CHAPTER 7--HEMODYNAMIC DYSFUNCTION = 2 Q'S Flashcards
CELLS & TISSUES are dependant on
- Normal Fluid Environment = increase edema and decrease dehydration
- Adequate Blood supply
- Thrombosis
- Embolism
- Infarction
- Hemorrhage
know
______–Accumulation of excess fluid (transudate, exudate, lymph) in the intercellular (interstitial) tissue spaces and body cavities:
Body cavities are:
- pleural cavity (hydrothorax)
- peritoneal cavity (ascites )
- pericardial cavity (hydropericardium)
**Edema can be local or generalized
EDEMA
Pitting edema of the leg
reflects the “________” of the fluid- filled tissue
in-elasticity
Pathogenesis of Edema
- INCREASE capillary hydrostatic pressure (hemodynamic edema): protein-poor transudate
- INCREASE capillary permeability (inflammatory edema):protein-rich exudate
- DECREASE collodial osmotic pressure of plasma proteins: liver (dec. protein synthesis), kidney (nephrotic syndrome)
- INCREASE tissue osmotic pressure (sodium retention)
- obstruction of lymphatics (lymphedema): in malignancy, surgery, radiation therapy, or filariasis
KNOW
Causes of generalized edema
1. Cardiac = Left ventricular failure + Right ventricular failure
2. Renal–Acute glomerulonephritis & Nephrotic syndrome
3. Hepatic:–decreased protein synthesis & portal hypertension
4. 4. Nutritional: protein malnutrition
(kwashiorker or starvation)
KNOW
Causes of localized edema
1. Inflammatory edema
-INCREASE vascular permeability
-__________ hydrostatic pressure to arteriolar dilation
(= exudate)
2. Edema due to localized ________ obstruction
-thrombosis, varicose veins, compression
-hydrostatic pressure (= transudate)
3. Edema due to____________ obstruction
-surgery, cancer, parasites
-in early stage, edema is pitting ( = lymph)
-later, edematous tissue becomes fibrosed, thickened & non-pitting (elephantiasis)
INCREASE
venous
lymphatic
_________: INCREASE of blood due to active arterial dilation:
a. Physiologic : muscles during exercise
b. Pathologic: inflammation
__________: passive INCREASE of blood due to impaired venous drainage:
- –localized as due to venous obstruction, or
- -generalized as with right heart failure
Hyperemia
Congestion
Pulmonary congestion—Etiology: _____ ventricular failure (hypertension, myocardial infarction, rheumatic heart)
Alveolar capillaries: engorged, dilated, tortuous:
-edema of interstitial tissue
-transudate in alveoli
-hemorrhage
Left
Chronic passive congestion of the lungs
.
Increased venous pressure leads to extra vasation of
red blood cells into the alveoli and alveolar edema.
The hemosiderin formed from hemoglobin released from hemolyzed red blood cells is taken up by intraalveolar macrophages. These macrophages are
sometimes called “_____ _____ ______” because of
their association with pulmonary congestion with
congestive heart failure
.
“heart failure cells”
Liver congestion
Etiology—_______ side heart failure, pulmonary fibrosis, tricuspid stenosis, & thrombosis of hepatic vein or inferior vena cava
Right
Chronic passive congestion (nutmeg liver), gross. a “nutmeg” liver seen with chronic______ ________ of
the liver
.
passive congestion
__________— (blood clot):
A solid mass formed from blood constituents within heart and blood vessels during life. It is composed of layers of aggregated platelets and fibrin
Thrombus
Thrombosis is a normal hemostatic mechanism that stops _____-_____
bleeding:
Thrombosis is a normal hemostatic mechanism that stops bleeding.
- Formation of platelet plug:
-injury of __________ exposes subendothelial collagen
-adhesion of platelets to exposed collagen
-platelet release reaction: secretion of ADP platelet
aggregation (they aggregate on top of each other)
endothelium
Thrombosis is a normal hemostatic mechanism that stops bleeding.
- Coagulation of blood:
-activation of ________________ activates intrinsic pathway
-tissue thromboplastin released by injury activates
extrinsic pathway
3._________:—-prevents excess thrombus formation
Hageman factor (XII)
Fibrinolysis
Three important factors are involved in hemostasis
- Endothelial cells
- Blood platelet
- Coagulation factors
know
ENDOTHELI AL CELLS-Releasing antithrombotic or
thrombotic factors
A—-intact endothelial cells prevent thrombosis through;
1. Anti-platelet properties
2. Anti -coagulant properties
3. Fibrinolytic properties
B-Injured endothelial cells = initiate thrombosis
—Synthesize von WILLIBRANDS FACTOR–binds platelets to exposed subendothelial collagen (platelet adhesion)
-Release tissue factor (thromboplastin) = activates
__________ clotting pathway
:
extrinsic
PLATELETS—-Derived from cytoplasmic fragmentation of megakaryocytes
- platelet ________ to subendothelial collagen mediated by von W factor
adhesion
COAGULATION SYSTEM x 2
Intrinsic Pathway = Activation of XII
Extrinsic Pathway = Release of tissue thromboplastin
- **Coagulation is confined to site of injury through:
- natural anti-thrombin
- removal of activated factors (liver & phagocytic cells)
- dilution
know
THROMBOGENESIS Predisposing factors (VIRCHOW'S TRIAD)
- Endothelial injury
- Alteration of normal blood flow
- Hyper-coagulability of blood
know
Morphology of Thrombi
1. Arterial thrombi:
“ _______ ___ _____ “ which are the alternating pale pink bands of platelets with fibrin and red bands
of RBC’s forming true thrombus
- Venous thrombi—commonly (90% ) in veins of
lower limbs—almost always occlusive
lines of Zahn
________ veins of the legs = Severe varicosities of
the superficial leg veins have led to stasis dermatitis
and secondary ulcerations
Varicose
Fate of Thrombi x 5
- _______: accumulate more platelets & fibrin to obstruct a critical vessel
- Fibrinolysis: re-establishment of lumen (fibrinolytic
Activity) - Thromboembolism: partial or complete detachment
- ___________: inward growth of granulation
tissue - Recanalization: capillaries of granulation tissues form
anastomosing channels
Propagation
Organization (fibrosis)
EMBOLISM
______:–an insoluble mass (solid, liquid, gaseous)
circulating in the blood
.
