bio 224 exam 1

cardiovascular sys. ch. 17-19

what makes up the cardiovascular system? (3 parts!)

• heart, blood vessels, & blood

Heart’s size & location

• Size: fist. abt. 250-350g

• Location: inferior mediastinum behind sternal attachments of ribs 2-6

  • Anterior surface is against the sternum. Posterior surface is against vertebral bodies

  • Apex/bottom of heart rests on the diaphragm. Top part (base) doesn’t rest on anything but has vessels

Pericardium

• Pericardium- a serous/mesothelial membrane that surrounds the heart

• Fibrous pericardium- made up of collagen fibers. Part of the parietal pericardium (the layer of the serous membrane away from the organ)

• Function: protects the heart by reducing friction. Since the heart is up against bones, it rubs against them while beating. Damage to the pericardium can be life-threatening!

• Layers (outer to inner): fibrous pericardium, parietal layer of pericardium, serous fluid, visceral layer of pericardium (aka epicardium)

Layers of the heart wall (outer to inner)

• Epicardium- same as visceral pericardium. Superficial layer made of SSE (simp. squam. epith.) & conn. tissue. Has coronary blood vessels

• Myocardium- cardiac muscle. Makes up 95% of the heart wall

• Endocardium- Inner layer that has specific areas where it’s modified. Closest layer to blood. Made of SSE

Heart chambers

• Atrium- upper chambers (shaped like an “a”)

• Ventricle- lower chambers (shaped like a “v”)

Valve

• a structure that prevents a fluid from moving backwards

  • for the heart, this fluid is blood

  • Valves prevent blood from moving back up into the atrium by using flaps

Endocardial modifications (made of tissue that isn’t SSE)

• Valves

  • Aortic valve- has no chords

  • Pulmonary valve- also has no chords

    • Aortic & pulmonary valves are semilunar valves that only have flaps (no chord or papillary musc.)

  • Mitral (bicuspid) valve- has 2 flaps. (Left A-V (atrium ventricle))

  • Tricuspid valve- has 3 flaps (right A-V)

    • this & mitral valve are the largest valves

• Parts of mitral & tricuspid valves

  • Chordae tendineae- tendonous chords. help hold valves closed

  • papillary muscle- attached to chordae tendineae & holds onto them. contracts & pulls chords tight to keep flaps closed

• Trabeculae carneae- trabeculae made of meat. Inside ventricles. Irregular shape on wall

• Musculi pectinati (pectinate muscles)- trabeculae made of mead inside of atria (plural from for atrium). Purpose isn’t known

What causes the heartbeat sound?

• Comes from valves closing (first, AV valves, then the semilunar valves)

  • murmur- extra heart sounds from turbulence of blood.

• Heart sound goes down, out

  • Atria contract & shove blood down into ventricles with AV valves

  • ventricles contract & shove blood out thru semilunar valves

Pathway of blood thru heart

• Great vessels- vessels attached to the heart’s chambers

• Color code guide: chamber & endocardial modifications

• Left side (brings blood from & to body) (doesn’t include lungs)

  • goes from left atrium, mitral/bicuspid valve, left ventricle, aortic valve, aorta (delivers blood to body (systemic))

    • Enters the heart again from the superior/inferior vena cava into the right atrium

• Right side (brings blood from & to lungs)

  • goes from right atrium, tricuspid valve, right ventricle, pulmonary valve, & pulmonary trunk

    • enters heart again from the pulmonary veins (carries blood from lungs)

• then it repeats! Can start from any point to practice

Characteristics of cardiac muscle

• striated, involuntary, not very long, uninucleate/binucleate, can branch, & loose T-tubule sarcoplasmic reticulum connections

  • this means a slower action potential

• Has lots of myoglobin & mitochondria. Means it can’t do anaerobic metabolism

• Has intercalated discs- type of cell to cell connection. Combo of desmosomes (protein stitches) & gap junctions (non-gated ion channels)

• 20% OF CA++ NEEDED IS FROM ECF (extracellular fluid)

  • PTH takes Ca++ from bones to keep brain & heart working.

