Hemodynamic Disorders

•Hemodynamic Disorders

•Thromboembolic Disease

•Shock

Overview• Edema (increased fluid in the ECF)• Hyperemia (INCREASED flow)• Congestion (INCREASED backup)• Hemorrhage (extravasation)• Hemostasis (keeping blood as a fluid)• Thrombosis (clotting blood)• Embolism (downstream travel of a clot)• Infarction (death of tissues w/o blood)• Shock (circulatory failure/collapse)

WATER• 60% of body• 2/3 of body water is INTRA-cellular• The rest is INTERSTITIAL• Only 5% is INTRA-vascular

EDEMA is SHIFT to the INTERSTITIAL SPACE• HYDRO-

– -THORAX, -PERICARDIUM, -PERITONUM,(ASCITES)– ( EFFUSIONS),

• ANASARCA(total body edema)

Fluid HomeostasisStarling’s Law

Homeostasis is maintained by the opposing effects of:

• Vascular Hydrostatic Pressure – and

• Plasma Colloid Osmotic Pressure

EDEMA

Increased hydrostatic pressure: – Impaired venous return – Congestive heart failure (poor right ventricular function) – Constrictive pericarditis – Ascites (peritoneal dropsy; e.g. from liver cirrhosis) – Venous obstruction or compression (thrombosis, external pressure, dependency of lower limbs)

Arteriolar dilation (heat; neurohumoral dysregulation)

Reduced plasma osmotic pressure (hypoproteinemia) – Nephrotic syndrome (protein-losing glomerulopathies) – Liver cirrhosis (ascites) – Malnutrition – Protein-losing gastroenteropathy

Increased fluid in the interstitial tissue spaces or body cavities.

Lymphatic obstruction – Interstitial fluids are removed via lymphatic drainage, to thoracic duct and left subclavian vein – Inflammation, neoplasm, surgery, irradiation

Sodium retention (water follows sodium) – Excess salt intake with renal insufficiency – Increased tubular reabsorption of sodium (renal hypoperfusion-- increased renin-angiotensin-aldosterone secretion) Inflammation (acute, chronic, angiogenesis)

CHF EDEMA

• INCREASED VENOUS PRESSURE DUE TO FAILURE

• DECREASED RENAL PERFUSION, triggering of RENIN-ANGIOTENSION-ALDOSTERONE complex, resulting ultimately in SODIUM RETENTION

HEPATIC ASCITES• PORTAL HYPERTENSION• HYPOALBUMINEMIA

RENAL EDEMA• SODIUM RETENTION

• PROTEIN LOSING GLOMERULOPATHIES (NEPHROTIC SYNDROME)

Transudate vs Exudate• Transudate

– results from disturbance of Starling forces– specific gravity < 1.012– protein content < 3 g/dl,

• Exudate– results from damage to the capillary wall– specific gravity > 1.012– protein content > 3 g/dl,

GENERALIZED EDEMA• HEART• LIVER• KIDNEY

Dependent Edema is a prominent feature of Congestive Heart Failure; in legs if standing or sacrum in sleeping patient

Periorbital edema is often the initial manifestation of Nephrotic Syndrome, while late cases will lead to generalized edema.

Pulmonary Edema

• is most frequently seen in Congestive Heart Failure– May also be present in renal failure, adult

respiratory distress syndrome (ARDS), pulmonary infections and hypersensitivity reactions

Pulmonary Edema• The Lungs are typically

2-3 times normal weight

• Cross sectioning causes an outpouring of frothy, sometimes blood-tinged fluid

• It may interfere with pulmonary

function

Pulmonary edema

Brain Edema• Trauma, Abscess, Neoplasm, Infection (Encephalitis due

to say… West Nile Virus), etc

The surface of the brain with cerebral edema demonstrates widened gyri with a flattened surface. The sulci are narrowed

Brain Edema

Clinical Correlation The big problem is: There is no place for the fluid to go!

• Herniation into the

foramen magnum will kill

SHOCK• Definition: CARDIOVASCULAR COLLAPSE• Common pathophysiologic features:

– INADEQUATE CARDIAC OUTPUT and/or– INADEQUATE BLOOD VOLUME

• Pathogenesis–Cardiac–Septic–Hypovolemic

GENERAL RESULTS• INADEQUATE TISSUE PERFUSION• CELLULAR HYPOXIA• UN-corrected, a FATAL outcome TYPES of SHOCK• CARDIOGENIC: (Acute, Chronic Heart Failure)

• HYPOVOLEMIC: (Hemorrhage or Leakage)

• SEPTIC: (“ENDOTOXIC” shock, #1 killer in ICU)

• NEUROGENIC: (loss of vascular tone)• ANAPHYLACTIC: (IgE mediated systemic vasodilation and increased

vascular permeability)