________:–occlusion or obstruction of a blood vessel by an embolus.
Embolus
Embolism
- THROMBOEMBOLISM
- Fragmented or _________ thrombi (98%)
- Site of embolism depends of origin:
i. pulmonary embolism
ii. systemic embolism
detached
- THROMBOEMBOLISM
Pulmonary embolism:
—Emboli are derived from thrombi of systemic veins,
mainly deep veins of legs (95%), superficial leg veins, pelvic,uterine, and periprostatic
–Multiple emboli over time may cause pulmonary
hypertension with ____ side heart failure
right
- THROMBOEMBOLISM
Systemic embolism:
-Emboli are derived from mural thrombi:
a. mural thrombi due to _______ ___________
b. mitral stenosis & atrial fibrillation
c. aortic aneurysm or atheromatous plaque
—–Impacted in cerebral, renal, intestinal & splenic
branches, more frequently (70-75%) in ________ limbs.
myocardial infarction
lower
- FAT EMBOLISM
-2nd most frequent type of emboli
-Fat globules enter blood after fracture of long bones
or extensive trauma to fatty tissue (burns or surgery)
-Effect: depends on their size:
More than 20 = Arrested in lung = Dyspnea
Less than 20 = Pass to systemic circulation
- AIR OR GAS EMBOLISM
a. _______
- Surgery or trauma to internal jugular vein
- During delivery or abortion: air enters ruptured uterine sinus
- Iatrogenic pneumothorax
b. ________:
(Caisson disease, Decompression sickness)
-occurs in caisson workers & sea divers
-breathing pressurized air = more air goes into solution in blood & tissues
-rapid decompression to sea level = dissolved gases come out of solution.
-because of low solubility of N2 = forms bubbles = act as emboli.
AIR:
GAS
________–Area of localized ischemic necrosis
produced either by occlusion of arterial supply or
venous drain
INFARCTION
Morphology of infarct
- ___________ coagulative necrosis (all infarcts) replaced by scar tissue
- Liquefactive Necrosis: in _____ or when infected.
Ischemic
CNS
Types of infarct x 2
- __________________infarct—arterial obstruction in
SOLID ORGANS with poor collateral circulation (end artery) e.g. spleen, heart, kidney, brain - ____________________infarct
-obstruction of venous outflow & congestion
-LOOSE ORGANS e.g. lung
-organs with double blood supply (liver, lung) or
collateral vessels (small intestine)
-twisted pedicle of ovary or test
Pale,white,anemic
Red,hemorrhagic
Septic infarct
- infected embolus
- organs normally containing ________ (e.g.intestine)
- bacteria from blood (secondary infection)
bacteria
SHOCK—DECREASE tissue perfusion associated with DECREASE in effective cardiac output.
3 Types of SHOCK
- Cardiogenic (decreased cardiac output)
- Hypovolemic
- Shock due to peripheral sequestration of blood volume
know
1.\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ shock Decreased cardiac output due to heart failure -myocardial infarction -massive pulmonary embolism -cardiac tamponade -arrhythmias
- ____________- shock
Decreased cardiac output due DECREASED blood volume
-hemorrhage
-fluid loss e.g. burn, diarrhea, vomiting - Shock due to _________ sequestration of blood
volume
-endotoxin of gram negative bacteria (septic shock)
-chemical mediators of allergy (anaphylacticsh shock)
-anesthesia, spinal cord injury (neurogenic shock)
Cardiogenic
Hypovolemic
peripheral
3 Stages of shock:
- compensation
- impaired tissue perfusion (decompensation)
- irreversible stage
know
3 Stages of shock:
- Stage of _____________
Decreased cardiac output = mild hypotension = reflex sympathetic stimulation.
-tachycardia
-peripheral vasoconstriction:
i. skin:cold & clammy
ii. renal arterioles: decreased glomerular filtration
= decreased urine output
compensation
3 Stages of shock:
- Stage of impaired tissue perfusion (stage of ______)
a. Prolonged stagnation & edema Vasoconstriction
b. Promotes anaerobic glycolysis = lactic acidosis, dilation of arterioles = Blood stagnation & edema
c. Tissue necrosis
decompensation
3 Stages of shock:
- ________ stage
a. Failure of peripheral vasoconstriction (capillary hypoxia & acidosis = vasodilation
b. fall in blood pressure
c. impairment of perfusion of brain (neuronal degeneration) & heart (further decrease in cardiac
output, death)
d. Full recovery is possible with the early detection and correction of the CAUSE of shock
Irreversible
High mortality rate x 2
- Cardiogenic shock— due to existing_______ diseases
- Septic shock—— due to the difficulty in ______ control
cardiac
infection
Factors that favor RECOVERY from shock X 3
- Availability of early treatment of
- Initiating cause
- Hypovolemia - Younger age
- Good general health
know
Factors that favor SHOCK FAILURE X 5
- Delay in treatment
- Failure in removing the initiating cause - Old age
- Poor health
- Pre-existing CVD & lung diseases
- Complications as infection & necrosis
know