• When one cell has an action potential, all other cells will have an action potential bc they all behave the same

• Electrically speaking, the entire myocardium behaves as a single unit

• Don’t need to be spit on by a motor neuron to contract bc they can contract on their own.

  • About 1% of our myocardium is made of autorhythmic cardiac musc. cells (contract on their own with greater leak channels for sodium. “spontaneously depolarizes”)

Intrinsic conducting system of the heart

• Autorhythmic cells: depolarize without any nervous control

  • Sinoatrial (SA) node- the pacemaker. Entire myocardium must follow that pace

  • Atrioventricular (AV) node

  • AV bundle

  • right bundle & left bundle branch

  • Purkinje fibers

• The pace of the heart can be controlled by controlling the SA node

Timing Issue

• Need to have all 4 chambers not contract all at once.

• Takes 0.03 seconds for SA node to get to AV node, then 0.10 seconds to get to the interventricular septum (0.13 seconds total)

  • AV has a build-in delay

• This delay allows for the 2 atria to finish contracting before the 2 ventricles contract

Heart’s electrical activity (with an ECG)

• P wave- atrial depolarization

• QRS complex- ventricular depolarization

  • atrial repolarization occurs during this. Covered up due to this wave & random electrical noise

• T wave- ventricular repolarization

Pre-ventricular contraction (PVC)

• QRS complex is too wide & invades the P wave.

• We can have PVSs once in a while (this is normal). If it occurs repeatedly, there’s an issue!!

Ventricular fibrillation

• Caused by repeated PVCs. Can lead to death.

• Looks like waves, but not like regular ECG trace. The heart is doing something, but is not pumping blood

Fibrillation & defibrillator

• Fibrillation- cardiac muscles are contracting independently of one another

• Defibrillator- helps counteract fibrillation by acting as a muscle stimulator & making all cardiac musc. cells contract at once.

  • Goal: return to SA rhythm

calcium channel blockers

• Reduces heart rate by slowing calcium ion entry

Lidocaine

when taken thru vein, used to correct abnormal heart rate

Systole vs Diastole

• Systole- heart chamber contracting

• Diastole- heart chamber relaxing

EDV, ESV, & SV

• End Diastolic Volume (EDV)- volume of blood in each ventricle at the end of Diastole (filling). Average=120ml

• End Systolic Volume (ESV)- volume of blood in each ventricle at the end of Systole (ejecting). Average=50ml (the amount that stays behind)

• Stroke volume(SV)- Volume of blood ejected by a ventricle. Average=70ml

Cardiac Output (CO) & Heart Rate

• Volume of blood ejected by a ventricle in one minute

• CO= heart rate * SV = ml/min (average: 4900ml/min)

• Heart rate= how many times a heart beats per minute. 70bpm is normal

Preload & Afterload (change the heart’s stroke volume) & Starling Law

• Preload- amount of stretching in myocardium

  • Starling Law: more blood in = more blood out (only true up to a certain point)

• Afterload- the pressure needed to open the semilunar valves (the door out of the ventricle) (how hard it is to open the door)

Extrinsic control of heart rate

• Nervous system:

  • Parasympathetic: spits ACh. Decreases heart rate

  • Sympathetic: spits NE. Increases heart rate

• Endocrine system:

  • Comes from adrenal gland spitting epinephrine (E). Speeds up heart rate

    • We have less receptors for E. This makes it easy to only stimulate the heart

Pulmonary circuit vs. systemic circuit

• Pulmonary circuit- blood goes to & from lungs

• Systemic circuit- blood goes to & from the rest of the body

How blood is supplied to the myocardium

• Blood is delivered to the myocardium thru the coronary vessels.

• Coronary arteries deliver oxygenated blood to the heart

• Coronary veins send deoxygenated blood away from heart.

• Found on outside of heart

Cardiac cycle

1. Ventricular filling phase- blood drains from atria to ventricles

2. Isometric contraction phase- AV valves close. Pressure in ventricles rise & ventricles begin to contract

3. Ventricular ejection phase- SL valves open & rapid outflow of blood from ventricles

4. Isometric relaxation phase- SL valves close. Constant volume since blood doesn’t enter or get ejected from ventricles.

