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BIOL 2200 > module 5: cardiovascular disorders > Flashcards

module 5: cardiovascular disorders Flashcards

1
Q

what is atherosclerosis?

A

principally a disease in the tunica intima of arteries that results in increased wall thickness, decreased elasticity, reduced vessel radius (flow), reduced flow rate, and ischemia to supplied organ/tissue

  • fibrous fatty lesions form in large/medium-sized arteries
    • aorta
    • femoral
    • carotid
    • coronary
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2
Q

describe the anatomy of a atherosclerotic plaque

A
  • aggregation of smooth muscle cells
  • macrophages
  • other leukocytes
  • elaboration of extracellular matrix
    • collagen
    • elastic fibers
  • intracellular/extracellular lipids
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3
Q
A
  • aggregation of smooth muscle cells
  • macrophages
  • other leukocytes
  • elaboration of extracellular matrix
    • collagen
    • elastic fibers
  • intracellular/extracellular lipids
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4
Q

what is the effect of atherosclerosis on the blood vessel wall thickness and elasticity, and on the rate of blood flow?

A
  • increased wall thickness
  • decreased elasticity
  • reduced vessel radius → reduced flow rate
  • ischemia to supplied organ/tissue
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5
Q

which four general blood vessels are principally affected?

A
  • aorta
  • femoral
  • carotid
  • coronary
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6
Q

describe the steps involved in the development of atherosclerosis

A
  • rated to endothelial cell damage
    • hyperlipidemia, cigarette smoke, immune mechanisms, turbulent blood flow, etc. can result in:
  1. increased endothelial cells permeability= substances can move into damaged cells = buildup of plasma proteins/lipids
  2. monocytes and other leukocytes come into the subendothelial layer due to the buildup of proteins and lipids (follows them into cells)
  3. monocytes turn into macrophages to ingest lipid and turn into lipid foam cells
  4. macrophages release growth factors to reproduce smooth muscle and reactive oxygen species, and other toxic substances
  5. progressive tissue damage and growth of plaque lesion
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7
Q

what is the significance of low-density lipoproteins to atherosclerosis?

A

associated with atherosclerotic plaques

  • high levels of LDLs are associated with damage of endothelial lining and depositing underneath = coronary artery diseases as a result of atherosclerosis
  • inflammatory reaction that’s going to cause plaque formation
  • LDLs are oxidized by ROS in plaques and then phagocytized by macrophages = an even bigger buildup of foam cells
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8
Q

name some predisposing risk factors for atherosclerosis

A
  • elevated cholesterol
  • high blood pressure increase endothelial cell damage
  • obesity
  • diabetes
  • smoking
  • sedentary lifestyle
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9
Q

what is coronary artery disease (CAD)?

A
  • ischemic heart disease = blocking blood flow to heart
  • cause of ischemic heart disease
  • third of all deaths in industrialized west
  • nearly all elderly have some coronary impairment
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10
Q

what is ischemic heart disease (IHD)?

A

a disease characterized by ischemia (reduced blood supply) of the heart muscle, usually due to coronary artery disease (atherosclerosis of the coronary arteries)

  • heart muscle not getting enough blood for tissue to work properly
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11
Q

describe the relationship between coronary artery disease and ischemic heart disease

A

since coronary artery disease is the major cause of ischemic heart disease, the two terms are often used interchangeably

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12
Q

Which regions of the heart are affected by blockages in the right coronary, and vessels leading from the left coronary arteries? (You don’t need to separate out the regions from the individual vessels leading from the left coronary artery.)

A
  • right coronary:
    • supplies mostly the right ventricle and posterior regions of the heart
    • blockage between right and left ventricle
  • left coronary arteries:
    • supplies mostly the left ventricle and interventricular septum
    • blockage of upper right left ventricle and lower left ventricle
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13
Q

Describe the mechanisms that regulate myocardial blood flow and identify when myocardial blood flow is the highest.

A
  • in strenuous exercise, coronary blood flow increases 3-4x
  • nervous control
    • autonomic control
    • local autoregulatory control
  • blood flow highest during diastole
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14
Q

describe the autonomic control of myocardial blood flow

A
  • parasympathetic via vagus nerve
  • sympathetic:
    • alpha receptors = constrict
    • beta receptors = dilate
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15
Q

describe local autoregulatory control for myocardial blood flow

A

local metabolism is a major control of myocardial blood flow

  • in local environment, metabolism can activate vasoactive mediators
  • vasoactive mediators produce vasodilation or constriction depending what those mediators are, to meet demand of heart
    • ex: adenosine and nitric oxide
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16
Q

Why is the subendocardial region of cardiac muscle most sensitive to ischemia?

A

they have most difficulty obtaining adequate blood flow

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17
Q

Why is the collateral circulation of the myocardial blood flow a potential life-saving feature?

