
Q

What are some of the other causes of of valve disease besides infective endocarditis and rheumatic fever?

A

Connective tissue defects
Rupture of papillary muscles
Damages from an MI
Congenital malformations
Calcifications

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108
Q

What are the valves most commonly affected by valve disease?

A

Mitral and Aortic

(think entrance and exit of left ventricle)

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109
Q

What are some of the variables when it comes to manifestations of valve disease?

A

Valve involved
Severity of Damage
Rapidity of onset
Compensatory mechanisms

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110
Q

A valve that develops _______________ is much more _____________ than one that develops ____________.

A

A valve that develops acutely is much more serious than one that develops chronically.

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111
Q

What is infective endocarditis?

A

A rare but life threatening infection of the endocardium that is often caused by the bacteria staphylococci, streptococci or enterococci

(just remember it ends in -cocci)

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112
Q

How does one contract infective endocarditis?

A

The person requires an already-damaged endocardium and an entry point for bacteria to enter into the circulatory system

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113
Q

What does infective endocarditis do to the heart?

A

bacteria and resulting inflammation create vegetations on heart valves that can look like nodules or cauliflower. Patient may have systemic infection symptoms and well as heart murmer

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114
Q

How is infective endocarditis diagnosed?

A

Blood cultures and an echocardiogram

115
Q

What is acute rheumatic fever?

A

A systemic inflammatory disease that may occur after group A beta hemolytic streptococcal pharyngitis (strep throat)

116
Q

What is the theory on why this strep causes rheumatic fever?

A

the theory is that the infection causes a type II or III autoimmune response

117
Q

What is Rheumatic Heart disease?

A

The cardiac manifestation of RF and may involve all three layers of the heart where autoantibodies react with host tissue causing damage to the valves that results in stenosis or regurgitation

118
Q

What is mitral valve stenosis?

A

Resistance to blood flow from LA->LV that causes the LA to work harder and becomes dilated and thickend due to hypertrophy

The pressure from the LA backs into pulmonary circulation and causes pulmonary pressures to rise

119
Q

What are the symptoms of mitral valve stenosis?

A

Enlarged LA
pulmonary congestion/edema
Reduced cardiac output
Increasing exertional dyspnea]
Tachycardia
Atrial dysrhythmia

120
Q

While Mitral valve stenosis starts out as a pressure problem, how does it turn into a volume problem?

A

The blood will eventually back up into the lungs

121
Q

What is mitral regurgitation?

A

during systole, some blood flows backward into the LA instead of moving forward through aortic valve because RHD has caused mitral prolapse

122
Q

During mitral regurgitation, the LA dilates to accomodate backflow, but what happens if this fails?

A

The pressure in the pulmonary circuit rise and left sided heart failure occurs

123
Q

Acute mitral valve regurgitation is usually?

A

Fatal

124
Q

What is one of the classic reasons for heart failure?

A

Aortic stenosis

125
Q

What is aortic stenosis?

A

a narrowed aortic valve obstructs blood flow into the aorta from LV during systole

126
Q

What will occur to the left ventricle if experiencing aortic stenosis?

A

hypertrophy

127
Q

When do symptoms of Aortic Stenosis occur?

A

at ~50% narrowing

128
Q

What are the symptoms of Aortic Stenosis?

A

Angina
Syncope
LV failure
Loud Systolic murmur

129
Q

What is the survival rate upon the onset of symptoms of Aortic Stenosis?

A

5 year survival rate

130
Q

Heart failure is defined as?

A

The chronic complex syndrome that involves imparments of ventricular filling or ejection of blood from ventricles

131
Q

What is an ejection fraction?

A

a measurement of the amount of blood that is pumped out of the heart with each contraction, as a fraction of the total amount of blood in the left ventricle. It is expressed as a percentage, and a normal EF is typically around 55-70%.

132
Q

Patients with heart failure have a greatly reduced?

A

cardiac reserve

133
Q

HFrEF is what part of the ejection fraction?

A

The systolic

134
Q

HFpEF is what part of the ejection fraction?

A

diastolic

135
Q

_________________ or_________________ tells us if the heart is failing to pump out enough blood or failing to accept enough blood from the body/lungs.

A

HFrEF or HFpEF

(systolic or diastolic)

136
Q

A reduced ejection fraction tells us?

A

That the issue is systolic and is an issue with contractility

Also called a “pumping problem”

137
Q

A preserved ejection fraction tells us?

