Midterm 1 - Amanda Flashcards
(106 cards)
1
Q
Left Ventricle
A
systemic circulation. Contraction 120 mm Hg and Relaxation 80 mm Hg. Three times thicker than right ventricle. Circular in cross-section to create a pressure pump to maximize pressure.
2
Q
Right Ventricle
A
pulmonary circulation. Contracting 24 mm Hg and Relaxation 8 mm Hg. Lower pressure to prevent net loss of fluid into alveoli. Thinner walled than the left ventricle. Crescent shaped cross-section maximizes volume of blood. Volume pump.
3
Q
Atria
A
Thin-walled and stretchy to accumulate blood. Is responsible for final 20% of ventricle filling (first part is due to suction when ventricle relaxes)
4
Q
Veins
A
thinner walled but larger than corresponding artery. High compliance - stretch easily.
- Superior and Inferior Vena Cava: Return blood to the right atrium
- Pulmonary veins: return blood from lungs to left atrium. Total of 4.
- Coronary sinus: returns blood from the heart muscle into the right atrium
5
Q
Arteries
A
Elastin which is much more compliant. Stretchy but springy which is important for blood pressure.
- Pulmonary trunk: carries blood from the right atrium to the lungs
- Aorta: carries blood from the left atrium through systemic circulation
- Coronary arteries: two. Found at the beginning of the aorta and carry blood to the heart muscle.
6
Q
Atrioventricular Valves
A
separates atrium and ventricles.
Right side is tricuspid and left is mitral.
Form puckered-lip funnel like structure.
To prevent from blowing backwards are secured to papillary muscle by chordae
7
Q
Aortic Valve
A
separates left ventricle from aorta.
three leaflets that meet at thickened edges.
When there is back-flow the leaflets balloon down which allow the edges to push together to prevent opening.
8
Q
Pulmonary Valve
A
separates pulmonary trunk and right ventricle.
9
Q
Functions of valves lying in a plane
A
First is support of the valves.
Second is to electrically separate the atria and the ventricles.
10
Q
Echocardiography
A
ultrasound of heart. Can add doppler to track flow of blood. Transducer placed under the left ventricle so on a echocardiography the transducer is the peak of the pyramid so see heart upside down.
11
Q
Normal Heart Sounds
A
S1: AV valves closing as ventricles start to contract. beginning of systole
S2: moment ventricles start relaxing and aortic and pulmonary valves start to close. beginning of diastole
systole: S1 to S2
diastole: S2 to next S1
12
Q
Split Sound (Heart)
A
asymmetry in closing of both valves. Occurs on deep inspiration and abnormally with bundle branch block.
13
Q
S3 Abnormal Heart Sound
A
Occurs in diastole during the rapid, passive phase of filling. Often heard in kids but more pronounced in elderly persons with an expanded ECF volume and those people with CHF
14
Q
S4 Abnormal Heart Sound
A
Occurs in diastole during atrial contraction because of stiff ventricles.
15
Q
Gallop Heart Sound
A
Here all four S’s
16
Q
Laminar Flow
A
blood is moving straight through vessels as if they were smooth sheets and not changing directions. most efficient movement and does not produce noise. Normal pattern of flow in the cardiovascular system.
17
Q
Turbulent Flow
A
pattern of laminar flow breaks down and blood cells swerve around bouncing off walls and causing noise.
18
Q
Stenosis
A
generic term meaning narrowing. With a valve it means that a valve can’t open fully and blood flow is narrowed.
AV = diastolic
pulmonary or aortic = systolic
19
Q
Insufficiency
A
Also called regurgitation. Valves do not close properly and blood flows backwards.
AV = systolic
aortic or pulmonary = diastolic
20
Q
Senile Aortic Valve
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Occurs in elderly (70s - 80s). stenosis and fibrosis leads to calcification of valves.
Calcification causes left ventricle hypertrophy (thicker) to generate more pressure. High pressures in the left ventricle lead higher pressures in the pulmonary circulation which can cause pulmonary edema and congestive heart failure.
