Hemodynamic Disorders 2007

8/4/2019 Hemodynamic Disorders 2007

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Todays Quranic verse

And hold fast, all together, by the rope which God

(stretches out for you), and be not divided among

yourselves; and remember with gratitude God'sfavour on you; for ye were enemies and He joined

your hearts in love, so that by His Grace, ye

became brethren; and ye were on the brink of the

pit of Fire, and He saved you from it. Thus dothGod make His Signs clear to you: That ye may be

guided. [003:103]


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If one advances confidently in the direction

of his dreams, he will meet with a successunexpected in common hours

"Shoot for the moon."Shoot for the moon. Even if you missEven if you miss

it, you will land among the stars.!"it, you will land among the stars.!"


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HEMODYNAMIC

DISORDERS


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THROMBOSIS


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DEFINITION:

It is the process of formation of solid mass in circulation

from the constituents of flowing blood (within a blood

vessel or cardiac chamber, in a living organism-always

formed ante-mortem). The mass itself is called Thrombus.

Blood clot: mass of coagulated blood formed in vitro

Hematoma: extravasular accumulation of blood clot into tissues.Hemostatic plugs: simplest form of thrombus formed in healthy individuals at the site of bleeding


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COMPOSITION OFTHROMBUS

Fibrin, Platelets, RBC's(Hemostatic plug formation: endothelial injury, platelet aggregation, fibrin meshwork )

LOCATION OFTHROMBIArteries, veins, heart chambers, heart valves

TYPES OFTHROMBIArterial vs. venous;

bland vs. septic


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PATHOGENESIS OF THROMBOSIS(Predisposing Factors)

Virchows TriadEndothelial injury

Stasis or turbulence of blood flow

Blood hypercoagulability


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Endothelial Injury

Tissue Damage (Surgery, Fractures, Burns)

Atherosclerosis

HypertensionToxic Products (cigarettes, homocysteine etc. )


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Abnormal Blood Flow

Turbulence of Blood Flow Swirls, Eddies and increased pressure are injurious

These changes occur in arteries and the heart

Atherosclerosis, Aneurysms, Myocardial Infarction, Cardiac Valve Lesions

Hyperviscosity Syndromes e.g. Sickle Cell Anemia, Polycythemia

Stasis of Blood Flow More commonly a problem on the venous side leading to Venous Thrombosis

Can occur in the heart (Atrial Fibrillation or Infarction)

Pregnancy, long plane ride, immobility after surgery

Turbulence and Stasis : Disrupt normal laminar flow and bring platelets in contact with endothelium Prevent dilution of activated clotting factors

Retard the inflow of clotting factor inhibitors and permit thrombi build-up

Promote endothelial cell activation


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Hypercoagulability

Any alterations of the coagulation pathways that predispose toThrombosis

Primary (Genetic) or Secondary (Acquired) Disorders

FactorVLeiden mutation is the most common inherited cause ofhypercoagulability, it is resistant to the anti-coagulant effect of Activated

Protein C

Lack of Protein S, Protein C and Antithrombin III, patients present with

venous thrombosis and recurrent thromboembolism in adolescence and early

adulthood Lupus Anticoagulant with Lupus Erythematosus is associated with arterial

and venous thrombosis & recurrent abortion

Smoking, Obesity, Oral Contraceptives (BCP)


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Lupus -Anticoagulant

Called an Anticoagulant because it interferes with a Coagulation Test, artificially

prolonging It.

But It Is Not an Anticoagulant. It Is a Procoagulant

HIT syndrome3-5% population

Un-fractionated heparin for therapeutic anticoagulation induces circulating

antibodies resulting in platelet activation & endothelial cell injury ending up

in prothrombotic state


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HEMOSTASIS


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Hemostasis & Thrombosis

Hemostasis is the normal, rapid formation of a

localized plug at the site of vascular injury

Thrombosis is thepathologic formation of a blood

clot within the non-interrupted vascular system ina living person


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Hypercoagulable StatesInherited

