exam 2 - intro to med (blood vessels)

circulatory system

blood vessels and heart

diseases of blood vessels and heart

• leading cause of morbidity and mortality

• account for more than 1/3 of death after birth

• impair the circulation of blood and delivery of oxygen and nutrients to tissues/organs → leads to decreased function of cells and organs

impaired perfusion

due to obstruction of blood vessels, rupture of blood vessels, or failure of the heart to pump blood

“cardiovascular disease” is an umbrella term for:

stroke, myocardial infarct, and atherosclerotic diseases of heart or blood vessels (arteries)

arteries

• blood vessels that carry blood AWAY from the heart TOWARDS the peripheral tissues

• normally carry OXYGEN-RICH BLOOD

• thick walls and elastic

veins

• blood vessels that carry blood TOWARDS the heart

• normally carry oxygen poor (DEOXYGENATED) blood

• thick walls NOT elastic

pulmonary arteries

• thick wall blood vessels

• carry OXYGEN-POOR blood

• venous blood

pulmonary veins

• thin wall vessel

• carry OXYGEN-RICH blood

blood vessels have 3 layers:

• intima (inner layer)

• media

• adventitia (outside layer)

superior vena cava

• collects blood from the upper body

• goes to the right atrium

inferior vena cava

• collects blood from the lower body

• goes to the right atrium

aorta

• exits the left ventricle

• supplies different blood vessels

ABC’s of the aortic vessels

• A = aorta

• B = brachiocephalic trunk

• C = carotid artery (left)

• S = subclavian artery (left)

brachiocephalic trunk

• supplies the right arm (subclavian) and right side of brain and face (carotid)

coronary arteries

how the heart is supplied with blood

coronary sinus

collects venous blood and transports it to the ventricle

circumplex artery

goes around the heart and supplies the back

edema

abnormal accumulation of fluid in interstitial tissues or tissue space

hemorrhage

• undesired loss of blood

• can be acute or chronic (internal bleeding)

• due to the rupture or injury of a blood vessel

• may be external, internal, or into tissues (hematoma)

• less than 20% can be tolerated in adults, but now in small children

• bleeds outside = not dangerous; bleeds inside = DANGEROUS

thrombosis

occlusion of blood vessels by local blood clot

types of thrombosis

• venous thrombosis (deep venous thrombosis = DVT) → can develop to pulmonary embolism

• arterial thrombosis (stroke, MI)

embolism

• blockage of a blood vessel by circulating blood clot

• can be due to: fat, air, and amniotic fluid embolism’s

types of embolisms

• venous thrombus

• arterial thrombus

venous thrombus

• (right side of the heart) will end up in the lungs (pulmonary arteries) and lead to pulmonary embolism

• makes it to the heart and leaves the heart through pulmonary arteries and into the lungs

• BIG = gets stuck and will cut off blood and oxygen supply

arterial thrombus

(left side of the heart) can result in arterial thrombosis anywhere in the body

• can go anywhere (up or down)

• can form a stroke in many places

infarction

tissue necrosis due to occlusion of arterial blood supply leading to tissue ischemia

shock

dramatic drop in blood pressure leading to hypoperfusion (not enough blood supply in an organ) of vital tissues

edema in body cavities

• hydrothorax = chest

• ascites = abdomen

• Hydropericardium = heart

factors that lead to edema

• inflammation

• salt retention

• increased hydrostatic pressure

• reduced plasma oncotic pressure

• lymphatic obstruction

lymphatic obstruction

removal of lymph nodes → edema

reduced plasma oncotic pressure

fluid leaves blood vessels

pitting edema

present when a depression remains upon pressure

lymphedema

• “non-pitting”

• will not dent when finger is pressed on skin

ascites

fluid in the stomach

hemorrhage types

• petechiae

• purpura

• ecchymosis (bruise)

• bleedings in body cavities

petechiae

• very small, 1-2 mm

• hemorrhage in skin and mucous surface

• cause: low platelet counts, platelet defects, some milder clotting factor deficiencies, increased blood pressure

purpura

• > 3 mm

• cause: low platelet counts, platelet defects, some milder clotting factor deficiencies, increased blood pressure

• vascular inflammation (vasculitis)

• increased fragility of vessels

• can be slightly raised

• thrombocytopenic purpura

ecchymosis (bruise)

• > 1cm

• bleeding into tissues (subcutaneous)

• after injury

• bleeding disorders

bleeding in body cavities

• hemothorax (chest)

• hemopericardium (heart)

• hemoperitoneum (abdomen)

• hemarthrosis (bleeding into joints)

hematoma

• pocket full of blood

• often pain or tenderness

• can be external or internal

• can be felt when touched

ecchymosis

• cannot be felt

• not painful or tender

hemostasis

normal mechanism of how bleeding is terminated

primary hemostasis

platelets bind to damaged/inflamed vessel wall and form a platelet plug (occurs in seconds)

secondary hemostasis

coagulation cascade forms a fibrin clot that stabilizes (“cements”) the platelet plug (may take minutes)

thrombosis

undesired activation of the coagulation system that leads to the occlusion of vessels and hypoperfusion

important factors that contribute to blood coagulation

• blood vessels: contract

• blood platelets: form a blob

• the coagulation system: glues the platelets in place

sequence of events (blood coagulation)