CARDIOGENIC shock• MI• VENTRICULAR RUPTURE• ARRHYTHMIA• CARDIAC TAMPONADE• PULMONARY EMBOLISM (acute RIGHT heart

failure or “cor pulmonale”)

HYPOVOLEMIC shock• HEMORRHAGE, Vasc. compartmentH2O• VOMITING, Vasc. compartmentH2O• DIARRHEA, Vasc. compartmentH2O• BURNS, Vasc. compartmentH2O

SEPTIC shock• OVERWHELMING INFECTION• “ENDOTOXINS”, i.e., LPS (Usually Gm-)• Degraded bacterial cell wall products• Also called “LPS”, because they are Lipo-Poly-Saccharides• Attach to a cell surface antigen known as CD-14

• Gm+• FUNGAL• “SUPERANTIGENS”, (Superantigens are polyclonal T-lymphocyte activators

that induce systemic inflammatory cytokine cascades similar to those occurring downstream in septic shock, “toxic shock” antigents by staph are the prime example.)

Effects of LipopolysaccharideLPS = lipopolysaccharide

TNF = tumor necrosis factor

IL = interleukin

NO = nitric oxide

PAF = platelet-activating factor

SEPTIC shock events(linear sequence)

• SYSTEMIC VASODILATION (hypotension)

• ↓ MYOCARDIAL CONTRACTILITY• DIFFUSE ENDOTHELIAL ACTIVATION• LEUKOCYTE ADHESION• ALVEOLAR DAMAGE (ARDS)• DIC• VITAL ORGAN FAILURE CNS

NON-PROGRESSIVE• COMPENSATORY MECHANISMS• CATECHOLAMINES• VITAL ORGANS PERFUSED

PROGRESSIVE• HYPOPERFUSION• EARLY “VITAL” ORGAN FAILURE OLIGURIA

ACIDOSIS IRREVERSIBLE• HEMODYNAMIC CORRECTIONS of no use

CLINICAL STAGES of shock

Morphologic Features of Shock• Brain: ischemic encephalopathy• lung :DAD (Diffuse Alveolar Damage,)• Heart: subendocardial hemorrhages and

necrosis• Kidneys: acute tubular necrosis or diffuse

cortical necrosis• Gastrointestinal tract: patchy hemorrhages and

necrosis• Liver: fatty change or central hemorrhagic

necrosis• DIC• MULTIPLE ORGAN FAILURE

CLINICAL PROGRESSIONof SYMPTOMS(linear sequence)• Hypotension • Tachycardia • Tachypnea • Warm skin Cool skin Cyanosis• Renal insufficiency• Obtundance• Death

Embolism • Embolism refers to the transport of an

intravascular solid, liquid or gaseous mass in the blood – to a site distal to its point of origin.

• Thromboembolism refers to the transport of a thrombus; The thrombus becomes a thromboembolus.

• At least 90% of all emboli are thromboemboli.• Emboli eventually cause some kind of

downstream vascular obstruction and this is their clinical significance.

• Embolism is a cause of sudden death.

Types of Embolism

• Thromboembolism (most common)• Fat embolism• Amniotic fluid embolism• Gas embolism• Cholesterol embolism• Septic embolism• Foreign body embolism• Bone marrow embolism

SOURCES AND EFFECTS OF VENOUS EMBOLI

SOURCES OF ARTERIAL EMBOLI

PULMONARY THROMBOEMBOLISM• The commonest type of thromboembolism• A common complication in hospitalized patients, especially in post

operative and chronic bedridden settings.• The most common source is the deep leg veins.• Large thromboemboli can obstruct the bifurcation of the main pulmonary

artery (saddle embolus) causing sudden death.• Small PTE obstruct distal (small) arteries and are often clinically silent. • Medium-sized PTE may also cause death or cardiovascular collapse. • Progressive obstruction of the distal pulmonary bed by small TE may lead to

pulmonary arterial hypertension.• Most non-fatal TE do not cause pulmonary infarcts because of the dual lung

circulation; Infarcts are more likely to occur when there is a co-morbidity such as heart failure or COPD.

THROMBOEMBOLUS BLOCKING PULMONARY ARTERY

R Ventricle Embolus from Leg Vein

SYSTEMIC (ARTERIAL) THROMBOEMBOLISM

• Refers to TE traveling in the systemic arterial circulation.

• About 80% arise from intracardiac mural thrombi.

• About 2/3s are associated with left ventricular infarcts.

• The remainder arise from ulcerated atherosclerotic plaques with or without attached mural thrombi, including from mural thrombi lining aortic aneurysms.

• A relatively small number arise from thrombotic lesions on cardiac valves (vegetations).

• Arterial thromboemboli impact in downstream arterial beds, such as cerebral, splenic, renal, intestinal or distal limb beds - causing infarcts in most cases.

• The most common sites are the lower extremity (75%) and the brain (10%).

