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SMP - APP Part 2 > Lectures 1-4 - Cardiovascular Pathophysiology I-IV > Flashcards

Lectures 1-4 - Cardiovascular Pathophysiology I-IV Flashcards

1
Q

What are the 3 layers of a vessel wall? List from outer to inner. What to note?

A
  1. Tunica intima
  2. Tunica media
  3. Tunica adventitia

NOTE: structure of the wall varies greatly between types and sizes of vessels

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2
Q

2 parts of tunica intima?

A
  1. Endothelium

2. BM

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3
Q

2 parts of tunica media?

A
  1. Smooth muscle

2. Elastic fibers

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4
Q

What is the tunica adventitia made of?

A

Areolar connective tissue

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5
Q

3 characteristics of vascular smooth muscle cells?

A
  1. Contractile
  2. Secretory: matrix, growth factors, proteases
  3. Plastic: hypertrophy, proliferation, large changes in phenotype
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6
Q

Basal state of the VSMCs?

A

Contractile

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7
Q

When are VSMCs secretory?

A

Usually when injured

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8
Q

2 factors affecting the vascular tone of the VSMCs?

A
  1. Intrinsic factors: myogenic tone

2. Extrinsic factors: neurogenic and humoral tone

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9
Q

What does vasomotion mean?

A

Change in caliber of a BV

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10
Q

4 roles of the endothelium in BVs?

A
  1. Barrier
  2. Secretory and modulatory for vascular smooth muscle tone and growth, and platelet function
  3. Metabolic: processing of vasoactive factors like ACE production of angiotensin II and breakdown of bradykinin (inflammation)
  4. Plasticity: angiogenesis in response to injury and ischemia
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11
Q

4 secretions of the endothelium?

A
  1. Endothelial-derived vasodilators: nitric oxide (NO) and prostacyclin (PGI2)
  2. Endothelial-derived vasoconstrictors: endothelin
  3. Anti-aggregatory for platelets
  4. Anti-mitogenic for vascular smooth muscle
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12
Q

What is flow through a region mainly governed by?

A

Mainly governed by the resistance of the microcirculation

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13
Q

What is Poiseuille’s Law?

A

(P1 - P2) = 8.η.L.Q / (π.r^4)

r = vessel radius
‎η‎‎ = fluid viscosity 
L = length of the vessel
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14
Q

How can turbulent flow cause BV damage?

A

Causes shear stress on the endothelium causes inflammation and diminished function

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15
Q

3 controls of local blood flow?

A
  1. Metabolic regulation through local metabolites (primarily vasodilation)
  2. Autoregulation through transmural pressure causing vasoconstriction
  3. Shear stress-induced vasodilation due to the longitudinal pressure gradient
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16
Q

Other name for autoregulation of local blood flow?

A

Myogenic regulation

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17
Q

Hydrostatic pressure at the beginning and end of a capillary bed?

A

Beginning: 32 mmHg

End: 25 mmHg

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18
Q

Oncotic pressure at the beginning and end of a capillary bed?

A

25 mmHg constant throughout

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19
Q

Is there a net fluid loss at capillary beds?

A

Not usually, but in the lower extremities the hydrostatic pressure due to gravity may favor filtration, which is usually compensated for

This can cause issues, for example during thermoregulation

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20
Q

In what vein does the thoracic duct drain?

A

Left subclavian vein

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21
Q

What is an edema?

A

Increased fluid in interstitial spaces

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22
Q

6 possible causes of edema? Provide examples for each.

A
  1. Increased hydrostatic pressure: impaired venous drainage or arteriolar dilation
  2. Decreased plasma oncotic pressure: protein-losing glomerulopathies (nephrotic syndrome), liver cirrhosis (ascites), malnutrition, protein-losing gastroenteropathy, reduced albumin
  3. Increased capillary permeability: burns, allergic inflammation reactions => increased tissue oncotic pressure and lymph obstruction
  4. Lymph obstruction: inflammation, neoplasticity, post-surgery, post-irradiation
  5. Sodium retention: excessive salt intake with renal insufficiency, increased tubular reabsorption of Na+, renal hypoperfusion, increased RAA secretion
  6. Inflammation: acute, chronic, or due to angiogenesis
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23
Q

5 subtypes of edema?

A
  1. Lymphedema: normally localized
  2. Subcutaneous edema: either regional due to heart or systemic due to kidneys
  3. Pulmonary edema: due to left ventricular failure or ARDS
  4. Brain edema: either local due to abscesses or neoplasms or generalized due to trauma
  5. Anasarca: extreme generalized edema
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24
Q

Clinical relevance of edema?