Abnormality Approximate Rate

Factor VLeiden - APCR (Caucasion) 15-30%Prothrombin Gene Mutation 8-13%

Protein C Deficiency 5-6%

Protein S Deficiency 5 - 6%

Antithriombin Deficiency < 1%Hyperhomocysteinemia 3 - 5 %

Rogers: Am J Hem 41: 113, 1992


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EFFECTS OFTHROMBI

Stenosis or blockage of arterial lumen

ischemia, infarction

Venous occlusion

local congestion and edema and/or pulmonary embolism (travels)

Left heart valve & chamber thrombi

systemic embolism


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MORPHOLOGY OF THROMBITHROMBI DEVELOP

IN THE CARDIOVASCULAR SYSTEM

Lines of ZahnAlternating Pale Layers of Platelets & Fibrin With Darker Layers of Rbcs

(seen in areas with active blood flow like heart, aorta & large arteries not in veins)

*Postmortem clots are gelatinous with a dark red dependent portion & yellow chicken fatsupernatant, usually not attached to the underlying wall

*Thrombi in heart chamber/aortic lumen are applied to the underlying structure, mural thrombi(non-occlusive)

Arterial thrombi are Occlusive/Non-occlusive, begin at site of endothelial injury and grow alongflow of blood & typically are firmly adherent to the injured arterial wall (atherosclerotic plaque)

Venous thrombi are almost always Occlusive- 85-90% of venous thrombi form in lower extremities


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Atheroma with Thrombosis:Atheroma with Thrombosis:


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Thrombus(Lines of Zahn)


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Layering(Lines of Zahn)


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Cardiac Mural Thrombus


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Cardiac Mural Thrombi

Notice underlying endocardial fibrosis

Right

Left


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Aortic Aneurysm

Mural Thrombus


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CLINICAL SETTING FOR CARDIAC /ARTERIAL

THROMBUS FORMATION

Myocardial Infarction (MI)Rheumatic Heart Disease

Atherosclerosis

Rare large round thrombus obstructing mitral valve is called ball-valve thrombus

Thrombi formed in ventricles just before death composed of mainly fibrin Agonal thrombi


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VENOUS THROMBOSIS

Superficial Veins of the Lower Extremities Cause Pain, Swelling - Rarely Embolize

Associated With Varicosities Abnormally Dilated, Tortuous Veins

Increased Risk of Infections

Increased Risk of Varicose Ulcers

Deep Veins of the Lower Extremities Thrombi in Deep Veins (Popliteal, Femoral, Iliac Veins) More Likely

to Embolize About 50% Are Asymptomatic (Formation of Collaterals)

May Produce Edema, Pain and Tenderness


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PhlebothrombosisIt is due to stasis of blood in un-inflamed veins,

particularly the calf veins.

Thrombophlebitis

It is related to inflammation of the vein walls.


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PHLEBOTHROMBOSIS THROMBOPHLEBITIS

Main cause Stasis Inflammation

Primary thrombus Small Larger-depends on extent

of phlebitis.

Propagated clot Long/poorly anchored Usually none-if presentshort and well-anchored

Emboli Common, may be massive Rare unless infective

Sterile

Site Usually calf veins Anywhere

Clinical Often silent Pain

Signs of inflammation


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CLINCAL SETTING FOR VENOUS

THROMBUS FORMA

TION

Cardiac Failure (CHF)

Trauma

SurgeryBurns

3rd Term Pregnancy and Postpartum

Cancer (migratory thrombophlebitis-Trousseaus Syndrome)

Bed RestImmobilization


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Valvular Thrombi (vegetations)

Infective Endocarditis

Non-bacterial Thrombotic Endocarditis (NBTE)-Seen in patients dying of chronic debilitating diseases- advanced cancer (50% cases) &

other end stage diseases (cachectic, marantic or terminal endocarditis)

Atypical Verrucous Endocarditis (Libman-sacks)-Seen in 50% of acute SLE, Systemic sclerosis, TTP, Collagen diseases

Capillary thrombiMinute thrombi composed mainly of packed red cells in vasculitis & DIC


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FATE OF THROMBOSIS

Resolution (Dissolution)

Recent thrombi can undergo total lysis by activation of fibrinolytic system (mostly small venousthrombi). After the first 2-3 h, thrombi wont undergo lysis.

