Test 1

Chapter 17-20

Prefixes and Suffix for Blood

• Prefixes

  • “heme-”

  • “hemo-”

• Suffix

  • “-emia”

Functions of blood

1. Transport

   1. Oxygen and nutrient delivery to tissues

   2. Waste removal from tissues

   3. Hormone transport from endocrine organ to target organs

2. Maintenance

   1. Body temperature

   2. pH

   3. Fluid Volume

3. Protection

   1. Blood clotting

   2. Infection

Waste products removed by blood

• CO₂

• _{Nitrogenous Waste}

  • Uric Acid

  • Urea

How does blood function to maintain body temperature?

• Blood is mostly water, water absorbs heat

• Moves blood

  • Closer to skin if hot (heat radiates)

  • Deeper if cold (less heat lost and preserves vital organs)

Bloods maintenance of fluid volume

• effects blood pressure

• maintain correct amount of fluid in tissues

  • Abnormal increase of fluids in tissues = edema

Characteristics of Blood

• Scarlet to dark red in color

  • Can vary due to amount of oxygen

• Total amount: 5.25L (in an average 150lb-180lb person)

• pH range: 7.35-7.45

  • Considered neutral range for blood (even though its slightly basic)

  • Maintained by urinary system and lungs

• Viscous due to erythrocytes

  • Blood is thicker than water

Which drop of blood has more oxygen?

• The lighter one on the left

• the darker the color the less oxygen

Blood Composition

• Blood Plasma

• Blood Cells

  • Erythrocytes (RBC)

  • Leukocytes (white blood cells)

  • Thrombocyte (platelets)

Blood Plasma

• Fluid (non-living) portion of blood

• When blood is centrifuged, it is the clearish yellow portion

• Composition

  • 90% water

  • 6 solutes found in plasma

    • Electrolytes

    • Nitrogenous substance (urea, uric acid, etc)

    • Organic nutrients (glucose, amino acids, triglycerides, etc.)

    • Respiratory gases

    • Hormones

    • Plasma proteins

    • Every night owl really hates possums

Plasma Proteins

• huge compared to other solutes in plasma

• make up most of the mass of plasma

• Most produced by liver

• Several types of plasma proteins

  • Albumin

  • Fibrinogen

  • Globulins

Albumin

• specific type of plasma protein

• major transport protein of blood and contributes to water content in blood

  • attracts water

What would happen to water content of the blood plasma if albumin were absent?

• decrease in blood volume blood pressure would decrease

• cause H₂O to leave blood and fallow the high salt concentration into tissues

Fibrinogen

• specific type plasma proteins

• soluble protein that functions in blood clotting

Globulins

• general class of plasma proteins

• transport proteins, antibodies (immune defense), etc

What do all blood cells have in common

• short-lived

• non-mitotic

Types of blood cells

1. Erythrocytes (red blood cells)

   • Transports oxygen

   • False cells: no nucleus therefore no mitosis

2. Leukocytes (white blood cells)

   • Protection and defense

3. Thrombocytes (platelets)

   • Blood clotting

   • False cells: no nucleus therefore no mitosis

Hematocrit

• portion of total blood volume made up by erythrocytes

  • composition of blood that is only red blood cells

• Males ~ 47%

• Females ~ 42%

• If too low will lead to hypoxia and anemia

Hematopoiesis

• production of blood cells (all 3 types) in red bone marrow

• All blood cells arise from hematopoietic stem cell (hemocytoblast)

  • Hematopoietic stem cells eventually become ”committed” to forming a certain type of blood cell

    • Once committed, the cell cannot become any other cell type

• Red marrow produces billions of new blood cells per day!!

• Fairly efficient

Erythrocytes

• RBCs

• Blood cell type responsible for respiratory gas transport

• Nuclei and most organelles removed during cell development

  • Increase the open space for hemoglobin to filled

Features that make erythrocytes ideal for gas exchange

1. Large surface area relative to volume

   • Oxygen has to cross the membrane

   • Gives more space for oxygen to cress

2. Flattened disc-shape

   • Oxygen closer to the membrane to leave

3. Anaerobic mechanism of energy production by RBC

   • RBCs use glycolysis

   • Do not use any of the oxygen they carry

Hemoglobin

• Hb

• Protein responsible for O2 transport in blood

• Is composed of heme pigment bound to globin protein

  • A globin protein is made up of 2 alpha chains and 2 beta chains

    • Each chain binds to 1 heme group

  • Each heme group has Fe+ ion at center

    • Each Fe+ can bind one molecule O2

• 1 hemoglobin can bind to 4 oxygen molecules

  • 250 million hemoglobin in 1 RBC = 1 billion oxygen molecules

• Bind and breaks free of oxygen very easily allowing easily oxygen transfer to and from tissues

