Dr. D.'s Overhead Lecture Notes                                Section 2 - REPLACE PAGE NUMBERS WITH PAGES FROM SIXTH EDITION2
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Abnormal accumulation of fluids
A. Congestion = hyperemia
    - excess blood in vessels
   1. Active congestion = active hyperemia
       - arteries/arterioles dilate -> excess delivery of blood
       - causes
           - inflammation, hypoxia, pH, temp., emotions
       - effects = adaptive
           Active hyperemia  - due to a usually beneficial increased input of blood from arteriolar and capillary dilation
        Example - for inflammation
            1. Erythema, gross
            2. Erythema and edema, gross
                    Example - for temperature regulation by integumentary vasodilation
            17.Hyperthermia, scene
                    Harmful example - edema blocks airway
            13. Edema in larynx, gross

   2. acute passive congestion
       - local - blockage of veins
       - reduced drainage of area
            - e.g. tumors, posture, clothing
       - systemic - reduced heart function ( cardiac output)
            - reduced drainage of veins
                - e.g. heart attack, valve disease
       - effects = detrimental   (1, 2, & 3)
          1. slow flow -> decr. O₂, incr. CO₂, decr. nutrients, incr. wastes -> cell injury/cell death -> pain and  decr. function

           2. slow flow  ->  thrombosis(Fig. 7-4 p.98)
           3. incr. volume  -> incr. pressure  -> edema
        Note: acute = short term -> no lasting effects

   3. chronic passive congestion
       - local - blockage of veins
       - systemic - decr. heart function
       - effects = detrimental  (1, 2, & 3)
           1. slow flow -> pain,  decr.function
           2. slow flow  ->  thrombosis
           3. incr. volume  -> edema, varicose veins
    Note: chronic = long term -> lasting effects
    Examples - liver
           3. Normal liver, cut surface, gross
                Note the color and the smooth homogeneous structure of the brown liver tissue.
           55. Chronic passive congestion (nutmeg liver), gross
                Note the spotty color and the uneven structure of the liver tissue.
           4. Normal liver zones, microscopic*
                The liver cells make up the prominent pink strands of material. Each liver cell can be identified by its small round blue nucleus. The more open streaks between the strands of liver cells are large capillaries (i.e., liver sinusoids) that contain some blood cells. The large vessels in the lower left region carry blood to the liver sinusoids, and the large vessel in the upper right drains blood from the sinusoids. Note that the liver cell cytoplasm appears solid in color and that most of the liver consists of liver cells and sinusoids.
           56. Chronic passive congestion, liver, microscopic*
           57. Centrilobular necrosis, liver, microscopic*
           58. Chronic passive congestion with "cardiac cirrhosis", liver, microscopic*
        Example - spleen
           22. Splenomegaly with portal hypertension, gross
                    Portal hypertension means high blood pressure in the hepatic portal veins. These veins carry blood to the liver from the spleen, the pancreas, and much of the GI tract between the esophagus and the anus. The high pressure in the portal veins develops because of passive congestion. The passive congetoins develops because fibrosis in a liver with cirrhosis blocks liver vessels, preventing blood in the spleen and digestive system organs from going to the liver.

      Effects on veins = varicose veins = permanently and excessively dilated veins
            Examples - esophagus
           1. Normal esophagus, gross
           12. Esophageal varices, gross
            Examples - hemorrhoids
           118. Prolapsed true hemorrhoids, gross
            Examples - skin
           20. Caput medusae of skin with portal hypertension, gross

   B. edema = excess fluid between cells
       i.e., incr. interstitial fluid
           11. Edema, gross
           2. Erythema and edema, gross
           31. Anaphylaxis with acute laryngeal edema, gross
                    Examples in lungs - pulmonary edema
           4. Normal lung, microscopic*
                    Note the thin membranes and open air spaces
           5. Lung, edema, microscopic*
                    This is at high magnification, note the thick membranes and filled air spaces
       - mechanisms (1, 2, or 3)
           1. incr. BP (hydrostatic pressure)
               (e.g. inflammation, hypertension, passive congestion)
           2. decr. COP (colloidal osmotic pressure)
               (e.g. inflammation, malnutrition, proteinuria, cirrhosis)
           3. blocked lymphatics
               (e.g. cancer, surgery, infection)

       - effects
           1. discomfort
           2. in lungs = pulmonary edema (p.726) (sketch)

            4. Normal lung, microscopic*
                    Note the thin membranes and open air spaces
           5. Lung, edema, microscopic*
                    This is at high magnification, note the thick membranes and filled air spaces
           6. Lung, passive congestion, microscopic*
                    This is at high magnification, note the thick membranes and filled air spaces
           14. Pleural effusion, serous, gross [XRAY]
                    Fluids has leaked into the pleural cavity
           115. Lung, interstitial fibrosis, microscopic*
                    Chronic pulmonary edema can cause pulmonary fibrosis.