Thus the use of tPA is only effective in the first 1-3 hours

Organization and recanalizationReplacement by granulation tissue followed by recanalaization or healing totally to leave only a

small fibrousLump as evidence of a previous thrombus

PropagationAccumulation of more platelet & fibrin and obstruction

EmbolizationEarly & infected thrombi may detache from site of origin and may block distal vesseles

Hyalinization & Calcification

(Degraded thrombus with superadded bacterial infection may lead tomycotic aneurysm)


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Thrombus Propagated into the

Inferior Vena Cava


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CLINICAL SIGNIFICANCE:

Obstruction of arteries or veins can cause

ischemia, infarction, or may embolize

Venous thrombi may lead to congestion, poor wound healing, skin ulcers and painful

thrombosed veins

Microthrombi in microcirculation (capillaries) may cause DIC


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DIAGNOSIS:

Clinical signs are unreliable.

Phlebography using a contrast medium.

Radioactive iodine-labelled fibrinogen test.

Doppler ultrasound.


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EMBOLISM


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EMBOLISM

It is the process of carrying an abnormal mass (embolus)

in the blood stream to a point distant from its origin.

*An embolus is a detached intravascularsolid, liquid or gaseous mass that

is carried by the blood to a site distant from its point of origin


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TYPES OF EMBOLI

Gas(air, nitrogen , other gases)

Liquid

(amniotic fluid, radiographic contrast material, fat after soft tissue trauma / fracture, bone marrow )

Solid(thrombus-- most common, foreign body- bullet, catheter; also atheroematous material, tumor cell

clumps, tissue fragments, parasites, bacterial clumps etc.

99% are dislodged thrombusRarely: Bullets, Fat, Air, Atherosclerotic Fragments, TumorFragments, Bone Marrow

Emboli can be Bland (sterile) or Septic (infected)


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ORIGIN & SITES OF EMBOLIZATION:

Venous: Systemic veins Pulmonary arteries

Arterial: Heart or aorta Systemic circulation

Paradoxic: Systemic veins (through septal defect in heart or

AV shunts in lungs) systemic circulation

*Retrograde: Embolus traveling against the flow of blood (metastatic deposits in spine fromcarcinoma prostate due to retrograde embolism through intraspinal veins from large thoracic

& abdominal veins due to increased pressure in body cavities: during coughing or straining)


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EFFECTS OF EMBOLISM

Ischemia

Infarction

Sepsis if infected

(example: pulmonary embolism with pulmonary infarction)


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Thromboembolism

A detached thrombus or part of thrombus constitutes the most

common type of embolism

*Arterial (systemic) thromboembolism(from within heart & arteries)

*Venous thromboembolism Pulmonary thromboembolism

(from veins of lower legs & upper limbs, pelvic vein, cavernous sinus of brain, right side of heart)


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Systemic Thromboembolism

Emboli traveling within the arterial circulation

80% arise from intra-cardiac mural thrombi (myocardial infarction)

Vegetations on the heart valves (mitral/aortic) & prosthetic heart valves mayembolize to the systemic circulation

Infective endocarditis, Cardiomyopathy & CHD may be cause Emboli developing in relation to atherosclerotic plaques, aortic aneurysms,

pulmonary veins and paradoxic emboli

Major site of embolization are lower extremities (75%), brain (10%), intestine,kidney & spleen

Leads to infarction of the affected organs, gangrene, arteritis & mycoticaneurysm, myocardial infarction and sudden death.


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Emboli can arise from--


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Pulmonary Thromboembolism

Generally originate from deep leg veins (popliteal, femoral & iliac)Usually pass through the right heart Into pulmonary vasculature

60% Pulmonary Arterial obstruction usually leads to sudden death, RVF

Most pulmonary emboli (60-80%) are clinically silent because of small size

May occlude main pulmonary artery, across the bifurcation (SaddleEmbolus) or pass into the smaller branching arterioles

Embolic obstruction of medium-sized arteries may result in hemorrhagewithout infarction because of intact bronchial circulation. If bronchialcirculation is compromised as in left heart failure it results in infarction

Emboli obstructing small end-arteriolar pulmonary branches usually result inassociated infarction

Multiple pulmonary emboli over time may cause pulmonary hypertensionand right heart failure