A

The issue is diastolic and is an expansion issue because the LV is not able to relax and fill with blood.
Also called a “filling problem”

138
Q

What are the common causes of Systolic HF?

A

Ischemic heart disease
Dilated cardiomyopathy
Extreme stress
Viral infections

139
Q

What are the common causes of Diastolic heart failure?

A

Long term hypertension resulting in hypertrophy of LV

Aortic Stenosis

Aging

140
Q

The pressure in the aorta must be __________ than the pressure in the left ventricle or blood will stop flowing.

A

less

141
Q

What are the diagnosing criteria of heart failure?

A

signs and symptoms related to reduced cardiac output
lab results
ejection fraction measured by echocardiogram

142
Q

What is a normal ejection fraction?

A

Normal is 60-70%

Or as Dr. Cuter said “2/3”

143
Q

In the classification of Heart failure, if you see ‘refractory’ what does this tell you?

A

The heart disease has progressed to be untreatable

144
Q

What are the compensatory mechanisms of heart failure?

A

Frank-starling mechanism
SNS activity
RAA mechanism
Natriuretic peptides: ANP, BNP
Endothelin
Myocardial hypertrophy/remodeling

145
Q

What are the good parts of the Frank-Starling mechanism?

A

The increased sodium and water retention by the kidneys due to low perfusion increases blood volume.

This increase in blood volume increases the end-diastolic volume (pre-load) leads to increased contractility and stroke volume.

146
Q

What are the bad parts of the Frank-Starling mechanism?

A

Increased cardiac muscle stretch->Wall tension->Increased O2 demand->EDV and ESV increase->Increased myocardial consumption

Because the increased cardiac muscle stretching leads to wall tension.

This wall tension increases O2 demand.

The end Diastolic and systolic volume increase because the myocardium can’t handle increased volume.

This leads to pulmonary congestion and increased myocardial oxygen.

147
Q

Decreased cardiac output leads to __________________ perfusion.

A

renal

148
Q

What are the good parts of the RAA Mechanism?

A

Kidneys release renin in response
Vasoconstriction leads to increase in BP

149
Q

Aldosterone release results in Na+ _______________ by kidney.

A

Reabsorption

150
Q

The increase in blood pressure and reabsorption of Na+ increases preload and theroretically ________________ and __________________.

A

stroke volume
cardiac output

151
Q

What are the bad parts of the RAA system?

A

The progressively weakening myocardium cannot contract or dilate well enough to handle increasing volume.

This increase in systemic venous return increases afterload (the workload on the heart)

152
Q

What are the Natriuretic Peptids?

A

ANP
BNP

153
Q

When are the natriuretic peptides released?

A

In response to atrial stress, pressure or volume overload

154
Q

What do the natriuretic peptides promote?

A

Vasodilation and inhibits sodium reabsorption and leads to natriuresis (excretion of sodium in the urine)

155
Q

In what patients do you see elevated levels of natriuretic peptides?

A

Patients with chronic HF

156
Q

What are Endothelins?

A

Endothelins have a role in the development of pulmonary hypertension because their release leads to vasoconstriction and results in cardiac myocyte hypertrophy and fibrosis.

The have an overall negative effect on symptoms and progression of heart failure

157
Q

HEART FAILURE:
JVD is a classic manifestation of what type of heart failure?

A

Right sided heart failure

158
Q

What occurs in Diastolic left sided heart failure?

A

The LV does not accept enough blood from lungs causing the body to lack blood and the lungs fill with fluid.

159
Q

What occurs in Systolic left sided heart failure?

A

The left ventricle does not pump enough blood to the body, causing blood to back up behind the LV.

160
Q

What occurs in Diastolic right sided heart failure?

A

The Right ventricle doesn’t accept enough blood from the body causing the blood to back up behind the RV.

This causes the body to fill with blood creating systemic edema and the lungs do not oxygenate enough blood.

161
Q

What occurs in Systolic right sided heart failure?

A

The right ventricle does not pump enough blood to the lungs and the blood backs up behind the RV.

This causes the body to fill with blood creating systemic edema and the lungs do not oxygenate enough blood.

162
Q

What is the difference in left vs. right sided heart failure?