Erythropoiesis

• the production of red blood cells

• Hematopoietic stem cell “commits” to a proerythroblast

• Strictly regulated process

Steps of erythropoiesis

1. Starts with stem cell (Hematopoietic stem cell/hemocytoblast)

2. Commits/differentiates (Proerythroblast)

3. Developmental pathway

4. Becomes Erythrocyte

• has nucleus for a lot of the steps

  • nucleus directs development and differentiation

  • kicks out nucleus at end of developmental pathway

How is erythropoiesis controlled

• Hormonal control

  1. Erythropoietin

  2. Testosterone

• Dietary needs must be met also

Erythropoietin affect on erythropoiesis

• EPO

• directly stimulates erythrocyte production

• produced and released by kidneys

• only simulates cells already committed to becoming erythrocytes

• small amount almost always present in blood to set basal rate of production

  • increase of EPO is negative feedback mechanism

    • excessive oxygen supply suppresses EPO release

Testosterone affect on erythropoiesis

• enhances production of EPO

• Males generally have more erythrocytes and Hb than females

  • Helps males be better athletes with more oxygen to expend

Dietary needs for normal erythrocyte production

• General nutrients: amino acids, lipids, carbohydrates necessary for cell synthesis

• B-complex vitamins: B12 and folic acid

  • Necessary for normal DNA synthesis

• Iron

  • 65% of body’s iron supply is in Hb

    • Remainder stored in liver, spleen, etc.

  • “Free” iron bound to protein transferrin—erythrocyte takes up iron as needed

    • Iron cannot circulate on its own and unbound

    • Iron is toxic in high amounts

Death of Erythrocytes

• Average lifespan: ~120 days

  • Over time, Hb begins to degenerate & RBC becomes less flexible

• Macrophages engulf & destroy cell

  • Heme group splits free from globin protein

    • Heme broken down to bilirubin in the liver & excreted to intestines → leaves body in feces

    • Globin proteins broken down to amino acids & released to circulation

• Fe²⁺ saved for reuse

  • temporarily bonds to transferrin

Why do RBCs need to be flexible

• blood vessels can be very tiny

  • need to be able to fold in half to fit

• if cannot fold are more likely to block blood flow

Bilirubin

• substance created by the break down of heme from erythrocytes destroyed by macrophages

• produced in liver and excreted to intestines

• leaves body in feces, gives the brown color

Homeostatic Imbalances of erythrocytes

1. anemia

   • too few erythrocytes

2. polycythemia

   • too many erythrocytes

Anemia

• insufficient oxygen supply to meet body needs

• not really disease or disorder…more a symptom

• Symptoms: paleness, cold, short-of-breathe, tired

Causes of Anemia

1. Blood loss (hemorrhage)

   • Acute hemorrhagic anemia: severe, swift blood loss (bleeding to death, requires blood transfusion)

   • Chronic hemorrhagic anemia: slow, persistent blood loss (long term, usually internal)

     • Ex: ulcer bleeding, hemorrhoids

2. Inadequate erythrocyte production

   • iron-deficiency anemia (nutritional origins - usually due to diet)

   • renal anemia - kidney failure (little/no EPO release)

3. Excessive erythrocyte destruction/deformation

   • autoimmune

   • Ex: sickle-cell anemia

Sickle-cell anemia

• erythrocyte deformation

• genetic condition

• single point mutation

  • change in confirmation of protein

    • different shape and less flexible

    • pulls on cell membrane

• Hypoxic condition

• Circulation problems

• Can hook together

  • Forming clots

• Symptoms: pale, short of breath, pain (not enough blood blow), cold hands and feet

• No cure, treat symptoms

  • Nitroxide

  • dilate vessels for easier blood flow

Polycythemia

• increased number of erythrocytes

• blood is thicker

  • harder to pump → heart works harder

  • increased blood pressure

  • increased risk of heart diseases and heart attack

• Types

  • Polycythemia vera

  • secondary polycythemia

  • temporary polycythemia - blood doping

Polycythemia vera

• hematocrit level ~80% (almost double - blood is practically sludge)

• blood volume doubles - vascular system engorges with blood and impairs circulation

• effects

  • increased blood pressure

  • increased risk of heart attack

  • increased risk of stroke

  • increased risk of kidney issues

• treatment

  • therapeutic phlebotomy (routinely get blood drawn/removed)

  • chemotherapy drugs to kill RBCs

  • Aspirin

Secondary Polycythemia

• Increased EPO release due to low oxygen availability

• Caused by: high altitude living, etc.