A

It points to an underlying disease, and is commonly associated with diminished inflammatory processes, e.g., impaired wound healing and ability to fight infection

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25
Q

Treatment for edema?

A

Albumin IV

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26
Q

4 possible causes of impaired venous return causing edema?

A
  1. CHF => increased central venous pressure => increased capillary pressure
  2. Constrictive pericarditis
  3. Ascites (liver cirrhosis)
  4. Venous obstruction or compression: thrombosis, external pressure (e.g. mass), lower extremity inactivity with prolonged dependency
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27
Q

2 possible causes of arteriolar dilation causing edema?

A
  1. Heat

2. Neurohumoral dysregulation

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28
Q

Describe the shock pathway.

A

Widespread vasodilation increases capacity of vascular bed => systemic hypoperfusion (due to reduced CO or circulating BV?) => hypotension => impaired tissue perfusion => cellular hypoxia (initially reversible), but if sustained => irreversible tissue injury => death

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29
Q

5 types of shock? Describe each.

A
  1. Cardiogenic: pump failure (intrinsic myocardial damage, ventricular arrhythmias, outflow obstruction)
  2. Hypovolemic: loss of blood or plasma (hemorrhage, severe burns, trauma)
  3. Neurogenic: anesthetic/spinal cord injury causing an imbalance between sympa and parasympa stimulation => loss of vascular tone and peripheral pooling of blood
  4. Anaphylactic: generalized IgE hypersensitivity => systemic vasodilation and increased vascular permeability
  5. Septic: systemic microbial infection (gram negative or positive endotoxins and fungal)
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30
Q

What is shock the common final pathway for?

A

Many severe events like hemorrhage, trauma, burns, myocardial infarctions, pulmonary embolism, sepsis, etc.

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31
Q

Describe the pathway of cardiogenic shock.

A

Decreased CO => RAA, ADH, catecholamine, and splenic discharge compensation => increase in BV and decrease in SVR => increased preload, SV, and HR =>

  1. Systemic and pulmonary edema => dyspnea
  2. Increased myocardial O2 requirements => decreased CO and EF => decreased BP => decreased tissue perfusion => ischemia and impaired cellular metabolsim => myocardial dysfunction => decreased CO and EF => vicious cycle
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32
Q

Describe the pathway of anaphylactic shock.

A

Allergen => IgE production => complement, histamine, kinins, prostaglandins system activation (aka inflammation) =>

  1. Increased capillary permeability => extravasation of intravascular fluids => edema + hypovolemia
  2. Peripheral vasodilation => decreased SVR => hypovolemia
  3. Constriction of extravascular smooth muscle => bronchoconstriction, laryngospasm, GI cramps

Hypovolemia => decreased CO => decreased tissue perfusion => impaired cellular metabolism

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33
Q

What is responsible for most ICU deaths?

A

Septic shock

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34
Q

Describe the pathway of septic shock.

A

Bacterial wall LPS released when cell walls are degraded => toxic FA core and polysaccharide coat unique to species induce an inflammatory response (cytokine cascade) =>

  1. Systemic vasodilation
  2. Increased vessel permeability
  3. Pump failure
  4. DIC
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35
Q

Septic shock mortality rate? What is it associated with?

A

25-50% mortality rate and is associated with multi-organ system failure (liver, kidneys,
CNS)

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36
Q

What does DIC stand for? What is it?

A

Disseminated intravascular coagulation = widespread activation of thrombin (coagulation factor) within the microcirculation (more so than antithrombins) causing diffuse circulatory insufficiency (brain, heart, lung, kidneys) leading to:

  1. Ischemia/micro infarcts
  2. Hemolysis
  3. Widespread injury to ECs
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37
Q

What are the 3 different exposure to LPS and their effects?

A
  1. Low: monocyte/macrophage/neutrophil activation, endothelial cell activation, complement activation => local inflammation
  2. Moderate: fever (brain effect), acute-phase reactants (liver effect), and lymphocytes => systemic effects
  3. High: low CO, low SVR, blood vessel injury, thrombosis, DIC, ARDS => septic shock
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38
Q

What are the 3 stages of shock?

A
  1. Nonprogressive stage
  2. Progressive stage
  3. Irreversible stage
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39
Q

What is hemorrhage?

A

Extravasation of blood due to a rupture in the vessel wall

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40
Q

What is a hematoma?

A

Blood accumulation within a tissue

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41
Q

How are hemorrhages classified?

A

By their relative size:

  1. Petechiae (1-2mm): minute, happen into skin, mucus or serosal membranes
  2. Purporas (3-5mm)
  3. Bruises (1-2cm): subcutaneous hematomas with RBC deposition, which are then phagocytosed by macrophages => Hb released metabolized into bilirubin which is then converted to hemosiderin (golden brown)
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42
Q

Other name for bruises?