A

Left sided causes diminished output via the aorta and a backup of blood volume/pressure into the pulmonary circulation

Right sided often occurs following left sided, but the diminished output via pulmonary arteries that causes systemic congestion and edema

163
Q

What occurs during Pulmonary edema?

A

Capillary fluid
Stiffened Lungs
Harder to exhale (decreased compliance)
Less gas change in alveoli
Crackles on auscultation
Frothy pink sputum

164
Q

What are the three categories of pleural disorders?

A

Pleuritis/Pleuritic chest pain
Pleural Effusions
Pneumothoraxes

165
Q

What is Pleuritis?

A

Localized inflammation that has a sudden onset that can be due to trauma or infection that is usually on one side.

166
Q

What is the pain of pleuritis like?

A

Acute pain upon inspiration in a very specific place because the pressure is highest at inspiration

167
Q

What are the 3 types of Pneumothoraxes?

A

Spontaneous
Traumatic
Tension

168
Q

Pleural Effusions are different from edema in what way?

A

Plueral Effusions are more like a ‘pocket’ unlike edema which is kind of like an area

169
Q

What is a pleural effusion?

A

A collection of fluid in the pleural cavity that decreases lung expansion during inspiration

170
Q

What are the different types of exhudate from plueral effusions?

A

Transudate
Exudate
Empyema
Hemothorax

171
Q

What is Transudate (hydrothorax) exudate?

A

Exudate that is mostly plasma that normally comes from fluid volume overload

172
Q

What is Exudate?

A

Fluid filled with cellular debride

173
Q

What is Empyema?

A

Fluid created from an infection in the plural lining that contains WBC, Plasma, Debride and glucose.

In severe cases infection can cross over into plural cavity

174
Q

What is hemothorax?

A

Blood in plural linging

175
Q

What is the V/Q mismatch for Pleural effesions?

A

Ventilation effected so V/Q ratio goes down

176
Q

What are the manifestations of Pleural Effusions?

A

Decreased lung expansion will affect gas exchange

Dull Percussion and reduced breath sounds over fluid

Dyspnea when infusion is large

Compensatory tachypnea possible

177
Q

A patient is admitted with bilateral pleural effusions. What other symptoms would the nurse expect?

A

Reduced breath sounds
Dyspnea

178
Q

What is a pneumothorax?

A

A buildup of air inside the pleural cavity that restricts lung expansion

179
Q

A spontaneous pneumothorax is?

A

Unexpected
No obvious cause

180
Q

What may a spontaneous pneumothorax occur from?

A

Blebs (Air blister on the surface of the lung that can burst)

neoplasms (Malignant tumors can be related to formation of pocket)

181
Q

What is a traumatic pneumothorax?

A

A pneumothorax created due to a chest wall injury (injury may penetrate the chest wall)

182
Q

An example of an injury that could cause a traumatic pneumothorax is?

A

A gunshot/car accident/hit with bat

183
Q

What are the two subcategories of a traumatic pneumothorax?

A

Open traumatic pneumothorax

Tension traumatic pneumothorax

184
Q

An open pneumothorax means?

A

the injury penetrates the plural lining creating a channel

This creates a loss of seal, but still has bidirectional movement of air

185
Q

A tension pneumothorax is?

A

A tension pnemothorax is an EMERGENCY

Air has entered the pleural cavity with each inhalation, but cannot exit.

186
Q

What are the side effects of a tension pneumothorax?

A

The air entering the effected lung stays compressed, but eventually the air will continue to build up and both sides will become compressed and displaced.

187
Q

What is the treatment for a tension pneumothorax?

A

A chest tube

188
Q

What are the manifestations of a tension pneumothorax?

A

Displaced trachea
Hypoxemia
typnea
Tachacardia
Difficulty breathing

189
Q

What happens to the V/Q ratio during a tension pneumothorax?

A

The ratio will go down

190
Q

To which direction will the trachea deviate towards in a tension pneumothorax?

A

Towards the unaffected side

191
Q

How is a tension pneumothorax diagnosed?

(What machine)

A

Diagnosed by Chest Xray or chest CT

192
Q

What is Atelectasis?

A

A sequela of several respiratory disorders that is the collapse of sections of alveoli due to underinflation of the lung.

193
Q

What are the two causes of Atelectasis?

A

Compression
Obstruction

194
Q

How does compression cause Atelectasis?

A

The extrinsic pressure pushes air out of alveoli and causes them to collapse

195
Q

What are 3 respiratory disorders that could cause Atelectasis?