Systolic murmur
21
Q
Bicuspid Aortic Valve
A
Form of aortic stenosis caused by a bicuspid valve versus the normal three leaflets. Systolic murmur. Treatment usually involves replacement in middle age.
22
Q
Rheumatic Heart Disease
A
Cause is an acute streptococcal infection involving pharyngitis (strep throat). Rheumatic fever develops 2-3 weeks afterwards and carditis causes mitral stenosis. Pressure in the left atrium increases, increasing the pressure in the pulmonary circulation causing pulmonary edema. Common symptom is shortness of breath, dyspnea. Progression leads to congestive heart failure. Diastolic murmur
23
Q
Infective Endocarditis
A
Common cause is nosocomial which is medical treatment in a hospital that results in bacteria in the blood. Vegetations form at inflamed valve leaflets. Can lead to aortic or mitral insufficiency (systolic) as well as pulmonary edema.
24
Q
Artificial Valves
A
- bi-leaflet: completely artificial valve made out of carbon fibers.
- biological valve: less problematic but shorter duration. Source is pig or cadaver. No immunological problems because endothelium is removed.
- Transcatheter aortic valve replacement: TAVR. only choice where the chest does not have to be cracked open and don’t have to open the heart.
25
Myogenic Cardiac Cell
cardiac muscle can begin a contraction on its own. Early embryonic heart is always myogenic and normal hearts have specialized cardiac muscle that is myogenic.
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Intercalated Disk
interconnect cardiac muscle and allow action potential to conduct over whole heart.
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Sinoatrial Node (SA Node): Natural pacemaker of heart which has myogenic properties. Produces action potentials at 100/min with no outside feedback. Parasympathetic nerves innervate SA Node and slow to about 70/min
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Atrioventricular Node (AV Node): Inherent rate is 60/min. May act as pacemaker if SA Node is damaged, but isn't normally because is in a refractory period while SA node initiates action potential.
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AV Bundle (of His): Muscle fibers run through the barrier of atrial and ventricular muscle cells (which are physically separated). Muscle fibers are bigger than the SA and AV node. Inherent rate of 30/min.
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Right and Left Bundle Branches: Branches from AV bundle and has similar large muscle fibers as AV bundle. Fast conduction.
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Purkunje Fibers: conduction is on inner surface of ventricles. Travels downward to bottom of ventricles than up outer walls of ventricles
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Cardiac Action Potentials
Ventricles: all are voltage-gated
A: Na+ channel opens causing an upsweep of depolarization. Fast.
B: Ca++ channels slowly open and slowly close causing the action potential to last for an extended period of time (causes plateau).
C: slow K+ channels open causing repolarization.
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Cardiac Action Potentials
SA node or any injured or sick cardiac muscle
B: slow Ca++ channels open and slowly close.
C: K+ channels open causing repolarization
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Cardiac Action Potentials
```
Pacemaker Potentials (seen in SA Node action potentials)
1. Parasympathetic Innervation: slow down pacemaker potential (less steep slope) causing longer time between heart beats. Nt is ACh with GPCR which opens the K+ channels.
```
2. Sympathetic Innervation: faster depolarization of pacemaker cells to reach threshold faster to produce faster heart rate. Nt is norepinephrine with GPCR which opens Calcium channels.
3. Adenosine: drug that opens potassium channel through GPCR to slow heart rate.
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Refractory Period in Cardiac Action Potentials
period of time when ion channels aren't back to normal state and are incapable of producing an action potential.
Ventricles have to have a refractory period before action potential or else tetanus would occur where there is steady contraction with one action potential after another which wouldn't allow the blood to pump any blood.
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Lidocaine
Blocks opening of voltage-gated ion channels in cardiac ventricular action potentials as well as in skeletal muscle.
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Introduction to Electrocardiograms
Lead II: most common
P wave: action potential moving through the atria
QRS wave: action potential moving through the bulk of the ventricles
T wave: repolarization of ventricular tissue.
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First Degree AV Block
Conduction velocity is greatly slowed so have a large interval between P and QRS wave.
Often is benign (athlete with good vagal tone). Can be due to heart disease (schema) or a variety of drugs including beta blockers, CCB's and digoxin.
