sine intellectus nihil est = without understanding memory is nothing

M131: Disease & the Human Body

Fall 2021

Part I. Cardiovascular Diseases

A. cardiovascular anatomy & physiology

Why is understanding the circulatory system important?

it is the main cause of death

1) structure of the heart
right atrium->left atrium
right ventricle -> left ventricle
atria right atrium left atrium
*BOTH contract from top to bottom*
- Contract first atrioventricular valves
- Relatively weak
- Role is to “top off” the ventricle volume tricuspid valve bicuspid
pulmonary aortic
Ventricles semilunar semilun
- Stronger valvue right ventricle left ventricle ar
- Contract second valve
semilunar valves (pointing out)
- Very thick walls made of muscle
- one way
- Higher pressure than atrium
- pulmonary: towards lungs
- Role; propel blood away from the
- aortic: towards aorta
heart(more blood= stronger
contraction) Vena cavae blood from body Pulmonary vein
- Oxygen out carbon dioxide in -Blood from lungs
2) cardiac muscle - Into right atrium -Oxygenated blood
- Fills atrium quickly (low volume -Into left ventricle
role = generate
Text pressure capacity) Aorta
Cardiac muscle -Carries blood to the body
- Opens av valve leading to pulmonary
Muscle fibers are directly connected
artery
Branch structure helps protect
some important muscle contents: pulmonary
- myoglobin - blood to lungs
moves oxygen through muscle
-oxygen provides energy
- troponin
helps shorten muscle when it contracts

- creatine kinase
generate energy

Why do we care about muscle contents?

to know how to diagnose someone
 pink- full phase of activity of ventricle,
electrocardiogram
time length between beginning to end of
3) cardiac muscle diagnostics: EKG
contraction and relaxation
p wave- atrial contraction (doesnt show
qt interval
r strength)

QRS complex- ventricle contraction-

depolarization

t wave- relaxation of ventricle

repolarization
p wave t wave
the pause, flatline, time between
contraction and relaxation
q st segment
s
chamber volume (ventricle and atria) +muscle contraction(squeezes on chamber and generate pressure, moving the blood) = ejection of blood
concept application

ejection of blood
chamber volume + muscle contraction = ________________________________
(ventricle and atria) (squeezes on chamber and generate pressure, moving the blood)
i stroke volume (SV) = any chambers amount of blood that leaves the chamber in a single contraction(heart beat)
SV decreasing= less blood leaving the ventricle, less
"absolute" number of mL, coming from chamber
efficient, cardiac output is lower-> blood delivered less
varies from person to person and situation to situation
efficiently... increase the heart rate to make up for it.
How would you measure efficiency of the contraction?
(mostly looking at the left ventricle due to sending blood all over the body)
compare it to the chamber volume (starting amount of blood vs blood that moves)

i ejection fraction = stroke volume- blood that left the chamber

total chamber volume

84mL
example for LV: = 60% was successfully moved into the artery
140mL
*50%-60% is normal*
exercise also bumps it up

4) heart rate (HR) = number of chamber contractions per minute(all of the chambers)

2 sources of heart rate control

1) intrinsic
SA node- (natural pacemaker) muscle fiber in the right atrium
naturally send out electrical signals

2) extrinsic
regulate the heart rate, controlling SA node and determining rate of the signals
autonomic systems( regulation)
- sympathetic - increase heart rate and responds to fight or flight
- parasympathetic - resting heart rate, slows down heart rate
 5) cardiac arrhythmias when there is a physical or electrical issue w heart tissue causing heart rate change
slow heart
bradycardia atrial fibrillation(a-fib)- no flatline, extra electrical activity
*70-75 bpm slower than normal heart rate at rest
is regular* random electrical signal
heart rate 60 or below at rest is considered bradycardia
- most common in older adults
stronger heart= stroke volume goes up= lower heart rate
tachycardia -defibrillator treatment (shocks muscle fibers to get them on
high speed heart rate at rest same beat)
100 beats or above ventricular fibrillation (v-fib)- fake, no pressure is generates,
semilunar valves never open,can be caused by chemical
fibrillation imbalances
all of the muscles are contracted but not synchronized
instead of a single contraction there are multiple random ones

concept application
ejection of blood per minute(CO)
heart rate + stroke volume = _________________________________

i cardiac output (CO) = amount of blood leaving a chamber in a minute, mostly looking at the left ventricle,
- 5-6 liters/ minute multiply heart rate x stroke volume
equal between right and left ventircles

6) blood composition

- red blood cells (erythrocytes) from lungs to tissue, deliver oxygen

hematocrit = % of red blood cells in someones whole blood(entire volume of blood)

low hematocrit means oxygen isnt delivered properly
blood plasma 55%
= low iron- anemia
- white blood cells (leukocytes) immune system, fight off infection, primary job is
to clean up
platelets, white
- platelets stopping bleeding, form cloths that block damaged vesicles blood cells<<1%

red blood cells 45%

- plasma
higher CO2 =blood pH is going to drop
6) blood composition (cont.)

