Cardiovascular System

Front 1

Functions of the cardiovascular system:

Back 1

MAIN FUNCTION = TRANSPORT
-brings O2 from lungs to cells
-brings CO2 from cells to lungs
-brings fuels to cells/brain
-brings nutrients into the body
-removal of waste products
-circulation of hormones
-circulation of immune cells and antibodies
-regulation of electrolytes
-regulation of pH
-H2O balance
-thermoregulation
-among many, many more

Front 2

why doesn't an amoeba need a cardiovascular system?

Back 2

-so small that oxygen can diffuse.. same with CO2 and other substances like food

Front 3

The Insect Heart

Back 3

-single vessel
-goes towards head of animal
-open circulation (blood flows out of circulation system and percolates through insect)

Front 4

Piscine Circulation

Back 4

Fish has closed circulation
-1 loop
-2 chambers (atrium and ventricle)

Front 5

Amphibian and Reptile Circulations:

Back 5

-double-loop circulation
-3 chambers (left and right atrium, a single ventricle)
-disadvantage: oxygenated blood and deoxygenated blood is somewhat mixed (not as efficient as it could be).. we have septum to create left and right ventricles

Front 6

Avian and Mammalian Circulations:

Back 6

-closed circulations
-2 loops
-4 chambers
*we have two hearts in our body.. left heart and right heart
-right heart: pulmonary circulation
-left heart: systemic circulation

Front 7

Where is the blood in our circulation system?

Back 7

-only about 10% of the blood is in the heart
-10% in the lungs
-10% in arteries
-10% in capillaries
wheres the rest??
-venous system= 60% of blood is found here
-often called capacitance system (hold the blood)
-arterial system= resistance

when we lose a lot of blood, the body will squeeze down on the veins to get more blood to the heart to circulate

Front 8

What is average cardiac output at rest?

Back 8

5L/min

Front 9

Flow:

Back 9

-flow = change in volume / change in time
-flow = area x MEAN velocity

*flow = perfusion pressure / resistance

Front 10

Pressure:

Back 10

-pressure = force / area
-s.i. unit: pascal
-practical unit: cm H2O; mmHg

-Blood Pressure: 120/80 mmHg
-Central Venous Pressure: 6 cm H2O

Front 11

Perfusion Pressure:

Back 11

-perfusion pressure = inlet pressure - outlet pressure

-perfusion pressure = arterial pressure - venous pressure

*since arterial pressure >> venous pressure; perfusion pressure ~ arterial pressure

Front 12

Resistance:

Back 12

Resistance = perfusion pressure / flow

Front 13

Laminar or Parabolic Flow

Back 13

flow is not equal across all of the cross-sectional area
-it moves fastest in the middle
-as you move outwards from the center, the value decreases

Front 14

Poiseuille's Law

Back 14

R = 8vL / 4(pi)r^4

so R is related to 1 / r^4

*since radius is to the 4th, small changes in radius can cause large changes in Resistance

Front 15

Control of Vessel Resistance:

Back 15

-arterioles will dilate to get a greater flow of blood

-if you are in the cold, flow will decrease (to maintain core temp) so arterioles leading to the skin will constrict

-by decreasing the radius by 20% (so it is at 80%) resistance goes up 2.5 times

Front 16

Resistance in Series:

Back 16

when you have two vessels in series, the resistances add (so the overall resistance will be greater than in either component)

Front 17

Resistances in Parallel:

Back 17

-with two vessels in parallel, the flow in will be the same as the flow out

-combined resistance of the system is less than the resistance of either of the two components

-why our arterioles branch (smaller pressure to get the same flow)

Front 18

Valves of the heart:

Back 18

tricuspid valve: between right atrium and right ventricle

mitral valve: between left atrium and left ventricle

aortic valve: between left ventricle and aorta

pulmonary valve: between right ventricle and pulmonary artery

*all valves are found in the "fibrous ring" of the heart

Front 19

Papillary Muscles and Chordae Tendinae:

Back 19

These muscles pull the tricuspid and mitral valves closed

-the chordae tendinae connect the papillary muscles to the valves

Front 20

Valve eversion / valve prolapse

Back 20

retrograde flow from ventricle to atrium

can be caused by papillary muscle rupture
-treatment= mitral valve replacement

Front 21

Are our hearts cardiogenic or neurogenic?