Fat Embolism

• Minute globules of fat can often be demonstrated in the circulation following fractures of the shafts of long bones (which have fatty marrows) and, rarely, with soft tissue trauma and burns

• Traumatic fat embolism can be demonstrated anatomically in approximately 90% of individuals who sustain severe skeletal injuries, only about 1% of these individuals manifest clinical signs or symptoms known as fat embolism syndrome

Fat Embolism Syndrome• Is characterized by pulmonary insufficiency,

neurologic symptoms, anemia, and thrombocytopenia. Typically, the symptoms appear after a latent period of 24 to 72 hours after injury.

• There is the sudden onset of tachypnea, dyspnea, and tachycardia. Neurologic symptoms include irritability and restlessness, which progress to delirium or coma. Petechial skin rash is common.

• The fat embolism syndrome is fatal in about 10% of cases.

Fat Embolus to Lung

Air Embolism• Bubbles of air or gas within the circulation obstruct

vascular flow and damage tissues just as as thrombotic masses

• The injury is referred to as barotrauma • Air or gas may gain access to the circulation• (1) during delivery or abortion when it is forced into

ruptured uterine venous sinuses by the powerful contractions of the uterus,

• (2) during the performance of a pneumothorax when a large artery or vein is ruptured or entered accidentally,

• (3) when injury to the lung or the chest wall opens a large vein and permits the entrance of air during the negative pressure phase of inspiration.

• Large quantities of air, about 100 cc, are required to produce problems.

• A specialized form of gas embolism known as decompression sickness occurs in persons exposed to sudden changes in atmospheric pressure

• scuba and deep sea divers• When the gas is breathed under high pressure, increased amounts

dissolve in the blood, tissue fluids, and fat. • If the individual decompresses too rapidly, the gases come out of solution

as minute bubbles.• The acute form is commonly known as “the bends” or “the chokes.” The

acute obstruction of small blood vessels in and around the joints and skeletal muscles causes severe pain; a similar process may produce acute respiratory distress, while involvement of the cerebral vessels may lead to coma and sometimes death

• The chronic form of decompression sickness is more properly referred to Caisson Disease. Here, the presumed persistence of gaseous emboli leads to multiple foci of ischemic necrosis throughout the skeletal system

Amniotic Fluid Embolism• An extreme complication usually of labor and the

immediate postpartum period is a major cause of maternal mortality

• Uncommon, (1 per 50,000 deliveries), but has a mortality rate of 86%.

• The clinical presentation is striking: suddenly and without warning, profound respiratory difficulty with deep cynanosis and cardiovascular shock appear, followed rapidly in some cases by clonic-tonic convulsions and profound coma.

• The underlying cause is the infusion of amniotic fluid with all of its contents into the maternal circulation following a tear in the placental membranes and rupture of uterine and/or cervical veins

HEMORRHAGE• EXTRAVASATION beyond vessel• “HEMORRHAGIC DIATHESIS”• HEMATOMA (implies MASS effect)• “DISSECTION”• PETECHIAE (1-2mm) (PLATELETS)• PURPURA <1cm• ECCHYMOSES >1cm (BRUISE)• HEMO-: -thorax, -pericardium, -peritoneum, HEMARTHROSIS

• ACUTE, CHRONIC

EVOLUTION of HEMORRHAGE

• ACUTE CHRONIC• PURPLE GREEN BROWN• HGB BILIRUBIN HEMOSIDERIN

Hemorrhage Ruptured vessels, usually from trauma or infection or

atherosclerosis – Can lose 20% of blood volume (more if slow lose) with little effect on health – Great blood loss >> hypovolemic shock (hemorrhagic shock)

Hemorrhagic diathesis: tendency to bleed with minor injury

Hematoma: localized pool of blood outside vessels (e.g. bruise) – If severe: death from blood loss (e.g. dissecting aortic aneurysm)

Hemorrhage (Haemorrhage) Rupture of Blood Vessels

TermTerm DescriptionDescription Main Cause(s)Main Cause(s)

PurpuraPurpura(2-10mm)(2-10mm)

Focal hemorrhage Focal hemorrhage (submucosal, etc.)(submucosal, etc.) Vessel fragilityVessel fragility

PetechiaePetechiae(1-2 mm)(1-2 mm)

Focal hemorrhageFocal hemorrhage(submucosal, etc.)(submucosal, etc.)

Increased pressure, small Increased pressure, small vessel disease platelet vessel disease platelet no.&function defects.no.&function defects.

EcchymosisEcchymosis Widespread surface Widespread surface petechiaepetechiae Same as aboveSame as above

PurpuraPurpuraColonic PetechiaeColonic Petechiae

Telangiectasia(Blood in Vessels)

ThrombocytopeniaThrombocytopeniaIdiopathic Thrombocytopenic PurpuraIdiopathic Thrombocytopenic Purpura