• composition increases to 50% because of less oxygen being available

• will take care of itself if individual moves to lower elevation

Temporary Polycythemia - blood doping

• Individuals (usually professional athletes) inject synthetic EPO/oxygen carriers or use of blood transfusions

  • autologous transfusion (from same individual) harder to trace

• Risks: stroke, heart failure

Body compensating for blood loss

• Body compensates for blood loss 2 ways:

  1. Decreasing blood volume to injured blood vessel(s)

     • rapid constriction

  2. Increasing red blood cell production by red bone marrow

     • kidneys stimulated to release increased amounts of erythropoietin

  • Only for regular scraps and cuts

• The body can only compensate so much

  • Losing 15-30% total blood volume leads to weakness

    • slow and sluggish and tired

    • decreased nervous system

  • 30%+ loss leads to severe shock (possibly death ← Hypovolemic shock)

    • Organs (BRAIN) are not getting oxygen

    • Blood pressure drops, blood flow slows and eventually stops

• Whole blood transfusions are rare

  • More often, red cell transfusions are used

Blood transfusion

• not 1 size fits all

• Erythrocytes have very specific extracellular markers called antigens

  • ABO antigens, Rh antigens, etc. etc.

  • allows our immune systems to identify our cells as us

  • more than 20 to 30 types of antigens but most are very rare or benign

• Transfusions between two people with different antigens usually cannot occur

• Medical field is mostly concerned with ABO Blood groups & Rh Blood groups

  • generally strongest immune response if mismatched

ABO Blood Groups

• Blood type A: have “A” antigen

• Blood type B: have “B” antigen

• Blood type O: do not have any antigen

• Blood type AB: have “A” and “B” antigen

Agglutinins

• immune system antibodies that will attack mismatched blood cells

  • work as red flags

• Person with Type A blood has anti-B antibodies

• Person with Type B blood has anti-A antibodies

• Person with Type AB blood has neither type of antibody

• Person with Type O blood has both anti-A and anti-B antibodies

• Donation rules

  • A can receive A, O

  • B can receive B, O

  • AB can receive A, B, AB, O

  • O can receive O

Rh Blood Groups

• Five antigens make up this blood group → C, D, E, c, and e

  • D antigen is Rh+

  • C, E, c, or e antigen is Rh-

• Donation rules

  • Rh- can only receive Rh-

  • Rh+ can receive Rh- and Rh+

• Blood types are identified as a combination of ABO blood groups and Rh blood groups

Blood acceptance practice

A- ←→ B-

A- ←→ A+

A- ←→ O-

A- ←→ AB-

• A- → B-

  • No: A blood can not be given to anti A

• A- ← B-

  • No: B blood can not be given to anti B

• A- → A+

  • Yes: A blood can be given to anti B, - can be given to +

• A- ← A+

  • No: A blood can be given to anti B but, + cannot be given to -

• A- → O-

  • No: A blood cannot be given to anti A anti B

• A- ← O-

  • Yes: O blood can be given to anti B, - can be given to -

• A- → AB-

  • Yes: A blood can be given to anti none, - can be given to -

• A- ← AB-

  • No: AB blood cannot be given to anti B

Transfusion Reaction

• Mismatching blood types can lead to transfusion reaction

• Antibodies attack “foreign” donor blood cells (immune system tries to kill what doesn’t belong)

  • Foreign erythrocytes are clumped together via agglutination → clumps of RBCs will ”clog” blood vessels

    • like shooting fish in a barrel

  • “Foreign” blood cells will eventually start to lyse → releases free hemoglobin to blood stream

    • Results: Free hemoglobin does not bind to oxygen outside of the cell, Decreased oxygen transport & hemoglobin causes damage to kidneys (clogs them)