Back 21

cariogenic.. our hearts can pump outside of our bodies.. other animals have neural signals firing from brain to tell heart to pump

Front 22

Activation Sequence of the Heart:

Back 22

Sinoatrial node (SA node) in right atrium is pacemaker cells (individual cells will beat by themselves under microscope)

Atrioventricular node (lower in the right atrium.. muscle cells that carry nerve impulse to:
-Bundle of His= bundle of muscle cells (specialized)
-bundle of His bifurcates into right and left bundle branches.
-break into tree-like branches of Purkinje fibers

Front 23

Name some special features of the joining of myocardial cells:

Back 23

-Intercalated Discs: zigzagging interactions

-Nexus or Gap Junction: same as above

-Connexons or Hemi-Junctions: connect between two cell membranes to create a junction
-these channels are huge (not small ion channels)
-any ion can go through
-even small molecules like ATP

Front 24

Local Circuit Currents:

Back 24

resting potential of cardiac cells: -90millivolts
-cells are short compared to axons of neurons (no specialized discs)

for propagation to occur, you need both intra- and extra-cellular flow of current

Front 25

electrocardiograph vs electrocardiogram:

Back 25

electrocardiograph is the instrument in which you use to obtain the measurement electrocardiogram

Front 26

Activation Sequence and ECG:

Back 26

PQRST:

1. Sinus node fires= ECG picks up nothing (bc SA node is so small, currents that leak out are small)

2. Action potential to right and left atrium = P wave

3. short period of no electrical current on ECG between P and QRS as action potential goes through AV node and Bundle of His because they too are so small

4. QRS wave = action potentials in ventricular muscle (right ventricular wall, left ventricular wall, septum)

5. T wave is from repolarization

Front 27

Bipolar Limb Leads:

Back 27

I = LA - RA
II = LL - RA
III = LL - LA

Front 28

The Clinical 12-Lead ECG:

Back 28

-leads, I, II, and III are bipolar limb leads

-aVR, aVL, aVF (voltage on left foot)

-V (1 thru 6) = unipolar chest leads

Front 29

Ventricular Action Potential:

Back 29

-steep upstroke
-plateau
-repolarization

*.250-.300 milliseconds (compared to nerve impulses of a millisecond or so)

Front 30

Ionic Basis Underlying the Ventricular Action Potential:

Back 30

resting potential: negative at rest (-90mV)

sodium channels are closed at rest, when voltage reaches threshold (about -70mV) they open (lots of them and open very very quickly). Sodium ions rush into the cell (from the electrical gradient and the concentration gradient as well). happens within a millisecond or so
*same as a neuron

potassium channels react slower and begin to open (a lot more K inside the cell than outside) so potassium rushes out of the cell. the voltage across the membrane becomes repolarized

Cardiac cells in addition to sodium and potassium they also have calcium channels. Calcium channels are much slower than the sodium. L type channel means that is is long-lasting.

P(K) >> P(Na) and P (Ca)
so: V ~ E(K)

Front 31

Sinus Node Action Potential:

Back 31

*never at rest (continuously changing their voltage)

no resting potential!!! instead it is the pacemaker potential

systole = heart contraction
dystole = resting
*spontaneous diastolic depolarization

Front 32

Ionic Basis Underlying the SA Node Action Potential:

Back 32

upstroke is slower than in atrial cell or ventricular cell
-this is because they don’t have sodium channels
-slower voltage change
-they still have calcium L channel

If (pacemaker current)
-f stands for funny
-activated by hyperpolarization
-both sodium and potassium can pass
-but sodium will be the ion to flow into the cell
-this influx will repolarize

anti-tachycardiac agent (slows heart rate) in Europe there is a drug that blocks If channels.

Front 33

Fast and Slow Action Potentials:

Back 33

"SLOW"
-0.01 to 0.05 m/sec
-1-10 V/sec
-SA node, AV node

"FAST"
-0.5 to 5 m/sec
-100-1000 V/sec
-ventricular muscle, atrial muscle, bundle of His, Purkinje Fibers

Front 34

Sinus Bradycardia:

Back 34

<60 bpm

-physiological bradycardiac arrhythmia is from being fit (or during sleep)

Front 35

Sinus Tachycardia:

Back 35

>100 bpm

-physiological tachycardiac arrhythmia can be from working out (or if you have a fever)

Front 36

2:1 Atrioventricular Block:

Back 36

2:1 atrioventricular block (there is no QRS on every second P wave)
-there is no problem with SA node
-no problem with atria
-Where is the block?
-somewhere in AV node, bundle of His, bundle branches
-if it is in the AV node it isn’t such a big deal and can usually resolve itself. If it is in the His-Purkinje system it can be a bigger problem leading to complete atrioventricular block

Front 37

Complete Atrioventricular Block:

Back 37

need an electronic pacemaker

Front 38

What is defibrillation? What is Cardioversion?