A
  • there are many connections called anastomoses between smaller. coronary arteries
  • during acute ischemia, anastomoses dilate fast to shunt blood to an alternative path to help bring blood to heart when there is another blockage
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18
Q

Define angina pectoris and differentiate between stable angina and unstable angina

A
  • angina pectoris: chest pain from a gradual hardening and narrowing of the coronary arteries
    • can lead to complete occlusion (blockage) = myocardial infarction
  • stable: chest pain caused by transient myocardial ischemia
    • not severe enough to cause necrosis
  • unstable: atherosclerotic plaque still in coronary artery and small portions of the plaque can break off (thromboses) and move through circulation = periods of occlusion
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19
Q

describe the underlyng pathology of stable angina

A
  • transient myocardial ischemia
  • brought on through physical exertion/emotional stress
  • myocardial blood flow cannot responf to increased demand for blood due to narrowing of one or more coronary arteries by atherosclerotic plaque
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20
Q

describe the underlying pathology of unstable angina

A
  • atherosclerotic plaque sheds and leads to a development of small thromboses = periods of occlusion
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21
Q

describe the distinctive diagnostic clinical features of stable angina regarding: the pattern and duration of pain

A
  • pain radiates from the sub-sternal regian of the chest to the jaw and down the arms
  • symptoms last less than 15 minutes
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22
Q

describe the distinctive diagnostic clinical features of stable angina regarding: the effect of exercise and emotional strss on the signs/symptoms

A

pain brought on through physical exertion/emotional stress

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23
Q

describe the distinctive diagnostic clinical features of stable angina regarding: the effect of short acting vasodilators such as glycerol trinitrate (GTN) on the signs and symptoms

A

symptoms relieved by GTN vasodilator

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24
Q

describe the distinctive diagnostic clinical features of unstable angina regarding: the pattern and duration of pain

A
  • chest pain is sudden and unpredictable
  • pain generally more severe, lasting longer than 20 minutes
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25
Q

describe the distinctive diagnostic clinical features of unstable angina regarding: the effect of exercise and emotional stress on the signs/symptoms

A

chest pain is not in response to exertion or stress, but is spontaneous

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26
Q

describe the distinctive diagnostic clinical features of unstable angina regarding: the effect of short acting vasodilators such as glycerol trinitrate (GTN) on the signs and symptoms

A

requires immediate hospitalization for rest, observation, and treatment: nitrates (vasodilator)

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27
Q

what is acute coronary syndrome?

A

a spectrum of ischemic heart diseases ranging from unstable angina to myocardial infarction

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28
Q

describe the differences in underlying pathology of acute coronary syndrome regarding: unstable angina

A
  • atherosclerotic plaque is still in the coronary artery
  • small portions of the plaque can break off = small thromboses
  • small thromboses move through circulation = blockages in blood vessels
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29
Q

describe the differences in underlying pathology of acute coronary syndrome regarding: non-ST segment myocardial infarction (Non-STEMI)

A

sometimes thrombus disintegrates before complete tissue necrosis = only sub endocardium affected

  • don’t see ST elevation because thrombus in blood vessel sometimes disintegrates before complete damage
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30
Q

describe the differences in underlying pathology of acute coronary syndrome regarding: ST-segment elevation myocardial infarction (STEMI)

A

most serious heart attack

  • the clot lodges permanently in the vessel and the entire thickness of the myocardium becomes ischemic
  • requires immediate emergency intervention
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31
Q

describe the distinctive diagnostic clinical features for unstable angina regarding: the pattern and duration of pain

A
  • chest pain sudden and unpredictable
  • pain generally more severe, lasting longer than 20 minutes
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32
Q

describe the distinctive diagnostic clinical features for unstable angina regarding: whether the event occurs at rest or only as a result of stress

A

chest pain is not in response to exertion or stress, but is spontaneous

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33
Q

describe the distinctive diagnostic clinical features for unstable angina regarding: the effect of short acting vasodilators such as glycerol trinitrate (GTN) on the signs and symptoms

A

requires immediate hospilization: nitrate (vasodilator)

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34
Q

describe the distinctive diagnostic clinical features for non-STEMI regarding: the pattern and duration of pain

A

sometimes thrombus disintegrates before complete tissue necrosis: only sub endocardium affected

  • lasts over 20 minutes
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35
Q

describe the distinctive diagnostic clinical features for non-STEMI regarding: whether the event occurs at rest or only as a result of stress

A

can happen at rest

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36
Q

describe the distinctive diagnostic clinical features for non-STEMI regarding: the effect of short vasodilators such as glycerol trinitrate (GTN) on the signs and symptoms

A

not relieved by GTN

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37
Q

describe the distinctive diagnostic clinical features for STEMI regarding: the pattern and duration of pain

A
  • serious: requires immediate emergency intervention
  • duration over 20 minutes
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38
Q

describe the distinctive diagnostic clinical features for STEMI regarding: whether the event pccurs at rest or only as a result of stress

A

pain occurs at rest

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39
Q

describe the distinctive diagnostic clinical features for STEMI regarding: the effect of short acting vasodilators such as GTN on the signs and symptoms

A

not relieved by GTN

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40
Q

Describe the ECG changes related to myocardial infarction and distinguish between STEMI and Non-STEMI ECG traces.

A
  • non-STEMI: sometimes transient ST elevation, the T wave inversion
  • STEMI: ST segment elevation on ECG
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41
Q

what are serum cardiac biomarkers?

A

markers produced when there’s nectrotic tissue

  • if seen in lab, it means there’s necrotic tissue going on
  • ex: troponin T
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42
Q

Describe the changes in serum cardiac biomarkers in relation to myocardial infarction and how these are used to differentiate MI from unstable and stable angina.

A
  • both Non-STEMI and STEMI present cardiac biomarkers
  • different MI to angina since biomarkers are able to distingush necrotic tissue
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43
Q

Describe the usual manifestations of ACS

A
  • abrupt onset
  • severe and crushing pain, usually substernal, radiating to the left arm, neck, or jaw
  • gastrointestinal complaints
  • complaints of fatigue and weakness
  • tachycardia, anxiety, restlessness, feelings of doom
  • pale, cool, and moist skin
  • a “silent MI” occurs when the person is asymptomatic
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44
Q

what are atypical symptoms of ACS?