           3. in brain   ->  increased pressure -> a or b
                a. damages neurons
                b. compresses vessels  -> decr. flow

Hemorrhage = blood leaks from vessels
    - general causes  (1, 2, & 3)
        1. trauma to vessel (e.g. cut, crush)
        2. disease weakens vessel
        3. low clotting ability
           Normal peripheral blood, segmented neutrophil and band neutrophil, high power microscopic
                    The small blue specks are platelets. Substances released by platelets start the clotting process.
           39. Hematoma, toenail, gross
                    A hematoma is a blood clot outside blood vessels or the heart but enclosed in the body.
           37. Petechial hemorrhages, epicardium, gross
           38. Ecchymoses, skin of arm, gross
           34. Hemorrhagic pulmonary infarction, gross
           35. Hemorrhagic pulmonary infarction, gross
    - local effects  (1 or 2) (sketch)
       1. Hb injures cells
       2. volume disrupts function
           127. Hemothorax, gross
                    This hematoma inhibits filling of the lungs during inspiration. It caused the lungs to collapse (atelectasis).
           20. Hemopericardium, gross
                    This hematoma around the heart inhibits filling of the heart during diastole.
    - systemic effects  (1 or 2)
       1. rapid massive leak  -> shock
       2. slow chronic leak  ->  anemia

    - fates of hemorrhaged blood (1, 2, or 3)
       1. peel off (e.g., scab)
       2. removal of hematoma (ex. "black + blue" mark fades)
       3. organization of hematoma (ex. scar formation replaces hematoma)

Blood clot in vessel = thrombus 
          Normal peripheral blood, segmented neutrophil and band neutrophil, high power microscopic
                The small blue specks are platelets. Substances released by platelets start the clotting process.
           36. Platelet, electron micrograph *
           33. Recent thrombus with lines of Zahn, microscopic *
           7. Severe coronary atherosclerosis, gross
           9. Coronary thrombosis, gross
           40. Disseminated intravascular coagulopathy (DIC), fibrin thrombus in lung, high power microscopic *
    general causes  (1, 2, & 3) (sketch)
       1. rough lining of vessel or heart
           - breaks platelets  ->  clotting
       2. slow flow (p. 98, Fig. 7-4)
           - clotting factors build up
       3. chemical imbalance
           - breaks platelets  ->  clotting
    effects  (1 or 2)
        1. block vessel at site (p. 100)
        2. block vessel at other site (sketch)
            - embolus     - embolize
           10. Coronary thrombosis, gross
           11. Coronary thrombosis, microscopic *
           Renal vein thrombosis, gross
           Hyaline thrombus in glomerulus with thrombotic thrombocytopenic purpura (TTP), microscopic *
    fates of thrombi  (1 or 2)
        1. dissolved
        2. organized
           78. Lung, remote organized pulmonary artery embolus, gross
           6. Coronary atherosclerosis with thrombosis, microscopic *
    types of emboli
        1. thrombi
            Thromboembolus - moving blood clot in a blood vessel
                Pulmonary embolus
           27. GIF animation of pulmonary thromboembolus, diagram
           28. Pulmonary thromboembolus, gross
           29. Pulmonary thromboembolus, gross
           30. Pulmonary thromboembolus, gross
           31. Pulmonary thromboembolus, microscopic *
           32. Pulmonary thromboembolus, microscopic *
           27. GIF animation of pulmonary thromboembolus, diagram
           69. Lung, pulmonary thromboembolus, gross
           70. Lung, pulmonary thromboembolus, gross
           73. Lung, pulmonary thromboembolus, gross
           74. Lung, pulmonary thromboembolus, low power microscopic*
           78. Lung, remote organized pulmonary artery embolus, gross
        2. gas bubbles
        3. plaque (from atherosclerosis)
        4. fat droplets (from trauma)
           1. Fat embolism, lung, high power microscopic *
           2. Fat embolism, lung, Oil red O stain, high power microscopic *
           3. Fat embolism, glomerulus, high power microscopic *
           4. Fat embolism, brain, gross
           5. Fat embolism, brain, gross
           6. Fat embolism, brain, high power microscopic *
        5. cancer cells (from metastasis)
           44. Metastatic adenocarcinoma, liver, gross [CT]
           45. Metastatic adenocarcinoma, liver, gross
           46. Metastatic adenocarcinoma, liver, gross [CT]
           47. Metastatic adenocarcinoma, liver, microscopic*

    effects of emboli
        - block vessels

Diseases of vessel walls - arteries
    Arteriosclerosis = "arterial scarring"
    Atherosclerosis = arteriosclerosis of large arteries

    contributing factors =  risk factors (p. 463)
        ** 1. smoking
        ** 2. high blood pressure = hypertension
        ** 3. high blood LDLs ~ high blood cholesterol
          * 4. genetic predisposition = runs in families
          * 5. diabetes mellitus
            6. being male
            7. age
            8. obesity
            9. high fat diet
            10. sedentary lifestyle
            11. stress
            12. "the pill" + smoking
            13.