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Thromboembolism


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Pulmonary

Embolus


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Saddle

PulmonaryEmbolus


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Fat embolism syndrome

Microscopic fat globules derived from long bone fractures (fatty marrow) or

rarely from soft tissue trauma and burns

10% of cases show clinical findings

Clinically characterized by

Pulmonary insufficiency, neurologic symptoms, anemia & thrombocytopenia

Symptoms appear 1-3 days after injury

PathogenesisMechanical obstruction in pulmonary & cerebral microcirculation and chemical

injury to endothelium by free fatty acids resulting in skin rash


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Air embolism

Gas bubbles within the circulation can obstruct vascular flow to cause distal

ischemic injury

Air can enter the circulation duringChest wall injury, Operation on neck & head, Obstetrical operation & trauma, Intravenous

infusion, Sudden atmospheric pressure changes in scuba & deep sea divers, underwaterconstruction workers and in individual in unpressurized aircraft in rapid ascent (Decompressionsickness- Caisson disease)

Clinically characterized byBends due to rapid gas bubble formation within skeletal muscle & about joint

Chokes due to respiratory distress caused by edema, hemorrhage, focal atelectasis, emphysema

CNS & CV effects due to focal ischemia

Multiple foci of ischemic necrosis specially in heads of femur, tibia, humerus etc

Clinical effects observed with air in excess of 100 ml


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Amniotic Fluid Embolism

Torn placental membrane- amniotic fluid release

Rupture of uterine veins

Infusion of amniotic fluid into maternal venous circulation

Morphologically characterized by

Lungs show squamous cells, lanugo hair, fat from vernix caseosa & mucin from GIT & RS

pulmonary edema, diffuse alveolar damage, systemic fibrin thrombi

Clinically characterized by

Severe dyspnea, cyanosis, hypotensive shock, seizures, coma & DIC

Mortality rate> 80%


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Disseminated Intravascular Coagulation (DIC) Sudden widespread fibrin deposition in microcirculation

Rapid consumption of platelets and coagulation proteins

Secondary massive fibrinolysis, all the little thrombi dissolve

Clotting Disorder Turns Into a Bleeding Disaster

Sepsis is common cause of DIC (30-50% of patients with gram negative sepsis)


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Disseminated Intravascular Coagulation

Schistocytes

Microthrombi


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Clinical Consequences of DIC


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Tumor Embolism

Tumor EmbolismLymphatics (Carcinoma)

Blood vesseles (Sarcoma)

Common sitesLiver (Carcinoma)

Lung (Carcinoma & Sarcoma)Bone (Prostate, Thyroid, Breast, Kidney, Lung


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INFARCTION


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INFARCTION

An infarct is a localized area of ischemic necrosis caused by

occlusion of either the arterial supply or venous drainage in a

particular tissue

90-99% of all infarcts due to arterial thrombotic or embolic events

Less common causes of infarction are vasospasm, hemorrhage in atheromatous plaque, twisting

of vessel, extrinsic compression or traumatic rupture of blood supply

Coagulative necrosis is characteristic of hypoxic death in all tissues except CNS

All infarcts tend to be wedge-shaped, with the occluded vessel at the apex


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TYPES OF INFARCTS:

Bland vs. Septic

(assumed to be bland unless specified as septic)

Arterial (usually white/pale) vs. Venous (red/hemorrhagic);

Bland and arterial most common

Organs with a single venous outflow channel (testis & ovary) are predisposed to infarction

caused by venous thrombosis


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MORPHOLOGY OF INFARCTS

White/Pale:

Occur with arterial occlusion or in solid organs with single blood supply (ex: kidneys, spleen)

Red/Hemorrhagic:Occur with venous occlusion, in loose tissues, tissues with dual circulation, in tissues previously

congested and when flow is re-established to a site of arterial occlusion & necrosis.

All infarcts are wedge shaped, poorly defined & hemorrhagic in initial stage, later margins are

better defined revealing hyperemia, become pale & sharply defined in solid organs and firmer &

browner in spongy organs

Microscopic evidence is visible after (12-18) hours if patient survives

Characterized by coagulative / liquefactive necrosis surrounded by inflammatory zone, later there

is evidence of regeneration & repair. Most infarcts are ultimately replaced by scars tissue.

