PHYL 142 Exam #3

Heart valves

Atrioventricular valves: Tricuspid, Mitral (bicuspid)

Semilunar: Pulmonary, Aortic

Trace the path of blood through the heart

(oxygen-poor) superior vena cava, Right atrium, Tricuspid valve, Right ventricle,

Layers of the heart wall

Epicardium, Myocardiuim, Endocardium

Epicardium

aka visceral pericardium, Mesthelium, Areolar tissue

Myocardium

Cardiac muscle tissue, made of cardiac muscle cells & connective tissues

Endocardium

Made up of Areolar tissue, Endothelium, Deep (heart chamber)

Location/function intercalated discs

Located in between epicardium and endocardium, holds adjacent muscle cells together

Skeletal muscle

Striated, multi-nucleated, voluntary

Cardiac muscle

Non-striated, uni-nucleated, involuntary

Atria

Thin walled chambers that receive blood from the veins

Ventricle

Thick walled chambers that pump blood out of the heart

Left ventricle vs. Right

Left: thicker, carries oxygen rich blood, pumps blood to the body

Right: thinner, oxygen poor blood, pumps blood to the lungs

Epicardial fat

Located between heart wall 7 pericardial sac

Excessive fat leads to obesity & heart disease

\#1 leading cause of death in the U.S

Heart disease

Myocardial infarction

Caused by cardiac ischemia, blood flow to tissue is dec., nutrients to tissues are decreased, cardiac muscle cells die from lack of O2 & nutrients

Ischemia in the coronary arteries

cause everything downstream to lose out on oxygen & nutrients

Deadliest myocardial infarction location

Left anterior descending artery blockage

LAD supplies left ventricle with O2 & nutrients and most of the interventricular septum

Blockage of LAD means L ventricle & interventricular septum may die due to lack of nutrients, which are the parts that pump blood to the rest of the body

What leads to a myocardial infarction

Ischemia

How the heart & body adapt to a MI

MI cause cardiovascular tissue to die -> Fibrous scar replaces dead tissue, area becomes thin & elongated->Heart compensates by causing surrounding cardiomyocytes to thicken

Signs & symptoms of myocardial infarction

Symptoms: Chest pain, dizziness, nausea, vomiting, Jaw/neck/back pain, pain in arm/shoulder, shortness of breath

Demographic differences in MI symptoms

Females more likely to exp. shortness of breath, nausea/vomiting, back/jaw pain,

Avg age to develop MI

males: 65 years

females: 72 years

MI treatments

Drugs & medication, Angioplasty & stents, Coronary bypasses

Drugs & medication for a MI

Anticoagulants: may help dissolve clot which caused ischemia/MI

Beta-blockers: causes heart to ease up, reducing O2 consumption

Angioplasty & stents

Inflatable balloon widens blocked area, stent wrapped around balloon helps hold the vessel open

Coronary bypass

Uses blood vessels from somewhere else to deliver blood around blockages

Diastole

Pressure inside dec. normal relaxation occurs

Systole

Pressure inside inc. contraction occurs

Cardiac cycle

how the heart contracts & pumps blood

Phases of the cardiac cycle

Atrial systole, Isovolumetric ventricular contraction, ventricular ejection, isovolumetric ventricular relaxation, ventricular filling, atrial systole

Atrial systole

Atrias squeeze, inc. pressure inside the atrium forcing the blood into the ventricles (Tricusp/Mitral valves open, pulm/aortic valve closed)

Atrias in systole leading it to have higher pressure than the ventricles, blood flows from high → low

Isovolumetric ventricular contraction

Ventricles are squeezing, everything is shut, pressure is inc. (all valves shut)

Atria are relaxing

Valves cause first heart sound (tricuspid/mitral)

Ventricles in systole, atria in diastole, ventricles have higher pressure than atria

Ventricular ejection

Pressure builds up in ventricles

Pulm/aortic valve open, blood rushes through the valves due to built up pressure

Atria in diastole, Ventricles in systole,

Isovolumetric ventricular relaxation

Ventricles are relaxing

All valves shut

Valves cause 2nd heart sound (Pulm/Aortic)

Atria & ventricles in diastole

Ventricular filling

Pressure in ventricles drop, atria have greater pressure

Mitral/tricusp. Valves open since atria have greater pressure than ventricles

Blood flows into atria then into ventricles

Tricusp/mitral valves open

Atria & ventricles in diastole

Heart sounds

lub: caused when tricuspid & mitral valve close during Isovolumetric ventricular contraction

dub: caused when pulm & aort valve close during isovolumetric ventricular relaxation

Parts of the electrical conduction system of the heart

SA node, Internodal pathways, AV node, AV bundle (bundle of His), Bundle branches, Purkinje fibers

Phases of authorhythmic cardiac muscle action potentials

Prepotential, Depolariztation, Repolarization

Cardiac muscle prepotential

Gradual slow increase in membrane potential toward threshold (due to slow influx of NA+ & CA2+)

Cardiac muscle Depolarization

Fast calcium channels open once threshold is reached (rapid influx of Ca2+) causes depolarization

Cardiac muscle Repolarization

K+ ion channel opens as Ca2+ rushes into cell causing K+ to rush out making cell more negative

Autorhythmicity

Ability of pacemaker cells to trigger their own action potentials

What regulates the heartbeat

SA node, contains pacemaker cells which can generate electrical signals and therefore contract by themselves