Back 38

shock the heart with AED (automatic external defibrillator)
the shock is so big that it “resets” the impulses of the heart to make it begin again in rhythmic beats
-this is called defibrillation

can be used for v-tachycardia too. (but use less current)
-this is called cardioversion

Front 39

Reentrant Ventricular Tachycardia:

Back 39

scar tissue = "anatomical obstacle"
-circus movement reentry

put “sock” on heart in open chest.
-it has 64 electrodes on it
-records in 1/5th of a second in a circular movement
-you will be able to see if there is a scar
-surgeon cuts out scar area and sews the two healthy parts of myocardial tissue together

Front 40

Pulmonary Vein Ablation for Treatment of Atrial Fibrillation:

Back 40

-atrial fibrillation is often triggered by premature atrial contraction

-to treat take a probe that is either very hot or very cold and kill the cells around pulmonary veins (ablation) so propagation cannot occur.

-atrial fibrillation is the most common arrhythmia
why is it bad?
-blood against atrial walls is static and is prone to clotting.
-these clots could go into the ventricles and from the ventricles could possibly go to brain and kill them

Front 41

Excitation-Contraction Coupling

Back 41

EC coupling: process by which action potentials is converted into mechanical contraction:

1. "Excitation" (depolarization of plasma membrane)
2. Opening of plasma membrane L-type Ca++ channels in T-tubules
3. Flow of Ca++ into cytosol
4. Ca++ binds to Ca++ receptors (RYANODINE RECEPTORS) on the external surface of the sarcoplasmic reticulum... calcium channels intrinsic these receptors open
5. Flow of Ca++ into cytosol
6. Increase in cytosol Ca++ leads to contraction

Front 42

Mechanical Activity lags behind Electrical Activity:

Back 42

activation does not equal contraction

QRS complex can occur without a pulse

Front 43

Systole:

Back 43

"to draw together, to contract"
1. isovolumetric ventricular contraction = volume is fixed
-AV valve = closed
-Aortic and pulmonary valves = closed

2. Ventricular Contraction (blood flows out of ventricle)
-AV valves = closed
-Aortic and pulmonary valves = open

Front 44

Diastole:

Back 44

"A putting asunder, separation, expansion, dilation"

1. isovolumetric ventricular relaxation:
-AV valves = closed
-Aortic and pulmonary valves = closed
(atria are filling)

2. Ventricular Filling (blood flows into ventricles):
-AV valves = open
-aortic and pulmonary valves = closed

Front 45

Stroke Volume:

Back 45

SV = End diastolic volume - end systolic volume

SV = 120mL - 50mL = 70mL

Front 46

Ejection Fraction:

Back 46

EF = stroke volume / end systolic volume

EF = 70mL / 120mL = 0.6 (60%)

Front 47

Cardiac Output:

Back 47

CO = heart rate x stroke volume

CO = 70bmp x 70mL = 4900 ml/min
~5L/min

Front 48

Starling's Law of the Heart:

Back 48

Starling’s Law of the Heart: if there is a greater end diastolic volume, the stroke volume will increase (stretch the heart and fill it more, the harder the contraction and the more blood will be pumped out).
-during exercise the amount of blood coming back to the heart goes up, increases SV

Front 49

"pre-load"

Back 49

“pre-load” = the load on the muscle before it starts to contract
= EDV, Pressure of right atrium, ...

right atrial pressure is a good indicator of pre-load

Front 50

Stenotic Valve:

Back 50

Narrowed valve
Turbulent Flow = murmur

stenotic valve: valve doesn’t open completely.. flow of blood is the same, but cross sectional area is smaller. Fluid speeds up and becomes turbulent

Front 51

Insufficient Valve:

Back 51

Leaky valve
Turbulent Back flow = murmur

Insufficient valve: when valve is supposed to be closed, it will leak in the backwards direction. small opening will cause increased fluid speed causing turbulence

Front 52

Mean Arterial Pressure

Back 52

MAP = diastolic pressure + 1/3(pulse pressure) = 100 mm Hg

Front 53

3 ways to measure Blood Pressure:

Back 53

1. Palpation: use aneroid sphygomanometer... pump cuff to pressure higher than systolic (completely occlude artery).. slowly release pressure while palpating artery. when you feel pulse you have found systolic pressure (NOTE: this method you cannot find diastolic pressure)

2. Auscultation: in addition to above, also use a stethoscope (put over brachial artery)... korotkoff sounds: when artery opens up barely, you will have a high pressure and small surface area so fast flow which causes turbulence which causes a sound. When pressure in cuff reaches diastolic pressure the flow is no longer turbulent. There are no more sounds.