Septic infarction results from embolization of infected vegetation from heart valve or if microbes

seed area of necrosis abscess organization


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FACTORS AFFECTING INFARCTS:

Nature of the vascular supply (dual arterial supply)

Collateral circulation

Rate of development of occlusion

Duration of occlusion

Metabolic needs of the tissue/organ Vulnerability of the tissue to hypoxia

Brain - < 3 minutes

Heart 0.5-2 hours

Kidney 2-3 hours

Skin fibroblasts - < 24 hours

Oxygen content of blood


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Hemorrhagic Lung Infarct Pale Splenic Infarct


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Myocardial Infarction


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MYOCARDIAL INFARCTION


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RENAL INFARCT

ION


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Lung Infarct

Wedge Shape...


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Infarcted Colon

OK Colon


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CLINICAL SIGNIFICANCE OF INFARCTION

Usually causepain;

May cause loss of function (example: myocardial infarct maycause heart failure);

May cause hemorrhage or sepsis (examples: lung infarct causes

hemoptysis, bowel infarct causes GI bleeding or sepsis).


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Marker Initial elevationafter AMIMean time topeak elevation

after AMI

Time to return to baselineafter AMI

Myoglobin 1 - 4 h 6 h 18 - 24 h

CK-MB 3 - 12 h 10 - 24 h 48 - 72 hMB-isoform 1 - 6 h 4 - 12 h 38 h

cTnI 3 - 12 h 10 - 24 h 5 - 10 days

cTnT 3 - 12 h 12 - 24 h 5 - 14 days

DIAGNOSIS OF INFARCTION

Depends on the organ involved

MI (ECG, Serum markers)

Common serum markers used to detect AMI


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SHOCK


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SHOCK

It is defined as systemic hypo-perfusion due to reduction either in

Cardiac Output or Effective Circulating Blood Volume.

The End Results are:

Hypotension, followed by

Impaired Tissue Perfusion and Cellular

Hypoxia

Reversible Cellular Injury Irreversible Tissue Injury Death

Non-Progressive Stage, Progressive Stage, Irreversible Stage


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TYPES OF SHOCK

Three Main Categories:

Cardiogenic,

Hypovolemic, and

Septic

Others:

Neurogenic Shock (anesthetic and spinal cord injury) & Anaphylactic Shock


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CARDIOGENIC SHOCK

Results From Severe Myocardial Failure Due to:

Intrinsic myocardial damage (myocardial infarction, ventricular

rupture, arrhythmia) Extrinsic Compression (cardiac tamponade)

Outflow Obstruction (pulmonary embolism)


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HYPOVOLEMIC SHOCK

Results From Loss of Blood or Plasma Volume:

- Hemorrhage

- Fluid Loss (severe burns, trauma, vomiting, diarrhea etc.)


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SEPTIC (ENDOTOXIC) SHOCK

Most common cause of death in ICUs in the US

Dissemination of infection into the vasculature

Caused by overwhelming systemic microbial infection, mostoften by Gram-negative infection (Endo-toxic Shock) but can

also occur with Gram-positive and fungal infections

Spread & expansion of localized infection (abscess, peritonitis,

pneumonia) into the blood stream.


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Pathogenesis Of Septic Shock

Endotoxins are bacterial wall lipopolysaccharides (LPS) whichconsists of a toxic fatty acid (Lipid A) core and a complexpolysaccharide coat (unique to each species). Gram-positivebacteria and fungi have analogus molecules.

High quantities of LPSp (TNF & IL-1 IL6 & IL8)-Systemic vasodilation (hypotension),

-Diminished cardiac contractility,

-Widespread endothelial injury and activation (SLA, ARDS, DAD),

-Activation of coagulation system (DIC)

Multi-organ system failure and death


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Effects of Shock on Tissues

Brain -- ischemic encephalopathy --> confusion, obtundation;

Heart -- subendocardial ischemia, infarction; contraction band

necrosis --> decreased output

Kidneys -- acute tubular necrosis --> oliguria, anuria and electrolytedisturbances

Lungs -- diffuse alveolar damage (DAD) --> adult respiratory

distress syndrome (ARDS) --> hypoxia

GI tract -- mucosal necrosis, hemorrhages Liver -- central necrosis, fatty change

Coagulation system -- disseminated intravascular coagulation (DIC)


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Morphology

of Shock


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Clinical Course of Shock

Hypotension

Weak, rapid pulse, tachycardia

Rapid shallow respiration Drowsiness, confusion & irritability

Cool, clammy skin

In septic shock the skin is initially warm and flushed

secondary to peripheral vasodilation

Multi-organ failure ensues if shock continues


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EDEMA


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EDEMA

Excess accumulation of fluid in the interstitial tissue spaces.Increased intracellular accumulation (edema) is generally termed as hydropic change.