Type O blood

• ”universal donor”

  • O- is the most universal

  • can donate to anyone

• Neither antigen is present on blood cell surface

• Most common

• Worst receiver, can only receive O

Type AB blood

• ”universal recipient”

  • AB+ is the most universal

  • can receive from anyone

• Neither antibody is present

• Least common

• Worst donor, can only donate to AB

Leukocytes

• White blood cells (WBCS)

• responsible for defending the body

Characteristics of Leukocytes

1. Not restricted to the blood vessels (can leave)

   • Use vessels as transport to various parts of the body

   • Can leave vessels via capillary walls

   • Uses blood as highway then squeezes through blood vessel wall straight to the infection or bacteria

     • This way can get to the problem before it infects the blood

2. Can be produced very quickly

   • the number in the body can double within 2-3 hours

   • Leukopoiesis is very fast

   • Prevents spread of infection

3. Average lifespan: 13-20 days

   • if used, lifespan is even shorter

   • many die in battle

Categories of leukocytes

• granulocytes

• agranulocytes

Granulocytes

• type of leukocytes

• spherical in shape, large, and packed with granules

  • granules full of different substances

• looks grainy under microscope

Types of granulocytes

1. Neutrophils (bacteria killer)

2. Eosinophils (parasite killer)

3. Basophils (have histamines)

Neutrophils

• Type of granulocyte

• bacteria killer

• 50-70% of total leukocyte population

• Chemically attracted to sites of inflammation - Chemotaxis

• granules contain defensins - antimicrobial protein

  • kill of bacteria by punching holes in membrane

    • water rushes into the cell, cell swells and burst open

• Can become phagocytic

  • breaks them down with digestive enzymes

Eosinophils

• Type of granulocyte

• Parasite killer (like worms ewwwww)

• 2-4% of leukocyte population

• lysosomes in cell contain digestive enzymes

  • Do not have enzyme that kills bacteria

  • digestive enzymes released will digest body wall of parasitic worms

    • only effects worms

Steps of getting infected by tapeworm

1. consume under cooked meat (eggs are in the meat)

2. eggs develop to larvae in lungs

3. coughs up the larvae and end up swallowing them

4. larvae go through digestive tract

5. hook on to the walls of small intestine

6. worms steal nutrients

Basophils

• Type of granulocyte

• 0.5-1% of leukocyte population

• have histamine-containing granules

  • Histamine release causes vasodilation & attracts other leukocytes to area

    • Tigger itch receptors

    • Blood vessels widen, so WBCs transport there faster

    • more WBCs better fight of illness

Explain how seasonal allergies work

• basophils are being dramatic

• think pollen will kill you

• has full histamine response

• itchy, red eyes, sneezing, puffy, etc

Agranulocytes

• Type of leukocytes

• lack visible granules

  • mainly just nucleus

Types of Agranulocytes

1. Lymphocytes

   1. T-lymphocytes

   2. B-lymphocytes

   3. Natural Killer cells

2. Monocytes

Lymphocytes

• Type of agranulocytes

• 25% of leukocyte population

• Hang out in lymphatic system

  • migrate into and out of blood continuously

• Types

  1. T-lymphocytes (T-cells)

  2. B-lymphocytes (B-cells)

  3. Natural Killer cells (NK)

• Between T-cells and NK cell about 12 types of cancer are killed in a person lifespan

T-lymphocytes

• T-cells

• act against virus-infected cells and tumor cells

  • specifically infected own body cells or cells that have grown into tumors

B-lymphocytes

• B-cells

• produce antibodies released into the blood

• attach as red flags to ID things that should be destroyed

Natural Killer Cells

• NK cells

• act against virus-infected cells and tumor cells

• same function as T-cells

Monocytes

• Type of agranulocytes

• 3-8% of leukocyte population

• Differentiate into macrophages as they leave bloodstream and enter damaged/infected tissue

