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Pathophysiology > Week 3 (ch. 12 CVS Disorders) > Flashcards

Week 3 (ch. 12 CVS Disorders) Flashcards

1
Q

Heart function

A

The pump for both systems and pulmonary circulations

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2
Q

Left ventricle: anatomy and function

A

LV is thicker

Eject blood into extensive systemic circulation

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3
Q

How many valves in the heart?

A

4 valves - ensure one way blood flow

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4
Q

Describe the conduction system of the heart

A
  • Ensure both atria and ventricles contract as desired for efficient filling and emptying
  • originates at SA node
  • conduction impulses produce electrical activity picked by up electrodes = electrocardiography
  • abnormal variations (arrhythmia or dysthymia) may indicate acute problems
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5
Q

Cardiac Control Center: where is it location?

A

Medulla of the brain

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6
Q

Cardiac Control Center: function

A

Controls heart rate and force of contraction

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7
Q

Baroreceptors

A

Detect change in BP

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8
Q

Cardiac Control Center: what does it response through and how

A

SNS

  • increased HR (tachycardia) and contractility
  • any stimulation of the SNS (stress, fever, exercise, pain)

PSNS
- decrease HR (bradycardia)

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9
Q

Coronary Circulation: Right and left coronary arteries —> part of what

A

Systemic circulation
- many small branches extend from these arteries to supply the myocardium and endocardium

** cardiac muscles requires constant supple of o2 but have limited storage ability. Any BF interference affects heart function

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10
Q

Coronary Circulation: Right and left coronary arteries —> where are they

A

They branch off aorta immediately distal to the aortic valve

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11
Q

Left coronary artery divides into what

A

Left anterior descending or inter-ventricular artery, Left circumflex artery

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12
Q

Right coronary artery branches into what?

A

Right marginal artery, Posterior inter-ventricular artery

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13
Q

What is the cardia cycle coordinated by?

A

Conduction system
Systole: cardiac contract
Diastole: cardiac relaxation

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14
Q

Describe how heart moves through ventricles and atria, starting with Atria relaxed, filling with blood

A
  1. Atria relaxed, filling with blood (diastole?)
  2. AV valves open
  3. Blood flows into ventricles
  4. Atria contract, remaining blood forced into ventricles (systole?)
  5. Atria relax
  6. Ventricles contract
  7. AV valve closes
  8. Semilunar valves open
  9. Blood into aorta and pulmonary artery
  10. Ventricles relax
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15
Q

Heart sounds: “lubb-dub”

A

Heart with stethoscope
“Lubb” = closure of AV valves, ventricular systole
“Dub” = closure of semilunar valves, ventricular diastole

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16
Q

Heart sounds: murmurs - cause

A

Caused by incompetent valves or hole in septum

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17
Q

Heart sounds: pulse

A

Indicates heart rate

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18
Q

Pulse deficit

A

Difference in rate between apical and radial pulses

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19
Q

What is BP

A

Pressure of blood against the systemic arterial walls

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20
Q

What does BP depend on

A

Cardiac output and peripheral resistance

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21
Q

Peripheral resistance

A

Force opposing blood flow

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22
Q

Systolic pressure

Diastolic pressure

A

Higher number
- pressure entered by blood when ejected from LEFT VENTRICLE

Lower number
- pressure that is sustained when ventricles are relaxed

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23
Q

Pulse pressure

A

Difference between systolic and diastolic BP

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24
Q

Does LOCAL vasoconstriction affect systemic BP

A

No

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25
Q

Changes in blood pressure: sympathetic branch of ANS

Describe how this changes blood pressure

A

Increased output —> vasoconstriction and increased BP

Decreased output —> vasodilation and decreased BP

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26
Q

BP is directly proportional to what

A

Blood volume

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27
Q

Changes in blood pressure: hormones - which ones and their impact on BP

A
  1. Antidiuretic hormone
    - increased BP
  2. Aldosterone
    - increases blood volume
    - increases BP
  3. Renin-angiotensin-aldosterone
    - vasoconstriction
    - increases BP
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28
Q