A

Ecchymoses

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43
Q

Important to keep in mind with hemorrhages?

A

The cavity size: thorax, peritoneum, etc.

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44
Q

What 3 elements in the blood will lead to clot formation? What is this regulated by?

A
  1. Platelets
  2. Clotting factors
  3. Dysfunctional endothelium

Regulated by the inflammatory system (including monocytes, neutrophils, and lymphocytes)

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45
Q

Purpose of clot formation?

A

Preventing blood from moving from the intravascular space to the extravascular space

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46
Q

What is hemostasis?

A

Clot formation

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47
Q

What is thrombosis? What is it described by?

A

Clot formation as a result of dysregulation of hemostasis, described by Virchow triad:

  1. EC injury: perturbation of balance via hypertension, shear stress, turbulent flow, or bacterial infection
  2. Alterations in blood flow: turbulence and stasis (due to atherosclerotic plaques, aneurysms, MI, and mitral valve stenosis) => contact of activated platelets with EC => prevents dilution of clotting factors, retards inflow, promotes EC and platelet activation
  3. Hypercoagulability: contributes less frequently, yet is an important aspect comprised of genetic (V and prothrombin gene) and acquired components
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48
Q

Can lymphocytes and platelets spontaneously activate? How is this controlled?

A

YUP

Role of endothelium to keep them in check

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49
Q

What 6 processes may occur following thrombus formation? Describe each.

A
  1. Propagation: due to the accumulation of platelets and fibrin
  2. Embolization: resulting from a dislodged clot
  3. Dissolution: can occur with adequate fibrinolytic activity
  4. Organization: due to inflammation, fibrosis, and EC and SMC ingrowth, and
    incorporation into the thickened vascular wall, followed by recanalization and subsequently re-establishing blood flow
  5. Infarction: downstream results
  6. Hemorrhage: inability to form a proper clot => can lead to shock
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50
Q

How can cardiac dysfunction cause thrombi? 3 examples?

A

Cardiac dysfunction is often the origin of arterial thrombi with formation beginning at the site of injury (plaque) or turbulence (bifurcation), and is associated with retrograde growth

Examples include:
1. MI: dyskinetic contraction of myocardium + damage to endocardium => mural thrombus

  1. Rheumatic heart disease => mitral valve stenosis => left atrial dilation with atrial fibrillation => atrial blood stasis, resulting => mural thrombus
  2. Atherosclerosis => EC injury and abnormal blood flow
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51
Q

Effect of stasis on endothelial cells?

A

It causes them to die faster because they have reached their “quota” of platelet deactivation

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52
Q

How is venous stasis different from arterial stasis? What does this mean for the thrombi?

A

In venous blood there are many toxic waste substances, including CO2 which can be converted to H+ by carbonic anhydrase => wastes and metabolic acidosis can cause inflammation => increased work of endothelium => die faster

Venous thrombi commonly occur at sites of stasis, and extend in the direction of growth/blood flow with the propagating tail not well attached and is therefore prone to embolus, cast formation (hardening of the thrombus)

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53
Q

2 examples of venous thrombi?

A
  1. Superficial (varicosities) vein thrombi

2. Deep vein thrombi of the leg

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54
Q

What is a platelet disorder and its 2 subtypes?

A

Thrombocytopenia

  1. Immune thrombocytopenic purpura (ITP)
  2. Thrombotic thrombocytopenic purpura (TTP)
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55
Q

What is thrombocytopenia? What is it often secondary to?

A
  • Platelet count < 100K/mm3 (normal is 300K/mm3)

- Often secondary to congenital/acquired conditions which ↓ platelet synthesis or platelet survival

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56
Q

What is ITP?

A

Autoimmune platelet destruction

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57
Q

What is TTP? What to note?

A

Platelets inappropriately activate, aggregate and occlude arterioles and capillaries

Note: usually increased interaction with Von Willebrand factor

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58
Q

Other name for platelets?

A

Thrombocytes

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59
Q

At what platelet count does spontaneous bleeding occur?

A

10-15k/mm3

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60
Q

What does purpura refer to?

A

Discoloration due to the accumulation of blood

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61
Q

2 types of TTP?

A
  1. Chronic relapsing

2. Acute idiopathic

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62
Q

Is DIC a primary disease?

A

NOPE

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63
Q

What is a consumptive coagulopathy? Example?

A

Multiple thrombi form causing rapid concurrent consumption of platelets and coagulation proteins

Example: DIC

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64
Q

What is released in DIC?

