Cardiac week 1 Flashcards by adam koraym

The heart

2 pumps:
RA, and RV: pump blood to lungs (pulmonary artery)
Low resistance, low pressure

LA and LV: pumps blood to organs (aorta)
High resistance, high pressure

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Heart sounds

Caused by the closing of valves
Valves close because the pressure pushing back is greater than the pressure pussing forward

S1: closing of A-V valve at the begining of ventricular contraction

S2: closing of the aortic valve at the end of ventricular contraction

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Cells of the Heart

Pacemaker cells: in the SA and AV node, have unstable resting membrane potential, spontaneously depolarize. Control heart rate

Myocytes: generate contractile force

Conducting cells: bundle of His and Purkinje fibers, cause rabid depolarization

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Myocyte Structure

Striated with actin and myosin filaments (like skeletal muscle)
Cells separated by intercalated disks containing gap junctions (fast spread of current from cell to cell) functions as a syncytium

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Action potential transmission in the heart

Action potential is generated at the SA node in the Right Atrium then travels through the internodal fibers then to the AV node then to the purkinje fibers where they transmit the AP to the ventricles

The AP is delayed at the AV node to allow ventricles to completely fill with blood during diastole

Ventricles contract in bottom-up fashion: apex to base contraction is neccessary to propel blood upward toward pulmonary artery and aorta

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Cardiac Muscle Action potential

Phases:
0: Fast Na channels open (upstroke, Na comes in)

1: Fast Na channels close (brief initial repolarization caused by the fast K out, and decrease in Na coming in)
2: Ca channels open and fast K channels close (plateau transient increase of Ca conductance, inward Ca and K out (but inward and outward are equal so Vm is stable)
3: Ca channels close and Slow K channels open (repolarization, Ca decreases, K increases and predominantes and leaves cell)
4: resting membrane potential

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Nodal Fiber Electrophysiology

Unstable Resting potential (sits at -40 as opposed to -90) (Funny Sodium Channels) If cause a slow influx of sodium until threshold is reached

When Threshold is reached, Voltage-gated calcium channels open leading to an influx of Calcium generating an AP

\
Phase 0: upstroke of AP, caused by an increase in Ca conductance. The increase causes an inward Ca current that drives the membrane potential towards the Ca equilibrium potential (not NA)

Phase 3 repolarization (caused by an increase in K conductance)

Phase 4 slow depolarization/automacity (AV node and Purkinje His are latenet pacemakers that can override SA), accounts for pacemaker activity of SA node, caused by an increase in Na conductance which results in an inward Na current via If (turned on by repolarization)

NO PHASE 1 AND 2

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Cardiac Excitation Contraction Coupling

extracellular calcium is required
AP spreads from Cell membrane into T tubules during plateau . Depolarization activates L type (DHP) Calcium Channels that cause an influx of Ca from extracellular fluid, which triggers even more calcium influx from SR via RyR channels (calcium induced calcium release
Relaxation occurs when the Calcium is pumped out of the cytoplasm into SR (via Ca ATPase)

Calcium binds to troponin C which moves tropomyosin out of the way and allows for actin and myosin binding (similar to skeletal muscle)

Intracellular calcium is porportional to contractile force of the heart

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Stroke volume, ejection fraction, and cardiac output

SV: blood ejected in one contraction of the L ventricle (End diastolic volume - End systolic Volume= SV)

Ejection Fraction: percent of Blood ejected from LV
(Stroke volume/ EDV) usually 55%

Cardiac output: Stroke volume x HR = usually 5 L/min

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Preload

amount of blood that stretches the ventricles

Preload will be increased with increased venous tone, and increased circulating blood volume

Pre load will be decreased with hemorrhage

an increase in pre load increases stroke volume

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afterload

back pressure exerted by the blood in the arteries (Arterial pressure)

If you increase afterload you decrease stroke volume (because you need a higher pressure to open the aortic valve)

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Contractility

contractile force generated by the muscle

its increased with catecholamines, and increased intracellular Ca

its decreased with heart failure and hypoxia

Increased ability of the heart to pump-> greater ejection fraction-> larger stroke volume

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ECG vs Action potential

ECG: represents the movement of current through the heart, the ecg measures the summated depolarizations of myocytes, its measuring the potential difference in membrane depolarizations between two location on the membrane (depolarized= -, repolarization= +)

AP: represents the change in membrane potental of one cell

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The ECG

P wave: Atrial depolarization, SA node fires (atrial repolarization burried in QRS segment)

PR Segment: represents the delay of the signal at the AV node to allow the ventricles to fill (from end of P to start of Q)