Diagnostics: Electrocardiography

A

Initial diagnosis and monitoring of dysrhythmias, myocardial infarction, infection, and pericarditis

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29
Q

Diagnostics: Ausculation

A

Determines valvular abnormalities or abnormal shunts of blood that cause murmurs

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30
Q

Diagnostics: Echocardiography (echo)

A

Used to record heart valve movements, blood flow, and cardiac output

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31
Q

Diagnostics: exercise stress tests

A

Used to assess general CV function

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32
Q

Diagnostics: Chest X-Ray films

A

Used to show shape and size of heart

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33
Q

Diagnostics: Cardiac catheterization

A

Measures pressure and assesses valve and heart function

- determines central venous pressure and pulmonary capillary wedge pressure

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34
Q

Diagnostics: Angiography

A

Visualization of blood flow in the coronary arteries

Can complete corrective treatment procedures

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35
Q

Diagnostics: Doppler studies

A

Assess blood flow in peripheral vessels

Record sounds of blood flow or obstruction

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36
Q

Diagnostics: Blood tests

A

Assess levels of serum triglycerides, cholesterol, sodium, potassium, calcium, other electrolytes

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37
Q

Diagnostics: Arterial blood gas determination

A

Checks the current o2 level and acid-base balance

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38
Q

General treatment measures: dietary modifications

A

Decrease fat intake, general weight reduction, reduce salt intake

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39
Q

General treatment measures: regular exercise program

A

Increase HDL, lowers serum lipid levels, reduces stress level

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40
Q

General treatment measures: cessation of smoking

A

Decreases risk of coronary disease

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41
Q

General treatment measures: many different drug therapies

A 
º vasodilators 
º beta-blockers
º calcium channel blockers 
º digoxin
º anti-hypertensive
º adrenergic blocking
o ACE inhibitors 
º diuretics 
º anticoagulants 
º cholesterol lowering
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42
Q

Coronary Artery Disease (CAD): what is the basic problem
Or Ischemic Heart Disease (IHD)
Or Acute Coronary Syndrome

A

Insufficient O2 for the needs of the heart muscles

  • common cause of disability and death
  • leading cause of death for men and women in US
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43
Q

Coronary Artery Disease (CAD)
Or Ischemic Heart Disease (IHD)
Or Acute Coronary Syndrome

What can it lead to

A

Heart failure
Dysthymias
Sudden death

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44
Q

Arteriosclerosis

A

General term for all types of arterial changes

  • degenerative changes in small arteries and arterioles
  • loss of elasticity
  • lumen gradually narrows and may become obstructed
  • cause of increased BP
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45
Q

Atherosclerosis

A

Presence of atheromas in large arteries

  • plaques consisting of lipids, calcium, and possible clots
  • related to diet, exercise, and stress
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46
Q

Lipids are transported in combination with what?

A

Proteins

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47
Q

Serum lipids: low density lipoprotein

A

Transports cholesterol from liver to cells

Major factor contributing to atheroma formation

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48
Q

Serum lipids: high density lipoprotein

A

Transports cholesterol away from the peripheral cells to liver
Catabolism in liver and excretion
- “good” lipoprotein

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49
Q

Atherosclerosis: risk factors

A

Non-modifiable = age, gender, genetics

Modifiable = obesity, sedentary lifestyle, smoking, diabetes mellitus, poorly controlled hypertension, combination of oral contraceptives and smoking

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50
Q

Atherosclerosis: diagnostic tests

A

Serum lipid levels (LDL and HDL)

Exercise stress testing (screening for arterial obstruction)

Nuclear medicine studies (determine the degree of tissue perfusion)

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51
Q

Atherosclerosis: treatment

A 
Weight loss
Exercise 
Diet
Lower Na intake
Stop smoking
Control hypertension
Control of primary disorder
Antilipidemic drugs
Surgical prevention (coronary artery bypass grafting)
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52
Q