    pathogenesis (p. 462)
       cause(s) ->  deposits in tunica intima  -> (1 and 2) (sketch)
            1. inward growth of plaque   ->  (a and b) (sketch)
                 a. narrowness  ->  *low blood flow (p. 103)
                    1. Normal coronary artery, microscopic *
                    2. Mild coronary atherosclerosis, microscopic *
                    3. Severe calcific coronary atherosclerosis, microscopic *
                    4. Coronary atherosclerosis, cross sections, gross
                    9. Coronary thrombosis, gross
                    10. Coronary thrombosis, gross
                    11. Coronary thrombosis, microscopic *
                    Left anterior descending coronary artery, advanced atherosclerosis, gross.
                 b. roughness  ->  thrombus  ->  *low blood flow (p. 100, p. 102, p. 103) (sketch)
                    9. Coronary thrombosis, gross
                    10. Coronary thrombosis, gross
                    11. Coronary thrombosis, microscopic
                    Left anterior descending coronary artery, recent thrombus, microscopic. *
            2. outward growth of plaque   ->  (c & d) (sketch)
                 c. stiffness   ->  decr. dilation ->  *low blood flow when more is needed
                    1. Normal coronary artery, microscopic *
                     2. Mild coronary atherosclerosis, microscopic *
                     3. Severe calcific coronary atherosclerosis, microscopic *
                     4. Coronary atherosclerosis, cross sections, gross
                 d. weakness   -> bulge = aneurysm   -> 1, 2, or 3 (sketch)
                    22. Aorta, atherosclerotic aneurysm, gross
                        1. thrombus  -> *low blood flow
                        2. pressure on structures
                        3. rupture  ->  hemorrhage -> a, b, or c
                                a. Hb injures cells
                                b. blood disrupts structure
                                c.  decr. decr. BP  ->  shock
          Pathogenesis
            Normal aorta, elastic tissue stain, low power microscopic
            1. Normal coronary artery, microscopic *
            2. Mild coronary atherosclerosis, microscopic *
            3. Severe calcific coronary atherosclerosis, microscopic *
            4. Coronary atherosclerosis, cross sections, gross
            5. Coronary atherosclerosis, plaque with thrombus, microscopic *
            6. Coronary atherosclerosis with thrombosis, microscopic *
            7. Severe coronary atherosclerosis, gross
            8. Coronary atherosclerosis with hemorrhage into plaque, gross
            16. Aorta, lipid streaks, gross
            17. Aorta, lipid streaks, gross
            18. Aortas with mild, moderate, and severe atherosclerosis, gross *
            19. Aorta, atheromatous plaque, medium power microscopic *
            20. Aorta, atheromatous plaque, high power microscopic *
            21. Aorta, atheromatous plaque, high power microscopic *
            Aortic atherosclerosis demonstrated in three aortas, gross.
        *Note*: *low blood flow = ischemia

    - areas commonly affected by atherosclerosis =
        heart (p.103), brain (p.100), kidneys (pp. 687, 710), legs (pp.529,535), aorta (p. 102)

    ischemia= inadequate blood flow
        local causes  (1 or 2)
            1. blocked artery (ex. compression, thrombus, embolus, plaque)
            2. blocked vein (e.g., compression, gravity, passive congestion)
        systemic causes (1, 2, or 3)
            1. heart failure =  decr. cardiac output
            2. vasodilation =  decr. peripheral resistance
            3. loss of fluid =  decr. blood volume
                ex. hemorrhage, diarrhea