A
  1. Tissue factor by endothelium in response to activation by inflammatory cells => sets off coagulation cascade
  2. Thromboplastic agents = prothrombotic factors
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65
Q

How can DIC affect pregnancy?

A

During birth there is massive blood loss with the placenta causing obstetric complications

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66
Q

What 5 factors can induce endothelial release/activation of tissue factor?

A
  1. Cytoplasmic granules of leukemic cells
  2. Carcinomas
  3. Bacterial sepsis
  4. Massive tissue destruction
  5. Endothelial injury
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67
Q

Clinical relevance of DIC?

A
  1. Shock
  2. Hypotension
  3. Increase in fibrin degradation products (FDPs) (e.g. D-dimers)
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68
Q

Treatment for DIC?

A
  1. Treat the underlying disorder
  2. Anti-coagulation therapy
  3. Fresh frozen plasma (FFP)
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69
Q

What is the fibrinolytic system? What does its activation cause?

A

Clot degradation system primarily mediated by plasmin

Activation causes split products that inhibit thrombin, platelet aggregation, and fibrin polymerization

70
Q

What can vascular occlusion lead to in DIC?

A
  1. Microangiopathic hemolytic anemia

2. Ischemic tissue damage

71
Q

What are 5 types of major disorders associated with DIC?

A
  1. Obstetric complications
  2. Neoplasms
  3. Massive tissue injury
  4. Infections
  5. Miscellaneous
72
Q

What are 5 obstetric complications associated with DIC?

A
  1. Abruptio placentae
  2. Retained dead fetus
  3. Septic abortion
  4. Amniotic fluid embolism
  5. Toxemia
73
Q

What are 2 neoplasms associated with DIC?

A
  1. Carcinomas of the pancreas, prostate, lung, and stomach

2. Acute promyelocytic leukemia

74
Q

What are 3 massive tissue injuries associated with DIC?

A
  1. Trauma
  2. Burns
  3. Extensive surgery
75
Q

What are 6 infections associated with DIC?

A
  1. Sepsis (gram + / -)
  2. Meningococcemia
  3. Rocky Mountain spotted fever
  4. Histoplasmosis
  5. Aspergillosis
  6. Malaria
76
Q

What are 8 miscellaneous major disorders associated with DIC?

A
  1. Acute intravascular hemolysis
  2. Snake bite
  3. Giant hemangioma
  4. Shock
  5. Heat stroke
  6. Vasculitis
  7. Aortic aneurysm
  8. Liver disease
77
Q

Describe the pathway of endothelial injury.

A
  1. Endothelium stops making normal antithrombic and vasodilatory substances (e.g. NO and prostaglandins)
  2. Leukocytes and macrophages adhere to the endothelium and release cytokines => inflammation => progressive vessel damage
  3. Oxidation and phagocytosis of LDL => foam cells
    4a. Fatty streak accumulates foam cells => progressive vessel damage
    4b. Smooth muscle proliferation => abnormal vasoconstriction

=> progressive vessel damage => fibrosis and calcification => plaque => ulceration/rupture/thrombosis

78
Q

How does age affect hypercoagulability?

A

As we get older the genetic effects decrease and the acquired factors increase

79
Q

6 effects of superficial venous thrombi or in deep veins of the leg?

A
  1. Local congestion
  2. Pain
  3. Swelling
  4. Tenderness
  5. Rarely embolize
  6. Edema and impaired venous drainage predispose skin to infection from slight trauma, and development of varicose ulcers
80
Q

3 effects of deep thrombi in larger leg veins above the knee?

A
  1. Embolize
  2. Asymptomatic, realized after
  3. With stasis and hypercoagulability => cardiac failure
81
Q

What are bypass channels?

A

Opening of collateral vessels to bypass the venous clot

82
Q

Definition of embolism?

A

Detached intravascular solid, liquid or gaseous mass

83
Q

What is a pulmonary thromboembolism? Consequence?

A

Thrombus from deep vein in leg to lungs (commonly have multiple)

If > 60% of pulmonary circulation is obstructed => sudden death, cor pulmonale, or CV collapse

84
Q

Why are pulmonary thromboembolisms clinically silent?

A

Due to bypass channels and vessel calibers

85
Q

What happens when an embolism occurs in a medium sized pulmonary vessel?

A

Collateral flow, not usually infarct, but problematic with LV failure

86
Q

What happens when an embolism occurs in a small sized pulmonary vessel?

A

Associated with infarct and if multiple of them => pulmonary HT with RV failure

87
Q

What are the types of systemic thromboembolism? What does each cause?