Angina Pectoris

A

Chest pain; deficit of O2 to meet myocardial needs

  • recurrent, intermittent brief episodes of substernal chest pain
  • triggered by physical or emotional stress
  • attacks vary in severity and duration but become more frequent and longer as disease progresses
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53
Q

Angina Pectoris: s/s and how is it relieves

A

S/s = pallor, nausea, diaphoresis (excessive sweating), chest pain

Relieved by rest and administration of coronary vasodilators

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54
Q

Angina Pectoris: describe the way chest pain may occur in different patterns

A 
Classic or exertional angina 
Variant angina (vasospasm occur at rest)
Unstable angina (prolonged pain at rest; may precede myocardial infarction)
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55
Q

Angina Pectoris: Treatment

A

Rest
Sit in upright position
Nitroglycerin (sublingual)
Check pulse and respiration
Administer O2
If patient known to have angina - second dose of nitroglycerin
Pt. Without history of angina - emergency medical aid

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56
Q

Myocardial infarction

A

Occurs when coronary artery is totally obstructed

  • atherosclerosis is most common cause
  • thrombus from atheroma obstructs artery
  • vasospasm is caused in small %
  • size and location of the infarction determine the damage
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57
Q

Myocardial infarction: signs

A

Feeling pressure, heaviness, or burning in chest - especially with increased activity
— sudden SOB, weakness, fatigue
— nausea, indigestion
— anxiety/fear

Pain may occur and, if present, is usually substernal, crushing, radiating

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58
Q

Myocardial infarction: diagnostics

A

Changes in ECG
Serum enzyme and isoenzyme levels
Serum levels of myosin and cardia troponin are elevated
Leukocytosis, elevated CRP and ESR common
Arterial blood gas measurements may be altered
Pulmonary artery pressure measurements are helpful

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59
Q

Myocardial infarction: complications

A

Sudden death
Cardiogenic shock
CHF
Rupture of necrotic heart tissue/cardiac tamponade
Thromboembolism causing CVA with left ventricular MI

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60
Q

Myocardial infarction: treatment

A 
Goal: reduce cardiac demand
O2 therapy
Analgesic 
Anticoagulants 
Thrombolytic agents can be used
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61
Q

Medications are given to help treat Myocardial infarction along with secondary problems such as?

A

Medication to treat:

Dysrhythmias, hypertension, CHF

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62
Q

Cardiac Dysrhythmias (Arrhythmias)

A

Deviations from normal cardiac rate or rhythm

  • reduces the efficiency of the hearts pumping cycle
  • many types of abnormal patters exist
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63
Q

Cardiac Dysrhythmias (Arrhythmias): cause

A

Electrolyte abnormalities, fever, hypoxia, stress, infarction, infection, drug toxicity

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64
Q

Cardiac Dysrhythmias (Arrhythmias): diagnostics

A

Electrocardiography (ECG/EKG) - for monitoring the conduction system
- detects abnormalities

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65
Q

Cardiac Dysrhythmias (Arrhythmias): SA node symptoms

A

Bradycardia, tachycardia, sick sinus rhythm

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66
Q

Cardiac Dysrhythmias (Arrhythmias): Atrial symptoms

A

Premature atrial contraction, atrial flutter, atrial fibrillation
- most common

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67
Q

Cardiac Dysrhythmias (Arrhythmias): Atrioventricular

A

Heart blocks

- 1st degree, 2nd degree, 3rd degree

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68
Q

Cardiac Dysrhythmias (Arrhythmias): Ventricular

A

Bundle branch block, ventricular tachycardia, ventricular fibrillation, premature ventricular contractions

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69
Q

Cardiac Dysrhythmias (Arrhythmias): Asystole

A

Cardiac arrest

  • no conduction, flat ECG
  • immediate loss of consciousness
70
Q

Cardiac Dysrhythmias (Arrhythmias): treatment

A

Determine cause

  • fix electrolyte imbalance
  • drug therapy changes (i.e., change drug dose of certain medication)
  • antiarrhythmic / antidysrhythmic drugs
  • pace maker
71
Q

What are examples of anti-arrhythmic drugs

A

Beta-adrenergic blockers
Calcium channel blockers
Digoxin

72
Q

In what type of arrhythmia would a defibrillator placement be useful for

A

Ventricular fibrillation

73
Q

What arrhythmia’s require pacemaker

A

SA nodal problems

74
Q

CHF: what is it?