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Second Degree AV block
Some of the action potentials never get to the AV node (see a P with no QRS). P to QRS interval is variable.
Causes can be schema, benign, or drug effect that reduces excitability of the heart including BBs, CCB's and digoxin.
40
Third Degree AV Block
Prolonged and misshaped QRS waves. Action potential never gets through the AV node so other specialized tissue (probably bundle branch) is causing the QRS waves.
Causes can be mild MI.
Ectopic focus in ventricles.
41
Premature Atrial Contraction
extra contraction due to an ectopic focus in atria, causing an extra heartbeat.
Cause: heart disease or benign
Longer pause after premature contraction leads to more filing of ventricles. Person may feel next beat as a little pulsation in the chest.
42
Premature Ventricular Contraction
ectopic focus in ventricle shows as a prolonged and misshapen QRS wave.
Shape of the QRS wave can be upwards or downwards or both depending (two ectopic focus) on which side of the heart.
Cause: heart disease or benign.
43
Bundle Branch Block
bundle branch damaged resulting in both ventricles contracting in a desynchronized fashion. Hear split heart sounds.
Normal rhythm but QRS wave would be prolonged and misshapen.
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Sinus Bradycardia
slow heart rate. less than 50/min
May be normal in younger healthy individuals.
Sick sinus syndrome in elderly may could bradycardia and the individual would need a pacemaker.
Other causes are hypothyroidism or certain drugs including BBs, CCBs and digoxin.
Symptoms include fatigue and fainting (syncope).
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Supraventricular Tachycardia
heart rate over 100/min
Paroxysmal: most typical are episodes that show up maybe due to stress or caffeine.
No changes in blood vessels so ventricles don't fill properly and usually are pumping less blood than normal. May have syncope.
Most common cause is AV node re-entry. May have a fast and slow pathway in AV node. Fast pathway causes an action potential and then after the refractory period the slow pathway creates the next action potential.
46
Wolff-Parkinson-White Syndrome
Type of supraventricular tachycardia
Rare cause is an accessory pathway that creates a loop from the normal pathway then after the action potential goes through the ventricles it exits back into the atria through an accessory pathway. Cure is ablation which is to destroy the tissue that holds the accessory pathway.
47
Ventricular Tachycardia
Ectopic focus in ventricle that is constantly producing an action potential.
Cause can be due to an MI, or may be genetic (abnormal ion channel "myopathy")
Will lapse into ventricle fibrillation which is death. Treatment is to have a pacemaker/defibrillator combination that blasts an action potential into the heart to wipe the slate clean if an individual goes into ventricular tachycardia.
48
Atrial Fibrillation
Action potential continues over atria indefinetly and cause the atria to quiver instead of pumping.
Periodiacally the action potential hits the AV node causing contraction
ECG is a random action potential frequency.
May or may not be symptomatic.
49
Treatments for Atrial Fibrillation
Aspirin (thromboxane) and clopidogrel (blocks ADP)
Warfarin (vitamin K antagonist to reduce prothrombin). Narrow therapeutic index and constant measurement of prothrombin time.
Dabigatran. direct thrombin inhibitor
Apixaban. inhibits factor X.
Ablation and/or pacemaker.
50
Ventricular Fibrillation
lethal arrhythmia
Causes include MI, myopathy leading to ventricular tachycardia.
Treatment: pacemaker with a defibrillator.
51
Pharmacology of Arrhythmias
Na+ Channel blockers: lidocaine, flecainide
Beta Blockers: propranolol, metoprolol, etc...
Prolong repolarization to increase refractory period: amiodarone
Calcium Channel Blockers to reduce excitability of heart: Verapamil
Open K+ channels: adenosine.
52
Valves and Heart Sounds in the Cardiac Cycle
All occur at the very end of the peak of the QRS wave.
AV Valve: The AV valve is closed. Ventricular pressure increases. Atrial pressure remains low and constant. When ventricular pressure falls below atrial pressure the AV valve opens.
Aortic Valve: Left ventricular pressure increases. When left ventricular pressure is higher than aortic pressure the aortic valve opens. When the left ventricular pressure falls below aortic pressure the aortic valve closes.