• actively phagocytic

  • destroy bacteria, viruses, sources of chronic infection

• more or less specialized

Leukopoiesis

• production of leukocytes

• takes place in red bone marrow

• Stimulated by 2 chemical messengers

  • Interleukins

  • Colony-stimulating factors

    • e.g: erythropoietin

• Leukocyte differentiation

Leukocyte differentiation

• Hematopoietic stem cell can form either

  1. Myeloid stem cell

     • Commits to either myeloblast or monoblast

  2. Lymphoid stem cell

     • Commits to either B-lymphocyte or T-lymphocyte precursor cells

Steps of leukocyte differentiation

1. Start with Stem Cells - Hematopoietic stem cells (hemocytoblast)

2. Slightly differentiate - Myeloid stem cells or Lymphoid stem cells

3. Cells commits

   • Myeloid Stem Cells to Myeloblast or Monoblast

   • Lymphoid Stem Cells to B lymphocyte precursor or T lymphocyte precursor

4. Developmental Pathway

5. Final Stage

   • Granular leukocytes form from Myeloblast

     • Eosinophils

     • Basophils

     • Neutrophils

   • Agranular leukocytes form from Monoblasts, B lymphocyte precursors and T lymphocyte precursors

     • Monocytes

     • B lymphocytes

     • T lymphocytes

Homeostatic Imbalances of Leukocytes

1. Leukemia

Leukemia

• cancer resulting in over-production of abnormal leukocytes

• “Extra cells originate from single abnormal cell

• Abnormal leukocytes remain unspecialized, proliferate extensively

  • Cancerous leukocytes crowd red marrow & immature leukocytes flood bloodstream

    • Other blood cell types are crowded out of blood, resulting in anemia & bleeding problems

• Do not defend the body as they shouldinfection & hemorrhage occurs

Way Leukemia is named

• according to how fast cells proliferate and the type of cell involved

• Rate of proliferation:

  • Acute leukemia: derived from stem cells

    • Primarily affects children

    • Severe and progresses quickly

  • Chronic leukemia: derived from later cell stages

    • Primarily affects the elderly

    • Takes longer to progress

• Type of cell involved:

  • Myeloid leukemia: involves myeloid stem cell descendants

  • Lymphocyte leukemia: involves lymphocyte

Thrombocytes

• Fragments of large cells (megakaryocytes)

  • Megakaryocyte is fragmented into smaller platelet “cells”released to blood

• Average lifespan: about 10 days if unused (shorter if used)

• Function: Initiate blood clot formation after damage to blood vessel wall

  • When blood vessel wall is damaged/torn → platelets stick to each other & to injury site

  • With no damage → prostacyclin and nitric oxide prevent platelets from sticking together

    • Prevents unnecessary and unwanted blood clots

Platelet formation regulated by

• Hormone thrombopoietin

Steps of platelet formation

1. Start with stem cell - Hematopoietic stem cell (hemocytoblast)

2. Developmental pathway results in Megakaryocyte (stage IV)

3. Bits and pieces breakoff - Platelets

Hemostasis

• blood clotting

• the process by which bleeding is stopped after blood vessel rupture occurs

• very very highly localized response that progresses very quickly

Steps of Hemostasis

1. vascular spasm

2. platelet plug formation

3. coagulation

Vascular Spasm

• first step of hemostasis

• rapid constriction of a damaged blood vessel

• Triggered by:

  1. injured smooth muscle tissue

  2. chemicals released by damaged cells in vessel wall (inflammation)

  3. reflexes from local pain receptors (pain indicates damage)

Platelet Plug Formation

• second step of hemostasis

• platelets stick to each other & to fibers in blood vessel wall to form a plug in a damaged blood vessel

• Platelets release the following in response to injury:

  1. ADP: causes more platelets to stick to site of injury

  2. Serotonin & thromboxane A₂: increase vascular spasm & platelet aggregation

• Platelet plugs are only good for general wear & tear and small injuries

  • Not particularly strong

  • Larger injuries require more severe mechanism to stop bleeding (i.e., coagulation)

Coagulation

• third step of hemostasis

• formation of a true blood clot

• The Process:

  1. Clotting factors (I-XIII) form prothrombin activator

     • Clotting factors produced by liver

     • All clotting factors needed for coagulation!