PR interval: begining of P to begining of Q (ventricular filling, atrial contraction)-depends on AV node conduction velocity (if decreased in heart block, PR int increases in size)

QRS interval: ventricular depolarization/ contraction

ST segment: end of S to begining of T (no current is observed because in plateau phase of AP

T wave: ventricular repolarization

ECG reading: one small box =.04 sec
large box =.2 sec
5 box= 1 sec
HR: 300/(# of big boxes from peak to peak)

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ECG leads

look at study guide diagrams

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Difference in pulmonary/systemic circulation and Vascular beds/systemic circulation

Pulmonary and systemic circulation are in series

Vascular beds within the systemic circulation are in parallel (blood will not pass through every vaascular bed, allows for independent regulation of blood flow for each vascular bed/organ)

Blood flow through the body

Arteries-> arterioles-> capillaries-> venules-> veins

Arterioles: main control mechanism for regulating blood flow to specific vascular beds by changing resistance (dilating/contracting)

Capillaries: where nutrient and fluid exchange occurs

Veins: major reservoir for extra blood (very compliant) can constrict, pushing more blood back to the heart, increasing venous return (increasing preload), which increases stroke volume

Blood flow

Velocity of blood flow can be expressed as v=Q/A
v (velocity;cm/sec), Q (flow; L/min), A (total cross sectional area cm^2)- capillaries have the highest total cross sectional area

Blood flow equation/ Ohms law equation:
Q= dP/R , Q (flow; L/min), dP (pressure gradient; mmHg), R (resistance/TPR; mmHg/L/min)

the pressure gradient drives blood flow (no gradient= no flow blood HAS to flow from high pressure to low pressure)

Resistance (poiseuille’s law)

R= (8nl)/ (Pi * r^4)

n= viscosity, l=length of blood vessel, r= radius

Resistance in parallel: systemic circulation, total R is less than the greatest resistance an individual artery

Resistance in series: blood vessels in one organ: largest proportion of resistance is in the arterioles

Laminar vs Turbulent Flow

Laminar flow is in a straight line, Turbulent flow is not

Laminar flow: friction from the vessel walls slows down flow on the outside, creating a parbolic flow distribution

Turbulent flow: rate of blood flow too great, passes obstruction in vessel, rough surface, makes a sharp turn

high reynolds number=high turbulence

Turbulence is increased by decreasing blood viscosity and by increasing blood velocity

Shear: the difference of speed of blood of adjacent layers in the tube (blood at the wall is slow, blood at the center is fast)

Capacitance/ Compliance

distensibility of blood vessels, inversely related to elastance(stifness)

Compliance= volume change/ pressure change
compliance is much greater in veins than arteries (why more blood is carried in the unstressed volume as opposed to the stressed volume) capacitance in the artery decreases with age

Pressure decreases as you go along through the circulation due to increased resistance (greatest pressure drop occurs across arterioles bc they are the site of highest resistance)

Mean pressures: Aorta (100), Arterioles (50), Capillaries (20), Vena cava (4)

Arterial pressure

its pulsatile, not constant during a cardiac cycle

Systolic pressure (highest arterial pressure, measured during contraction/ejection of blood in the arteries)

Diastolic Pressure (lowest arterial pressure, measured when the heart is relaxed and blood is returned to heart)

Pulse pressure: the difference between systolic and diastolic pressure, most important determinant of pulse pressure is stroke volume (pulse pressure increases to the same extent as systolic pressure)

decreases in capacitance (aging)increase pulse pressure

Mean Arterial Pressure: average arterial pressure with respect to time, NOT AVERAGE OF DIASTOLIC AND SYSTOLIC, (greater fraction of cardiac cycle is spent in diastole) diastolic + .3 pulse pressure

Arterial pressure tracing

See study guide

Shape of tracing is determined by:
Stroke volume
Contractility

Heart Rate- if too fast, less time to allow blood flow into venous system, leading to increased diastolic pressure

Arterial Resistance: if high, blood is unable to flow into circulation, higher diastolic pressure

Arterial Compliance- if low, leads to higher systolic pressure (less able to accomodate increased volume)

Dicrotic notch- slight backward flow from aorta to L ventricle before valve closes

Abnormal Arterial Pulse Contours

Diseases that cause change in Systolic pressure:

Arteriosclerosis: hardening of Arterial vessels, decresed compliance leading to increased systolic pressure
Aortic Stenosis: aortic valve doesnt open, decreased arterial systolic pressure

Diseases that cause change in Diastolic pressure:

Patent Ductus arteriosus (AV shunt): decreased arterial resistance, decreases Diastolic, increases systolic