Venous return

amount of blood returning to right atrium from systemic circuit. Influences EDV

Endocarditis

inflammation of endocardium’s valve’s & chambers

Ectopic pacemaker

extra pacemakers other than the SA node. Can result in irregular heart rhythms

Pericarditis

inflammation of pericardium

angina pectoris

chest pain caused by decreased blood flow to myocardium

myocardial infarction

heart attack caused by obstruction of blood flow to myocardium

myocardial ischemia

decrease of blood flow to myocardium due to plaque

cardiac tamponade

condition where pericardial cavity has excess fluid. Compromises amount of blood pumped each beat.

stenosis of a valve

calcium deposits build up in cusps, making them hard & inflexible

coronary thrombosis

blood clot forms inside coronary artery

valve insufficiency

Valve fails to fully close, causing blood to leak backwards

heart failure

heart can’t pump blood as well as it should

heart block

heart’s normal conduction pathway is disrupted by blockage or accessory pathways between atria & ventricle

tachycardia vs bradycardia

• Tachycardia- heart rate is over 100bpm (faster)

• bradycardia- heart rate is under 60bpm (slower)

coronary angiography

medical imaging to see the blood flow thru arteries

coronary angioplasty

Keep artery open using balloon & stent

ventricular tachycardia

type of arrythmia. Can be life-threatening

What type of tissue is blood?

Connective tissue

Blood is a…

• fluid (it flows)

• mixture (has more than 1 thing in it)

• suspension (has things floating in it)

• solution (has things dissolved in it)

all at the same time! Think of it as the “river” of life

average blood volume in a human

4-6L

Composition of human blood & definition of hematocrit

• 55% of blood is plasma & 45% of blood is cells (red & white blood cells)

  • Hematocrit= % of whole blood that is RBC (red blood cells) (usually 45%)

    • The percentage for the buffy coat (white blood cells or WBC) is usually less than 1%, so it’s negligible

functions of blood (& functions of cardiovascular system)

• Transport- can transport multiple different things (whatever it can carry. ex. nutrients, waste, etc)

• Homeostasis (maintain standard body temperatures)

• Protection (ex. WBC can fight off pathogens. Protects us from blood loss thru clotting)

Plasma (percentages & protein functions)

• 90% is water, 9% is proteins, 1% is other stuff

• Blood proteins:

  • Albumins: maintain osmotic pressure (think about hyper/hypotonic solutions & what would happen to blood in those types of solutions)

  • Immune proteins: antibodies. Immunity. Igs. (think of IgA, IgG, etc.)

  • Transport proteins: bind to & transport things

  • Clotting proteins: fibrinogen (inactive version) & prothrombin (early version)

Hemopoiesis/Hematopoiesis & hematopoietic stem cell

• Hemopoiesis/Hematopoiesis- The formation of blood cells

  • Starts with hematopoietic stem cell (or hemocytoblast)

    • Has the potential to become any type of blood cell (but not other types of cells like a muscle cell or neuron)

    • Undergoes “understood mitosis” so we don’t run out of stem cells

• Formation of blood cells occurs in red bone marrow (RBM)

  • Found in skull bones, sternum, vertebral bodies, os coxae, & proximal ends of humerus & femur

    • for red bone marrow extractions, os coxae & humerus/femur are preferred due to lower risk

• Most of the cells will become RBCs, but they can also become WBC or platelets

  • Determined through chem. instructions from ligands

EPO- erythropoietin

• protein from kidney

• Creates more RBCs

• Can be abused as a drug enhancer since RBCs hold oxygen. Can result in too much clotting.

blood doping

injecting oxygenated blood into an athlete to enhance performance

Thrombopoietin

• Protein from liver

• Tells stem cells to become platelets

White blood cells (WBCs) are driven by…

CSFs (colony stimulating factors) & interleukins

Erythropoiesis (definition & intermediate steps)

• Formation of erythrocytes (RBCs)

• Intermediate steps:

  • Late erythroblast- has nucleus

  • Reticulocyte- loses nucleus (got spat out) (means RBC can’t repair itself, divide, etc)

Leucopoiesis

Formation of leucocytes (WBCs)

Platelet formation

• Megakaryocyte- large nucleus cell.