• after injury arteries initially constrict

• the injury to blood vessels exposes extracellular matrix and tissue factors that activate blood coagulation

• platelets adhere to site of injury and become activated and release granules that activate even more platelets

• fibrin is produced by the coagulation cascade and stabilizes the platelet thrombus

most important factor of coagulation cascade

factor 10 (Xa)

coagulation pathways

• tissue factor TRIGGERS coagulation

• contact activation SUSTAINS coagulation

tissue factor pathway

• “jump starts” coagulation

• primary job is to generate “thrombin burst”

• tested by the PT test = prothrombin time

what inhibits vitamin K dependent factors (II, VII, IX, X)

coumadin

contact activation pathway

• activated by thrombin

• tested by PTT (aPTT) = activated partial thromboplastin time

hemophilia A

deficiency of factor VIII

hemophilia B

factor IX

hemophilia lab tests

• aPTT prolonged

• PT normal

• platelets normal

• bleeding time normal

• factor VIII or IX reduced

aPTT prolonged

measures contact activation (factor 8 or 9)

PT normal

measures tissue factor

thrombus

• intravascular blood clot

• may form in veins, arteries, or the heart

• thrombi (plural)

three main factors that contribute to thrombus formation (virchow’s triad)

• stasis of the blood flow (creates turbulence)

• endothelial injury (artherosclerosis, inflammation, smoking/nicotine)

• blood hypercoagulability

stasis of the blood flow

• platelets are forced against blood vessel walls and in contact with endothelium which may activate them

• anti-clotting factors are diluted and endothelial cells activated

• forces platelets outside its normal location

endothelial injury

• more important for thrombus in the arterial system

• exposure of extracellular matrix activated platelets and clotting system

blood hypercoagulability

• genetic or acquired

• elevated prothrombin

• autoimmune diseases like SLE can produce antibodies against anti-coagulation factors

risk factors for thrombosis/embolism

• prolonged bed rest or immobility

• status after surgery, fracture, burns

• underlying conditions (age + smoking + sitting in the same position)

DVT clinically

swelling, pain, redness

DVT diagnostic

• ultrasound

• elevated D-dimers levels (>300 ng/mL)

• intravenous venography

• negative D-dimers rule out thrombosis

what are D-dimers

fibrin breakdown products created by plasmin digesting blood clots

DVT therapy

• short term: heparin (PTT test)

• long term: warfarin (coumadin- PT test)

• thrombolysis: extreme situations

• PREVENTION: MOVE AROUND

pulmonary embolus

• blood clot from DVT dislodges and ends up in the lungs

• major artery in the lungs is occluded: pulmonary trunk, pulmonary arteries

pulmonary embolus (clinically)

• sudden onset of shortness of breath (dyspnea)

• chest pain

• rapid breathing (tachypnea)

• tachycardia

• dizziness

• cyanosis (blue skin tint)

pulmonary embolus (diagnosis)

• pulse oximetry, chest X-ray

• CT scan

• ventilation-perfusion scan (V/Q scan)

• ECG

• echocardiography

• blood tests

pulmonary embolus (treratment)

• thrombolysis

• oxygen

• analgesia

• anticoagulation

• surgical removal of embolus

most important cause for thrombus formation (arterial thrombus/embolus)

atherosclerosis of arterial blood vessels

ischemic necrosis

tissue death due to infarction

causes of infarction

• thrombosis

• embolus

• twisting of vessels

• entrapment of a vessel

infarction symptoms

depend of the tissue and its blood supply

• MI

• bowel infarction

• gangrene of a limb

• stroke

infarction

death of tissue due to lack of blood supply

anemic (white) infarct

arterial occlusion of organs that have only one arterial supply (heart, kidney, spleen)

hemorrhagic (red) infarct

tissue is infarcted and then blood flows back in from another artery that supplies this tissue

atherosclerosis

is a form of arteriosclerosis

arteriosclerosis

hardening of arteries

three main types of arteriosclerosis

• atherosclerosis

• arteriolosclerosis

• monckeberg’s medial calcific sclerosis

Atherosclerosis

• most frequent form of arteriosclerosis

• hardening of arteries due to atheromatous plaques

monckeberg’s medial calcific sclerosis

calcium deposits in muscular arteries

arteriolosclerosis

• affects small arteries

• thickening of the walls found in diabetes and hypertension

fat embolism

• microscopic emboli of fat droplets after fracture of large bones

• fat obstructs/inflames blood vessels, veins, arteries, capillaries

air embolism

• most common

• arteries or veins

• during surgical procedures, chest wall injury

• decompression injury after diving = nitrogen bubbles in the blood

amniotic fluid embolism

• cause: amniotic fluid or fetal tissue enters into maternal blood circulation due to rupture of uterine veins or tear in placental membranes

• complication of labor or immediate postpartum

epidural hematoma

bleeding between skull and dura mater; typically arteries

• pushes the brain to the side

• arterial blood

subdural hematoma

bleeding between dura mater and arachnoid mater; typically veins

• bleeds much slower

• venous blood

clinical presentation of epidural hematoma

initial loss of consciousness → lucid interval (patient is like normal) → followed by decline in mental status