A

Pleural Effusion
Pneumothorax
Severe Abdominal Distension

196
Q

How does obstruction cause Atelectasis?

A

The airway to the alveoli is blocked

197
Q

What are 3 things that could cause obstruction Atelectasis?

A

Mucous Plug
Increased secretions
Narrowed Airways

198
Q

What kind of Atelectasis is preventable after surgery and how?

A

Obstruction Atelectasis
Prevented by use of a spirometer to help keep those airways clear

199
Q

What are the manifestation of Atelectasis?

A

Tachypnea (abnormal rapid breathing)
Tachycardia (rapid heart rate)
Dyspnea (difficult/labored breathing)
Hypoxemia
Possibly Cyanosis

200
Q

If Atelectasis is large enough, what is it referred to as?

A

A collapsed lung

201
Q

Airway _______________ makes expiration difficult.

A

Obstruction

202
Q

What are the common obstructive disorders?

A

Asthma
Emphysema and chronic bronchitis (COPD)

203
Q

The two common signs of an airway obstruction are?

A

Dyspnea
Wheezing

204
Q

What is a respiratory disorder that is common in children but can develop as an adult, and can “flare up” or be exacerbated?

A

asthma

205
Q

What is Asthma?

A

An inflammatory response in the airways causing hyperresponsiveness and narrowed airways

206
Q

What are the two ways Asthma is characterized and why?

A

Extrinstic-Type 1 hypersensitivity reaction to an external antigen

Intrinsic-A non-immune reaction to various other airway irritants

207
Q

What is the common type of immune cell seen in asthma?

A

Mast cells are very active and release inflammatory mediators into airway

208
Q

What are the effects of asthma?

(Like what is actually happening in the lungs)

A

swelling of mucousal lining
Swelling around bronchioles
Secretion of mucosa/exudate
Smooth muscle contration

209
Q

What are the phases of Extrinsic asthma?

A

Early phase: Asthma lasts minutes to hours

Late Phase: Acute problems resolve several hours to days. The risk of a flare up is high here

210
Q

If asthma is left untreated it can cause long term airway damage known as?

A

Airway remodeling

211
Q

Airway remodeling is seen as?

A

Airways loose flexibility, get stiffer, stenotic, and more and more progressive damage occurs

212
Q

What are the manifestations of asthma?

A

Dyspnea
Persistant cough
Tachypnea, tachycardia
Wheezing
Diminished breath sounds
Chest tightness
Prolonged expiratory phase

213
Q

Why do people suffering from asthma experience a prolonged expiratory phase?

A

Because of the swelling in the airways, the patient is having to use their muscles to force air out

214
Q

How is asthma diagnosed?

A

Pulmonary function tests

215
Q

What type of asthma would exercise induced asthma be considered?

A

Intrinstic because inspiration in these pts is not normal but expiration is worse

216
Q

Are the two categories of Chronic Obstructive Pulmonary Disease?

A

Emphysema
Chronic Bronchitis

217
Q

A respiratory disease that has a long preclinical period until progressive airflow limitations that smoking is the primary cause of is?

A

COPD

218
Q

What respiratory disease is the leading cause of disability and death?

A

COPD

219
Q

Since both Emphysema and Chronic bronchitis are both considered COPD, do patients just have one or the other?

A

Majority of patients have bronchitis and emphysema, and a selects few have just one

220
Q

What are the Types of Emphysema?

A

Primary (1-3%)
Secondary (97-99%)

221
Q

What is primary emphysema?

A

Genetic breakdown of a maintenance enzyme that leads to breakdown of elastin

222
Q

What is the maintenance enzyme that keeps up elastin in the lungs?

A

Alpha 1 Antitripsin

Breakdown of this enzyme can cause primary hypertension

223
Q

What is secondary emphysema?

A

Breakdown of elastin due to direct effects of cigarette smoking or air pollution

224
Q

What is elastin?

A

Connective tissue that allows to the lung to return to its normal size after stretching

225
Q

90% of secondary emphysema cases are what age?

A

Age 45 and older

226
Q

What are some direct effects of emphysema?

A

Expiration is directly impacted
Hyperinflated Lungs
Increase in total lung compacity
Chest enlarges
Alveoli enlarge
Blebs and Bulla may form on lung surface

(Every Hippopotamus Is Crunching Apples & Bananas)

227
Q

What is a tell tale sign that a patient has ephysema and not Chronic Bronchitis?