3. Oscillometry: this is an automatic system (patient can do it to themselves)
looks at rate of change of pressure and computes diastolic and systolic pressures

Front 54

autoregulation of important organs:

Back 54

Some important organs keep flow constant, despite fluctuations in Pa (“autoregulation”) i.e. the brain, heart, kidneys
-senses drop in pressure, the arterioles will dilate and the flow will go back up
-if pressure goes up, constricts the smooth muscles to bring flow back down

Front 55

The mechanisms of autoregulation:

Back 55

Metabolic: O2, increase in metabolites
Myogenic: decrease in vessel-wall stretch in organ

Front 56

Total Peripheral Resistance:

Back 56

TPR: total peripheral resistance: the resistance that the left ventricle has to pump against

R = change in perfusion pressure / flow

-perfusion pressure: mean arterial pressure - pressure in right atrium
-flow is cardiac output

* TPR = mean arterial pressure / cardiac output

Front 57

pulse pressure

Back 57

difference between systolic and diastolic pressures

Front 58

parasympathetic control of the heart rate

Back 58

1. from medulla
2. through vagus nerve (pre-ganglionic nerve)
3. releases acetylcholine to nicotinic receptor on post-ganglionic nerve)
4. postganglionic nerve innervates SA node vis muscurinic receptor (acetylcholine)

*ACh leads to potassium channels opening which leads to hyperpolarization (slows down heart rate)

Front 59

Atropine

Back 59

patients with sinus bradycardia, inject with atropine. Atropine is a competitor with acetylcholine.. so ACh binds less, more potassium channels stay open, and heart rate increases

Front 60

Sympathetic control of the heart rate

Back 60

1. from spinal cord
2. preganglionic nerve releases ACh to postganglonic which releases norepinephrine to SA node
3. B-adrenergic receptor on SA node binds NE and increases heart rate

*increases Ca-L current (which generates upstroke of A.P.) so heart rate increases

Front 61

Beta-agonist and Beta-antagonist

Back 61

Beta-agonist: increases heart rate (activates beta-receptors)

Beta-antagonist: decreases heart rate (bind to beta-receptors but has no effect so it is a competitor and thus will decrease the heart rate).. also decreases contractility of heart, so beta-antagonist is used to treat people with high blood pressure

Front 62

Sympathetic control of vessel tone

Back 62

-Most blood vessels in the body have alpha-adrenergic receptors
-norepinephrine binds to alpha-adrenergic receptors and causes smooth muscle to constrict

Front 63

alpha agonist and alpha blocker

Back 63

1. alpha agonist: constricts vessels.. increases TPR. so blood pressure will go up. this is used only in emergencies since an increased blood pressure can kill organs

2. alpha blocker: binds to receptor but no effect so no constriction. TPR will fall and so blood pressure falls

Front 64

Adrenal glands (effect of stimulation on cardiovascular system)

Back 64

-stimulated by sympathetic nervous system
-secretes NEP (1/3) and EP (2/3)
-NEP is beta agonist and alpha-agonist
-EP is beta and alpha-agonist

Front 65

What is the quick response to blood pressure regulation?
What is the long-term response to blood pressure regulation

Back 65

Short term:
-baroreceptor reflex (why we don't feint when we stand up)

Long term:
-kidneys

Front 66

What are baroreceptors? where are they located? how do they function?

Back 66

Baroreceptors are are specialized nerve receptors that interpret stretch

They are located in the carotid sinus and the aortic arch

every time the heart beats, arterial walls stretch and these receptors fire signals to the brain (how we know what the blood pressure is on a beat to beat basis)

Front 67

Baroreceptor response to decreased blood pressure:

Back 67

-decrease in arterial pressure will result in a decrease in firing of arterial baroreceptors.

-this will lead to a decrease in parasympathetic outflow to heart (increases HR)

-also will lead to an increase in sympathetic outflow to heart, arterioles, veins (also increases HR)
-increase in contractility
-increase in vasoconstriction
-increase in venoconstriction

Front 68

"Buffer Reflex"

Back 68

when the nerve to baroreceptors is cut, the blood pressure will not remain constant, it will fluctuate.