        effects =

            Infarction
           17. Coagulative necrosis, adrenal infarction, microscopic *
           18. Coagulative necrosis, splenic infarctions, gross
           19. Small intestinal infarction, gross
           52. Small intestinal infarction, gross
           59. Infarction, liver, gross
                Heart
           Interventricular septum, recent myocardial infarction, gross.
           5. Hypertrophy, heart, gross
           1. Left ventricular hypertrophy, heart, gross
                Brain
           22. Liquefactive necrosis, cerebral infarction, microscopi *
           23. Liquefactive necrosis, cerebral infarction, microscopic *
           24. Liquefactive necrosis, cerebral infarction, gross *
           25. Liquefactive necrosis, cerebral infarction, gross *
                Kidneys
           15. Coagulative necrosis, renal infarction, gross
           Acute renal infarction, gross
           Acute renal infarction, gross
           Acute renal infarction, microscopic *
           Massive renal infarction, gross
                Lungs
           1. Normal lungs, gross
           2. Normal lung, cross section, gross
           4. Normal lung, microscopic*
           26. Abscess formation, lung, gross
           27. Abscess formation, lung, gross
           28. Abscess formation, lung, gross
           34. Hemorrhagic pulmonary infarction, gross
           35. Hemorrhagic pulmonary infarction, gross
           14. Lung, abscesses, gross
           15. Lung, abscesses, gross
           71. Lung, hemorrhagic infarct, gross
           72. Lung, hemorrhagic infarct, gross
           1. Normal lungs, gross
           2. Normal lung, cross section, gross
           4. Normal lung, microscopic*
                Leg
           31. Gangrenous necrosis, foot, gross
           32. Gangrenous necrosis, lower extremity, gross
           33. Gangrenous necrosis, low power microscopic *

Basic of circulation to service body cells:

incr. BP -> incr.blood flow  -> incr. BP (blood pressure) ->
                                                   incr. BP blood flow (mls/minute)

decr. BP -> decr. blood flow (mls/minute) (trouble area)

incr. CO -> incr. BP -> incr. blood flow (mls/minute)

decr. CO -> decr. BP ->
                     decr. blood flow (mls./minute) (trouble area) 

CO =  SV x HR
                CO = cardiac output = mls/minutes
                SV =  stroke volume = mls/beat
                 HR = heart rate = beats/minute

Consider SV first  

incr. SV -> incr. CO -> incr. BP -> incr. blood flow (mls./beat)

decr. SV -> decr. CO -> decr.BP -> decr. blood flow (trouble area)

SV depends upon (1) preload, (2) contractility, and (3) afterload

    (1) preload = stretch of cardiac muscle (p. 426, 427) (sketch)
                - can be changed by dilation
             Normal cardiac muscle, medium power microscopic *
             Heart, dilated cardiomyopathy, gross [XRAY]
             Heart, dilated cardiomyopathy, gross

           

    (2)  contractility = strength based on chemistry (O₂, ions, hormones, pH, etc.)
           - can be changed by hypertrophy
            5. Hypertrophy, heart, gross
            Heart, hypertension with left ventricular hypertrophy, gross
            Heart, cardiomyopathy, microscopic *

    (3) afterload = resistance to emptying from chamber diameter (ventricular radius), BP in aorta or pulmonary artery, wall thickness and stiffness (p. 427 ) 
            - can be changed by dilation and hypertrophy (sketch)
           Heart, dilated cardiomyopathy, gross [XRAY]
           Heart, dilated cardiomyopathy, gross
           5. Hypertrophy, heart, gross
           Heart, hypertension with left ventricular hypertrophy, gross

Chapters 28-29

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Within normal limits, a little increase in stretch = a little increase in preload, which is a GOOD thing

incr. stretch -> incr. preload -> incr. strength  -> incr. SV  -> incr. CO  -> incr. BP  -> incr. blood flow
(i.e., normal heart adjusts preload to increase or decrease CO as needed {e.g., exercise, rest})

With excess blood in the heart  (i.e., excess End Diastolic Volume {EDV}) -> excess stretch -> excess preload, which is a BAD thing

incr. incr. stretch -> incr. incr. preload -> decr. strength -> decr. SV -> decr. CO -> decr. BP -> decr. blood flow (trouble area)

                     
                                              

Compensation  - a little increase in stretch -> 
                             a little increase in preload -> a GOOD thing

incr. needed flow -> incr. venous return -> incr. stretch -> incr. preload -> incr. blood flow

Above normal limits,  -  excess stretch -> excess preload -> 
                                                                         a BAD thing
  e.g.,

  *(1) incr. incr. DILATION from ischemia = passive congestion

    (2) very high BP
    (3) injured heart cells
    (4) arrhythmias
    (5) bad valves
    (6) weak cells from low contractility

incr. incr. EDV -> incr. incr. stretch -> incr. incr. preload  -> decr. strength -> decr. SV -> decr. CO -> decr. BP -> decr. blood flow (trouble area)

acutely, decr. SV from one beat  ->incr. incr. ESV for next beat ->  incr. incr. EDV  ->  incr. incr. incr. stretch  ->  incr. incr. incr. preload  -> decr. decr.  blood flow -> etc., etc.

(i.e., one weak stroke -> an even weaker next stroke -> 
                                           an even weaker next stroke -> etc.)