A

Heart is unable to pump sufficient blood to meet metabolic demands of the body

Usually a complication fo another cardiopulmonary condition

75
Q

CHF how does it happen in the heart?

A

One side usually fails first and the other side follows

- left sided CHF / right sided CHF

76
Q

CHF: what happens when the heart cannot maintain pumping capability

A

Cardiac output (stroke volume) decreases

Backup and congestion develop as coronary demands for O2 and glucose are not met

  • output from ventricle is less than the inflow of blood
  • congestion in venous circulation draining into the affected side of the heart
77
Q

CHF: s/s

A

Forward effects (similar with failure on either side)

  • decreased blood supply to tissues (general hypoxia)
  • fatigue and weakness
  • dyspnea and SOB
  • decreased cell function
  • mild acidosis develops
78
Q

CHF: compensation mechanisms

A 
Tachycardia 
Cutaneous and visceral vasoconstriction
Daytime oliguria (low urine output)
79
Q

CHF: Left-sided failure s/s

A

Dyspnea and orthopnea
- develop as fluid accumulates in the lungs

Cough
- d/t fluid irritating the respiratory passages

Paroxysmal nocturnal dyspnea

  • indicates the presence of acute pulmonary edema
  • usually develops during sleep
  • excess fluid in lungs frequently leads to infections such as pneumonia
80
Q

CHF: left sided failure is related to what?

A

Pulmonary congestion

81
Q

CHF: right-sided failure is dependent on what

A

Edema in feet, legs, or buttocks

82
Q

CHF: Right-sided failure s/s

A
  • increased pressure in jugular veins —> distention
  • hepatomegaly and splenomegaly —> digestive disturbances
  • ascites (accumulation of fluid in peritoneal cavities; marked abdominal distention)

Acute right-sided failure: flushed face, distended neck veins, headache, visual disturbances

83
Q

CHF: diagnostics

A

X-Ray —> shows cardiomegaly or fluid in lungs

Cardiac catheterization —> measures pressures in circulation

ABG (arterial blood gases) —> measures hypoxia

84
Q

CHF: treatment

A

Treat underlying problem
Reduce workload of heart
Preventative measures (flu shot, pneumonia, vaccine)
Cardiac support (drug therapy)

85
Q

Congenital Heart Defects (CHD): cardiac anomalies

A

Structural defects in the heart that develop during the first 8 weeks of embryonic life

86
Q

Congenital Heart Defects (CHD): congenital heart disease

A

Valvular defects
Septal defects
Detected by the presence of heart murmurs
If untreated, child may develop heart failure

87
Q

Congenital Heart Defects (CHD) may be what

A

Cyanotic or acyanotic, depending on the direction of shunting

88
Q

Congenital Heart Defects (CHD): s/s

A

Pallor, Tachycardia, Dyspnea on exertion

Squatting position (toddlers / children)
- appears to modify blood flow, makes more comfortable

Clubbed fingers
Intolerance for exercise and exposure to cold weather
Delayed growth and development

89
Q

Congenital Heart Defects (CHD): diagnostics

A

Severe are often diagnosed at birth/in utero, others may not be detected for some time (I.e., murmur caught on assessment)

90
Q

Congenital Heart Defects (CHD): examination techniques

A 
Radiography 
Diagnostic imaging
Cardiac catheterization
Echocardiography 
Electrocardiography
91
Q

Congenital Heart Defects (CHD): treatment

A

Surgical and medical

92
Q

Rheumatic fever —> rheumatic heart disease: what is it and what does it involved?

