cardio physio Flashcards
What is MAP?
Mean arterial pressure has a goal of 60-70 mmHg
What is the direction of blood through the heart?
What is the equation for the volume of blood moved per unit of time?
F= deltaP/R
F= volume of blood moved per unit of time
P=pressure
R= resistance
Blood desires to move from an area of higher pressure to lower pressure
Flow is directly proportional to changes in pressure and is inversely proportional to resistance
What is the epicardium?
Visceral layer of pericardium
What are the factors that determine resistance?
Blood viscosity, total blood vessel length, Blood vessel radius (most important) because of dilated vessels= decrease and constricted vessels= increase. High sugars, flow is like maple syrup
What is the myocardium?
Circular or spiral bundles of contractile cardiac muscle cells (myocytes). Myocardium has two systems or types of cells. Conducting (SA node, AV node, etc) cells and contractile (myocytes) cells
What is the endocardium/endothelium?
Innermost layer, is continuous with endothelial lining of blood vessels
What are intercalated discs?
Are connecting junctions between cardiac cells that contain: desmosomes that hold cells together, prevent cels from separating during contraction. Gap junctions allow ions to pass from cell to cell, electrically couple adjacent cells
What allows the heart to be a functional synctium?
A functional synctium is a single coordinated unit or “function in synchrony” and the one in the heart is made up of intercaletd discs, desmosomes, and gap junctions (use calcium)
What is the conduction system of the heart?
Conducting system→ SA (pacemaker) → (pause) AV → bundle of HIS → R/L bundle branches → Purkinje fibers
The conducting system initiates the depolarization and the transfer of signal
Conducting system→ SA (pacemaker) → (pause) AV → bundle of HIS → R/L bundle branches → Purkinje fibers
Opening of sodium channels and the opening of potassium channels
Influx of calcium ions leads to depolarization
Inactivation of K and Ca channels
There is no flat line, this is pacemaker potential always flowing up and down.pacemaker potential is setting all this up and is due to sodium channels opening. The depolarization is then carried out by calcium and the repolarization phase is done by potassium.
What is the cardiac plexus?
Cardiac plexus→ branches of the vagus nerve and sympathetic trunk
The vagus nerve and the sympathetic trunk have fibers. The sypathethic trunk releases norepi or epi for beta adrenergic receptors of the heart to speed it up, and increase what we call contractile cells of the heart which is the strength of contraction.
Parasympathetic fibers release Ach onto muscarinic receptors to slow down heart rate for rest and digest. So, we have this intrinsic system, but we can also modify it as needed.
What is the contractile system?
In the cell of a myocyte. Calcium flows into the cell and triggers the release of more calcium from the sarcoplasmic recticulum (SR). Cross bridging of contraction of myocytes, actin and myosin activated and calcium is released for SR. The magnitude of contraction is directly proportional to the amount of calcium released, which makes these a great target for calcium channel blockers. The cross bridges of actin and myosin allow for contraction of the cardiac myocytes.
Inotropes act here (contractilty effects)
Pronotropes affect heart rate
What is the contractile system?
Rapid depolarization from sodium, then the sodium channels are inactivated, and then there is a plateau phase. The plateau phase represents the opening of calcium and potassium channels shortly after that. The potassium flowing out, finally starts cell repolarization and especially speeds up when calcium channels close. The one thing we do have here in the contractile cells of the heart are refractory periods. The pink is the absolute refractory period and the sand is the relative refractory period (strong enough stimulus will cause contraction). The heart cannot experience tetany.
What are the phases of blood movement through the heart?
Atrial systole→isometric ventricular contraction→rapid ventricular ejection → reduced ventricular ejection → isometric ventricular relaxation (blood is sucked back in some in order to close the valves)→ rapid ventricular filling
What are the 4 determinants of cardiac output?
Afterload, preload, contractility, and heart rate
What is cardiac output?
Volume of blood pumped out of each ventricle per unit of time. CO= HR x SV. Chronotropy- refers to the contractility, HR
Mostly influenced by heart rate
Normal cardiac output is about 5.25 Liters
What is stroke volume?
Volume of blood each ventricle ejects during contraction. SV= EDV-ESV, inotropy (stretch and contract back)
End diastolic volume - the end systolic volume
What are the chronotropic effects on the heart?
What is preload?