Decompensation

chronically, long term incr. EDV or long term ischemia  -> permanent DILATION   ->incr. incr. incr. stretch ->  incr. incr. incr. preload  ->decr. decr. decr. blood flow -> etc., etc.

        Normal cardiac muscle, medium power microscopic *
        Heart, dilated cardiomyopathy, gross [XRAY]
        Heart, dilated cardiomyopathy, gross

Compensation – an increase in contractility (strength) is always a
                          GOOD thing because contractility = strength  
                              (e.g., by vasodilation of coronary arteries)

incr. needed flow or mild ischemia from work  -> incr. coronary vasodilation -> incr. contractility -> incr. blood flow
(i.e., normal heart contractility to increase or decrease CO as needed {e.g., exercise, rest})

acutely, - a decrease in contractility (strength) is always a BAD thing

decr. O₂ (ex. respiratory problems, narrow vessels from thrombus)  -> decr. contractility -> decr. blood flow

chronically, (with atherosclerosis) 
- a decrease in contractility (strength) is always a BAD thing

incr. needed flow or mild ischemia from work -> no coronary vasodilation  -> decr. contractility (ex. O₂, incr. CO₂, pH)  -> decr. blood flow -> etc., etc.

Decompensation – from hypertrophy, which raises heart O₂ use above blood supply to heart muscle

chronically, a decrease in contractililty (strength) is a BAD thing

incr. incr. overwork (ex. high BP, bad valves)  -> incr. incr. cardiac HYPERTROPHY -> incr. incr. O₂ demand -> decr. decr. contractility -> decr. decr. blood flow -> etc., etc.

           5. Hypertrophy, heart, gross
           Heart, hypertension with left ventricular hypertrophy, gross
           Heart, cardiomyopathy, microscopic *

                          

To make matters worse,  excess decreased contractility + 
                                           excess preload is a VERY BAD thing

decr. contractility -> decr. SV -> incr. incr. ESV -> incr. incr. EDV -> incr. incr. preload -> decr. decr. blood flow -> etc., etc.

i.e., one weak beat -> an even weaker next beat -> 
                                      an even weaker next beat -> etc.

Afterload (resistance) is ALWAYS a bad thing, so an increase in afterload is always a BAD thing

incr. afterload -> decr. SV -> decr. CO -> decr. BP -> decr. blood flow

NORMAL

Compensation - preload and contractility overpower 
                              (compensate for) afterload
(i.e., normal heart adjusts preload and contractility to compensate for normal increase or decrease in afterload)

incr. ventricular radius  -> incr. afterload but also  incr. preload ->
                  incr. SV -> incr.  CO -> incr. BP -> incr. blood flow

incr. BP -> incr. afterload but also incr. contractility from coronary vasodilation
                     -> incr. SV -> incr. CO -> incr. BP -> incr. blood flow

 ABNORMAL

acutely, 
- excess preload is a BAD thing, which also increases afterload ->
 a VERY BAD thing

-  decreased contractility is a bad thing, which also increases afterload -> a VERY BAD thing

              

incr. incr. EDV from excess preload or bad contractility (DILATION) -> incr. incr. afterload incr. incr. incr. preload  -> decr.  SV -> decr. CO -> decr.  BP  -> decr. blood flow and  incr. incr. incr. ESV  -> incr. incr. incr. EDV for next beat -> incr. incr. incr. afterload and incr. incr. incr. preload  ->  etc. etc.

i.e., one weak beat -> an even weaker next beat -> 
                                       an even weaker next beat -> etc.

Decompensation

- excess preload is a BAD thing, which also increases afterload ->
                 a VERY BAD thing

- decreased contractility is a bad thing, which also increases
                 afterload -> a VERY BAD thing

- excess preload and decreased contractility are BAD things,
    which also increase afterload -> a VERY VERY BAD thing

chronically, DILATION from long term ischemia or HYPERTROPHY from long term overwork  -> (sketch)
incr. incr. afterload with   incr. incr. preload and  decr. decr. contractility -> decr. SV -> decr. CO  -> decr. BP  -> decr. blood flow

i.e., one weak beat -> an even weaker next beat -> 
                                        an even weaker next beat -> etc.

