Phys Exam 2 Flashcards
Nonmodifiable risk factors or CVD
Gender, age, family history
Modifiable risk factors of CVD
Hypertension, dyslipidemia, cigarette cooking, obesity (metabolic syndrome, diabetes ,management), physical activity, sleep disorders, mental stress and depression, oral health.
Materials transported in the cardiovascular system
Oxygen, nutrients and water, wastes, immune cells, antibodies, clotting proteins, hormones, stored nutrients, metabolic wastes, heat, CO2
Closed loop system
Several “sub loops” or sections within the CV circulation have unique functional significance. Systemic system, coronary system, portal systems.
What is a pulmonary embolism
A clot in the pulmonary system
What is the difference between a traveling and stationary clot
An embolism is a solid fragment traveling through vessels until it gets lodged into a narrow vessel and becomes a clot.
Clot on the venous side of circulation
Will always result in a pulmonary embolism
Portal systems
Any part of the systemic circulation in which blood draining from the capillary bed of one structure flows through a larger vessel to supply the capillary bed of another structure before returning to the heart. Departing, renal, hypothalamic-hypophyseal.
Does the venous or arterial system have a higher pressure
Arterial
Average pressure in arteries is
Approximately 10th mmHg
Average pressure in veins
0 mmHg
What way does blood/fluid flow
Down a pressure gradient
During the final months of pregnancy is its best for the mother to sleep in which position? Why?
Lying on the left side because it avoids compression of the vena cava
What is static system pressure influenced by
Fluid volume, wall compliance
What is a static system pressure influenced by
Fluid volume and wall compliance (stretch-ability)
What is a flowing system pressure influenced by
Driving force/pressure, pressure gradient, resistance to flow.
What influences resistance to flow
Diameter of vessel, total length of vessel, viscosity of fluid
What affects wall compliance of vessels
Age, plaque B/U, some genetic factors.
What is the driving force of blood pressure
Pressure created by heart muscle contractions in the ventricle moves the blood
What chamber of the heart drives systemic circulation
Left ventricle
**Flow is __________ proportional to the change pressure gradient and ________ proportional to the resistance of flow
Directly and inversely
What results in increased flow
Higher system pressure gradient
What decreases flow
Higher resistance
Resistance to flow
Is a function of vessel length, blood viscosity, vessel diameter.
What is the most significant influence on resistance
Radius/diameter of the vessel
What happens to this pressure if the blood vessels constrict
Blood pressure increases
What happens to blood pressure if blood vessels dilate
Blood pressure decreases
What controls blood vessel radius/diameter
Autonomic nervous system? Sympathetic and parasympathetic
Additional changes to _________ and __________ can also affect blood pressure
Volume of blood and vessel wall compliance
What happens to blood pressure when someone is dehydrated or is taking a diuretic medication
Blood pressure decreases
Which organ system of the body is most responsible for regulation blood volume
Kidneys
How would atherosclerosis of numerous arteries affect blood pressure
Increases it
How much does small vessel change in radius change resistance to flow
To the 4th power
If the radius of tube A changes from 1 to 3 what happens
Resistance changes to 1/3^4
flow rate equals
The volume of blood that passes a given point in the system per unit time
Flow velocity
Is the distance a fixed volume of blood travels in a given period of time
at a constant flow rate ….
The velocity of flow through a small tube will be faster than through a larger tube
Major component of the heart
Myocardium
Atrioventricular valves
Between atria and ventricles. Tricuspid of right and bicuspid on left
Semilunar valves
Between ventricles and the two main arteries exiting the heart. Aortic and pulmonary
What is the function of the papillary muscles and Cordae tendinae
They connect to valves and hold them closed to prevent back flow
Myocardial contractile cellls
Majority of heart cells and are striated fibers organized into sarcomeres
Myocardial autorythmic cells (pacemaker cells)
Approximately 1% of heart cells. Smaller and fewer fibers and dont have sarcomeres. Signal contraction/set rate of beat.
SA node
Controls heart beat (70-80 BPM)
AV node
40-60 bpm, if the SA node is not working the AV node can take over and get enough blood to the brain
Bundle branches and purkinje fibers
20-40 bpm. These cells can contract on their own but not enough to keep the heart going
What neurons control the heart
Autonomic
What is the hormonal influence on contraction of the heart
Epinephrine
Contraction speed of the heart
Intermediate compared to skeletal and smooth
Does the force of myocardial contractile cells vary
Yes. Force generated by cardiac muscle is proportional to the number of myosin/actin cross bridges that are active.
What is the number of active cross bridges in cardiac muscle determined by
The amount of Ca++ available to bind to troponin
Where does intracellular Ca++ come from in cardiac muscle
The sarcoplasmic reticulum
How can you increase contraction of the heart
Increase stretch
Myocardial contractile cell similarities to neurons and skeletal muscle cells
Depolarization is die to Na+ entry and repolarization is due to K+ exiting.