Edema Fluid can be

A transudate (protein-poor fluid -specific gravity 1.020)


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SPECIAL TYPES OF EDEMA

Pleural effusion (hydro-thorax)

Pericardial effusion (hydro-pericardium) Ascites (edema in peritoneal cavity)

Anasarca (widespread edema)

Cerebral edema (in brain, intra- and extracellular)


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Normal Microcirculation

Capillary Arterial Venous

Hydrostatic Pressure + 36 + 16

Oncotic Pressure - 26 - 26

Net filtration Pressure + 10 mmHg - 9 mm Hg(leak-out) (Reabsorb)


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Homeostasis is maintained by the opposing effects of vascular

hydrostatic pressure and plasma colloid osmotic pressure


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Pathophysiologic Categories of Edema

I. Increased Hydrostatic Pressure

II. Reduced Plasma Osmotic PressureIII. Lymphatic Obstruction

IV. Sodium Retention

V. Inflammation


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Increased Hydrostatic Pressure

A. Congestive Heart Failure

B. Portal Hypertension

C. Venous Thrombosis


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Congestive Heart FailureInability ofHeart to Pump blood in systemic circulation

Blood backing up into the lungs

Blood backing up into the venous circulation

Increasing Central Venous Pressure (CVP)

Increased capillary pressure (Hydrostatic Pressure)

Edema

Cardiac Output Decreased Arterial blood volume Decrease Renal perfusion

Activates the Renal Defense Mechanisms

Renin-Angiotensin-Aldosterone Axis, Renal Vasoconstriction, Increased ADH


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Congestive Heart FailureRenin-Angiotensin-Aldosterone Axis

Renin AldosteroneRenal Na

reabsorption

Renal retention of

Na + H2O

Plasma volume

Transudation EDEMA

Decreased Renal Perfusion


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Congestive Heart FailureRenal Vasoconstriction

RenalVasoconstriction

GlomerularFiltrationRate (GFR)

Tubularreabsorption of

Na + H2O

Plasma volume

Transudation EDEMA


Renal retention of

Na + H2O


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Congestive Heart FailureAnti-Diuretic Hormone

Anti-DiureticHormone (ADH)

Renal retention ofH2O

Plasma volume

Transudation EDEMA


Renal retention of

Na + H2O


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Central

Venous

Pressure

Renal

Perfusion

Renin Renal

Vasoconstriction

ADH

Congestive Heart Failure


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Clinically initially cardiac edema can be demonstrated in legs or sacrum


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Portal Hypertension

Portal Hypertension is Increased resistance to portal blood flow The most common cause of Portal Hypertension is CIRRHOSIS

Results in Ascites

Pathogenesis of Ascites is complex Increased Portal Pressure (hydrostatic pressure) leads to increased liver sinusoidal

hypertension. Fluid moves into the Space of Disse then into lymphatics

The hepatic lymph percolates into the peritoneal cavity Normal thoracic duct lymph = 1 Liter/d

In cirrhosis, hepatic lymph flow far exceeds Thoracic duct capacity

Cirrhosis hypoalbuminemia decrease in plasma osmotic pressure ascites decrease in blood volume decreased renal perfusion secondary hyperaldosteronism(increased renin etc.)

AscitesAscites


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AscitesAscites


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Portal Hypertension

SinusoidalHypertension

Renal

Perfusion

Hepatic Lymph OverwhelmsThoracic Duct

Aldosterone

ASCITES

Cirrhosis

SerumAlbumin


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Venous Thrombosis

Impaired venous outflow increases hydrostatic pressure

Reduced Plasma Osmotic Pressure


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Reduced Plasma Osmotic Pressure

Albumin is the serum protein MOST responsible for the maintenance ofcolloid osmotic pressure.