A
  • GI complaints
  • complaints of fatigue and weakness
  • tachycardia, anxiety, restlessness, feelings of doom
  • pale, cool, and maist skin
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45
Q

what does the term “silent MI” mean?

A

occurs when a person doesn’t experience any symptoms or has atypical symptoms

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46
Q

identify the three main causes of death through myocardial infarction. Which one is the most common cause of death?

A
  1. decreased cardiac output
  2. fibrillation of the heart
  3. rupture of the heart

most common cause of death: VF = ventricular fibrillation

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47
Q

describe decreased cardiac output

A

decreased cardiac output → cardiogenic shock

  • pumping ability reduced
  • maybe exacerbated by “systolic stretch” = dead muscle
    • when the heart goes to contract, there’s dead muscle= no contraction = bulge & pooling of blood
  • when cardiac output is inadequate to the needs of tissues heart failure and peripheral ischemia result = cardiogenic shock
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48
Q

describe fibrillation of the ventricles after MI

A
  • main cause of death in STEMI is VF = ventricular fibrillation
  • cardiac output is zero
  • due to erratic electrical impulses and abnormal conduction pathways in damaged myocardium
  • dangerous periods of VF to occur are after first 10 minutes then after 1 hour or so
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49
Q

describe rupture of the infarcted area

A
  • can occur several days after infarct as muscle fibres necrose and degenerate and the heart wall stretches thin
  • systolic stretch increases to the point when finally the heart ruptures
  • one way of assessing severe MI is by cardiac imaging to monitor the degree of systolic stretch
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50
Q

List the measures involved in immediate care of ACS.

A
  • nitroglycerin (GTN)- fast acting vasodilator
  • bed rest
  • pain relief - morphine
  • 12 lead ECG and ECG monitoring
  • oxygen therapy - to increase oxygen
  • beta blockers - slows HR, lengthen diastole
    • beta adrenergic receptor antagonists
  • anticoagulant therapy
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51
Q

Describe the key aspects of care and their rationale

A

less strain on the heart

  1. cellular death determines by:
  • degree of ischemia due to infarct
  • workload on the heart since it increases O2 demand
  • lower workload = lower injury from ischemia
  1. when the heart becomes highly active, coronary arteries dilate to supply healthy muscles with O2 and nutrients
    * this reduces collateral circulation that may be assisting the damaged muscle during recovery = not good
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52
Q

describe the importance of pain relief for ACS management

A
  • normally we cannot “feel” our heart - but ischemic myocardium can produce severe “crushing” pain
  • believed to releate to release of lactic acid (anaerobic respiration) and mediators of inflammation
    • ex: histamine, kinins
  • pain rrlief in itself is important for comfort, but also because pain increases stress = cardiac output = increase workload on the heart
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53
Q

Describe the clinical manifestations that occur with atherosclerosis of the aorta

A
  • in large vessles, thrombus formation could lead to hypertension or emboli and weakening of the vessel wall could lead to aneurism
  • in smaller blood vessels, can also get weakening of vessel wall = bursting of wall (on top of thrombus/emboli)
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54
Q

Describe the clinical manifestations that occur with atherosclerosis of the cerebal arteries

A

in medium-sized arteries, mainly ischemia and infarction due to vessel occlusion

  • coronary = heart attack
  • cerebral - stroke
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55
Q

Describe the clinical manifestations that occur with atherosclerosis of the peripheral arteries

A

can cause significant pain and disability

  • especially prevalent in diabetics
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56
Q

Describe the clinical manifestations that occur with atherosclerosis of the coronary arteries

A

CAD (coronary artery diseasse) caused by atherosclerosis is the major cause of myocardial ischemia

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57
Q

Define hypertension and identify medical conditions that someone with hypertension may be at increased risk for.

A
  • hypertesion = a consistent elevation of systematic arterial blood pressure
    • >/= 140/90
  • increased risk for MI, kidney disease, and stroke
  • commonly divided into categories of primary (idiopatheic) or secondary (resulting from another disorder)
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58
Q

Are most cases of hypertension due to primary or secondary causes?

A

primary (95%) due to a combination of genetics and the environment

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59
Q

What factors can lead to primary hypertension?

A
  • family history
  • age
  • gender
  • race
  • high dietary sodium intake
  • insulin resistance
  • cigarette smoking
  • obesity
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60
Q

The increase in blood pressure is due to one or both of what 2 changes in the circulatory system?

A
  1. increase in circulating blood volume (volume of blood gone up)
  2. increased peripheral resistance (blood vessels are constricted/extra resistant to the amount of blood coming in)
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61
Q

describe 3 factors that can interact to produce changes to blood pressure

A
  1. sympathetic nervous system - increases heart rate and vasoconstriction
  2. overactivity of renin-angiotension-aldosterone system (RAAS) - increases blood volume and pressure (retain water in kidneys), increases vasoconstriction
  3. chronic inflammation results in smooth muscle contraction
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62
Q

Why is hypertension called the “silent disease”? Give examples of damage that can be caused by sustained hypertension

A
  • “silent disease” = early stages have no symptoms/signs, other than elevated blood pressure
  • damage due to sustained hypertension:
    • coronary heart disease
    • kidney disease
    • CNS dysfunction (stroke)
    • impaired vision
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63
Q

How is hypertension diagnosed and how is it typically treated?