A

Little cough or sputum*

228
Q

What is a common stance that emphysema patients tend to take?

A

They lean forward in a tripod position with pursed lips

229
Q

What is chronic bronchitis?

A

The other end of the COPD Spectrum were irratants such as smoking, air pollution cause increased mucus production and the size and number of mucous glands

230
Q

How does mucus effect the lungs in chronic bronchitis?

A

The thick copious mucous impairs the cilia

231
Q

A key feature of Chronic Bronchitis compared to Emphysema is?

A

A productive cough lasting at least 3 consecutive months/years for at least 2 consecutive years

232
Q

What occurs to the lungs over time from chronic bronchitis?

A

The bronchial walls become thickened from edema and inflammation and fibrosis occurs. Eventually increased mucus and narrowed bronchioles result in obstruction of large and small airways

233
Q

What are the manifestations of Chronic bronchitis?

A

Wheezing and SOB
Chronis productive cough
Frequent pulmonary infections
Polycythemia
Cyanosis
Decreased exercise tolerance

The wheezing blue man coughs alot due to his frequent infections that don’t let him exercise

234
Q

Compare and contrast Emphysema and Chronic Bronchitis.

A

Emphysema:
-increase respirations to maintain oxygen levels
-Dyspnea
-Accessory muscles are used to aid breathing

Chronic Bronchitis:
-Cannot increase respirations enough to maintain oxygen levels
-More cyanosis and polycythemia are seen
-Cor pulmonale, fluid volume overload

235
Q

Both Emphysema and Chronic bronchitis tend to retain more CO2, and therefore they tend to stay in a state of?

A

Respiratory Acidosis

236
Q

What is something in concern to oxygen therapy and COPD?

A

You can’t give them too much supplemental oxygen or their respiratory rate will drop

237
Q

A DVT from the leg can NOT?

A

Cause a stroke in the brain

238
Q

What is a pulmonary embolus?

A

A blockage that develops in the pulmonary circulation

239
Q

What kind of material can cause a Pulmonary embolus?

A

Blood
Fat
Amniotic fluid
Air

240
Q

What are the signs and symptoms of a pulmonary embolus?

A

Restlessness (Feeling of something is wrong/impending doom)
Dyspnea
Tachycardia
Tachypnea
Pleuritic pain

A restless man who’s heart is beating really fast feels doomed complaining of pain in his lungs and fast or difficult breathing.

241
Q

What is the V/Q mismatch for a Pulmonary Embolus?

A

Ratio goes up because decrease in perfusion=decrease in Q

242
Q

A _______________ _______________ will not impact breath sounds.

A

pulmonary embolus

243
Q

What are the primary and secondary causes of pulmonary hypertension?

A

Primary:Genetic, idiopathic
Secondary: Due to other lung disease, left ventricle disfunction, chronic PEs

244
Q

What is Cor Pulmonale?

A

Failure of the RIGHT ventricle due to primary lung disease or pulmonary hypertension

245
Q

What are the signs and symptoms of pulmonary hypertension?

A

Systemic edema
SOB
Hypoxemia

246
Q

What is Acute Respiratory failure?

A

A failure of the lungs to efficently perform gas exchange and generally the final complication of other lung diseases.

247
Q

What is the V/Q mismatch on Acute Respiratory Failure?

A

Depends on the case, it can go either way

248
Q

In Acute respiratory failure, where does the impaired gas exchange occur?

A

At the aveoli

249
Q

What PaO2 stat would indicate acute respiratory failure?

What PaCO2?

A

Under 50-60mmHg

Over 50mmHg

250
Q

Acute respiratory failure patients may be hypoxemic or hypercapnic. Why?

A

If the ARFs patients are just experiencing a gas exchange failure they will just be hypoexemic only.

If they are experiencing a ventilatory failure they can be hypoxemic/hypercapnic/

251
Q

In just a gas exhange issue in acute respiratory failure, what do we generally see in the blood?

A

The oxygen is not able to cross into the blood, but the CO2 can cross-giving high levels of CO2 in the blood.

252
Q

What is the order of symptoms of hypoxia related acute respiratory failure?

A

Neurological changes are prominent then cardiovascular follows

253
Q

What are the signs and symptoms of hypercapnia acute respiratory failure?