A decrease in osmotic pressure can result from increased protein loss ordecreased protein synthesis

Increased albumin Loss: Nephrotic Syndrome

Increased protein permeability of the glomerular basement membrane

Protein losing gastroentropathy

Reduced albumin synthesis Cirrhosis

Protein malnutrition


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Inflammation

Both Acute and Chronic Inflammation are associated with Edema

Generalized edema in systemic infections, poisoning, certain drugs

& chemicals, anaphylactic reactions and anoxia

Localized edema in infections, allergic reactions, insect bite,

irritant drugs & chemical and Angioneurotic edema*

*It involves skin of face & trunk and may involve lips, larynx, pharynx, lung etc


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Angioedema


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Angioedema


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Elephantiasis


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Elephantiasis (filariasis)


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peau dorange appearance in breast cancer

S di & W t R t ti


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Sodium & Water Retention

Contributory factors in several forms of edema

Salt retention may be primary cause of edema

Post-streptococcal glomerulonephritis & Acute Renal failure

Increased salt with accompanying water cause increase hydrostatic pressure

and decreased vascular colloid osmotic pressure leading to edema


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EDEMA

INCREASED

HYDROSTATIC

PRESSURE

Congestive Heart Failure

Portal hypertension (Ascites)

Venous Obstruction

HEART

LIVER

KIDNEY

INFLAMMATION

Increased permeability

DECREASED

ONCOTIC

PRESSURE

Nephrotic SyndromeCirrhosis (Ascites)

Protein Malnutrition

LYMPHATICOBSTRUCTION

Inflammatory

NeoplasticSALT & WATER RETENTION


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GENERALIZED EDEMA

HEART

LIVER

KIDNEY

Edema Morphology


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Edema Morphology

Edema of the Subcutaneous Tissue is most easily detected Grossly (notmicroscopically)

Push your finger into it and a depression remains (pitting)

Swelling and wetness of the tissues

Subtle cell swelling with clearing and separation of extracellular elements

Dependent Edema is a prominent feature of Congestive Heart Failure (legs instanding & sacrum in recumbent position)

Periorbital edema is often the initial manifestation of Nephrotic Syndrome,later affecting all parts of body


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Pitting edema


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Pulmonary Edema

Pulmonary Edema is most frequently seen in Congestive Heart Failure (LVF)

May also be present in Mitral Stenosis, Cardiac Surgery, Renal failure,Adult Respiratory Distress Syndrome (ARDS), Pulmonary Infections,Inhalation of toxic substances, Aspiration, Radiation injury, Shock, Uremia,High altitude edema and Hypersensitivity reactions.

The Lungs are typically 2-3 times normal weight

Cross sectioning causes an outpouring of frothy, sometimes blood-tinged fluidrepresenting mixture of air, edema fluid & extravasated red cells

Microscopically alveolar capillaries are congested and there is collection ofeosinophilic, granular and pink proteinaceous material (edematous fluid) ininterstitial and alveolar spaces


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Pulmonary Edema

P l EdN l L


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Pulmonary EdemaNormal Lung


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Pulmonary Congestion

and Edema


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Edema of the Brain

Localized: Abscess, Neoplasm

Generalized: Encephalitis, Hypertensive crises, Obstruction of

venous outflow, Trauma

In Generalized edema brain is grossly swollen with narrowed

sulci and distended gyri showing flattening against skull

Vasogenic & Cytotoxic edema


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Brain edema

C i i C i


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Clinical Correlation

Subcutaneous Edema-Annoying but Points to Underlying Disease

However, it can impair wound healing or clearance of Infection

Pulmonary Edema-May cause death by interfering with Oxygen

and Carbon Dioxide exchange & Creates a favorable environmentforinfection

Edema of Brain-The big problem is: There is no place for the fluid togo! Herniation into the foramen magnum will kill or brain stemvascular supply can be compressed and damage vital centers

i & C i


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Hyperemia & Congestion

Increased volume of blood in an area compared to normal

HyperemiaH

yperemia is an active process resulting from augmented tissue inflowdue to arteriolar dilation (e.g. Acute inflammation, Exercising muscles,

Blushing, Sexual arousal)

Congestion

Congestion is a passive process resulting from impaired outflows from atissue (cardiac failure-systemic or venous obstruction-local)

Both can be Local or Diffuse

MORPHOLOGY OF HYPEREMIA &


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MORPHOLOGY OF HYPEREMIA &

CONGESTION

Hyperemia: tissue is red or purple, engorged with oxygenated blood,

swollen, often edematous. Examples- Lungs.