A
  • diagnosis:
    • several BP measurements at different times
      • 3-5 visits depending on the measurement
    • complete blood count (CBC)
    • urinalysis
    • blood chemistry
    • ECG
  • treatment:
    • exercise
    • lose weight
    • stop smoking
    • diuretics
    • other antihypertensives
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64
Q

Describe the two classifications of hypertension during pregnancy

A
  1. pre-existing: present before pregnancy, or appears before 20 weeks of pregnancy
  2. gestational: occurs at or after 20 weeks of pregnancy - due to the pregnancy
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65
Q

Why would hypertension develop during pregnancy and be familiar as to what conditions it might lead

A
  • unknown: thought to be due to a decrease in placental blood flow = release of toxic compounds that causes changes in blood vessel walls throughout the body
  • conditions: risk for development of many pathological effects
    • preeclampsia = danger zone
    • liver failure
    • kidney failure
    • heart disease
    • respiratory distress
    • DIC
    • generalized edema
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66
Q

What manifestations would result in the diagnosis of preeclampsia?

A
  1. hypertension - once you see hypertension, have to check for proteinuria and other conditions
  2. proteinuria - protein high in the urine
    1. liver beinf affected
    2. kidney is being affected
  3. adverse conditions such as persistent or new headache, visual disturbances, persistent abdominal pain, elevated liver enzymes, etc.
67
Q

Describe eclampsia and its possible cause

A
  • eclampsia = the occurence of convulsions (CNS shuts down) and possible coma
  • possibly brought about through the development of blood clots in cerebral vessels
68
Q

What is the effect of gestational hypertension on the fetus?

A
  • decrease in placental blood flow
  • results in infants who are small for gestational age, and the frequent need for early delivery
69
Q

What is the definitive cure for preeclampsia?

A

birth of baby and accompanying delivery of placenta

70
Q

Define orthostatic (postural) hypotension

A
  • specific decrease in blood pressure within 3 mins of moving to a standing position, causing dizziness, fainting, etc.
71
Q

What is the pathophysiology behind orthostatic hypotension?

A
  • more frequently observed in elderly (age)
    • mechanisms that increase BP decline as we age
  • medications
  • other medical conditions
72
Q

Give a common cause for orthostatic hypotension and describe how it is treated

A
  • common cause = certain medications
  • treatment = alleviating the cause (aka change the meds)
    • can be managed by learning ways to cope
73
Q

what is an aneurism?

A

local outpouring of vessel or heart chamber, usually in the abdominal aorta

74
Q

describe the causes of an aneurism

A
  • atherosclerosis
  • hypertension
75
Q

describe the manifestations of an aneurism

A
  • depends where the aneurism is
  • involve the production of pressure on local structures
    • depends where the weakness is in order to see different effects
  • rupture causes exteme pain and hypotension
76
Q

Define thrombus. What can cause thrombi and what can they do?

A
  • thrombus = blood clot
  • caused by any condition that promotes activation of coagulation
  • can occlude the artery/vein, or can break off to form an embolus
77
Q

define embolism

A

obstruction of a vessel by an embolus

  • no matter how times, it will eventually lodge in a vessel
78
Q

describe the difference in origin between pulmonary and arterial emboli

A
  • pulmonary emboli- arise from the venous side, or in the right heart (goes to the lungs)
  • arterial emboli - arise from the left heart and are associated with thrombi that occur after heart trauma
    • go back through coronary artery = MI
    • go back to the brain = stroke
79
Q

Define varicose veins

A

veins in which blood pooled, producing distended (widen), tortuous (twisted), and palpable vessels

80
Q

Describe two reasons for why varicose veins commonly occur in the legs

A
  1. there are no valves in the inferior vena cava or the common iliac veins = veins in the legs responsible for supporting the blood in these vesels = increase pressure in abdomen = increase strain on valves
  2. standing for long periods of time puts extra strain the these valves since leg muscles are not being used to pump blood back to the heart
81
Q

Describe how varicose veins develop

A
  • pressure from the valve damage increases pressure down to the legs because of gravity
  • vein swells = edema in the surrounding tissues
  • edema = damage to the remaining upstream valves in the vein
  • damage to upstream valves = unable to maintain normal venous pressure
82
Q

Describe some risk factors for developing varicose veins

A
  • standing long periods
  • crossing legs at knee
  • age
  • females
  • family history
  • obesity
  • pregnancy
  • deep venous thrombosis
  • previous leg injury
83
Q

describe treatment for varicose veins

A
  • compression stockings
  • physical exercise
  • surgical ligation (clipping off vein)
  • vein stripping
84
Q

Define CVI

A
  • CVI = chronic venous insufficiency
  • inadequate venous return over a long period of time, which impairs blood flow to the area
85
Q

To what two complications can CVI lead? What is a symptom of CVI?

A
  • complications
    • impaired tissue nutrition
    • edema and venous hypertension = inflammation in the vessels and tissue
  • symptoms
    • darkening of the skin of the feet and ankles
86
Q

what is a stasis ulcer?

A

when circulation becomes so poor that any trauma or pressure can lower the delivery of oxygen to the tissues to the point of causing necrosis

87
Q

If delivery of nutrients to the tissues becomes sufficiently poor, what two problems can result?

A

trauma or pressure can lower the delivery of oxygen to the tissues to the point of causig necrosis (stasis ulcer) and infection

88
Q

Define DVT. Name some risk factors

A
  • DVT = deep venous thrombosis
    • the development of a thrombus in deep vein- occurs primarily in lower extremit
  • risk factors:
    • venous stasis = not able to move a lot because muscle can’y help w/o movement
    • impaired cardiac function = not enough pressure to extremeties to get blood back up in the end
    • venous endothelial damage
    • hypercoagulable states
89
Q

Describe the development of DVT

A
  1. clotting fators and platelets accumulate and form a thrombus
  2. inflammation around the thrombus promotes further platelet aggregation and the thrombus grows
  3. because the vein is deep in the leg, it is usually asymptomatic
90
Q

how can the risk of DVT be reduced?

