Hemodynamic Disorders and Shock -CIL


Hemodynamic Disorders and Shock -CIL

Mechanisms of Disease

May 5, 2003


Lori Wasson, D.O.

Scribe-Heather Volkman



Dr. Wasson went over her powerpoints for this lecture, as well as, questions from the Robbins Review book.



A 25-year-old IV drug abuser presents with high fever , chills and rigors.

On examination he is found to have a murmur in the tricuspid valve area. His face and extremities look flushed and blood pressure is 90/60.

Laboratory examination reveals an elevated leukocyte count with polymorphonuclear leukocytosis. Blood culture shows growth of gramnegative bacteria . He is treated with intravenous antibiotics. His blood pressure continues to fall and urinary output declines to 100 mL/24 hr.

He died 3 days later. i.

Acute infectious process due to fever, chills, rigor, and elevated

WBC count ii.

Septic shock iii.

Look at view of vegetations on tricuspid valve iv.

What might be the consequences of infective endocarditis with formation of vegetations on the right side of the heart? --embolism to the lung, causing infarction if it gets to the end arterioles –the bacteria on the vegetations might cause an abcess—septicemia due to gram negative rods v.

Look at view of acute (renal) tubular necrosis (ATN)

--it is pale due to low perfusion of kidneys vi. Why did this patient develop shock? –gram negative rods due to LPS activated macrophages which secreted IL-1 and TNF

(look at figure in book for LPS) resulting in hypotension and hypoperfusion vii. Look at high power of ATN—viable tubes next to necrotic tubes (at autopsy, can determine shock if viable next to necrotic tubes in kidney)

What might happen if the infected vegetation breaks loose from the valve and lodges in distant organs? (aortic valve) –systemically, most likely place, resulting in infarction or abcess

Rheumatic heart disease results in mitral valve stenosis with vegetations that are not infected (aseptic) i.

What complications might arise from this lesion? –mitral stenosis -

--can become infected and can embolize systemically –pulmonary

edema and hypertension –the mitral valve, chordae tendinae, or papillary muscles can rupture resulting in septicemia and ventricular failure ii.

Look at view of infective endocarditis at medium power

How is fibrin formed? And What are the categories of coagulant proteins? i.

Coagulation cascade with end of thrombin converting fibrinogen to fibrin. ii.

Three types of coagulant proteins (fibrin, active coagulation factors

(V,VIII), and cofactors) iii.

Look at infective endocarditis at high power –have necrosis and microorganism

--Could this person develop a cerebral infarct? What would the appearance of such an infarct of the brain? ---yes, liquifactive necrosis and abscess formation iv. Look at nonbacterial endocarditis picture --lots of fibrin


Questions from Powerpoints

note: non-bacterial endocarditis will not go on to become an abscess, however, infective endocarditis can become an abscess is breaks off

Question 1: A 21 year old female sustains multiple injuries, including fractures of the right femur, right tibia, and left humerous. The fractures are stabilized after surgery and she is in stable condition. However, 2 days

- after admission, she becomes severely dyspneic. What happened?

--she did not develop a PE (pulmonary embolism) due to time frame

--fat embolus, is the correct answer

Question 2: A 76 year old female fell and fractured she left femoral trochanter. After 2 weeks in the hospital, she left leg is swollen, particularly her lower leg below the knee. She experiences pain on movement of this leg, and there is tenderness to palpation. Which of the following complications is most likely to occur after these events? -PE

--What happened? a DVT (deep vein thrombosis)

--Will it cause gangrenous infection of foot? --no (from arterial circulation)

--note: most PEs comes from veins above the knee


Questions from Review Book

- Question 1: answer—vasoconstriction is the first thing that happens, then after a few minutes the platelets aggregate (adhesion then activation)

- Question 2: answer—liver (also, lung)—due to dual circulation

- Question 4: answer---congestive heart failure (also tricuspid valve stenosis)

- Question 5: answer—immobilization

- Question 6: answer—damage to endothelium (most likely causeatherosclerosis)

- note: very common cause of hypercoagulable state—factor V mutation

(Leiden mutation)

- Question 7: answer—t-PA (most common drug used now) (most are not using urokinase or streptokinase)

- note: t-PA should be given within 30 minutes of acute MI due to irreversible injury and hardened clot (criteria: ST segment elevation, etc) (diabetics can have silent MI and days later be diagnosed with MI—not candidate for t-PA)

- Question 8: answer—acute pulmonary congestion—therefore, congestion of alveolar capillaries with transudate in the alveoli (low protein) (not purulent or exudative)

- note: even if the congestion is chronic, don’t assume exudative effusion unless given information about fever or infection (even though increased risk due to chronic effusion)

-note: effusion can be exudative or transudative

- Question 9: answer—tissue nitrogen emboli (disease—the bends)

- Question 10: answer—lymphatic obstruction due to tumor cells in dermal lymphatics –inflammatory carcinoma (note: fine-needle aspirate is used to biopsy and retrieval of cells)

- Question 26: she did not like terminology in this question answer--lymphedema due to lymphatic obstruction

- Question 13: answer—factor V Leiden mutation (most common cause of hypercoagulable state)

- note: a woman with recurrent miscarriages and recurrent DVT--lupus anticoagulant or anti-phospholipid antibody syndrome (interchangeable)