- normal plasma contents

importance clinical significance

90%, as you dehydrate , your blood pressure also

water drops

electrolytes
highest concentration on the outside of cells,
creates electrical communication through
sodium
the body, hyponatremia- when the cell count
drops and electrical disturbances
the counter point of sodium, inside the cells,
its poisonous in high concentrations
potassium

contraction of muscle, signal neurons to storing it in the bones, bone mineral density drops
release chemical signals, after age 25
calcium

buffers acid in the blood, decreases the acids

effects,
bicarbonate acidosis- acid too low
alkalosis- acid too high

waste products

blood urea metabolic biproduct, only builds up when

nitrogen there is kidney failure,
(BUN)

metabolic biproduct, as levels rise cronic

creatinine kidney disease starts

produced in the liver, metabolic bi product,

bilirubin when it rises liver disease is inspected for the
patient
 water decreasing in the blood, heart rate drops

nutrients

sugar, easiessts for us to process and pull as glucose levels rise-> diabetes mellitus is a
glucose energy from possible problem

amino acids -> increase blood pressure or

amino acids stroke?

fats in the blood, fats we eat get absorbed provide an energy source for cells
triglycerides in the body too much-> increase chance of artery disease

plasma membranes, produce hormones too much -> increase chance of artery disease
cholesterol

builds red blood cells, deficient in iron is the

most common cause of
iron anemia-> = hematocrit drops
last about 120 days,

gasses

helps provide tissues the capacity to generate

oxygen energy-> hypoxemia= low blood oxygen

metabolic biproduct, as levels build up it changes

carbon blood pH and decreases=
dioxide

other solutes
small protein helping fight off infections can produce auatoimmune disorder, where
antibodies white blood cells start to attack healthy cells
reumitoid arthritis

within the blood

draws water towards it to delute it, helps with
proteins (if they rise to much- high blood pressure
water balance
(albumin) if its too low- low blood pressure and
changes in albumin levels indicate liver damage
oxygen delivery drops
7) structure of blood vessels
3 layers in larger arteries & veins:
tunica externa /adventitia
outside, connective protective layer and elastic layer

tunica media
smooth muscle

tunica interna /intima

elastic layer, innermost layer(endothelia layer)

tunica adventitia
tunica media
characteristics of large vessels
tunica intima

arteries
thick walls, space to move blood is small
immediately pushes back against blood pushing them-> high pressure

veins
thinner walls , lumina is much larger( amount of blood in vein> blood in an artery)
vein expands and doesn't move when blood pushes->little pressure
there are 1 way vowels inside preventing blood from going backwards

characteristics of capillaries
single cell layer joined , nutrients delivered ...
only thin enough to allow exchange of surface area
thin enough for exchange large enough surface area to make it efficent

8) vessel diameter

vasocontriction
tunica media becomes active and contracts, decreasing space in vessel, vessel gets narrower

vasodilation
tunica media is relaxed, as it relaxes space opens up, vessel diameter gets larger

Why do we care about vessel diameter?

relates to vessel resistance
 9) vessel resistance

opposite
as vessel diameter changes, resistance changes in the _______________direction.

decrease
therefore, vasodilation __________________ resistance

increase
vasoconstriction ____________________ resistance

How does that affect blood flow?

low resistance -> blood moves through arteries and towards veins easily
high resistance -> basoconstrict resisting blood flow, blood builds up within the
artery, leading to blood pressure rising, affecting the heart(left ventricle)

How does that affect the heart?

pressure in aorta rises -> increase work on ventricle to get same amount of blood delivered

concept application

pressure forces (BP)

resistance + blood flow = ______________________________________
& how the affect the ventricle
i blood pressure (BP) = the forces of blood pushing against the vessels walls ( mostly in arteries, thats where the
most pressure is)

clinical application

a. find your pulse

artery (you can only messure a pulse in an artery)_

b. what kind of vessel do you feel your pulse in? ____________________

c. explain what you're feeling

simply bamboozled, elastic stretching against the artery, stroke volume is felt in each beat and distributed to each artery

what changes vessel resistance ? vessel diameter.

resistance vs. blood pressure- increase resistance-> increase in blood pressure
why isnt blood pressure messure in veins ? veins collapse when pressure is applied, arteries maintain structure,
10) arterial blood pressure

systolic pressure = contraction phase of the heart, highest pressure we find in the artery( in the aorta)
ex; 120/80

diastolic pressure = dia- relaxation of the heart, minimum pressure,

Why do we care about blood pressure?