• Platelets are chunks of a cell or cell fragments

Red blood cells (erythrocytes)

• biconcave disc shape (a disc with 2 dents on it)

  • Gives us inc. surface area (cell membrane) & less volume

  • Gives up its nucleus to have this shape

• These cells can flex, bend, stack

• These are bags of Hemoglobin (Hb)

  • Hemoglobin is made up of 4 large protein arms & 4 heme groups

    • Iron (Fe) is in the central part of heme. Fe²⁺ is ideal to hold oxygen (so this is where oxygen sits!!)

      • Carbon monoxide has a stronger chem. attraction to iron than oxygen! It’s dangerous since it displaces O2 off the heme

    • CO₂ would be on the outside of protein arms, not hemes

  • OxyHb- hemoglobin that is carrying oxygen

  • DeoxyHb- hemoglobin that is not carrying oxygen

  • carbaminoHb- hemoglobin that is carrying CO2

Function of each human blood cell type

• erythrocytes: transport oxygen & bind & transport some carbon dioxide

• platelets: blood clotting

• Leukocytes:

  • neutrophil- releases chem. to attract other leukocytes & destroy bacteria. Also destroys bacteria thru phagocytosis

  • eosinophil- releases chem. in response to parasitic worm infections. Mediates allergic response

  • basophil- releases chem. that mediates inflammation

  • monocyte- becomes very active phagocyte in tissues

  • lymphocyte- activates all components of immune response & destroys virally infected & cancer cells. Secretes antibodies

Life cycle of erythrocytes

• Lifespan: 120 days

  • Gets damaged over time from bumping into each other so much

• Macrophage destroys RBCs that are damaged beyond repair. They get taken apart & parts get reused (like amino acids & iron) This is what happens to old RBCs

Terms related to RBC (anemia & polycythemia)

• anemia- any condition that redudces the blood’s ability to carry oxygen (ex. low iron, low Hb, damage to RBM, or misshapen RBCs, such as from sickle cell anemia)

• polycythemia- too many RBCs (hematocrit is too high & blood is too thick). (can cause heart attack, stroke, etc)

White Blood Cells (WBCs) (Leucocytes)

• Larger than RBCs

• Take stain

• Have a nucleus

• Can move (unlike RBCs)

• adhesion/margination (can stick to wall of blood vessel)

• emigration/diapedesis (leave blood stream)

  • Chemotaxis (follow a chemical trail)

Definitions for leucocytes (leukocytosis, leucopenia, & leukemia)

• Leukocytosis- too many WBCs

• Leucopenia- too few WBCs

• Leukemia- overproduction of abnormal (not functioning) WBCs (often with anemia) (cancer)

  • acts like both since it’s making too many blood cells, but symptoms are similar to leucopenia since they aren’t functioning

Platelets (definition, purpose, & lifespan)

• cell fragments

• Lifespan: 5-9 days

• Job: form platelet plugs & clots

  • Can stick to collagen & other platelets (when activated

Steps for hemostasis

• Vascular spasm, platelet plug formation, coagulation (forming clot), clot retraction, & thrombolysis

• Trigger for process: vessel injury exposes collagen fibers (platelets will stick to these, then activate)

  • Damaged endothelial cells release von Willebrand factor (vWF) (helps connect platelet to collagen by making collagen more sticky)

• Activated proteins spit out Ca++, some clotting factors, ADP, thromboxane, & serotonin

  • Vascular spasm- created by serotonin, thromboxane, & endothelin. Vessel contracts to reduce blood loss

  • ADP & thromboxane activate other platelets

  • An example of a positive feedback mechanism

• Damaged endothelial cells also release prostacyclins to limit platelet aggregation (built-in brakes)