A
  1. Intracardiac thrombi => LV wall infarct leading to dilated LA
  2. Ulcerated atherosclerotic plaques or aortic aneurysms
  3. Lower extremities, brain, intestines, kidneys and spleen => dependent on point of origin and relative blood flow
88
Q

What do the consequences of systemic thromboembolisms depend on?

A

Consequences dependent on collateral supply, caliber of vessel occluded

89
Q

1st step of atherosclerosis?

A

Damage to the endothelium

90
Q

4 steps of intimal thickening?

A
  1. Damage to endothelium => inflammation => unable to regulate smooth muscle cells of the tunica media => SMCs go from contractile to secretory
  2. Recruitment of smooth muscle cells or smooth muscle precursor cells to the intima
  3. Smooth muscle cell mitosis
  4. Elaboration of extracellular matrix
91
Q

What is an atheroma? Other name?

A

Intimal lesion from fatty streak with a lipid core covered by fibrous cap

= plaque

92
Q

What is the fibrous cap of the atheroma made of? 7

A
  1. SMCs
  2. MOs
  3. Foam cells
  4. Lymphocytes
  5. Collagen
  6. Proteoglycans
  7. Neovascularization
93
Q

What is the lipid core of the atheroma made of? 4

A
  1. Cell debris
  2. Cholesterol crystals
  3. Foam cells
  4. Calcium
94
Q

Where does the lipid core of an atheroma come from?

A

Oxidation of LDLs => phagocytosis by MOs that adhere to the dysfunctional endothelial cells and enter the intima => foam cells => inflammation => weakened blood vessel wall => foam cells deposit in the vessel wall => fatty streak => core of the plaque to form

95
Q

What happens to the lipid core of an atheroma with time?

A

If it is not receiving enough blood flow => necrosis

96
Q

Describe the 5 steps of atherosclerosis.

A
  1. Endothelial dysfunction
  2. Oxidization of LDLs
  3. Foam cell formation
  4. SMC migration, proliferation, and secretion (intimal thickening)
  5. Plaque formation
97
Q

What happens to more advanced plaques?

A

Internal and external elastic membranes are destroyed and the media is thinned

98
Q

When do plaques become an issue? 4 situations.

A
  1. When O2 demand of tissues increase
  2. When they rupture/erode and inflammatory cells are exposed to platelets => clot formation => BV obstruction
  3. When the plaque grows so much is causes critical stenosis
  4. When the plaque causes mural thrombosis, embolization, and wall weakening leading to aneurysm and rupture of the BV
99
Q

Is atherosclerosis a hyperinflammatory state?

A

YESSSSSSSSSSSSSS

100
Q

What 3 factors decrease coronary blood supply?

A
  1. Coronary plaques
  2. Decreased perfusion pressure
  3. Decreased arterial O2 content
101
Q

What 4 factors increase myocardial O2 demand?

A
  1. Increased HR
  2. Increased preload
  3. Increased afterload
  4. Increased contractility
102
Q

What can the imbalance of coronary blood supply and myocardial O2 demand cause?

A

Ischemia and anginal pain

103
Q

BP equation?

A

BP = CO x TPR

104
Q

What factors affect CO? 2

A
  1. BV: sodium, mineralcorticoids, ANP

2. Cardiac factors: HR, contractility

105
Q

What factors affect TPR? 3

A
  1. Humoral factors
  2. Local factors: autoregulation and ionic (pH, hypoxia)
  3. Neural factors: alpha-adrenergic (constrictors), and beta-adrenergic (dilators)
106
Q

5 humoral BV constrictors?

A
  1. Ang II
  2. Catecholamines
  3. Thromboxane
  4. Leukotrienes
  5. Endothelin
107
Q

3 humoral BV dilators?

A
  1. Prostaglandins
  2. Kinins
  3. NO
108
Q

Describe BP regulation by the RAAS.

A

Decrease in BP and/or distal tubular sodium => renin converts angiotensinogen to Ang I => ACE converts Ang I to Ang II => direct vasoconstriction + aldosterone secretion => increased Na+ reabsorption => increased CO => increased BP

109
Q

Other than normal factors, what pathologies can activate renin? 3

A
  1. Fibromuscular dysplasia
  2. Renal artery stenosis
  3. Renin-secreting tumor
110
Q

Effect of oral contraceptives on RAAs?

A

Increase in angiotensinogen

111
Q

Describe the pathogenesis of HT.

A
  1. Genetic influences:
    - defects in renal Na+ homeostasis => increased BV => increased CO
    - functional vasoconstriction => increased TPR
    - defects in vascular smooth muscle growth and structure => increased vascular wall thickness toward lumen => less vasoactive and decreased lumen diameter => increased TPR

+

  1. Environmental factors

= HT

112
Q

Common cause of aneurysm?