Heart Sounds: S1 is heard right at the closing of the AV valve. S2 is heard when both the AV valve opens and the aortic valve closes which occurs simultaneously.
53
Phase 1 of Cardiac Cycle
Isovolumetric Contraction: Phase 1. Systole. AV valve closes, aortic valve is closed and have S1 heart sound.
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Phase 2 of Cardiac Cycle
Ejection: Phase 2. Systole. Aortic valve opens. First half of ventricular pressure and second half is reduced.
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Phase 3 of Cardiac Cycle
Isovolumetric Relaxation: Phase 3. Diastole. Aortic Valve closes. Ventricular pressure drops.
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Phase 4 of Cardiac Cycle
Passive Filling: Phase 4. Diastole. Aortic pressure falls and atrial pressure starts rising. Split into rapid filling then passive filling.
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Phase 5 of Cardiac Cycle
Atrial Contraction: Phase 5. Diastole. AV valve open.
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Cardiac Output
Cardiac output is the amount of blood pumped per minute. Determined by heart rate (beats/min) and stroke volume (blood per beat). CO = HR \* SV
Average is about 5 L/min with no activity and resting. Young, healthy athlete can be around 20 L/min. World-class athlete is 35 L/min
59
Heart Rate Regulation
Heart rate: determined by pacemaker potential controlled by K+ channels (slowing) and Na+ and Ca++ (speeding). Voltage gated. GPCR.
parasympathetic input: Nt is ACh. Slows heart rate by opening K+ channels. Parasympathetic tone keeps heart rate low when at rest.
sympathetic input: Nt is norepinephrine. Increases heart rate by opening Ca++ channels
Beta-adrenergic receptors: epinephrine does same thing as sympathetic nerves
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Stroke Volume and Sympathetic input
sympathetic input: increased Ca++ release and storage.
Ejection fraction = stroke volume/end diastolic volume
End diastolic volume is how much blood is in the ventricle after filling.
61
Stroke volume and Afterload
If aortic pressure increases, volume of blood that flows through the aorta is reduced.
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Frank-Sterling Mechanism
Increased volume in central veins (superior and inferior vena cava)
Frank-Sterling Mechanism: as end diastolic volume increases so does stroke volume.
Heart responds to stretch by contracting more forcefully due to increased ATP expenditure.
Keeps the two ventricles pumping the same amount
63
What alters Stroke Volume?
Posture: lying on the floor causes increased SV due to an increase in central venous pressure and end diastolic pressure
Muscle contraction: muscle pumping works on veins that are large, highly compliant and have valves
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Systolic Heart Failure
Causes: MI, myopathy
Results: EF falls. Below 10% is considered to be cardiogenic shock. Ventricle dilates causing an increase in end diastolic volume but because the ventricle is weak do not see a normal Frank-Sterling response.
Law of Laplace: A dilated ventricle requires more tension in the wall to generate the same pressure. P = T/R. Ventricle must work harder to accomplish same thing.
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Abnormal Response in Heart Failure
Abnormal hypertrophy
fetal isoforms are synthesized.
Collagen damage including fibrosis.
Abnormal regulation leads to continue sympathetic activation. Result is angiotensin II over-production.
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Angiotensin II production in heart failure
Poor renal perfusion appears to kidney as low ECF volume. Kidney releases renin which acts to convert angiotensinogen to angiotensin I. ACE converts angiotensin I to angiotensin II which constricts arterioles (increases afterload) and expands ECF.
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Congestive Heart Failure
Increased ECF that causes pulmonary edema and other volume overload issues produces congestive heart failure
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Diastolic Heart Failure
EF is normal which defines as diastolic
compliance of ventricles decreases making them stiff and unable to relax and fill properly. Ventricle walls become thicker. EDV is decreased.
Cardiac output is decreased.
Causes: long-standing hypertension, valve problems, diabetes, obesity, elderly and women are more prone then men.