A

Acute systemic inflammatory condition; abnormal immune function
- involved heart and joints

93
Q

Rheumatic fever —> rheumatic heart disease: when can it occur

A

A. A few weeks after an untreated infection (usually group A beta-hemolytic Streptococcus)
— abnormal immune function

B. In children ages 5-15 y/o

94
Q

Rheumatic fever —> rheumatic heart disease: long term effects

A

Rheumatic heart disease

May be complicated by infective endocarditis and heart failure in older adults

95
Q

Rheumatic fever —> rheumatic heart disease: Acute stage

A

Pericarditis, myocarditis, endocarditis and incompetent heart valves

96
Q

Rheumatic fever —> rheumatic heart disease: other sites of infection

A

Large joints, erythema marginatum, non-tender subcutaneous nodules, involuntary jerky movements of the face, arms and legs

97
Q

Rheumatic fever —> rheumatic heart disease: s/s

A 
Low grade fever
Leukocytosis
Malaise
Anorexia 
Fatigue 
Tachycardia 
Murmur 
Epistaxis 
Abdominal pain
98
Q

rheumatic heart disease: diagnostics

A

Elevated serum antibody levels
Heart function test
Electrocardiography
Antibody titer

99
Q

rheumatic heart disease: treatment

A

Prophylactic antibacterial agents

Anti inflammatory agents

100
Q

Subacute Infective Endocarditis

A

Defective heart valves invaded by Streptococcus viridans, normal flora

101
Q

Acute Infective Endocarditis

A

Normal heart valves attacked by harmful organisms (I.e., staphylococcus)

  • severe tissue damage
  • difficult to treat
102
Q

Subacute and Acute infective endocarditis: basic effects

A

Same regardless of organism

103
Q

Subacute and Acute infective endocarditis: predispositions

A

Abnormal heart valves
Bacteremia
Reduced host defenses

104
Q

Infective Endocarditis: s/s (overall for both types)

A

Low-grade fever, fever, fatigue

Anorexia, splenomegaly, CHF

105
Q

Infective Endocarditis: subacute s/s

A

Insidious onset - increasing fatigue, anorexia, cough and dyspnea

106
Q

Infective Endocarditis: Acute s/s

A

Sudden, marked onset - spiking fever, chills, drowsiness

107
Q

Infective Endocarditis: diagnostics

A

Blood culture
Murmur
Transesophageal echo

108
Q

Infective Endocarditis: treatment

A

Antimicrobial

Drug therapy to promote heart function

109
Q

Pericarditis is usually what

A

Secondary to another condition classified by cause or type of exudate

110
Q

Acute Pericarditis: what is it and what happens?

A

Simple inflammation of pericardium
- may be secondary

Effusion may develop

  • large volume of fluid accumulates in pericardial sac
  • leads to distended neck veins, faint heart sounds, pulsus paradoxus
111
Q

Chronic Pericarditis: what is it?

A

Results from the formation of adhesions between the pericardial membranes

112
Q

Chronic Pericarditis: what happens?

A

Limiting movement of the heart during systole —> reduced cardiac output
— inflammation or infection may develop from adjacent structurea

113
Q

Chronic Pericarditis: s/s and cause

A

Fatigue, weakness, abdominal discomfort

Caused by systemic venous congestion

114
Q

Pericarditis: general s/s

A 
Tachycardia 
Chest pain
Dyspnea
Friction rub
Distended neck veins
Faint heart sounds 
Pulsus paradoxus (systole pressure drop by 10) 
Fatigue weakness abdominal discomfort
115
Q

Pericarditis: treatment

A

Treat primary cause

116
Q

How might you be able to diagnose Pericarditis

A

Fluid aspiration

117
Q

Secondary hypertension

A

Results from renal, endocrine, or pheochromocytoma of adrenal medulla or SNS chain of ganglia