Two main reasons that BP is important:

1. relates to the vascular health
analogy: what makes potholes occur ? wear and tear, weather, asphalt expands and contracts through the seasons(same thing
happens in your blood pressure)
*higher pressures damage blood vessels*
- brain> stroke
- eyes>blindness
- kidneys>renal failure
2.cardiac workload (left ventricle)
analogy: what happens when you crimp a garden hose ? low pressure> wont see much , high pressure> problems visible
*higher pressure ^ workload on the heart*
- fatigues& stresses the heart
- leads to pathological hypertrophy - enlargement of the muscle, increase in sum
^ chamber volume is smaller> less blood can be pumped out
clinical application
How would ventricular hypertrophy affect an EKG?
couldnt tell the stroke volume, or strength of contraction
QRS complex is elevates& longer QT interval
 affects the increase and decreases arterial blood pressure in untreated diabetes mellitus, increase of
glucose, filling up blood vessels-> high bp

11) factors affecting arterial blood pressure

1) cardiac output
- how fast are the arteries filling ?

2) resistance
- higher resistance> higher blood pressure
- how slow are arteries emptying ?
3) blood volume
- if there is less volume the pressure decreases
- how full are the vessels ?

B. vascular diseases

- ARTERIO-sclerosis
-hardening of the arteries, lack of elasticity
-doesnt expand as much as it should, narrower, resistance increases
-higher blood pressure
-ATHERO-sclerosis
-narrowing of the arteries, increase resistance, physically blocking blood flow
-can be seen

1) atherosclerosis progression

A B

1. begins in tunica interna 1. invasion of White Blood Cells(WBC)

inflammation is the trigger - absorb cholesterol>foam cells
- many indicators - collagen cap ("plaque") forms
-^high cholesterol/triglycerides, ^ high BP, trauma
C D

1. smooth muscle & more WBCs move in 1. significant vessel blockage

- more foam cells - increase risk of rupture
- calcification of the collagen cap(more of a rigid structure now) - increase of clot formation
- resistance has increases dramatically
 when walking in hot weather, the pressure of blood drops due to
sweat

2) atherosclerosis risk factors starting with inflammation

inherent risk factors
- age
- increase risk for males
- family history
- lifestyle
-smoking (resistance increase, increase pressure, chemicals in cigs)
- diets (trans fat)
-hypertension(more stress = more chance for inflamation)
-hyperlipidemia( too much fats and cholesterol)
- type 2 diabetes mellitus(increase glutcose=inflammation in vessels)
C. hypertension

1) symptoms
- often... none
- headaches
- tinnitus(ringing in the ears)
- edema(swelling in their ankles)
- nosebleeds
2) diagnosis
- blood pressure is the easiest way to measure it

*dont forget... pathological hypertrophy

ventricular hypertrophy & EKG
3) causes
elevated QRS+ longer QT interval

- intrinsic factors
- causing basocontriction and resistance
- increase of glucose *hypertension vs coronary artery disease*
similar: both be impacted by lifestyle, both
- extrinsic factors harmful
- smoking difference:hypertension is easier to diagnose,
- poor diet coronary has no symptoms, hypertension could
- too much fat and cholesterol
cause coronary artery disease
- stress
What do all of the causes have in common?
*angina vs heart attack
- cardiac output, resistance, volume
angina is the first step, angina cardiac muscle fiber
is healthy but during heart attack the muscle fiber
has died, angina has just enough oxygen to get by
similar: symptoms, both caused by decrease of
oxygen
 C. hypertension (cont.) medication examples
- lower hr or contraction force
4) treatments -beta blockers (decrease heart rate)
what would decrease bp ? - calcium (Ca2+) channel blockers
- lifestyle changes - decrease resistance
-medications -ACE inhibitors
-lower heart rate or contraction force -alpha blockers (prevents tunica media from contraction,
- decrease resistance relaxing smooth muscle in the blood vessel)
-decrease blood volume - decrease blood volume
- diuretic

D. coronary artery disease :narrowing of ateries bc of inflammation and plaque

1) coronary arteries
oxygen muscles need come from these arteries
atherosclerosis between these arteries
oxygen delivery to cardiac muscle decreases

2) symptoms / events
early part is asymptomatic
- 1st: angina (chest pain)
- decrease in oxygen to heart muscle
- not fatal, muscle fibers are healthy jut not happy
- feeling of heartburn, shortness of breath, nausea or fatigue
- "referred sensations" (tingling of the left side of jaw, shoulder, neck)
-2nd: myrocardial infarction
-not enough oxygen to tissue, cardiac muscle starting to die( doesn't come back)
- same symptoms but more intense