Myocardial contractile cell difference from neuron and skeletal muscle cells
Long AP (plateau) die to Ca++ entry in the cell to prevent tetanus.
What is tetanus and why is it important that the heart contraction does not reach a state of tetanus
A continuous tonic spasm of a muscle—it could result in fainting at minimum but could be fatal because the heart would be unable to pump blood to the brain.
Phases of myocardial contractile cell action potential
0-depolarization, Na+ channels open
1-initial repolarization, Na+ channels close
2-repolarization plateau, Ca++ channels open;fast K+ channels close
3-rapid repolarizatoin, Ca++ channels close; slow K+ channels open
4-RMP
How does lidocaine work in a local injection
Alters signal conduction in neurons by blocking the fast voltage gated Na channel in the neuronal cell membrane responsible for signal propagation
What is the greatest potential risk to performing too many intramural injections of lidocaine on a patient who is hypersensitive to the drug
Greatest risk is cardiac arrest, but more likely you will see decreased BP
What makes up the conducting system of the heart and what is the conducting system of the heart
Myocardial autorythmic cells and it is the SA, AV nodes and purkinje fibers
Pacemaker potential
Is an unstable membrane potential that cardiac autorythmic cells have.
AP of cardiac autorythmic cells
Pacemaker potential phase: Na+ flows in through ion funny channels, hyperpolarization, as membrane potential slowly rises I F channels close and slow Ca++ open
Depolarization phase: threshold is reached AP occurs due to opening of fast gated Ca++ channels
Rapid repolarization:peak AP, Ca++ close and K+ channels open causing repolarization. K+ channels close at the end of this phase
What effect would a drug that blocks the ion funny channels have on heart function
No response, heart rate would stop.
How does the rising phase of an AP in the heart differ form smooth and skeletal muscle
The heart has Ca++ entry, the others have Na+
What does ryania speciosa do
It enables calcium ions to exit the SR and enter the cytoplasm resulting in a sustained contracture of skeletal muscles w out depolarization of muscle cell membrane.
How do depolarizations of autorythmic cells spread to adjacent contractile cells
Through gap junctions
What would happen to conduction if the AV node malfunctioned and could no longer depolarize?
The electrical signal from SA node would stop at the AV node, ventricle would not receive a signal. Purkinje fiber pacemaker would take over and produce a very slow beat
Electrical conduction of the heart
SA node—>internodal pathway from SA to AV—>AV node—>AV bundle—>bundle branches—>purkinje fibers
How do the ventricles contract
From the bottom up
Waves of an EKG
Reflect depolarization or repolarization of the atria and ventricles. P wave, Q wave, and T wave
P wave
Atrial depolarization
QRS complex
Progressive wave of ventricular depolarization (atrial repolarization)
Q wave
Sometimes absent on normal EKG
T wave
Ventricular repolarization
Where is atrial repolarization represented on the EKG
It is part of the QRS complex but is overpowered by the ventricular activity
Segments of an EKG
Sections of baseline between waves.
Interval
A combination of a wave and segment
P-R segment
Conduction through AV node and AV bundle
What allows one to assess for abnormalities in an EKG
Segments
Are mechanical or electrical events lagging in the heart
Mechanical events lag slightly behind electrical
What does the EKG represents
The summed electrical activity of all the heart muscle cells
Standard EKG speed
Runs 1mm per .04 seconds
Arrhythmia
Irregular interval lengths
How can you tell heart rate from an EKG
Time between two comparable waves on the tracing. P or QRS, just use a consistent one.
Normal serum potassium range
3.5-5.0 mmol/L
What are serum potassium levels outside the standard range associated with
Cardiac arrhythmias. Hypo and hyperkalemic states can put patients at risk for sudden cardiac death.
Hypokalemia on EKG
Significant hypokalemia is associated with Q-T interval prolongation and subsequent risk of ventricular fibrillation
Hyperkalemia on EKG
Significant hyperkalemia is associated with peaked T waves and widened QRS complexes with subsequent risk for bradycardia and asystole.
What makes the “lub” sound
Closing of the AV valves
What makes dub sound
Closing of semilunar valves
Late diastole
Both sets of chambers relaxed and filling passively
Atrial systole
Atrial contraction forces a small amount of blood (20%) into ventricles
Isovolumetric ventricular contraction
First phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves
Ventricular ejection
As ventricular pressure rises and exceeds pressure in the atria, the semilunar valves open and blood is ejected.
Isovolumetric ventricular relaxation
As ventricles relax, pressure in ventricles falls, blood flows back into cusps of semilunar valves and snaps them clsoed.
Diastole
Cardiac muscle relaxes
Systole
Cardiac muscle contracts
Where does the right atria receive blood from
SVC and IVC
Where does the left atria receive blood from
Pulmonary veins
During atrial systole what creates a visible pulse
Some blood being forced back into the vena cava in the jugular vein if someone is laying supine.