  2. Prothrombin activator catalyzes conversion of plasma protein prothrombin into active enzyme thrombin

  3. Thrombin catalyzes transformation of soluble clotting factor fibrinogen (soluble) into fibrin (insoluble) molecules

     • Fibrin molecules link together to form long, insoluble strands that stick together

       • Factor XIII: enzyme that binds fibrin strands to one another (making very strong mesh work)

     • Fibrin strands also trap platelets & RBCs → forming a blood clot

Blood Clot Retraction

• the process of pulling damaged edges of blood vessel close together

• Platelets in blood clot have contractile ability (much less than muscle tissue)

  • Contraction pulls fibrin strands together & pulls edges of injury closer together

    • easier to repair small area

Platelet-derived growth factor

• causes increase in number of fibroblasts and smooth muscle cells in damaged area

• Forms connective tissue that will eventually form new blood vessel wall where damaged occurred

Fibrinolysis

• the removal of blood clot after healing is complete

• prevents blood clots form on top of old blood clots

• Plasmin: enzyme that digests fibrin

• Typically begins within 2 days of clot formation

  • Depends on extent of damage

Homeostatic Imbalances of Blood Clotting

1. Thromboembolic Disorder

   1. Thrombus

   2. Embolus

2. Bleeding disorders

   1. Thrombocytopenia

   2. Hemophilia

Thromboembolic Disorders

• formation of undesired/unnecessary blood clots

  1. Thrombus (stationary)

  2. Embolus (circulates)

Thrombus

• Thromboembolic Disorder

• formation of blood clot in unbroken vessel (*remains stuck to vessel wall*)

• Effect: blocks circulation

  • How bad depend on size of thrombus

Embolus

• Thromboembolic Disorders

• thrombus that breaks free & enters circulation

• Effect:

  • If small, embolus is generally not a problem

  • If large, can obstruct smaller blood vessels & block circulation

• Examples:

  • Pulmonary (lung): very bad, decreased oxygen supplied to body

  • Cerebral (brain): ischemic stroke

Bleeding disorders

• absence of desirable blood clots, leading to excessive bleeding

1. Thrombocytopenia

2. Hemophilia

Thrombocytopenia

• Bleeding disorder

• low number of platelets in circulation

• Limited ability of body to form platelet plugs → even “small breaks” can cause massive hemorrhage

• Caused by: anything that decreases red bone marrow will usually decrease platelet count

Hemophilia

• Bleeding disorder

• hereditary bleeding disorders

• Deficiency or absence of certain clotting factors causes extreme bleeding from small cuts/injuries

• Symptoms: prolonged bleeding into tissues, painful/disabled joints

• Types:

  1. Hemophilia A: deficiency of clotting factor VIII (sex linked on x chromosome, most dangerous)

  2. Hemophilia B: deficiency of factor IX (sex linked on x chromosome)

  3. Hemophilia C: lack of factor XI (least dangerous)

• Treatment:

  • all very expensive

  1. Plasma transfusions

  2. Injections of absent/deficient clotting factor

Prefix for heart

“cardio-”

Function of the heart overview

• movement of blood

• Multichambered

• Tissue: Cardiac Muscle Tissue

Circuits that move blood through the body

1. Pulmonary Circuit

2. Systemic Circuit

Pulmonary Circuit

• any of the blood vessels that carry blood to and from the lungs

  • to lungs supplies blood with O₂ and disposed of CO₂

  • away from lungs supplies the body tissues with O₂

• made up of

  • Pulmonary arteries

  • Pulmonary veins

Pulmonary arteries

• pump oxygen poor blood from right side of the heart to the lungs

Pulmonary veins

• pump oxygenated blood from the lungs to the left side of the heart

What side of the heart is part of the pulmonary circuit?

Right

Systemic circuit

• any of the blood vessels that carry blood to and from the tissues

• oxygenated blood leaves heart through aorta (and its branches) to body tissues

• oxygen poor blood returns to heart via superior vena cava & inferior vena cava

What side of the heart is part of the systemic circuit?

Left side

The right & left side of the heart pump roughly the __ volume of blood per minute, BUT:

• The right & left side of the heart pump roughly the _SAME_ volume of blood per minute, BUT:

• wall that immediately surrounds empty space is muscles

• The right side (pulmonic) is relatively low-pressure

  • smaller than left

  • thinner walls, less muscle, less force

• The left side (systemic) is high pressure

  • The walls of the left side of the heart (especially the ventricle) are very thick, more muscle, more force

• Why?

  • Right side delivers blood to in the same cavity, needs to travel shorter difference

  • Left side delivers blood to rest of body, head to toes, needs to travel farther

Gross Anatomy of the Heart

• Heart slightly on left side

• The heart is tipped in the thoracic cavity

  • Apex (inferior “tip” of the heart) points to left hip

  • Ensures blood vessels stay open and are not crushed