Congestion: tissue is blue-red in color due to accumulation of

deoxygenated hemoglobin in the affected tissues. Later on tissue becomes

brownish (iron deposition) & indurated (fibrosis).

Examples Liver, Legs, Lungs

PULMONARY CONGESTION


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Acute Pulmonary Congestion: engorged alveolar capillaries, alveolar septal edema, focal

minute intra-alveolar hemorrhage Chronic Pulmonary Congestion: thickened & fibrotic septa along with presence of

numerous hemosidrinladen macrophages (Heart Failure Cells)

HEPATIC CONGESTION

Acute Hepatic Congestion: central vein and sinusoids are distended with blood, centralhepatocytes may show degeneration & peripheral hepatocytes may develop fatty change

Chronic Passive Congestion of Liver: central regions of hepatic lobules are grossly red-brown, slightly depressed & surrounding uncongested zones reveal fatty change (nutmeg

liver). Microscopically there is centrilobular necrosis with hepatocyte drop out andhemorrhage & hemosidrin containing macrophages. Hepatic fibrosis (cardiac cirrhosis) may

be seen in heart failure.


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Hyperemia in Pneumonia

Hyperemia

Infection

(Pneumonia)


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Liver - Chronic Passive Congestion

Nutmeg Liver


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Nutmeg Liver

Cross Section of a NutmegNutmeg Liver


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Chronic Passive Congestion


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SIGNIFICANCE OF CONGESTION

If diffuse, usually indicates Heart failure;

If local, usually indicates a blockage upstream toward theheart;

Cirrhosis can cause Varices in esophagus

HEMORRHAGE


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HEMORRHAGE

Extravasation of blood due to rupture of blood vessels

Rupture of a large vessel: Trauma, Atherosclerosis, Inflammatory orNeoplastic Erosion

Rupture of small vessels: hemorrhagic diathesis

Hematoma is blood enclosed within tissue (red-blue blue-green golden brown)

Petechiae are minute (1-2 mm) hemorrhages into skin, mucous membranes

or serosal surfaces

Purpuras are larger (3-5 mm) hemorrhages

Ecchymoses are larger (1-2 cm) subcutaneous hematomas (bruises)

Hemothorax, Hemopericardium, Hemoperitonium and Hemoarthrosis are bleeding in one

or other body cavities.Hematochezia- bright red blood per rectum, Melena - dark black blood per rectum

Hematuria - blood, gross or microscopic in urine

Hemoptysis - coughing up of blood , Hematemesis - vomiting up of blood

CAUSES OF HEMORRHAGE


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CAUSES OF HEMORRHAGE

Trauma

Vascular diseases with rupture (atherosclerosis, arteritis,

aneurysms, etc.).

Low platelets (below 10-15,000/cu mm)

Coagulopathy (factors less than 10% activity)

Ulcers, tumors, coagulation factors, infarcts,

MORPHOLOGY OF HEMORRHAGE


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MORPHOLOGY OF HEMORRHAGE

Acute

Red or purple collection of blood in tissue

Chronic or old

Brown or maroon pasty material


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HemorrhageWhy do bruises change color

as they Resolve?

The RBCs in a hemorrhage are broken down:hemoglobin (red)pbilirubin (blue-green)p

hemosiderin (golden-brown)


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Clinical Effects of Hemorrhage


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Clinical Effects of Hemorrhage

20% blood loss hemorrhagic shock

Bleeding into the brainstem is fatal while same blood loss from a

finger cut is trivial

Chronic recurrent bleeding can lead iron deficiency anemia!


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Anemia from Blood Loss

This may be the only hint of Occult Cancer

Carcinoma of the Colon

Gastric Carcinoma (less common)

Documents

Hemodynamic Disorders 2007