118
Q

Secondary hypertension treatment

A

Treat underlying problem

119
Q

Malignant hypertension

A

Hypertensive emergency

  • extremely high
  • organ damage
  • CNS and renal system damage
120
Q

Primary hypertension: cause

A

Idiopathic

121
Q

Primary hypertension: values

A

140/90

122
Q

Primary hypertension is what

A

Increase in arteriolar vasoconstriction

123
Q

Primary hypertension: how does diastolic value increase (what causes it to increase)

A

**diastolic pressure indicates the degree of peripheral resistance and increased workload of left ventricle

There is an increase in arteriolar vasoconstriction

Decrease in diameter of arterioles - major cause in peripheral resistance - reduced capacity of system - increases diastolic pressure

Vasoconstriction leads to decreased blood flow through the kidneys - leads to increased renin, angiotensin, and aldosterone - leads to increased vasoconstriction further increasing BP

124
Q

Primary hypertension: long term effects

A

Damage to arterial walls

- sclerotic (hard and thick) narrowing of the lumen —> can form aneurysm or reduced blood flow

125
Q

Primary hypertension: areas frequently damaged

A

Kidneys, brain and retina

Retina: easily observed for sclerotic changes and rupture

126
Q

Chronic Primary hypertension can lead to what?

A 
Chronic renal failure
Stroke d/t hemorrhage
Loss of vision
CHF 
Decreased life span
127
Q

Primary hypertension: s/s

A

Asymptomatic early stage

Fatigue, malaise, morning headache

128
Q

Primary hypertension: treatment

A 
Lifestyle changes (decrease Na intake, weight, stress, fitness)
Drug therapy (diuretics, ACE inhibitors, combination drugs)
129
Q

Primary hypertension: compliance to treatment

A

Compliance is hard d/t lack of s/s

130
Q

Primary hypertension: prognosis

A

Depends on treating underlying cause and constant control / compliance of treatments

131
Q

Peripheral vascular disease is a what

A

Arterial disorder

132
Q

Peripheral Vascular Disease: what is it

A

Disease in arteries outside the heart

133
Q

Peripheral Vascular Disease: increased incidence with what

A

Diabetes

134
Q

Peripheral Vascular Disease: common sites

A

Abdominal aorta
Carotid arteries
Femoral arteries
Iliac arteries

135
Q

Peripheral Vascular Disease: diagnostic tests

A

Doppler studies and arteriography

Plethysmography - measures the size of the limbs and blood volume in organs/tissues

136
Q

Peripheral Vascular Disease: s/s

A 
Weakness of legs
Intermittent claudication (leg pain)
Associated with exercise
Sensory impairment
Weak peripheral pulses
Skin: pallor/cyanotic, dry, hairless, toenails thick and hard
137
Q

Peripheral Vascular Disease: treatment

A
  • control BG
  • control BMI
  • reduce cholesterol level
  • platelet inhibitors
  • anticoagulant meds
  • stop smoking
  • exercise
  • maintain dependent position for legs
  • peripheral vasodilators
  • observe skin for breakdown and treat prompts
138
Q

Peripheral Vascular Disease: what is something to keep in mind with the skin

A

Increased risk for ulcers or delayed healing (lack of blood flow)
If gangrene develops, amputation is required

139
Q

Aortic Aneurism is what

A

Arterial disorder

140
Q

Aortic Aneurism

A

Localized dilation and weakening of arterial wall

141
Q

Aortic Aneurism: how does it develop

A

From a defect in the medial layer of the arterial wall

142
Q

Aortic Aneurism: succular

A

Bulging wall on the side

143
Q

Aortic Aneurism: fusiform

A

Circumferential dilation along a section of artery

144
Q

Aortic Aneurism: dissecting aneurism

A

Develops when there is a tear in the intima of the wall and blood continues to dissect or separate tissues