A
  • most thrombi will eventually dissolve, but are associated with higher risk of pulmonary embolism
  • hard to detect, so prevention is important
91
Q

Define pericarditis and name some causes

A
  • pericarditis = acute inflammation of the pericardium = pain and fever
  • causes:
    • idiopathic
    • infection
    • surgery, etc.
92
Q

Define cardiomyopathy

A

diverse group of diseases the primarily affect the myocardium itself

93
Q

Describe two examples of cardiomyopathy and their effects on heart function

A
  • ex 1: dilated cardiomyopathy
    • ventricles are widening = muscle layer very thin = impairment of the systolic function of one or both ventricles (blood can’t get through the body)
    • ⅓ of cases are inherited
    • effects = orthopnea reduced exercise capacity
  • ex 2: hypertrophic cardiomyopathy
    • thickening of septum = decrease in left ventricular size = obstruct the outflow of the left ventricle
    • one of the most common types of cardiomyopathies and inherited
    • most people asymptomatic
    • effects = angina, dyspnea, reduced exercise capacity
94
Q

What is one of the most common acquired causes for valvular dysfunction?

A

through rheumatic heart disease

  • initial infection with streptococcus pyogenes, followed by molecular mimicry
95
Q

Which valves in the heart are most commonly affected by valvular dysfunction? Why?

A
  • aortic and mitral valve
  • because these valves are between the body (aorta) and atrium or lungs (mitral) and left ventricle..? IDEK
96
Q

Describe the two types of disruptions that can occur with a valvular dysfunction

A
  • stenosis: narrowing of valve opening, causing turbulent flow and enlargement of emptying chamber
  • incompetent (regurgitant) valve: permits backward flow
97
Q

what is a “heart murmur”?

A

sounds made by abnormal flow

98
Q

What is dysrhythmia/arrhythmia?

A

range from occasional “missed” or rapid beats to serious disturbances that impair the pumping ability of the heart

  • problem with conduction pathway
99
Q

What are the two general causes for disrhythmias?

A
  1. abnormal rate of impulse generation from thr SA node or other pacemaker
  2. abnormal conduction of impulses through the heart’s conduction system
    1. SA node working properly, but problem elsewhere
100
Q

Define sinus rhythm

A

the rhythm of your heartbeat, determined by the sinus node of your heart

101
Q

define bradycardia

A

slower than normal heart rate

102
Q

define tachycardia

A

faster than normal heart rate

103
Q

define sinus arrhythmia

A

a changing sinus node rate with the respiratory cycle, on inspiration and expiration

irregular heartbeat

104
Q

Describe atrial fibrillation. Why can this be sometimes asymptomatic? What is the greatest danger?

A
  • AFib = 400-600bpm
    • completely disorganized and irregular atrial rhythm accompanied by completely irrgular ventricular rhythm
  • greatest danger: causes pooling of blood in atria = risk for blood clot
  • may be asymptomatic because ventricular filling is not totally dependent on atrial contraction
105
Q

Describe atrioventricular node abnormalities (heart block)

A
  • atria contract ok, but AV node may be paused too long
  • “first, second, or third degree” = depends how long the pause is at AV node.. longer = worse
  • heart block occurs when ocnduction is excessively delayed or stopped at the AV node or bundle of His
106
Q

Describe ventricular fibrillation

A
  • conductions not going through ventricles = not contracting
  • ventricles quiver but do not contract = ineffective in ejecting blood
  • death within minutes if not corrected
107
Q

describe asystole

A
  • no electrical activity in the heart/absence of a heartbeat
  • “flatline”
  • worst case scenario
108
Q

What is heart failure?

A

when the heart is unable to generate an adequate cardiac output

109
Q

What two factors interact to produce cardiac output? Which of these factors is reduced in heart failure?

A
  1. stroke volume
  2. heart rate
  • cardiac output = stroke volume x heart rate
  • decrease in stroke volume
110
Q

Upon what three characteristics does stroke volume depend?

A
  • preload
  • afterload
  • myocardial contractility
111
Q

What are the two possible consequences of heart failure?

A
  1. inadequate perfusion of tissues
  2. increased pulmonary capillary pressures

**or both

112
Q

Describe some of the main causes and risk factors for heart failure

A
  • coronary artery disease
  • hypertension
  • dilated cardiomyopathy
  • valvular heart disease

risk factors:

  • ischemic heart disease
  • hypertension
  • T2DM
  • obesity
  • older age
  • lack of exercise
  • smoking
  • hyperlipidemia
113
Q

Define preload. What two factors determine preload?

A

volume of blood in the ventricle at the end of diastole

  • two factors
    • amount of blood entering ventricle during diastole
    • blood left in ventricle after systole
114
Q

What is the Frank-Starling Law of the Heart?

A

the more stretched the ventricle wall, the greater the force of the contraction (up to a maximum value) = the more blood in the ventricles, the stronger the contraction = greater stroke volume

115
Q

Define afterload and describe the characteristic that would be a good indicator of this

A

afterload = resistance to ejecion of blood from the left venricle (blood easy to push out = good)

  • peripheral vascular resistance is usually a good index of afterload
116
Q

Define inotropy. What is a synonym for inotropy?