Volume of blood filing the heart before contraction (aka venous return). If we fill up the heart more. What can impact preload? Increase blood volume, ADH, aldosterone, IV fluids. Increase preload- increase diastolic volume, hypovolemia
What is afterload?
Pressure the heart must pump against to eject blood (aka vascular resistance) what can increase afterload? Vasconstriction, aortic stenosis, hypertension, hyperlipidemia, plaques in the blood vessels, increase in blood viscosity. Vasodialtion- nitrates decrease afterload and dilates vessels of the heart. Increase afterload- increase systolic volume, increase resistance. To decrease afterload, we can dilate with things like nitrates (nitroglycerin), vasodilation.
What is inotropy?
Contractility of the heart
What are the formulas for stroke volume?
What are the inotropic effects on the heart?
digoxin and dobutamine increase contractility of the heart
What is the formula for cardiac output?
CO= HR x SV
What is the formula for stroke volume?
SV= EDV-ESV
What is the impact on stroke volume and cardiac output?
So in exercise, you’ll have increases in cardiac output modestly, so when youre compensating with exercise in the SVT at very high heart rates. Even though the HR x SV drops so significantly in SVT that CO drops. So at very extremely high rates where you’re uncompensated in situations such as SVT, you will have a decrease in CO despite the fact that your HR is high. In compensated situations such as exercise, your cardiac output will actually stay the same nad SV will increase. In exercise, your HR doesnt just speed up, contractility speeds up, you know, your pre-load increases.
There are situations where your strong contractility will not increase HR and thats in SVT for example. High HR results in a decrease in diastolic volume.
In parasympathetic effects, a decrease in HR gives more tiem for filling, but HR is decreasing and therefor CO will decrease, despite decrease in EDV.
Increase contractility, decrease ESV, so less blood left over after contraction and that’ll increase your cardiac output, because you have a very clear increase in stroke volume.
When we increase HR a lot, we decrease end diastolic volume and therefore decrease cardiac output. During moderate increase in HR like in exercising, we increase cardiac output. In the parasympathetic nervous system, when we decrease contractility, it doenst have many effects. It doesn’t really do much in regards to our cardiac output but when you start to add in things like heart failure, where the muscles get stretched out and they really cannot contract, then you start to see decreases in SV like in cases of heart failure. This will lead to a decrease in cardiac output and the ejection fraction is decreased
HR is really the biggest influence
Vascular smooth muscle is essentially afterload
Vasodilation is parasympathetic
What is the ejection fraction (EF)?
Quantification of contractility. EF= SV/EDV, 50-70%. This is measured on echo, or cardio MRIs, etc. Percent of blood that the LV ejects during contraction
What are the blood vessels?
Arteries, arterioles, capillaries, venules, veins
Artery use things like pressure, pumping of the heart, elasin and recoil to facilitate blood movement
Veins have valves, some smooth muscle changes and skeletal muscles
What is diastolic pressure (DP)?
Minimum arterial pressure reached just prior to ventricular ejection. Indicates recoil
What is systolic pressure (SP)?
Maximum arterial pressure reached during the peak of ventricular contraction and ejection (systole). Peak pressure during systole, aka when the left ventricle contracts and is ejecting blood. Indicates pressure
What is the formula for compliance?
compliance= delta volume/ delta pressure. Arteries are often called pressure reservoirs and so arteries have stretchability or compliance
What is arterial blood pressure (BP)?
Is stated as SBP/DBP = 120/80. Arteries are elastic and the stretch out, so we can measure a pressure when they are returned back
What is pulse pressure (PP)?
This is a good indicator for cardiovascular health. Difference between SBP and DBP. PP
Define blood pressure
SBP-DBP=120-80= about 40-60 mmHg. Consider: SV, speed of ejection, arterial compliance. A PP >60 mmHg is considered widened and may suggest arterio-(arteries stiffen) or atherosclerosis (narrowing and increased peripheral resistance), hypertension, or aortic regurgitation. A PP <25 mmHg is considered narrow and may indicate low cardiac output or blood loss (hemorrhage, suggesting in adequate perfusion)
Describe baroreceptor reflex
Decrease in firing of baroreceptors and that sensation goes back to the brain and the medulla will decrease output from the vagus nerve, through the sympathetic trunk. The barorecpetors reflex maintains MAP. We have a down regulation of sympathetic outputs from the sympathetic trunk and an increase in parasympathetic regulation.