• These steps lead to platelet plug and/or clot

Terms for platelets (platelet adhesion, platelet release, platelet aggregation)

• Platelet adhesion- platelets sticking to exposed collagen & vWF (these platelets will become activated platelets & change shape & start releasing chemicals)

• Platelet release- platelets (after activation) begin spitting out chemicals

• Platelet aggregation- platelets sticking in groups to each other

coagulation/clotting cascade

• Forming a clot (not a platelet plug. These are larger & require fibrin to make a clot

  • Fibrin clot acts like a net that catches blood cells & dams up wound

• Last steps in clotting pathway (common pathway part)

  • Last step: Make fibrin. fibrinogen —(thrombin)→fibrin

  • 2nd to last step: get enzyme thrombin. prothrombin—prothrombinase (X & V)→thrombin

  • fibrinogen & prothrombin are normally in plasma, they’re just inactivated til this event

• Clotting factors to know: calcium, fibrinogen, prothrombin, X & V

  • Most clotting factors are proteins made by liver. Many need vitamin K

• Fibrinolysis- destroying fibrin after wound is done (get rid of clot)

• Plasmin- takes apart fibrin. Inactive form of this is plasminogen

Extrinsic pathway vs Intrinsic pathway

• Extrinsic pathway

  • Starts with TF (factor III/thromboplastin)

  • Prots/lipids from damaged cells outside the blood vessels (extrinsic)

  • Faster due to fewer steps

• Intrinsic pathway

  • Starts with Factor XII (already in plasma) getting activated

  • normally in blood. Activated by collagen exposure and/or platelet chem. (intrinsic)

Note: both will still lead to the common pathway!!

Things that favor clots vs things that prevent/hinder clots

• Things that favor clots:

  • roughness

  • collagen exposure

  • gauze

• Things that prevent/hinder clots:

  • smoothness

  • some blood chemicals (ex. Heparin- blocks thrombin formation)

  • leeches

Terms to go with clotting (hemophilia, thrombus, embolus, & serum)

• Hemophilia- missing clotting factor (often VIII)

• Thrombus- stationary clot

• Embolus- moving blood clot

  • note for thrombus & embolus: location determines if it’s dangerous or not

• Serum- plasma without clotting proteins

Blood types (antigens, antibodies, & Rh factor)

• Antigens- proteins on the surface of cells. Used to identify blood type. (ex. Type A blood has A antigens on its surface)

• We make antibodies against antigens we DON’T have

  • ex. Type O blood has antibodies against A & B

  • Agglutination- clumping of RBCs caused by antibodies sticking to antigens. Can make a blood clot in bloodstream!!

• Rh factor- another antigen (positive or negative). A protein that can exist on the surface of cell

  • Usually must be sensitized to Rh factor before agglutination happens

    • Agglutination will occur during the 2nd time you receive blood, not the first, bc it needs to be exposed to Rh first before making antibodies against it

• O- = universal donor. AB+ = universal recipient

CBC

Complete blood count. Used to evaluate number & characteristics of blood cells

hemolysis

rupture of erythrocytes. Can occur naturally or after agglutination from receiving wrong blood

hypoxia

• Low levels of oxygen in the body’s tissues

• Sherpas don’t suffer from hypoxia as much as the people they guide because they’ve adapted to higher altitudes & can use oxygen more efficiently

• Olympic athletes live in high-elevation cities so their bodies can adapt to using less oxygen & improve athletic abilities

reticulocytes

• immature erythrocyte released into circulation. Still has nucleus & some organelles

HDN (hemolytic disease of the newborn)

Rh- mother gives birth to Rh+ fetus. The first pregnancy will be unaffected, but subsequent pregnancies can result in death of the fetus

thalassemia

• defective synthesis of hemoglobin.