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Treatment for Heart Failure
ACE inhibitors: diuretic that causes vasodilation of arterioles decreasing afterload
Beta-adrenergic blockers: address the continuous sympathetic stimulation
aldosterone antagonist: steroid hormone that normally acts to save sodium and expand ECF. Antagonistic activity will decrease these actions.
Diuretics: Furosemide. decrease ECF
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Hydrostatic Pressure
barrel with spout at the bottom. Pressure is created by the weight of the water.
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Electrostatic pressure
balloon and tension in the walls causes pressure. Pressure that we see in arteries.
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Resistance to flow
determined by diameter. Determines flow of fluid. If you reduce the diameter by 1/2 it reduces the flow of fluid by 1/16th. Hence, the smallest parts of the arteriole system determine flow.
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Arteries structure
Elastic Arteries: Aorta and major branches. Have a lot of elastin in the tunica media layer of the wall.
Muscular Arteries: Smaller arteries. Tunica media layer contains a lot of smooth muscle.
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Role of elastic arteries
expansion during systole to store pressure energy
when the aortic valve closes in diastole the walls are capable of giving back pressure energy by relaxing the elastin walls.
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compliance of aorta
compliance is higher in younger people.
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Mean arterial pressur
= CO + TPR. Where TPR is determined by the diameter of the smallest arteries, arterioles. Vasoconstriction of arterioles increases TPR and vasodilation decreases TPR
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Carotid Baroreceptor Reflex
Reflex that adjusts the mean arterial pressure back to a normal level. Sensors are in the carotid sinus and the integrating center is the medulla.
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Pulse Pressure
= SP- DP. Determined by stroke volume and compliance. Remember that flexible arteries have high compliance and stiff arteries have low compliance. Decreasing compliance increases PP.
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Claudication
While sitting the patient is fine, but when they start to walk after awhile pain is felt in the calves.
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Effects of Branching Arteries
In young healthy adult the reflective wave increases the diastolic pressure.
In the elderly with lower compliance, because the wave travels faster, the addition of the initial wave and the reflected wave gives a higher systolic pressure and a lower diastolic pressure. Coronary blood flow is driven by diastolic pressure.
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Atherosclerosis: sequence of events to form a fatty streak
Begins with damage to the endothelium resulting in an inflammatory response. LDL cholesterol and apolipoprotein apoB accumulates in the tunica intima. Macrophages begin to accumulate at the site. Macrophages take up so much cholesterol they are now called foam cells that start to accumulate in the growing plaque. This is seen as a fatty streak in the coronary arteries.
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Atherosclerosis: formation of a fibrous plaque
Growth factors secreted from the growing plaque cause smooth muscle cells to migrate to the tunica intima. Release of connective tissue begins to form a fibrous plaque.
The center of the plaque tends to become necrotic and releases crystalized cholesterol.
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Atherosclerosis: formation of the fibrous cap
Fibrous cap is the region between the necrotic tissue and the blood flow. Can be a thin or thick cap.
Thick caps tend to form ischemia.
Thin caps may rupture and expose extracellular lipids to the blood flow promoting clotting. If the clot breaks free it is called an infarction. Myocardial infarction occurs when the clot breaks free and clogs an artery. A stroke occurs when the clot breaks free in the common carotid.
With time the cap becomes calcified
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Ischemia
Symptoms of ischemia (inadequate blood flow): referred pain called angina pectoris, claudication (ischemia to legs) and syncope (ischemia to brain).
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Aneurysms
Local dilation of an artery at a weak spot. Aneurysms in the cerebral arteries are called berry aneurysms and are possible locations of a hemorrhagic stroke. Abdominal aneurysms are due to cholesterol plaques in the distal aorta.
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Atherosclerosis: risk factors
hypertension, diabetes, smoking, hyperlipidemia.
Farmingham risk calculator: assess risk with information such as age, BP, diabetes, LDL/HDL, gender and age.
Increases in plasma levels of C-reactive protein is a potential risk factor
Ankle/brachial index is also a risk assessment tool. Low ratios reveal significant levels of atherosclerosis.
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Atherosclerosis: treatments
Statins, fibrates, niacin, ezetimibe (reduces cholesterol uptake in GI).