#################################################################

NOTE: – in summary:

Preload

incr. preload -> slightly increased stretch ->  incr. strength -> incr. SV -> etc., etc. (GOOD)

incr. incr. preload -> excess stretch -> decr. strength -> decr. SV -> etc., etc. (from dilation) (BAD)

Contractility 

incr. contractility -> always incr. strength -> incr. SV ->
                                    etc., etc. (GOOD)

decr. contractility -> always decr. strength -> decr. SV -> 
                                    etc., etc. (from hypertrophy) (BAD)

Afterload 

decr. afterload -> always decr. resistance -> incr. SV -> 
                                 etc., etc. (GOOD) 

incr. afterload -> always incr. resistance -> decr. SV ->
                                 etc., etc. (BAD)
 (from either dilation or hypertrophy) (BAD)

Therefore, 

dilation + hypertrophy -> 
excess preload + decreased contractility + increased afterload ->
                                                   VERY VERY BAD

           Heart, dilated cardiomyopathy, gross [XRAY]
           Heart, dilated cardiomyopathy, gross
           5. Hypertrophy, heart, gross
           Heart, hypertension with left ventricular hypertrophy, gross
 

Variations in heart rate =  incr. HR  or  decr. HR

        CO = SV x HR
                  CO = cardiac output = volume/minute
                  SV = stroke volume = volume/beat
                  HR = heart rate = beats/minute

    normal = compensation
        incr.   HR   ->incr.  CO  ->incr.  BP  ->incr.  blood flow
        decr.  HR   ->  decr.  CO  ->  decr.  BP  ->  decr.  blood flow
(i.e., normal heart adjusts HR to increase or decrease CO as needed {e.g., exercise, rest})

    abnormal = decompensation (1, 2, & 3)
         incr. incr. incr. HR  -> decr. CO -> decr.  BP  -> decr. blood flow

    incr. incr. HR = tachycardia > 100 BPM at rest

              

  1.  incr. incr. incr. HR  -> decr. filling time  -> 
                                       decr. decr. EDV (decr. decr. preload) -> ??

  2.  incr. incr. incr. HR  -> incr. incr. O₂ demand -> decr. contractility -> ??

  3.  incr. incr. incr. HR  -> decr. decr.  diastole -> incr. vessel closure  -> 
                decr.  blood flow  -> decr. O₂ supply  -> decr. contractility -> ??

Therefore:  incr. incr. incr. HR -> decr. decr.  preload  &  decr. contractility -> decr.decr. decr.  SV ->  decr. decr. CO

also:  decr. decr. decr. HR  -> decr. decr. CO

        decr. decr. decr.  HR = bradycardia < 60 BPM

Definitions
    ejection fraction = fraction ejected per beat
            normal = 2/3

    abnormal (weak beat)  -> decr. decr. ejection fraction -> incr. incr. ESV  -> incr. incr. EDV -> incr. incr. preload

ventricular tension = diastolic BP

ventricular radius = "width of ventricle" (sketch)

    - abnormally
         incr. incr. ventricular tension  =  incr. incr. afterload  -> decr. SV  -> decr. CO

         incr. incr. ventricular radius (dilation) =  incr. incr. preload  &  incr. incr. afterload  -> decr. SV  -> decr. CO

cardiac reserve =  incr.  CO when needed (5X)
    abnormalities -> decr. cardiac reserve  ->  limited incr. CO when  incr. incr. CO is needed

Cardiac oxygen - supply vs. demand  (p. 461)
    - constant pumping  -> constant O₂ demand
    - O₂ for energy
    - if O₂ supply less than O₂ demand
        - low O₂ ->  low energy  -> decr. CO
        - low O₂ -> incr. lactic acid  -> cell injury/cell death

Factors affecting O₂ demand (p. 460)  (1, 2, 3, &4)
    1. heart rate -  incr. HR  -> incr. demand
    2. contractile force - incr. force  -> incr. demand
    3. muscle mass  -  incr. mass (hypertrophy)  -> incr. demand
    4. ventricular wall tension =  afterload
             - incr. afterload -> incr. demand
        -from ventricular radius & BP

Normal:
incr. O₂ demand  ->  coronary vasodilation -> incr. O₂ supply

Abnormal:
incr. O₂ demand  ->  low O₂ supply = ischemia

Factors in left ventricle  (1, 2, & 3)

    1. large mass = high O₂ demand
    2. large contractile force = high O₂ demand
    3. intermittent flow = low O₂ supply
        - systole ->  vessel compression

Coronary atherosclerosis

    Risk factors (see above)

    Development of atheroma(see above) (p. 462)

    Atheromas  -> decr. blood flow (see above)
        -narrowness (p. 103), roughness (p. 102), stiffness

Effects from ischemia (O₂ supply < O₂ demand)  (1, 2, & 3)
    1. weak contraction  (low contractility)
    2. dilation (distention) -> incr. incr. preload  and incr. incr. afterload
    3. wall rigidity  -> incr. incr. afterload  -> decr. decr. SV

            1. + 2. + 3.  -> decr. decr.  CO  ->  systemic ischemia

THEREFORE: cardiac ischemia  ->  1, 2, & 3

        1. initial decr. decr. CO from ischemia  +
        2. continued decr. decr. CO from cardiac decomp. +
        3. problems from  decr. respiratory function