A

Atherosclerosis

113
Q

What is an aneurysm?

A

Abnormal dilation of a BV

114
Q

3 types of aneurysms?

A
  1. Saccular true aneurysm
  2. Fusiform true aneurysm (circumferential dilation)
  3. False aneurysm: lumen does not dilate but a tear in the wall causes blood to extravasate and forms a hematoma surrounded by extravascular connective tissue (tunica adventitia is affected)
115
Q

What is a dissection?

A

Blood extravasate into the wall of the vessel and separates the tunica intima and media layers

116
Q

Most common vessel for aneurysms? Why?

A

Abdominal aorta due to bifurcation into iliacs causing turbulent flow and shear stress

117
Q

Describe the clinical course of an aneurysm. What can it lead to? 5

A

Dependent on size, location, and can lead to:

  1. Rupture
  2. Obstruction
  3. Embolism
  4. Impingement
  5. Formation of a mass
118
Q

2 types of failures in congestive heart failure? Describe each.

A
  1. Forward failure: fluid accumulation within LV => decrease in SV, CO, and EF => decreased oxygenation to tissues
  2. Backward failure: back up of fluid within LV => LA => lungs => right heart => venous system => arterial system
119
Q

3 examples of forward congestive heart failure?

A
  1. Systemic hypertension: increased overall pressure and peripheral resistance so the heart has to work harder
  2. Mitral/aortic valve disease: heart must pump harder to pump oxygenated blood through valves
  3. Ischemic heart: decreased blood flow going through heart because coronary arteries aren’t receiving adequate blood flow => increased O2 demand
120
Q

What are 2 adaptive mechanisms to congestive heart failure? What is this called?

A
  1. Neurohumoral responses
  2. Ventricular wall remodeling

= compensated heart failure

121
Q

2 types of ventricular hypertrophy in congestive heart failure? What is each due to? Purpose for each?

A
  1. Increased pressure load:
    concentric hypertrophy => initially the hypertrophy is made to increase the contractility, but eventually it causes smaller lumen => decreased SV
  2. Increased volume load:
    eccentric hypertrophy with increased lumen size and decreased wall thickness to accommodate large blood volume => decreased contractility => decreased SV => increased LV end systolic volume => further excacerbation => LA needs to work harder
122
Q

3 symptoms of congestive heart failure?

A
  1. Dyspnea during exertion due to decreased lung compliance (edema/congestion)
  2. Orthopnea due to increased venous return
  3. Can become cyanotic and/or acidotic
123
Q

What is decompensated heart failure?

A

Compensatory mechanisms are no longer enough leading to pulmonary congestion, edema, venous congestion, and systemic edema

124
Q

What is orthopnea?

A

Shortness of breath that occurs when lying flat

125
Q

What is ischemic heart disease?

A

Imbalance in myocardial O2 demand and supply commonly caused by a narrowing lumen of coronary arteries associated with atherosclerosis aka coronary heart disease

126
Q

What syndromes can develop from ischemic heart disease? What does this depend on?

A 
Depending on the severity of the narrowed lumen, as well as cardiac compensation, any of the following syndromes can develop:

1. Angina pectoris
2. Acute MI
3. Sudden cardiac death
4. Chronic ischemic heart disease
127
Q

What is angina pectoris? 3 different types?

A

Intermittent chest pain due to transient reversible myocardial ischemia due to 75% reduction in the lumen due to platelet aggregation, vasoconstriction, and/or formation of mural thrombus

  1. Stable: only upon exertion
  2. Variant: during rest or sleep
  3. Unstable: increased frequency of pain)
128
Q

Other name for acute MI?

A

Heart attack

129
Q

What is an acute MI?

A

Complete occlusion of coronary artery causing an area of ischemic necrosis

130
Q

What can cause sudden cardiac death? What does it lead to? 3

A
  1. PE
  2. Ruptured aortic aneurysm
  3. Infections

=> ventricular fibrillation

131
Q

What is chronic ischemic heart disease?

A

Congestive heart failure (ischemic cardiomyopathy) with progressive degeneration of the myocardium with angina or myocardial infarction

132
Q

What region is most susceptible to necrosis in acute MI? What is this region called? How does it move?

A

Region that is furthest away down stream (distal) to occlusion = zone of necrosis

It will gradually move toward the occluded blood vessel as the infarct becomes more severe

133
Q

What 3 plasma compounds are indicative of acute MI? Why? Different types?