Front 69

Kidney response to increase in blood pressure:

Back 69

1. arterial pressure increases
2. pressure diuresis increases and aldosterone secretion decreases (increased urinary loss of sodium and water)
3. decrease in plasma volume
4. decrease in blood volume
5. decrease in venous pressure
6. decrease in venous return
7. decrease in end-diastolic volume
8. decrease in stroke volume
9. decrease in cardiac output
10. blood pressure decreases (MAP = CO x TPR)

Front 70

The Renin-Angiotensin-Aldosterone (RAA) system and its response to decreased atrial pressure:

Back 70

1. arterial pressure falls: kidneys secrete more renin
-renin is an enzyme. it attacks angiotensin (polypeptide made in the liver). chops 2 of the amino acids off.. you now have angiotensin I (octopeptide)..

2. angiotensin goes to lungs where ACE (angiotensin converting enzyme) is produced.. it forms angiotensin II (active compound).

3. angiontensin II binds to smooth muscle and causes vasoconstriction (much more powerful than norepinephrine)

4. Angiotensin II promotes more production of ADH (which will preserve the conservation of water)

5. Angiotensin II binds to cells in adrenal glands and causes release of aldosterone. travels to kidneys and make kidneys excrete less salt and therefore secrete less water

**increases blood pressure

Front 71

RAA system as target for drugs:
1. ACE inhibitors
2. Angiotensin II receptor blockers
3. Renin-inhibitors

Back 71

1. ACE inhibitors.. if you give drug that blocks ACE, angiotensin circulating levels will fall. so blood pressure will fall

2. Angiontensin-II receptor blockers: binds to receptors all around the body. leads to less of an effect of AGII so blood pressure falls

3. Renin-inhibitors: inhibits action of renin. less angiotensin I.. less angiotensin II.. blood pressure will fall

Front 72

Orthostasis (definition and what happens when it occurs)

Back 72

definition: standing up

How it works:
**Arterial blood pressure remains constant (baroreceptors keep up from feinting)

-when we stand up we lose blood from central blood volume (blood located in the thorax)

-so you stand up and you have less blood coming back to the heart
so right arterial pressure will decrease when you stand (because the right atrium will not be as filled)

-end-diastolic volume would also decrease then... so stroke volume would also fall.. when you stand up your SV decreases by about 50% (blood goes to legs so heart isn’t as filled)

-blood leaves thorax and pools in legs, buttocks, etc

-we would expect CO to also fall by half since CO = SV x HR.

-but it only goes down less than 50%.. this is because heart rate has increased when you stand up (due to baroreceptor reflex)) also increased contractility

since MAP stays constant and we know that CO goes to 3/4 of what it was, TPR must have increased to 4/3 of what it was

Front 73

"Muscle Pump"

Back 73

the "3rd" heart in our body..
when standing in attention, you are supposed to contract calf muscle to increase pressure to get more venous return to the heart. The one-way valves in veins prevent reflux

Front 74

Chronic Venous Insufficiency:

Back 74

chronic venous insufficiency from vascular incompetence. leads to venous hypertension (which means pressure in capillaries will also be too high).. this leads to edema. if it goes for long enough it can lead to venous ulcerations.. can lead to amputation. (common in diabetes).

think of a grandma standing for too long and their ankles swell.

Front 75

Response to Aerobic Exercise:
1. Heart Rate
2. Stroke Volume
3. Cardiac Output
4. Arterial Pressure
5. Total Peripheral Resistance
6. Oxygen Consumption
7. Arteriovenous Oxygen Difference

Back 75

1. Heart rate increases 3X (max HR = 220 - age)

2. Stroke volume decreases at very high HR

3. CO increases 3X (from increase in HR)

4. arterial pressure increases by 1.2X

5. TPR decreases to 0.4X (due to skeletal muscle vasodilation

6. Oxygen Consumption increases 9X (increases 3X from increase in CO, the rest comes from the fact that at rest we only extract a quarter of available oxygen from the blood)

7. A-V O2 Difference increases by 3 (at rest we only extract a quarter of available oxygen from the blood.. this explains how oxygen consumption increases 9X when CO only increases 3X)

Front 76

Blood Flow to various organs during exercise:

Back 76

1. Muscles at rest receive about 20% of flow, this can increase up to 12 times)

2. Skin at rest receives 9% of blood flow, during exercise it can increase by 5X (this is needed to get rid of excess heat from metabolic activity)

3. Flow to the heart also increases by 3 or 4X

4. Flow to the brain stays pretty much constant

5. Flow to all other organs decreases due to constriction (they aren't needed during exercise)

Front 77

Neural Control of skeletal muscle tone:

Back 77

*alpha receptors (norepinephrine and epinephrine binds) causes constriction

*beta receptors (epinephrine binds) causes vasodilation

(there is so much muscle, that at maximum CO we can only work out half of our muscle at a time)

-not much neural or hormonal control during max effort ----> mostly LOCAL CONTROL

(non muscle and non-exercising muscles constrict exercising muscle won’t constrict due to increase in waste products from that muscle)

Front 78

Effect of training on heart rate? on stroke volume?