    S&S from coronary ischemia  (1, 2, & 3)

        1. angina (sublethal injury reversible)
        2. T-wave inversion (p. 467) (sketch)
        3. ST segment depression (p. 467) (sketch)

Effects from myocardial infarction (M.I.)
    - same as ischemia but WORSE!!
    - more severe  + longer lasting (cell death)

Therefore:  (1, 2, & 3)
        1. decr. decr. decr. CO  +
        2. incr. incr. incr. decomp. +
        3. decr. decr. decr. respiratory function

S&S from myocardial infarction (M.I.)  (1, 2, & 3)

    1. lasting pain (lethal injury irreversible)
        - also nausea, vomiting, panic, sweat
    2. EKG changes  (p. 471)
        - inverted T-wave (sketch)
        - ST-segment elevation (sketch)
     3. cardiac enzymes in blood

        1 + 2 + 3 = diagnostic triad

Compensatory responses  (1, 2, & 3)

    1. immediately  -> incr. sympathetic activity
        - incr. rate,  incr. force,  incr. vasoconstriction
        - decompensation from incr. incr. O₂ demand
    2. later -> incr. hormones
        - norepinephrine incr. CO,  incr. BP , mineralocorticoids incr. BP
        - decompensation from incr. incr. O₂ demand
    3. long term  ->  cardiac hypertrophy
        -decompensation from incr. incr. O₂ demand, incr. incr.afterload

Healing of infarct (2nd intention)  ->  scar

Complications from M.I.  (1 - 10)
    1. congestive heart failure
        - from gradual hypertrophy + dilation (sketch)
        - decr. decr. CO  &  pulmonary congestion  &  systemic congestion
           Heart, dilated cardiomyopathy, gross [XRAY]
           Heart, dilated cardiomyopathy, gross
           5. Hypertrophy, heart, gross
           Heart, cardiomyopathy, microscopic
           14. Remote myocardial infarction, gross
    2. cardiogenic shock
        -from rapid dilation
        - decr. decr. CO  &  pulmonary congestion  (& systemic congestion)
    3. papillary muscle dysfunction (p. 472) (sketch)
        - valve allows back flow of blood
            - overworked heart  &  systemic ischemia  &  pulmonary congestion
    4. ventricular septal defect (p. 472) (sketch)
        -blood from left ventricle to right ventricle
        - decr. decr. CO  &  overworked heart  &  pulmonary congestion
    5. cardiac rupture (p. 473) (sketch)
        - blood fills pericardial cavity
            - cardiac tamponade
        - prevents filling during diastole  ->  decr. decr.  CO + pulmonary congestion
    6. ventricular aneurysm (outpocketing) (p. 473) (sketch)
            - CHF  +  emboli  +  arrhythmias
           15. Left ventricular aneurysm, gross
    7. thromboembolism (sketch)
        - roughness ->  emboli  ->  strokes, etc.
    (8. pericarditis)
    (9. Dressler's syndrome)
    10. arrhythmias (pp. 476)
        - most common complication
        - abnormal rates (tachy., brady.)
        - abnormal sites of initiation
            - ectopic beats, escape beats, (PVC) premature ventricular contraction (sketch)
        - abnormal conduction  ->  decr. decr. CO
            - heart blocks (sketch)
                - 1st degree, 2nd degree, 3rd degree
                - bundle branch block

Treatment strategies (1, 2, 3, & 4)
     1. incr. contractility (incr. O₂ supply, meds.)
     2. decr. preload & decr. afterload (decr. O₂ demand)
          e.g., decr. fluids, decr. salt,  decr. BP,
     3. decr. workload (decr. O₂ demand)
          e.g., rest, mechanical pumps
     4. surgery
          e.g., bypass, valves, transplant, repair defects

Heart valve operation
    - direction of blood flow opens or closes
        - smooth flexible movable sheets
        - endothelium on connective
    1.  allows forward flow (sketch)
    2.  prevents back flow (sketch)

Causes of valvular heart disease  (1 - 5)
    1. rheumatic heart disease (most common)
        - Group A B-hemolytic strep. (sketch)
 

 (sketch)
    2. bacterial endocarditis(p. 99)
        infection on valve  ->  inflamed valve ->  scarred valve -> ??
    3. damaged papillary muscle(p. 472) (sketch)
        M.I. ->  damaged papillary valve ->  valve flips backward ->  regurgitation -> ??
    4. congenital defect (sketch)
        defect ->  stenosis &/or regurgitation-> ??
    5. autoimmunity ("in born error")
        immune attack on valve  ->  inflammation ->  scar on valve -> ??