Phases of contractile & autorhthmic cardiac muscle action potentials

Rapid depolarization, the plateau, Repolarization

Contractile depolarization

Na+ flows into cell causing depolariztation

Contractile plateau

Ca2+ channels open, calcium flows into cell, K+ channels open, potassium flows out of cell

Contractile repolarization

Ca2+ channels close ending the plateau leading to repolarization

Waveforms of an EKG

P, QRS, T

P wave

Atrial depolarization, Atrial systole-\> Atrial diastole

QRS complex

Ventricular repolarization

Ventricular diastole -> Ventricular systole

T wave

Ventricle repolarization, Ventricular systole -\> Ventricular diastole

Perfusion

Distribution of blood into capillaries so tissues can receive nutrients

Ischemia

Insufficient blood flow to tissues

Hemorrhage

Excessive bleeding, blood escapes from a vessel

External hemorrhage

Blood leaks from a vessel and appears on the outside of the body

Epistaxis

Nosebleed

Internal hemorrhage

Broken blood vessels, no broken

Shock

critical state where the body is not getting enough blood flow

Shock subtypes

Cardiogenic, Anaphylactic, Septic, Neurogenic, Hypovolemic shock

Cardiogenic shock

Heart problems, blood does not circulate properly

Anaphylactic shock

Allergies, severe allergic reactions can cause blood vessels to become leaky

Septic shock

Infection, can cause blood vessels to become leaky

Neurogenic shock

nervous system trauma

Hypovolemic shock

low blood volume

Cerebrovascular accident

(stroke) blockage of blood flow to brain, leads to cell death

Ischemic stroke

Caused by blockage and inadequate perfusion to brain tissue

Most common stroke type

Hemorrhagic stroke

Caused by brain blood vessel rupture & bleeding

Often caused by ruptured aneurysm

Blood leaks out, inc. fluid in brain, increases pressure in brain, causes inc. in cell damage & death in brain tissue

Fast Symptoms of stroke

face drooping, asymmetry/arm weakness, slurred speech, trouble seeing/walking/understanding

Long-term effects of a stroke

Impaired speech, restricted physical abilities, weakness or paralysis of limbs on one side of body, difficulty gripping or holding things, slowed ability to communicate

Stoke & MI similarities

Occlusion: blockage of blood vessels

Ischemia: lack of blood flow to tissues

Cell death

Artery

BV that conducts blood away from heart

Capillary

Smallest of BV where physical exchange occurs between blood & tissue cells surrounded by interstitial fluid

Vein

BV that carries blood to the heart

Tunics

Intima, media, externa

Tunica intima

Endothelium: thin layers of cells,

vein: smooth surface

artery: ripped surface, elastic membrane

Tunica media

Both have Smooth muscles, constricts BV,

artery: thicker muscle layer, elastic ECM fibers

vein: thinner muscle layer, collagen ECM fibers

Tunica externa

Both have collagen & elastic fibers

veins: smooth muscle cells, prevents vein from collapsing

System circuit

Aorta\> Arteries \> arterioles \> capillaries \> venules \> veins \> vena cavae

Blood pressure changes in systemic circuit

BP drops from Aorta -> Capillaries

BP drops close to 0mmHg from Capillaries-> veins

Hearts affect on BP

Heart squeezes: inc. blood pressure

Heart relaxes: dec. blood pressure

Aneurysm

Vessel enlargement due to vessel wall weakness, weak spots bulge due to pressure

Ruptured aneurysm symptoms

Hemorrhage, inc. pressure in surrounding tissues, sudden exteremly painful headache, typically happens without warning, often deadly

Cerebral aneurysms can lead to hemorrhagic stroke in the brain

Vasoconstriction

Contraction of vessel smooth muscle, dec. vessel diameter, inc. BP, dec. flow

stimuli ex: Epinephrine, sympathetic activity

Vasodilation

Relaxation of vessel smooth muscle, inc. diameter, inc. flow

stimule ex: vasodilators, cyclic GMP

Nitroglycerin

Nitric oxide & Vasodilation

Nitric oxide activates production of cGMP which causes vasodilation

Nitroglycerin & vasodilation

body metabolizes nitroglycerin into nitric oxide

Arterioles

relax-> open blood flow

contrict-> cut off blood flow

considered resistance vessels

resistance vessels

regulate resistance to blood flow

Capillaries

are thinner than other blood vessels

thinner walls= more diffusion

Continuous capillaries

little cracks, permit narrow range of substances to cross capillary walls

fenestrated capillaries

cracks & gaps/pores, allow large volumes of fluid & larger molecules to cross capillary walls

Sinusoid

many cracks/gaps, allow large substance to cross capillary walls

Precapillary sphincters

rings of smooth muscle that control blood flow to capillary beds, constrict to close blood flow & open when it needs to remove waste from capillary beds

venous valves

prevent blood from flowing backwards, compression around veins also helps return blood to the heart

Muscular compression

Compression around veins helps return blood to the heart, contraction of skeletal muscle surrounding veins inc. pressure within veins pushing open proximal valve & forcing blood toward the heart

Deep vein thrombosis

blood clot in a deep vein, usually in the legs

Deep vein thrombosis causes

sitting still for extended periods inc. risk, clots can result in an embolism

Embolism

blockage of an artery by an object (e.g thrombus, lipid globule, air bubble)

Avg. adult total blood volume

Male: 5-6 L

Female: 4-5 L

Blood volume distribution

Venous system\~ 60-65%

Heart, arteries, capillaries\~ 30-35%

Venous reservoir\~21% of your total blood volume