A
  • inotropy synonym = contractility (how good can your muscle fibres contract)
    • the ability of actin and myosin of the heart muscle to interact and shorten against a load
117
Q

Name two diseases that would affect inotropy and identify whether contractility would increase or decrease

A
  1. ventricular hypertrophy increases contractility
  2. myocardial infarction decreases contractility
118
Q

Define systolic heart failure

A

myocardial contractility is imparied, leading to a decrease in ejection fraction = decrease in cardiac output

  • normal = 65%
  • dysfunction = 40%
119
Q

Describe how systolic heart failure can lead to pulmonary/peripheral edema

A
  • decrease in ejection fraction = more blood left in the ventricle after contraction
  • more blood in the ventricle = increase of pre-load
  • increased pre-load = too much pressure in ventricles all the way to the lungs
  • increased pre-load = pulmonary/peripheral edema
120
Q

Identify (and understand the examples for each) three causes for systolic heart failure

A
  • decreased contractility = due to MI, cardiomyopathy
  • volume overload = due to valvular incompetence
  • pressure overload = due to hypertension
121
Q

Define diastolic heart failure

A
  • decrease in cardiac output that occurs on the left side
  • caused by decreased diastolic relaxation so that less blood enters the ventricle
122
Q

Identify (and understand the example for each) three causes for diastolic heart failure

A
  • decrease expansion of the ventricle = ex: pericardial effusion (pressure on the heart)
  • increase wall thickness and reduce chamber size = ex: hypertrophic cardiomyopathy (not able to pull as much blood)
  • delay diastolic relaxation (myocardial ischemia) = decreased energy for calcium pumps
123
Q

What is the result of diastolic heart failure, and how does this happen?

A
  • result = pulmonary edema
  • happens as blood backs up into pulmonary circulation = increasing pulmonary pressure
124
Q

Define left heart failure. What is left heart failure commonly called?

A
  • definition: decreased output to systemic circulation
  • commonly called congestive heart failure
  • can be systolic, diastolic, or both
125
Q

Describe the consequence of left heart failure, and how this arises

A
  • consequence = pulmonary edema
  1. blood accumulates in the left side, then in the pulmonary circulation = increased pulmonary venous pressure
  2. if this exceeds osmotic pressure in capillaries, fluid enters the lung tissue
  3. fluid enters lung tissue = pulmonary edema
126
Q

What are the common causes of left heart failure?

A
  • hypertension
  • acute MI
  • cardiomyopathy
127
Q

Define right heart failure

A

inability of right ventricle to move deoxygenated blood from systemic circulation into the pulmonary circulation

128
Q

Describe the consequences of right heart failure and how these arise.

A
  • consequences:
    • peripheral edema and congestion of the viscera
  1. right ventricle unable to movr deoxyginated blood to pulmonary circulation = pressure rise in systemic venous circulation
  2. pressure rise in systemic venous circulation = peripheral edema and congestion of the viscera
129
Q

Identify the most common cause of right heart failure and describe how this occurs

A
  • most commonly caused by left heart failure
  1. left heart failure increased pulmonary pressure
  2. backs up into the right ventricle which is poorly equipped to compensate = dilate and fail
130
Q

Define cor pulmonale and name some diseases that may be a cause

A
  • cor pulmonale = when right heart failure occurs independently of left heart failure, in response to pulmonary disease
  • diseases:
    • COPD
    • cystic fibrosis
    • ARDS (acute respiratory distress syndrome)
131
Q

what are the 3 compensatory mechanisms for heart failure?

A
  1. sympathetic nervous system activation
  2. RAAS activation
  3. hypertrophy
132
Q

describe the sympathetic nervous system activation compensatory mechanism for heart failure: why they are activated, or their purpose in being activated, and how they bring about harm to the heart

A
  • to increase blood pressure and cardiac output
  • harm: the increase in HR and contractility actually put more strain on the already weakened heart
133
Q

describe the RAAS activation compensatory mechanism for heart failure: why they are activated, or their purpose in being activated, and how they bring about harm to the heart

A
  • RAAS= renin-angiotensin-aldosterone-system
  • activated due to decreased cardiac output (decreased amount of blood going through kidney due to a decrease in BP)
    • aldosterone and ADH released = increase of vasoconstriction & blood volume = increase BP
  • harm:
    • vasoconstriction increased afterload = increases resistance to pushing blood out of the heart = heart working harder
    • increase blood volume = increase preload = heart working harder
134
Q

describe the hypertrophy compensatory mechanism for heart failure: why they are activated, or their purpose in being activated, and how they bring about harm to the heart

A
  • depending on the stimulus
  • heart working harder = disproportionate thickening of walls due to increase of muscle = ischemia or thinning of ventricular walls
  • ischemia or thinning of ventricular walls = dilations and impairment of heart contraction
135
Q

Explain the phrase “decompensated heart failure”

A

heart failure worsening

136
Q

Describe the symptoms for heart failure

A
  • dyspnea - SOB due to pressure on lungs
  • orthopnea- sitting up helps relive dyspnea (pressure on lungs)
  • fatigue and tires easily - reduction in blood flow = decrease oxygen to tissues
  • decreased urine output - kidney function
  • edema (especially in lower extremities) - fluid build up
137
Q

List the treatments for heart failure and explain why they would be used

A
  • salt restriction and diuretics, weight management - concentrates on decreasing preload and afterload
  • digitalis (improves stroke volume), beta-blockers, oxygen therapy
138
Q

Define shock

A

an acute failure of the circulatory system to supply the body with an adequate blood supply, resulting in cellular hypoxia