• Treatment depends on severity. Treatments include:

  • blood transfusions

  • removal of spleen

  • bone marrow grafting

edema

swelling from excess water in interstitial fluid

warfarin

inhibits production of Vit. K dependent clotting factors by liver. This is an anti-clot medication

antithrombin

anticoagulant. Binds & inhibits activity of factor Xa & thrombin

EDTA

prevents blood samples from clotting & removes calcium & lead from the body

septicemia

Blood poisoning, especially caused by bacteria or their toxins

jaundice

yellow discoloration of skin. Can be caused by excess RBC breakdown

thrombocytopenia

low blood platelet count

positive chemotaxis

Occurs if movement is toward higher concentration of chemical

petechiae

tiny spots of bleeding under skin

Structure & function between capillaries, arteries, & veins

• arteries & veins both have all 3 layers (tunica intima, tunica media, & tunica adventitia), but veins have much less tunica media

  • Tunica intima- endothelium touching blood

  • Tunica media- smooth muscle

  • Tunica adventitia- connective tissue

• Capillaries are the only blood vessels that allow exchange between the blood & environment. It’s a thin wall made of just SSE. It connects the arteries & veins

  • Continuous- most common

  • Fenestrated- have holes

  • they ALL LEAK!!!

• Arteries are distinctly round & circular while veins are pleomorphic (undefined shape), less round, & have a higher diameter lumen

• Veins have valves, which arteries don’t have

• Blood travels faster in arteries than veins due to a narrower hose

Corresponding pair & what influences blood flow

• Corresponding pair- carrying the same amount of blood in each direction. Otherwise, there’d be a swelling issue

• Speed of blood between arteries & veins is different due to how narrow or wide the hose is.

  • Hose is more narrow in arteries, so blood travels faster in arteries

• Narrower hose=faster blood flow & wider hose = slower blood flow

  • Inverse relationship

Elastic arteries vs muscular arteries vs arterioles

• Elastic arteries

  • Biggest, up to 2.5cm (~1inch)

  • Lots of elastin

  • Aorta, pulmonary, common carotid, common iliac, brachiocephalic, subclavian

  • Carried lots of blood at high pressure

• Muscular arteries

  • Other “named” arteries

  • Up to 0.5cm

  • Thicker tunica media

• Arterioles

  • Smallest arteries. Leads to capillaries

• It’s the muscular arteries & arterioles we change the size of (AKA constricting & dilating blood vessels)

Purpose of muscular pump & respiratory pump

• Blood can sometimes pool around the semilunar valves & bulge

  • Semilunar valves prevent blood from moving backwards

• Muscular & respiratory pump help get blood back into heart from veins

Blood pressure, sphygmomanometer, korotkoff sounds, systolic vs diastolic pressure, & vascular resistance

• Blood pressure- the outward force blood exerts on the walls of blood vessels. Measured in millimeters of mercury (mmHg). Regular blood pressure: 120/80 mmHg

• Sphygmomanometer- tool to measure arterial blood pressure

• Korotkoff sounds- sounds detected by stethoscope caused when blood flow thru brachial artery resumes at systolic pressure & becomes turbulent

• Systolic pressure- blood pressure in arteries when ventricles are in systole. Average- 110-120mmHg

• Diastolic pressure- blood pressure in arteries when ventricles are in diastole. Average- 70-80mmHg

• Vascular resistance- resistance in circulatory system used to create blood pressure

What influences blood pressure?

• The two major factors: heart rate & vessel size

  • These are controlled by the nervous system

  • Inc heart rate = inc blood pressure

  • Skinnier blood vessel size = inc blood pressure

• Smaller factor: changing blood volume

  • Controlled by endocrine system

Varicose veins

Dilated, bulging & often hardened veins. Often on superficial veins of lower limb

Phlebitis

inflammation of a vein, often in a leg

gangrene

tissue death due to lack of blood flow

anastomoses

communication between blood vessels or other hollow organs. It’s a system of channels formed between blood vessels

arteriosclerosis

hardening of arteries. Disrupts normal blood flow

atherosclerosis

caused by a buildup of plaques. Affects large & medium sized arteries

cerebrovascular accidents (CVAs)

stroke. Damage to brain caused by disruption to its bloodflow

ischemia

blood flow to heart is reduced