If someone is upright and you can see a pulse in the jugular vein what may be wrong
Above normal atrial pressure
Auscultation is using a stethoscope to listen to hear sounds through the chest wall. At which point in the heart cycle would you first begin to hear blood regurgitating through a faulty aortic SL valve back into the left ventricle
Isovolumetric ventricular relaxation
Does the L ventricle eject all of its blood by the end of ventricular systole?
No, there is always some blood in there. Around 65 mm
Stroke volume
Is the amount of blood pumped per contraction/beat
End diastolic volume
Is maximum amount of blood in a ventricle during a mechanical heart cycle
End systolic volume
Is the least volume of blood in a ventricle during a mechanical heart cycle
Why is there some residual blood left in the ventricle after systole?
Allows for compensatory change with change in vessel capacities. Safety mechanism.
How to find stoke volume
EDV-ESV
Is stroke volume a constant
No, it can increase up to 100mL during exercise and is controlled by many different factors
Cardiac output
Volume of blood pumped by one ventricle in a given period of time. BPM X SV
Four determinants of cardiac output
Heart rate
preload-more venous blood in
contractility-muscle contraction force
afterload-less vascular resistance out
What happens when one side of the heart begins to fail
Blood pools in the circulation behind the failing side because loss of cardiac muscle function
Heart rate
Highly variable, initiated by SA node, modulated by neuronal and hormonal input, SA node control typically dominated in the PNS.
What affect do sympathetic neurons have on HR
They bind to beta 1 receptors and increases Na+ and Ca++ influx, increase rate of depolarization, increase HR
What affect do parasympathetic neurons have on HR
Bind to muscarinic receptors and increase K+ efflex and decrease, decrease hyperpolarization cell and rate of depolarization, decrease HR
What does epinephrine do to hear rate
Depolarize the autorythmic cell and speed up the pacemaker potential, increasing the heart rate
How does an epi pen work
It relaxes smooth muscle in the airways to reduce wheezing and improve breathing. Constricts blood vessels which decreases swelling and increases BP
How do cholinergic agonist drugs or “parasympathetic drugs” work
Slows heart rate, causes vasodilation, constriction of pupils, secretion of sweat, saliva, tears, and mucus (in the respiratory tract) and constriction of bronchioles.
What part of the NS dominates tonic control of HR
Parasympathetic branch of the ANS
Chrontoropic
Means rate or timing of a physiological process. These drugs influence heart rate.
Chronotropic incompetence
Broadly defined as the inability of the heart to increase its rate commensurate with increased activity or demand
What controls the HR response during exercise
Catecholamines from the eternal glands, resulting in significantly slower increase of the HR at onset of exercise, reduced peak HR, and delayed return towards resting values after cessation of exercise.
What happens to nervous system control of heart rare in transplant patients especially during exercise
They faint because HR can’t adapt. Higher HR due to loss of parasympathetic control. Re-educated HR during exercise form chrontoropic incompetence due to denervation
Heart rate is under ANS and hormone control, this is also known as
Chronotropic
Preload and contractility are known are _______
Ionotropic
What determines preload
The volume of blood in the ventricular wall. Length tension relationship of myocardial cells.
What influences contractility of the heart
Influenced by stretch of muscle cells and chemical/electrical factors (drugs, hormones, SNS)
Frank starling law
States that stroke volume increases as EDV increase increases. EDV is determined by venous return. More ventricle stretch means more powerful contraction.
Venous return (preload) is affected by
Skeletal muscle pump, respiratory pump, sympathetic innervation of veins.
Skeletal muscle pump
Skeletal muscle contraction promotes venous return, especially in the lower limbs.
Respiratory pump
Lower atmospheric pressure in thorax with inhalation, decreases thoracic vena cava pressure which helps draw more blood into the vena cava. Also enhanced by higher abdominal pressure with diaphragmatic contraction.
Sympathetic innervation of veins
Vasoconstriction squeezes blood out of veins sending more blood into the right atrium of the heart
Length-tension relationships preload skeletal muscle
As skeletal muscle is stretched from very short lengths, its tension increases because excessive overlap of myofilaments is removed.
Length-tension preload relationship of cardiac muscle
As cardiac is stretched form very short lengths, its tension increases from removing interfering myofilament overlap and from increasing the number of active cross bridges by increasing sensitivity of myofilaments to Ca++
What is the difference in heart muscle tension development when it is stretched to 80% of maximum length compared to stretched at 95% max length
Cardiac muscle tension development/contractile force production is INCREASED significantly at 95% stretch compared to skeletal muscle. Necessary to pump additional fluid volumes
What is the length-tension relationship of preload known as
Starling curve
How would venous dilation affect stroke volume
Decreases stroke volume and reduces venous return
Inotropic
Modifying the force or speed of contraction of muscles. Any chemical that affects contractility is an inotropic agent
Positive inotropic drugs
Increase/strengthen contractility. Which pumps more blood with fewer heart beats.