139
Q

Describe the basic cellular effects of shock

A
  • lack of oxygen to cell = switch to anaerobic respiration = decrease ATP production
  • lack of ATP = cell’s sodium/potassium pump operates poorly
  • sodium/potassium pump affected & calcium not maintained = problems with functioning of nervous and muscular systems
140
Q

describe positive feedback loop #1

A
  • failure in circulation
  • losing water from interstitial fluid due to Na+ attracting water into the cell
  • lack of interstitial fluid = water being pulled from the vascular system
  • lack of fluid from vascular system = drop in BP
  • drop in BP and blood volume = lack of blood to tissues
141
Q

describe positive feedback loop #2

A
  • lysosomal enzymes are released, damaging tissues.. 2 ways:
  1. disruption of cell membrane = cellular swelling = burst cell = release of enzymes
  2. increase acidity due to increase lactic acid = change in pH = cells bursting = release lysosomal enzymes
  • lysosomal enzymes attack surrounding cells = inflammatory response = increase to tissue damage = further damage to cellular metabolism
142
Q

describe positive feedback loop #3

A
  • lactic acid buildup = lower pH
  • lower pH = decreased affinity (AKA binding ability) with o2 to hemoglobin
  • decrease of o2 binding to hemoglobin = decreased o2 carrying capacity of our blood = anemia
143
Q

What is the consistent sign of shock?

A

hypotension

  • arterial pressure below 60mmHg
  • normal = 70-110mmHg
144
Q

Describe some symptoms of shock

A
  • symptoms can be conflicting in nature
  • being sick
  • weak
  • cold
  • hot
  • dizzy
  • confused
  • afraid
  • thirsty
  • SOB

depends on the type of shock

145
Q

Describe the condition of cardiogenic shock and its effect on the heart

A
  • enough blood volume but decreased cardiac output due to decreased contractility increased preload, and increased afterload
    • as the heart is contracting, it is not able to pump blood to tissues efficiently
  • decrease in BP causes compensatory responses = increase o2/nutrient demand on the heart
  • increase o2/nutrient demand = further strain on the heart
  • further strain on heart = incapable of pumping an adequate volume of blood to the heart
146
Q

Identify the condition that often leads to cardiogenic shock

A

myocardial infarction

147
Q

Describe the condition of hypovolemic shock and its causes

A
  • not enough blood volume
  • caused by a loss of whole blood (hemorrhage), plasma (burns), or interstitial fluid (diarrhea/diuresis in large amounts
  • amount of volume of blood in your vascular system decreases by 20% = starts to get issues w/hypovolemic shock
148
Q

What compensatory mechanisms does the body employ to counteract hypovolemic shock?

A
  • HR and vasoconstriction increase
  • interstitial fluid moves into blood
  • liver and spleen add to blood volume
  • RAAS is activated, as is ADH
149
Q

Describe the condition of distributive shock

A
  • right amount of volume, but blood vessels are dilated throughout the body = ineffective movement of blood
  • ineffective movement of blood = lower BP and lack of nutrients to tissues
150
Q

what 3 shock states share the distributive shock mechanism?

A
  1. neurogenic
  2. anaphylactic
  3. septic
151
Q

Describe the condition of neurogenic shock and the potential causes

A
  • result of massive vasodilation resulting from overstimulation of parasympathetic nervous system and under stimulation of the sympathetic nervous system
  • rare and usually transitory
  • causes:
    • trauma to the spinal cord or medulla
    • anesthetic agents
    • severe pain
152
Q

Describe the condition of anaphylactic shock, its cause, and its treatment

A
  • results from a widespread hypersensitivity reaction
  • cause:
    • release of histamine by mast cells = type 1 hypersensitivity
    • type 1 hypersensitivity = vasodilation and vascular permeability
    • vasodilation and vascular permeability = peripheral pooling and tissue edema
    • smooth muscle constriction can result in laryngospasm, bronchospasm, and diarrhea
  • treatment:
    • epinephrine to cause vasoconstriction and reverse airway constriction
153
Q

Define the condition of septic shock

A
  • the most common type of vasodilatory shock
  • happens from infection
  • huge inflammatory response to microorganisms itself and antigens OR from toxins being released by microorganisms OR both
  • common cause of death in ICUs
  • skin is warm and flushed since septic shock produces dilation
154
Q

What manifestation differs between septic shock and other categories of shock?

A

skin is warm and flushes because septic shock produces dilation

155
Q

Describe the condition of obstructive shock and its most common cause

A
  • results from mechanical obstruction of the flow of blood through the central circulation (large veins)
  • most common cause = pulmonary embolism
  • elevated right heart pressure occurs
  • significant decrease in cardiac output
  • often classified under cardiogenic shock
156
Q

Describe the treatments for shock

A
  • must remove the underlying cause
    • know what type of shock we’re looking at/what is causing it
  • IV fluid to expand blood volume
    • because all shock has low BP
  • once positive feedback loops have been established, intervention is very difficult
157
Q

Mr. S. is a 65 yr old obese male, with a history of smoking. He has set up an appointment with his doctor due to his decreasing quality of life and concern about the increasing severity of several problems. He had suffered a myocardial infarction 6 years previously (and quit smoking at that time). Within the last several months, he has suffered increasing problems with his breathing, particularly at night (he now finds he can only sleep in the family room “easy chair”, in a semi-upright position). In addition, now his feet and legs are continually swollen, and he feels tired and weak all of the time.

Based on the described symptoms, what is Mr. S. likely experiencing? Support your decision by explaining all pathologic manifestations based on your diagnosis.