3) diagnosis

EKG
- compare resting to exercise(stress test) angiogram
- look for elevated ST segment
D. coronary artery disease (cont.)
3) diagnosis (cont.)

blood tests
check the blood for:
- presence of muscle contents
-troponin, creatine kinase, myoglobin, high cholesterol levels,
increase triglyceride level
angiogram
-use a radio-opaque dye & x-ray
easier to look at arteries and find differences

echocardiogram
using doppler ultrasound
can measure: stroke volume, chamber volume, ejection fraction, cardiac output

4) treatments

pharmaceutical intervention
- anti-hypertensives( relieves workload on the heart )
- statins( decrease cholesterol, very common, many benefits, decrease resistance, rare side effects )
- nitroglycerin( causes vasodilation, allowing more oxygen to be delivered to the tissue )
- anticoagulants( prevent clots, blood thinners)
- most commonly prescribed aspirin to prevent coagulation clots ( little side effects )
- antiplatelet drugs ( prevent clots )

angioplasty
-most common surgical technique used
- wire injected in the thigh, move wire ur to the heart with angiogram, worked
into coronary artery, expand the wire with balloon like item to push plaque to the side
- allowing bloodflow
-patient is usually awake and can tell more blood is flowing ( more energy )

coronary artery bypass graft (CABG)

extract vein, and stitch it into the artery to bypass blockage
two blockages - double bypass
- last resort to save the heart
 E. thrombosis & embolism

1) terminology

thrombosis =
- clot attached to walls of vessel
- clot- group of red blod cells bound together

embolism =
- part of a thrombosis that broke off the wall and travels through the blood stream
- increase change of it blocking the blood vessel

2) causes related to the rate of clots made

Virchow's triad
where does atherosclerosis fit ? between stasis and vessel injury

stasis- lack of flow creates signals

within the blood
3) symptoms

- arterial
- if you block an artery ... what effect with this have ? whatever part of the body the artery is on, the amount of oxygen
delivered is decreased, leading to tissue death
- oxygenated blood is blocked

- venous
- blocking a vein... what happens ? preventing deoxygenated blood from getting back to the heart
- the vein stretches increasing pressure, harder to get blood in the vein due to pressure
- impedes venous return
- deoxygenate blood is blocked.
E. thrombosis & embolism (cont.)

4) diagnosis
- D-dimer test
- results of natural break down of clot
- bits a pieces of broken clot
-a high count of d-dimer confirms clots
- dopler ultrasounds
- venogram

5) risk factors

- acquired
- age
- surgery/trauma
- immobilization
- obesity
- increases vessel inflammation, static blood flow
- oral contraceptives
- increases clotting of blood
- genetic
- family history
- coagulation (clotting) disorders
- thrombophillia- body clots much easier
-dont bleed as much, but internally can be a problem
- non-o blood types(A, AB,B)

6) common arterial examples

- myocardial infarction (heart attack) same symptoms ( lack of blood)

- ischemic stroke blood vessel in brain is being blocked

7) common venous examples

- deep vein thrombosis (DVT)

- not uncommon result of leg vein being blocked by embolism
- fluid that should go to heart instead is getting stuck in the leg
- symptoms: warm skin, swelling, person could have pain(more swelling -> pain)
E. thrombosis & embolism (cont.) not all embolisms hurt, depending on size
7) common venous examples (cont.)

- pulmonary embolism (PE)

- lodged into lungs
- embolism stops blood from getting deoxygenated
- symptoms: shortness of breath, fatigue, not fatal

8) treatments
- get rid of embolism
- thrombolytics - ("clot-buster")
-anticoagulants
- blood thinners, aspirin
- surgery (worst case scenario)
-deep vein thrombosis

F. ischemic stroke - a.k.a. cerebrovascular accident (CVA)

1) mechanism
- failing to deliver blood to specific part of brain
- neruons are now at severe risk( permenent damage)

2) symptoms
- sudden onset (rapid, acute, one side of the body)
- loss of function
- depend son area of the brain being infected
- usually no headache
-
F. ischemic stroke (cont.)

3) diagnosis

- physical exam
-what may be missing

- imaging
- CT scan or MRI
- some wont immediately show on
scans or not till after
-

4) treatment
- "time is brain"
- the longer you wait the worse the chances are
- as soon as a patient has these symptoms they need to be in the hospital in 30 minutes
- thrombolytics(clot-busters)
-tissue plasminogen activator(tPA)
- most effective within 3 hours
- anticoagulants
-prevent further clotting
-surgery(if possible)