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Arterioles: Local chemical factors
cause vasodilation and include CO2, H+, K+, adenosine and osmolarity
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Arterioles: sympathetic nerves
norepinephrine acting on alpha receptors causes vasoconstriction. Effect is strong on the skin, digestive tract and kidney
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Arterioles: Non-adrenergin, non-cholinergic autonomic nerves
release NO which is a vasodilator
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Arterioles: hormones
in blood vessels there are both beta-2 (vasodilation) and alpha (vasoconstriction) receptors. Important in skeletal muscles where activation preferentially activates beta-2 in exercise.
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Arterioles: kidney hormones
angiotensin II and vasopressin are vasoconstrictors
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Arterioles: Paracrines
inflammatory paracrines cause vasodilation and NO.
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Arterioles: distribution of blood to the skin
sympathetic nerves cause greater releases of norepinephrine resulting in vasoconstriction
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Arterioles: distribution of blood to the digestive tract
sympathetic nerves cause vasoconstriction
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Arterioles: distribution of blood to the skeletal muscless
Epinephrine causes vasodilation during exercise but the greatest effect is due to local chemical factors including increases in extracellular K+ and increased osmolarity.
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Arterioles: distribution of blood to other arterioles
Reactive hyperemia occurs when blood flow has been constricted to a region for a long time then is suddenly returned. Example is Raynaud's Disease which is the spasm of arterioles in the fingers/toes due to cold or stress.
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Arterioles: distribution of blood to brain
if CO2 levels fall as in hyperventilation vasoconstriction occurs
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Capillaries: permeability
anything smaller than a blood protein
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Capillaries: osmotic effect
Protiens in blood pull liquid into capillary but this is equally and oppositely balanced by the capillary blood pressure. Albumin, a protein formed in the liver also balances the osmotic effect.
101
Edema causes
Caused when more fluid leaves the capillaries and accumulates in tissue space.
most common cause is inflammation
Decreases in blood proteins: hemorrhage or starvation
Increases in ECF volume: congestive heart failure
Increases in venous pressure: standing for a long time while not contracting leg muscles
Blocked lymphatics
Hepatic portal hypertension causing abdomen edema or ascites.
102
Veins
compared to arteries: much thinner walled, higher compliance, larger, more anastomoses (vessels divide but reconnect later), more valves, and the amount of blood in much higher.
Sympathetic nerves: causes veins to become less compliant and they contract so as to allow for compensation in blood volumes. Also happens with angiotensin II.
103
Types of hypertension
"White-coat hypertension": elevated blood pressure in a healthcare setting so requires multiple at home readings to diagnose hypertension.
Secondary hypertension: resulting hypertension due to another disease. Kidney disease for example. Only 5% of cases.
Essential hypertension: Goal for hypertensive is less than 140/90 or less than 130/80 with other co-morbities. Usually causes increased CO although in the elderly will be increased TPR.
104
Treatment of hypertension
Thiazides: first choice, reduces ECF
Beta adrenergic blocker: if problem arises from heart condition
ACE inhibitors or angiotensin II antagonists: act on both ECF volume and TPR.
CCB
105
Syncope
sudden loss of consciousness and postural tone.
Vasovagal syncope: occurs due to abrupt bradycardia and vasodilation. Tilt table test is the primary diagnostic tool where you wait for an abrupt decreased heart rate and fall in arterial pressure.
Orthostatic Hypotension: also called postural hypotension. Faint on standing. typical cause is low ECF volume.
106
Cardiovasular result of exercise (6)
1. As a muscle begins contracting in exercise arterioles to that muscle dilate due to local chemical factors.
2. Carotid Baroreceptor reflex works to adjust the Mean arterial pressure but is not the only factor to keep it constant during exercise.
3. Feedforward signal called the central command anticipates changes in the mean arterial pressure.
4. Cardiac output is increased through sympathetic nerves.
5. Muscle pumping works through the Frank-starling method to increase cardiac output by squeezing blood back into the central veins.
6. Sympathetic vasoconstriction occurs in the gut, skin and inactive skeletal muscles to compensate for the increased usage in the exercising muscle.