Aortic regurgitation: aortic valve does not close all the way, allowing back flow into ventricle decreasing diastolic and increasing systolic

Right Atrial Pressure

Determined by: The ability of heart to pump blood out of the heart The flow of blood back into the heart from periphery Normal RAP= 0 mmHg ! When heart failure occurs, the heart can't pump blood out as fast as it is coming in from veins and blood backs up causing increased RAP

Gravity and arterial and venous pressure

Pressure due to gravity is proportional to the verticle distance above or below the heart Venous pressure at heart= 0 Arterial pressure at heart= 100 (generated by heart) Venous pressure at foot when standing= 100 (gravity hydrostatic pressure) Arterial pressure at foot when standing= 200 (hydrostatic pressure from gravity + pressure generated by heart)

Return of Blood from veins to the heart

The pressure gradient opposes the return of blood to the heart, contraction of skeletal muscle compresses veins and propels blood back to the heart, valves prevent backward flow

Structure of capillary beds

Metarterioles branch into capillary beds, at the junction of the arterioles and capillaries is a smooth muscle band called the precapillary sphincter true capillaries dont have smooth muscle, but have a single layer of endothelial cells surrounded by a basement membrane Flow through capillaries is slow due to large cross sectional area and allows for exchange of nutrients and waste products diameter of RBC is larger than capillary so they squish through, precapillary sphincters contract and relax to regulate blood flow through the capillaries Capillary flow is intermittent: flow is not always hapening due to regulation of metaarteriols and precapillary sphincters. Tissue oxygen levels determine precapillary sphincter and metaarteriol contraction (vaso motion)

passage of stuff across the capillaries

Capillaries are fully permeable to water, oxygen and CO2 Transport occurs through: Slit pores: mostly water soluble substances, NaCl, glucose, - capillary slit pores have different sizes depending on tissue/organ function Vesicle exchanger: for larger,, hydrophilic proteins Transcellular: lipid soluble substances simply diffuse through cell and basement membrane Fenestrae/aquaporins: for large amounts of water

Capillary pores in Different organs

brain: pores are tight allowing only small molecules liver: pores are open, allowing all dissolved substances including proteins intestines: pores allow for transmission of small proteins kidney/glomerular tufts: have fenestrae that allow ionic substances to pass thru pores differences in pores allow for different diffusion coefficients

Ficks law of Diffusion

Jx= Px ( [Xout] -[X in] ) Jx is fluid flux (+ when net flux out of capillary ie filtration, - when net flux into capillary) Px is the diffustion rate= DB/a a= surface area, D= coefficient, B donc, difference

Starling Forces

Net filtration= forces moving out- forces moving in 2 forces that want fluid to move OUT of capillary Capillary hydrostatic pressure, interstitial colloid osmotic pressure Two forces want fluid to move INTO the capillary Interstial fluid pressure (typically neg or 0 and draws fluid out of capillary), and plasma colloid osmotic pressure

Lymph

Normally filtration of fluid out exceeds absorbtion of fluid into the capillaries The excess filtered fluid is returned to the circulation via the lymphatics to the venous tract (accomodates upt to 7 mmHG) before edema occurs

Factors that influence lymph flow

Net filtration of fluid: elevated capillary pressure, decreased plasma colloid osmotic pressure, increased IF colloid osmotic pressure, increased permeability of CApillaries Lymph Pump: collecting lymphatics have myogenic responses, contraction of surrounding muscles, movement of body parts, pulsations of adjacent arteries, compression of tissues by external forces

Autoregulation

tissues maintain appropriate flow for a given amount of metabolsim if arterial blood pressure increases or decreases the blood flow needs to stay the same brain, heart and kidney have autoregulation if the blood pressure were to decrease, vasodialation of arterioles occur in those organs Myogenic autoregulation: when smooth muscle of vasculature is stretched, the smooth muscle will contract, to combat an increase in pressure in small arterioles

Metabolic autoregulation (maintanence of normal)

1. Vasodilator substances increased metabolic rate causes release of vasodilators that relax the precapillary sphincters, relaxing teh sphicters allows for more blood flow by decreasing resistance. Changes in pressure and flow affect the washout and buildup of the substances Vasodilators: lactate, adenosine, histamine, H, CO, and K 2. Oxygen deficit Works on negative feedback, if O2 is high, the tissues cause contraction of the arterioles because it doesnt need more O2, and vice versa

Active vs Reactive hyperemia (when more O2 is needed)

Active/functional: metabolic demand increases (exersize) blood flow increases Reactive: after a period of occlusion, blood flow increases

long term local changes

``` Increase in number of vessels (angiogenisis) vascular remodeling (hypertrophy) ```