Mitral Stenosis (see Course Booklet p. 36)

    Heart chamber that pumps blood through the diseased valve is affected most (pp. 491-496) (sketch)

        Heart, dilated cardiomyopathy, gross [XRAY]
        Heart, dilated cardiomyopathy, gross
        5. Hypertrophy, heart, gross
        Heart, cardiomyopathy, microscopic

Dangers from pulmonary edema

    immediate: thick membrane  +  filled alveoli  ->  decr. gas exchange (sketch)
           1. Normal lungs, gross
           2. Normal lung, cross section, gross
           4. Normal lung, microscopic*
                    Note the thin membranes and open air spaces
           5. Lung, edema, microscopic*
                    This is at high magnification, note the thick membranes and filled air spaces
           6. Lung, passive congestion, microscopic*
                    This is at high magnification, note the thick membranes and filled air spaces
    later: incr. fluids  ->  incr. risk of infection  ->  decr. gas exchange (sketch)
              17. Lung, bronchopneumonia, low power microscopic*
    chronic: incr. fluid  ->  pulmonary fibrosis -> decr. gas exchange (sketch)
           115. Lung, interstitial fibrosis, microscopic*
                    Chronic pulmonary edema can cause pulmonary fibrosis.

Degree of damage from atherosclerosis
    depends upon  (1, 2, & 3)
        1. severity
        2. tissue demand
        3. amount of collaterals

Reasons for S&S from ischemia
    - from chemical imbalance (decr. O₂,  incr. CO₂, etc.)
        - intermittent claudication
        - pain at rest
        - necrosis
        - atrophy
        - cyanosis
    - from low blood flow into area
        - weak pulse
        - pallor
        - coolness
    - from pulse wave hitting blockage
        - strong pulse above lesion
           1. Normal lungs, gross
           2. Normal lung, cross section, gross
           4. Normal lung, microscopic*
           5. Lung, edema, microscopic*
           6. Lung, passive congestion, microscopic*
           Foot with previous healed transmetatarsal amputation and recent ulcer, gross.
           Gangrenous necrosis and ulceration, lower extremity, gross.

Aneurysm  -  outpocketing of vessel (sketch)
        22. Aorta, atherosclerotic aneurysm, gross
    causes  (1, 2, 3, & 4)
        1. atherosclerosis
        2. trauma
        3. congenital defect
        4. syphilis
    effects  (1, 2, & 3) (sketch)
        1. thrombus
        2. pressure on nearby structure
        3. hemorrhage

Venous thrombosis
    causes  (1, 2, & 3)
        1. roughness
        2. slow flow
        3. chemical imbalance
        Renal vein thrombosis, gross
    consequences - block flow
        1. at site of formation (sketch)
        2. embolize to other sites (sketch)
            e.g. pulmonary embolus (p. 617)
           27. GIF animation of pulmonary thromboembolus, diagram
           69. Lung, pulmonary thromboembolus, gross
           70. Lung, pulmonary thromboembolus, gross
           73. Lung, pulmonary thromboembolus, gross
           74. Lung, pulmonary thromboembolus, low power microscopic*
           27. GIF animation of pulmonary thromboembolus, diagram
           28. Pulmonary thromboembolus, gross
           29. Pulmonary thromboembolus, gross
           30. Pulmonary thromboembolus, gross
           31. Pulmonary thromboembolus, microscopic *
           32. Pulmonary thromboembolus, microscopic *
           78. Lung, remote organized pulmonary artery embolus, gross

Varicose Veins (sketch)
    causes  (1 - 4)
        1. gravity - standing still
        2.  compressed veins
            - posture, tight clothing, pregnancy, tumor
        3.  back pressure
            - coughing, straining with defecation, constipation
        4.  blocked drainage
            - cirrhosis, heart failure
    pathogenesis (sketch)
        - chronic forced dilation  -> permanent distention (p. 547)
    complications
        - ischemia, edema, thrombosis, infarction, infection, hemorrhage, pain, cosmetic
           1. Normal esophagus, gross
           2. Normal esophagus, low power microscopic*
           12. Esophageal varices, gross
           13. Esophageal varices, gross
           14. Esophageal varices, with sclerotherapy, gross
           118. Prolapsed true hemorrhoids, gross
           21. Esophageal varices with portal hypertension, gross
           22. Splenomegaly with portal hypertension, gross
           20. Caput medusae of skin with portal hypertension, gross
Shock
    causes
        - hemorrhage, heart failure, pulmonary embolus, trauma, severe infection, stroke, etc.
    areas affected most
        - first
            1. brain (high O₂ demand)
            2. heart (high O₂ demand)
            3. lungs (pulmonary edema)
        - then
            4. kidney (decr. decr. BP  ->  decr. decr. filtration)
 
 

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