A
  • Heart failure: tired and weak (due to lack of blood supply to the body
  • Left side failure: trouble breathing (due to pulmonary edema as a result of backup of pressure from the left side of the heart into the lungs, increasing blood pressure in lungs)
  • Right side failure: swollen feet and legs (due to peripheral edema as a result of back-up of pressure from the right side of the heart into the veins of the body)
158
Q

Mr. S. is a 65 yr old obese male, with a history of smoking. He has set up an appointment with his doctor due to his decreasing quality of life and concern about increasing severity of several problems. He had suffered a myocardial infarction 6 years previously (and quit smoking at that time). Within the last several months, he has suffered increasing problems with his breathing, particularly at night (he now finds he can only sleep in the family room “easy chair”, in a semi-upright position). In addition, now his feet and legs are continually swollen, and he feels tired and weak all of the time

His condition has worsened: from difficulties with breathing to peripheral edema. Explain the pathophysiology behind this development

A

Left sided failure -> back-up of pressure into lungs -> increased venous pressure in lungs -> edema in lungs (difficulty in breathing) -> back-up of pressure into right ventricle -> right sided failure -> back-up of pressure into body -> increased venous pressure -> increased edema.

159
Q

Mr. S. is a 65 yr old obese male, with a history of smoking. He has set up an appointment with his doctor due to his decreasing quality of life and concern about increasing severity of several problems. He had suffered a myocardial infarction 6 years previously (and quit smoking at that time). Within the last several months, he has suffered increasing problems with his breathing, particularly at night (he now finds he can only sleep in the family room “easy chair”, in a semi-upright position). In addition, now his feet and legs are continually swollen, and he feels tired and weak all of the time.

what are the risk factors for his present condition?

A
  • age
  • obesity
  • smoking
  • previous MI
  • male
160
Q

Mr. S. is a 65 yr old obese male, with a history of smoking. He has set up an appointment with his doctor due to his decreasing quality of life and concern about increasing severity of several problems. He had suffered a myocardial infarction 6 years previously (and quit smoking at that time). Within the last several months, he has suffered increasing problems with his breathing, particularly at night (he now finds he can only sleep in the family room “easy chair”, in a semi-upright position). In addition, now his feet and legs are continually swollen, and he feels tired and weak all of the time.

why would an ACE inhibitor would very likely be included in the treatment of Mr. S’s condition and describe the initial compensatory effects that are caused by the named compound (not the ACE inhibitor).

A
  • An ACE inhibitor would very likely be included in the treatment of Mr. S’s condition
  • Angiotensin II causes increased vasoconstriction of arteries, leading to increased BP
  • Angiotensin II also causes release of aldosterone by adrenal cortex. Aldosterone causes kidney to retain sodium (water follows). This increases the blood volume, which increases BP
161
Q

Mr. S. is a 65 yr old obese male, with a history of smoking. He has set up an appointment with his doctor due to his decreasing quality of life and concern about increasing severity of several problems. He had suffered a myocardial infarction 6 years previously (and quit smoking at that time). Within the last several months, he has suffered increasing problems with his breathing, particularly at night (he now finds he can only sleep in the family room “easy chair”, in a semi-upright position). In addition, now his feet and legs are continually swollen, and he feels tired and weak all of the time.

Name and define the three terms involved in cardiac output

A
  • Preload – the volume of blood in the ventricle at the end of diastole.
  • Afterload – the force required to pump blood out of the heart, most easily connected to peripheral resistance.
  • Inotropy - ability of actin and myosin to interact and shorten against a load (force of contraction independent of Frank-Starling law).
162
Q

Mr. S. is a 65 yr old obese male, with a history of smoking. He has set up an appointment with his doctor due to his decreasing quality of life and concern about increasing severity of several problems. He had suffered a myocardial infarction 6 years previously (and quit smoking at that time). Within the last several months, he has suffered increasing problems with his breathing, particularly at night (he now finds he can only sleep in the family room “easy chair”, in a semi-upright position). In addition, now his feet and legs are continually swollen, and he feels tired and weak all of the time.

What changes in preload and afterload (i.e., increase? decrease?) will cause the heart to work harder, thus putting more stress on the heart?

A
  • Preload – increase
  • Afterload - increase
163
Q

Mr. S. is a 65 yr old obese male, with a history of smoking. He has set up an appointment with his doctor due to his decreasing quality of life and concern about increasing severity of several problems. He had suffered a myocardial infarction 6 years previously (and quit smoking at that time). Within the last several months, he has suffered increasing problems with his breathing, particularly at night (he now finds he can only sleep in the family room “easy chair”, in a semi-upright position). In addition, now his feet and legs are continually swollen, and he feels tired and weak all of the time.

id pre-load or after-load most directly related to the Frank-Starling law of the heart? Explain your answer, using the definition of the Frank-Starling law.

A

Pre-load. The Frank-Starling law of the heart is: the greater the stretch on the ventricle wall (the more blood contained in the ventricle prior to contraction), the greater the force of contraction, up to a maximum value. Preload is the volume in the ventricle just before contraction. As volume increases, stretch increases and the force of the contraction would increase

164
Q

Mr. S. is a 65 yr old obese male, with a history of smoking. He has set up an appointment with his doctor due to his decreasing quality of life and concern about increasing severity of several problems. He had suffered a myocardial infarction 6 years previously (and quit smoking at that time). Within the last several months, he has suffered increasing problems with his breathing, particularly at night (he now finds he can only sleep in the family room “easy chair”, in a semi-upright position). In addition, now his feet and legs are continually swollen, and he feels tired and weak all of the time.

Based solely on having suffered a previous myocardial infarction, is Mr. S.’s heart failure most likely systolic or diastolic in nature? Explain your answer using the definitions of systolic and diastolic heart failures.

A
  • It is systolic – failure in the ability of the heart to contract (caused in this case by a MI).
  • Diastolic – decreased volume (filling) in the left ventricle during diastole.

BIOL 2200 (12 decks)

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