A
  1. Creatine kinase: cytoplasmic cardiac enzyme released during necrosis (increases 2-4hrs after MI, peaks 24 hours post infarct, and returns to baseline by 72 hours)
    a. Dimer BB: brain and lung
    b. Dimer MB: primarily myocardium (increases 2-4hrs after MI, peaks 18 hours post infarct, and returns to baseline by 48 hours)
    c. Dimer MM: heart and skeletal muscle
  2. Cardiac troponins T and I: more specific (increases 2-4hrs after MI, peaks 18 hours post infarct, and returns to baseline by 4-7 days)
  3. Myoglobin: specific, but could be missed as it peaks right after and returns to baseline in less than 40 hours
134
Q

What is the location and severity of an acute MI dependent on?

A
  1. Location of vascular occlusion

2. Anatomy of coronary vasculature

135
Q

Clinical presentation of acute MI? 3

A
  1. Radiating severe chest pain, which may last from several hours to days
  2. Diaphoresis (sweating)
  3. Pulmonary edema/congestion
136
Q

4 possible causes of infarctions? Most common?

A
  1. ***Thrombotic/embolic events leading to arterial occlusion
  2. Local vasospasm
  3. Swelling of atheroma (hemorrhage within plaque)
  4. Compression of a vessel (tumor)
137
Q

How are infarctions classified? 2

A

Classification based on color:

  1. Hemorrhage => red and bland
  2. Microbial infection => white and septic
138
Q

4 factors affecting the severity of a myocardial infarction?

A
  1. Nature of vascular supply: alternative blood supply (dual arterial supply (liver, lungs, hands) vs. end arterial (renal and splenic)
  2. Rate of development of occlusion: slow less likely become MI due to development of alternative flow (pre-existing collaterals)
  3. Vulnerability to hypoxia (in order): neurons, myocardial cells, fibroblasts within myocardium
  4. O2 content of blood: anemia, cyanosis, CHF
139
Q

Definition of an infarction?

A

Area of ischemic necrosis due to occlusion of arterial supply or venous drainage

140
Q

How do infarctions impact cell metabolism?

A

Partially ischemic cells conduct anaerobic metabolism and accumulate lactate, which inhibits glycolysis => reduced ATP => ion leaks and hypocontractility

141
Q

What happens to totally ischemic myocardial cells?

A

No ATP => noncontractile and loss of membrane integrity => cell rupture and death

142
Q

4 treatments for occluded arteries? Describe each.

A
  1. Thrombolysis: administer drugs such as streptokinases and tissue plasminogen activators that enzymatically digest the thrombus
  2. Percutaneous transluminal coronary angioplasty (PTCA): physically scrape away at plaque build up to open the lumen of the artery
  3. Stent: a stent can be put in to prevent an occlusion from reoccurring
  4. Coronary artery bypass grafting: surgical placement of a new conduit bypass the occluded area of the artery
143
Q

Issue with stents and PTCA?

A

Re-stenosis is an issue with this because you are irritating the area, thus causing more inflammation

144
Q

What are cardiomyopathies?

A

Diseases related to the myocardium

145
Q

3 types of cardiomyopathies?

A
  1. Dilated
  2. Hypertrophic
  3. Restrictive
146
Q

What is dilated cardiomyopathy? What causes this? What to note?

A

Progressive form of cardiac hypertrophy associated with dilation and cardiac systolic dysfunction due to ineffective contraction

Environmental and genetic factors can cause it

NOTE: tends to affect all chambers of the heart

147
Q

Example of genetic cause of dilated cardiomyopathy?

A

If a person as a mutation that doesn’t allow them to produce dystrophin (contractile protein), they can get a weak functioning cardiac muscle fiber => heart will stretch easier but will not have the elasticity to recoil to its original shape => decreased contractility

148
Q

What is hypertrophic cardiomyopathy? What can it lead to?

A

Asymmetric septal hypertrophy or idiopathic hypertrophic sub-aortic stenosis =>

  1. Decreased diastolic filling
  2. Intermittent ventricular outflow obstruction

=> ventricular arrhythmias and sudden death

149
Q

Hereditary cause of hypertrophic cardiomyopathy?

A

Issues with sarcomeric contractile proteins

150
Q

What is restrictive cardiomyopathy? Causes?

A

Decrease in ventricular compliance which results in impaired ventricular filling during diastole without a forceful systole => myocardial contractility declines

Can be caused by endomyocardial fibrosis (innermost layer) or cardiac amyloidosis (protein deposits within the cardiac wall => thickening)

151
Q

Why does myocardial thickening cause arrhythmias?

A

Increased distance for electrical signal to travel

152
Q

What is cor pulmonale? Explain.