What happens to our pulse pressure with age?
It widens as we get older. What happens is, while the compliance decreases, the pressure inside increases. SVP is going to be higher. There is more stiffness
What is mean arterial pressure (MAP)?
Average pressure driving blood to the tissues overcardiac cycle. Approximation formula:
MAP = DBP + ⅓ PP= 80 + ⅓ (40) = 93 mmHg
MAP = CO x total peripheral resistance (TPR)
Vasodilation= decrease in MAP, decrease in total peripheral resistance
Vasoconstriction= increase in MAP
How does MAP directly realte to baroreceptors
What are arterial baroreceptor reflex compensation for hemorrahage?
In hemorrhage, SV decreases naturally. You see the sharp drop, your heart rate and baroreceptor response will go up. SV decreases because you dont have enough and you dont have enough preload. This is a great example. Your heart rate can bring out that CO only to a point. Your peripheral resistance will increase and so it will vasoconstrict because you have more volume.
Peripheral resistance will increase, so you’ll vasoconstrict and have an increase in MAP. Hemorrhage causes decrease in peripheral resistance so there will be a parasympathetic response.
What are arterial baroreceptor reflex compensation for increase in arterial blood pressure and blood volume?
So, we will have decrease in parasympathetic response and decrease the SA node of the atrial heart an increased sympathetic response, so HR. Our peripheral resistance mostly has to do with our arteries, so we increase our peripheral resistance to try to increase our MAP, our arterial pressure. Increase blood volume, increase blood pressure so we will increase baroreceptor finding. This is a negative feedback mechanism. Increase in blood volume like drinking water
How does arterial pressure work in the body to affect MAP?
So increase in blood volume so increase in blood pressure, so increased baroreceptor firing so increase baroreceptor firing, laws of increase in venous pressure, venous return, we have more blood volume and we increase our EDV and try to increase our cardiac output which will increase our arterial pressure. We need to regulate arterial pressure. Regulation of MAP through baroreceptors. The RAAS system used ADH and aldosterone for longer term regulation of blood pressure. It takes a little bit longer. Drop in blood pressure, inhibits baroreceptors, then sympathetic nervous system activity and then the renin from the juxtaglomerulus complex and will cause the conversion of angiotensin to angiotensin I and ACE from the lungsto angiotensin II which goes to the adrenal cortex for aldosterone that helps with sodium reabsorption, ADH will be released by posterior pituitary, etc, etc
What is ANP?
ANP is atrial naturetic peptide
What is hypovolemic shock?
Due to a decrease in blood volume secondary to hemorrhage or loss of fluid other than blood (hemorrhagic shock)
What is low-resistance shock?
Due to a decrease in total peripheral resistance secondary to excessive release of vasodilators, as in allergy and infection (like septic, infection, anaphylaxis)
What is cardiogenic shock?
Due to an extreme decrease in cardiac output from any variety of factors (for example, during a heart attack)
What is obstructive shock?
Due to an obstruction in blood flow, such as a blood clot, a tumor, or a collapsed lung
Describe some reasons for primary essential hypertension?
Genetic problems with RAAS, regulation of endothelial cell function, and arteriolar smooth muscle contraction. Increased total peripheral resistance caused by reduced arteriolar radius, obesity, isulin resistance (characteristic of Type 2 diabetes), chronic high salt inatke leading to overstimulation of the sympathetic nervous system, stress, smoking, excess alcohol or caffeine consumption, poor diet, low birth weight and not being breast-fed as an infant.
How do you control hypertension?
Primary hypertension can be managed with diet, exercise, and lifestyle changes, and with medication
What factors are involved in secondary hypertension include?
Damage to the kidneys or their blood supply can lead to renal hypertension, excess renal Na+ reabsorption, hypersecretion of cortisol, aldosterone, or thyroid hormone. The abnormal nightime sleeping pattern, sleep apnea. Secondary hypertension can be managed with medication.
What are the two types of congestive heart failure?
Diastolic and systolic heart failure
What is diastolic dysfunction?
Involves difficulty with ventricular filling, due to decreased compliance, reduced end diastolic volume leads to reduced stroke volume, often caused by the heart pumping against high arterial pressure (hypertension)
What is systolic dysfunction?
Involves difficulty with a ventricular ejection, due to damage to the myocardium, this can result from a heart attack, decreased contractility leads to a lower stroke volume at any EDV