145
Q

Aortic Aneurism: etiology

A 
Atherosclerosis 
Trauma
Syphilis 
Infections 
Congenital defects
146
Q

Aortic Aneurism: s/s

A

Bruit, pulse felt on abdomen

Usually asymptomatic until large or rupture

147
Q

Bruit

A

Blowing sound heard on auscultation with stethoscope

148
Q

Aortic Aneurism: what does rupture lead to

A

Moderate or severe bleeding, usually leading to severe hemorrhage or death

149
Q

Aortic Aneurism: diagnostics

A

Ultra sound, radiography, CT, MRI

150
Q

Aortic Aneurism: treatment

A

Maintain normal BP until surgical repair

Prevent stress, coughing, constipation, exertion

151
Q

Varicose veins is what type of disorder

A

Venous disorder

152
Q

Varicose Veins: what are they

A

Irregular, dilated, tortuous areas of superficial veins

153
Q

Varicose Veins: predisposing factors

A

Genetics
Increased BMI
Parity
Weight lifting

154
Q

Varicose Veins: in the legs (cause and appearance)

A

May develop from defect or weakness in vein walls or valves

Appear as irregular, purplish, bulging structures

155
Q

Varicose Veins: treatment

A

Keep legs elevated, compression stockings
Avoid restricted clothing and crossing legs
Surgery

156
Q

Thrombophlebitis is what type of disorder

A

Venous

157
Q

Thrombophlebitis: what?

A

Development in inflamed vein (e.g., IV site)

158
Q

Phlebothrombosis: what

A

Thrombus forms spontaneously without prior inflammation; attached loosely

159
Q

Factors for thromus development

A

Stasis of blood or sluggish blood flow
Endothelial injury
Increased blood coagulability

160
Q

Thrombophlebitis / Phlebothrombosis: s/s

A

Often unnoticed
Aching, burning, tenderness in affected legs
Systemic signs: fever, malaise, leukocytosis

161
Q

Thrombophlebitis/Phlebothrombosis: complications

A

Pulmonary embolism:

  • respiratory and cardiac complications
  • sudden chest pain and shock
  • life threatening
162
Q

Thrombophlebitis/Phlebothrombosis: treatment

A

Exercise, elevate legs
Anticoagulant therapy
Surgical intervention

163
Q

Hypovolemic Shock

A

Loss of circulating blood volume

164
Q

Cardiogenic shock

A

Inability of heart to maintain cardiac output to circulation

165
Q

Distributive, vasogenic, neurogenic, septic, anaphylactic shock

A

Changes in peripheral resistance leading to pooling of blood in the periphery

166
Q

Shock: Compensation Mechanisms

A
  1. SNS and adrenal medulla stimulated
    - increase HR, force of contraction, systemic vasoconstriction
  2. Renin secretion
    - increases vasoconstriction —> will decrease urine output
  3. Increased ADH secretion
    - will decrease urine output
  4. Secretion of glucocorticoids
  5. Acidosis stimulates increased respiration

These are mechanisms to INCREASE BP

167
Q

What happens with prolonged shock

A

Cell metabolism is diminished, waste is not removed, leads to lower pH

168
Q

Shock: early s/s

A 
Anxiety
Tachycardia 
Pallor
Light-headed
Syncope
Sweating
Oliguria
169
Q

Shock: complications

A
  1. Acute renal failure
  2. Shock lung (adult respiratory distress syndrome)
  3. Hepatic failure
  4. Paralytic ileus, stress or hemorrhage ulcers
  5. Infection / septicemia
  6. Disseminated intra-vascular coagulation
  7. Depressed cardiac function
170
Q

Shock: Treatment

A
  1. Emergency treatment
    - supine
    - keep warm
    - call for help
    - administer o2
    - determine underlying cause and treat it
  2. Depends on cause/type of shock
    - early stages of shock has good prognosis
    - decompensated shock, mortality is increased, renal failure or DIC

Pathophysiology (11 decks)

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