Do you get hyperplasia or hypertrophy from training?

Back 78

training does not increase heart rate capacity (max HR is 220-age).. however training does increase stroke volume

In a trained athlete, their heart rate will be less than an untrained individual for a given workload

Hear hypertrophies but no hyperplasia takes place from training.

Front 79

Regional Circulations
-Heart
-GIT
-Kidneys
-Brain
-Skin
-Lungs

Back 79

1. Heart: oxygen extraction is very high at rest, so flow must increase when oxygen consumption increases. MAINLY LOCAL FACTORS CONTROL.. autoregulation

2. GI system: liver has an artery that brings in 2/3 of blood to the liver.. the rest comes from the portal vein. (when you eat there is a diversion of blood to the gut)

3. Kidneys: autoregulation. Sympathetic nerves cause vasoconstriction

4. Brain: excellent autoregulation. controlled by local metabolic factors. vasodilation in response to CO2 in arterial blood

5. Skin: controlled mainly by sympathetic nerves... reflex vasoconstriction occurs in response to decreased arterial pressure or cold. Vasodilation occurs in response to heat.

6. Lungs: very low resistance compared to systemic system. fall in PO2 causes arterioles to dilate. Hypoxic vasoconstriction (everywhere else in the body, with low PO2 there is constrictions).

Front 80

Immediate Effect of hemorrhage (7 steps)

Back 80

Blood loss leads to:
1. decreased blood volume
2. decreased venous pressure
3. decreased venous return
4. decreased atrial pressure
5. decreased ventricular end-diastolic volume
6. decreased stroke volume
7. decreased cardiac output
End Result: decreased arterial blood pressure

Front 81

Acute Response to hemorrhage:

Back 81

-decreased arterial blood pressure leads to baroreceptors firing...
1. decreased parasympathetic discharge to heart (increase HR)
2. increased sympathetic discharge to heart (increase HR)
3. increased sympathetic discharge to veins (increased constriction of peripheral veins.. leads to increased venous pressure, increased venous return, increased EDV, increased SV)
4. decreased sympathetic discharge to arterioles (increased total peripheral resistance)

Front 82

Chronic Response to hemorrhage

Back 82

Negative Feedback Loop:
1. decreased blood volume
2. decreased venous pressure
3. decreased venous return
4. decreased end-diastolic volume
5. decreased stroke volume
6. decreased cardiac output
7. decreased arterial pressure
*8. decreased pressure diuresis in kidneys (decreased water loss from urine... also increased RAA)
9. increase plasma volume
10. increase blood volume

Front 83

Normal Blood Pressure Value
Hypertension Values
Prehypertensive value

Back 83

Normal: 120/80

Hypertensive:
-systolic greater than or equal to 140
-diastolic greater than or equal to 90

Borderline (prehypertensive):
-systolic 120-139
-diastolic 80-89

Front 84

4 basic facts about hypertension:

Back 84

1. a lot of people have high blood pressure (one in 3 adults)

2. about 1/4 of people over age of 20 have high blood pressure but are unaware that they have high blood pressure... this it is the “silent killer”

3. ”essential hypertension” in 9 out of 10 cases the cause of hypertension is unknown.. (this is the medical term for unknown)

4. high blood pressure is easily detected and usually controllable

Front 85

What causes angina pectoris?

How to treat?

Back 85

pain in the chest when you try to exercsie and the heart wants to increase flow but you can’t because of the stenosis... if the stenosis gets worse than you can get angina even at rest.

Treatments:
1. inject drug that will lyse (eat away) clot... = thrombolysis

2. angioplasty: push catheter through (with balloon on it)... when you get to the clot.. inflate the balloon.. the balloon will break up the clot. also called PCI (percutaneous coronary intervention).

3. stent: stent is collapsed to get it into an artery.. get to the area of stenosis and expand it (to hold the artery open)

4. bypass graft (CABG): take artery or vein from somewhere else in the body, attach it around the stenosis (bypass the stenosis)