A

Right-sided heart failure caused by lung disease:

Lung disease => increased pulmonary vascular resistance => right ventricle compensates by working harder to pump adequate blood, causing hypertrophy of the right side of the heart and/or dilation + pulmonary hypoxic vasoconstriction => pulmonary hypertension => exacerbation => peripheral edema

153
Q

What is valvular heart disease?

A

Stenosis of the mitral or aortic valve results in a decrease in blood flow through those areas

  • Hemodynamically significant aortic stenosis is normally associated with a transvalvular pressure gradient >50 mm Hg and an aortic valve orifice area < 1 cm2
  • Mitral valve stenosis is associated with a transvalvular pressure gradient of 6 mmHg instead of 0
154
Q

Triad of symptoms of valvular heart disease?

A
  1. Angina pectoris often in absence of ischemic heart disease
  2. Dyspnea on exertion
  3. Syncope
155
Q

2 common causes of valvular heart disease?

A
  1. Calcification of vessels (aortic)

2. Rheumatic heart disease (mitral or aortic)

156
Q

What is a valve raphe?

A

Partial fusion of heart valve due to calcification

157
Q

What is rheumatic heart disease?

A

Caused by the pathogen, hemolytic streptococcus, which invades system and triggers an immune response => body creates antibodies to fight off the pathogen, but because of molecular mimickery/cross reactivity, the antibodies we create also recognize myocytes in the mitral or aortic valve => antibodies travel to the valve where they recruit macrophages and neutrophils causing inflammation and eventually stenosis

158
Q

What is mitral valve stenosis due to?

A

Fusion of the mitral valve leaflets at the commissures

during the healing process of acute rheumatic fever

159
Q

Important 2 values of mitral valve stenosis?

A
  1. Mitral valve area is decreased

2. Mean left atrial pressure is high to maintain an adequate resting CO

160
Q

Complication of mitral valve stenosis? Symptoms?

A

Left atrial enlargement => predisposes to atrial fibrillation + stasis of blood in distended LA predisposes to the formation of thrombi (consider chronic anticoagulant therapy)

Symptoms: dyspnea on exertion and severe cases lead to CHF

161
Q

What is the mitral orifice called in mitral stenosis?

A

Fish mouth

162
Q

Describe how calcification can cause aortic stenosis.

A

Isolated non-rheumatic-aortic stenosis usually results from progressive calcification and stenosis of a congenitally abnormal bicuspid valve

163
Q

What is rheumatic fever causing aortic stenosis associated with?

A

Rheumatic fever-aortic stenosis due to rheumatic

fever almost always occurs in association with mitral valve stenosis

164
Q

What is mitral regurgitation due to? What is it associated with?

A

Due to rheumatic fever and almost always associated with mitral stenosis

165
Q

Pressure reading caused by mitral regurgitation?

A

Regurgitant flow is responsible for the V wave present on the recording of the PAOP (LA pressure) with the size of the V wave correlating with magnitude of regurgitant flow

166
Q

What is mitral valve prolapse?

A

Leaflets of the valves billow back into the atrium during left ventricular systole, allowing the leaflets to part slightly and permit regurgitation into the atrium => decrease in SV, CO, and oxygen supplied to the periphery

167
Q

2 types of aortic regurgitation? Describe each.

A
  1. Acute: infective endocarditis, trauma, dissection of a
    thoracic aneurysm
  2. Chronic: prior rheumatic fever, persistent systemic HT
168
Q

Pressures in aortic regurgitation?

A

High systolic pressures and low diastolic pressures

169
Q

Describe the nonprogressive stage of shock. What is primarily affected?

A

Compensatory mechanisms activated: neurohumoral for CO and BP to maintain perfusion

Primarily affecting cardiac, cerebral, pulmonary systems

170
Q

Describe the progressive stage of shock. What is primarily affected?

A

Tissue hypoperfusion and onset of worsening of circulatory and metabolic imbalances:

Aerobic to anaerobic respiration => lactic acid => decreased pH and metabolic vasodilation => pooling in microcirculation => decreased venous return, EC
injury, DIC

Vital organs affected, frequently with the patient in a confused state and decreased urine output reflecting renal damage

171
Q

Describe the irreversible stage of shock. What is primarily affected? 3

A
  1. Tissue/cellular injury too severe: necrosis => lysosomal leakage => exacerbation with decreased myocardial contractility due to NO synthesis
  2. Possibly with ischemic bowel allowing flora into circulation => superimposed endotoxic shock
  3. Renal shutdown due to acute tubular necrosis compounding

OVERALL: state that cannot be corrected by hemodynamics

172
Q

EKG changes due to MI?

A
  1. ST changes

2. Q waves

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