A

Cerebral Dilation
Increased Blood Flow
Increased intracranial pressure
Progressive sedation
Reduced LOC

254
Q

What is Acute respiratory distress syndrome (ARDS)?

A

ARDs is a specific type of respiratory failure resulting from many types of lung injuries and illnesses

255
Q

What is the MOA of ARDs?

A

Easy Explaination: Inflammatory rxn increases the capillary membrane of aveoli and causes lungs and aveoli to fill with fluid.

Slide Explanation:The massive inflammatory response increases the permeability of the alveolar capillary membrane resulting in fluid moving into the interstital and alveolar spaces

256
Q

What is the onset of ARDs?

A

Rapid onset of respiratory distress and failure (12-18 Hours) after a caustive event

257
Q

What is the end result of ARDs?

A

End result of ARDs is diffuse, noncardiogenic pulmonary edema and atelectasis

258
Q

What does noncardiogenic mean?

A

Not born from the heart

259
Q

What is the mortality rate for ARDs?

A

50-60%

260
Q

What are some specific things to remember about ARDs?

A

The Causes:
-ARDs is a specific type of respiratory failure resulting from many types of lung injuries and illnesses

Inflammation is not from the heart.

Similar concepts with pneumonia

261
Q

What is the volume per min for Ventilation (V)?

A

about 4L/min

262
Q

What is the volume per min for Perfusion (Q)?

A

about 5L/min

263
Q

What is the average fraction for V/Q?

A

0.8-0.9

264
Q

A low V/Q Ratio (<.8) indicates?

A

Inadequate ventilation in well perfused lungs

Sometimes “shunting”

265
Q

What are the causes of a low V/Q Ratio?

A

Atelectasis
Asthma (due to Bronchioconsriction)
Pulmonary Edema
Pneumonia

266
Q

A High V/Q Ratio (>.8) indicates?

A

Adequate ventilation but poor lung perfusion
“Aveolar dead space”

267
Q

What are the causes of a high V/Q Ratio?

A

Pulmonary Embolism
Shock

268
Q

Blood flow with no air would have which mismatch?

A

low V/Q

269
Q

Air but no blood flow would be which V/Q Mismatch?

A

High V/Q ratio

270
Q

An oxyglobin dissociation curve tells us?

A

How oxygenated our patient actually is

271
Q

96% SaO2 would indicate what PaO2 level?

A

around 80%

272
Q

A decreased affinity of hemoglobin for O2 means?

A

The O2 dissociates from RBCs more quickly and so there is more O2 available for cells.

273
Q

A decreased affinity of hemoglobin for O2 means what in regards to the oxyhemoglobin curve?

A

Visible shift as a right shift of the curve

274
Q

What causes a decreased affinity of hemoglobin for oxygen?

A

Acidosis
High PCO2 levels
Increased Temp
High 2,3-DPG

275
Q

An increased affinity of hemoglobin for O2 means?

A

O2 seperates from RBCs slower, therefore there is less O2 available for cells

276
Q

An increased affinity of hemoglobin for O2 does what in regards to the oxyhemoglobin dissociation curve?

A

Visible shift to the left of the curve

277
Q

What causes An increased affinity of hemoglobin for O2?

A

Alkalosis
Low CO2 levels
Decreased Temp
Low levels 2,3-DPG

278
Q

What are the steps to using the oxyhemoglobin dissociation curve?

A

1)What is factors are causing an increase or decrease for Hb for O2
2)How does this increase or decrease shift the curve
3)Use the curve to find PO2

279
Q

What are some of the manifestations of pulmonary disease?

A

Chest pain
Abnormal Sputum
Hemoptysis
Hypoventilation
Hyperventilation
Cyanosis
Clubbing

280
Q

What is hypercapnia?

A

High levels of CO2

281
Q

What is the property of all muscle tissue that is part of the Frank-Starling Mechanism?

A

The property of muscle fibers where they loosen a little bit before contraction, and this allows a stronger contraction.

282
Q

What is preload?

A

Preload refers to the volume of blood present in the ventricles of the heart at the end of diastole, which is the relaxation phase of the cardiac cycle.

283
Q

What is afterload

A

afterload refers to the pressure against which the left ventricle must pump blood during systole, which is the contraction phase of the cardiac cycle. The afterload is determined by the pressure in the aorta and the peripheral resistance in the arteries.

NURS 709 Pathophysiology (5 decks)

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