Cardiovascular Systems Physiology and Pathophysiology Flashcards by Joel Glotfelty

Describe the vasculature that blood passes through as it leaves the heart

Heart (oxygenated blood) —> arteries —> arterioles —> capillary beds (gas exchange) —> venules (deoxygenated blood) —> veins —> SVC and IVC

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What are the component of the microcirculation of blood?

Arterioles, capillaries, and venules

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The vena cava empty mixed venous blood (i.e.

deoxygenated blood from the superior and inferior circulatory beds) into the

Right atrium of the heart

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At any given moment in time, most of our blood is in the

Venous system

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Sequential blood flow through the central cardiovascular system during one complete cardiac
cycle is as follows:

Right atrium —> tricuspid valve —> right ventricle —> pulmonic semilunar valve —> pulmonary arteries (Deoxy) —> lungs —> pulmonary veins (Oxy) —> left atrium —> bicuspid valve —> left ventricle —> aortic semilunar valve —> aortic arch —> aorta —> arteries

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The heart functions as two pumps in series which allow for which two types of circulations?

) Pulmonary circuolation (Exchange of CO2 for O2)

2. ) Systemic circulation (exchange of O2 for CO2)

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In general, two phases of the cardiac pump occur and are defined by the properties of the ventricles. They are:

) Diastole: Ventriclular relaxation (low intraventricular pressure)
) Systole: Ventricular contraction (high intraventricular pressure)

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Cardiac muscle is known as

Myocardium

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Comprise the major portion of the ventricles by volume, however occupy only 25-30% by number

Cardiomyocytes (or just myocytes)

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The heart beats on average around 100,000 beats per day to circulate around 6 tons of blood per day. This is a metabolically expensive process that uses approximately

6 kg of ATP daily

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The substrate for all of this comes predominantly from

) Glucose (glycolysis)

2. ) Free fatty acids (FFA β-oxidation)

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Glucose and free fatty acids feed into oxidative phosphorylation for generation of

ATP

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In a healthy adult, approximately 60% of ATP is derived from

FFA β-oxidation

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Under conditions of stress (e.g., heart failure or ischemia), a shift occurs resulting in proportionally more ATP being generated from

Glucose oxidation

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This metabolic shift is important when you consider that glucose oxidation yields around

13% ATP per O2 molecule consumed than FFA β-oxidation

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The use of FFA for energy in the heart is energetically wasteful because FFA stimulate the synthesis of

Mitochondrial uncoupling proteins

-releases heat instead of ATP

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Collectively, the stressinduced shift from the β-oxidation of FFA to the oxidation of glucose results in the production of approximately

40% more ATP per O2 molecule

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Which has a thinner myocardium, atria or ventricles?

Atria

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What are the cells of the myocardium called?

Myocytes

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Contraction of the myocyte operates via the sliding filament model that depends on

Ca2+ and ATP-dependent cross bridge cycling

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The contractile element of the myocyte is referred to as the

Sarcomere

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Intercalated disks form the end borders between myocyte fibers; and the fibers are separated laterally by the

Plasma membrane-like Sarcolemma

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Cardiac muscle resembles a syncytium in that each fiber contains multiple nuclei; i.e. cardiac muscle fibers operate as a

Functional syncytium

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Cardiac muscle cells and fibers are joined by

Gap junctions

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Enable a high degree of electrical conductivity as well | as the free diffusion of very small molecules such as ions and some second messengers between cells

Gap junctions

Cardiac myocytes utilize oxidative phosphorylation for the production of ATP; thus, the cells are rich in

Mitochondria

Intracellular Ca2+ sinks that cab bolster sarcoplasmic Ca2+ concentrations

Mitochondria

An isoform of creatine kinase that is referred to as cardiac-specific CK

Creatine kinase MB (CK-MB)

What is the clinical importance of CK-MB?

CK-MB is dumped following a myocardial infarcation

How many hours from a myocardial infarction do we see: 1. ) Rise of CK-MB 2. ) Peak of CK-MB 3. ) Return to normal CK-MB

1. ) 3-8 hours 2. ) 24 hours 3. ) 48-72 hours

Since there are other CK isoforms, the ratio of CK-MB: total CK is measured. A reliable marker for myocardial injury is CK-MB : Total CK ratio of

> 2.5%

Cardiac muscle contains a T-tubule network as well as an abundant representation of

Sarcoplasmic reticulum (SR)

Cardiac muscle fibers are well vascularized, such that we have what type of correlation between capillaries and mucle fibers?

One capillary per muscle fiber

Like skeletal muscle, cardiac sarcomeres contain Z discs (Z lines) that anchor

Actin filaments

Like creatine kinases, there are specific cardiac | troponins. These are

1. ) Cardiac troponin 1 (cTn1) | 2. ) Cardiac troponin T (cTnT)

In the event of a myocardial infarction, cTn1 and cTnT will both rise. When will we see their 1. ) Rise 2. ) Peak 3. ) Return to normal

1. ) 3-4 hours post infarction 2. ) 18-36 hours post infarction 3. ) 10-14 days post infarction

What is the current gold standard for diagnosis of a myocardial injury?

Measurement of the cardiac troponins

Cardiac muscle fibers are strongest at the

Onset of contraction (from approximately L0)

Unlike skeletal muscle, we see a greater contractile force when cardiac muscle is

Stretched

This is because unlike skeletal muscle, a very slight stretch from L0 is one signal to the cardiomyocyte to

Release intracellular Ca2+ from SR and mitochondria

With increase intracellular Ca2+ comes

Increased contractile force

When compared to other muscle types, cardiac muscle can develop much more tension from

Stretch

Represents the phase following the ejection of blood from the left ventricle (LV)

Beinning of diastole

Diastole is considered the relaxed (resting) stage; hence the LV fibers have essentially no

Load

During diastole the 1. ) Aortic valve is 2. ) Mirtal valve is

1. ) Closed | 2. ) Open

During early diastole, the mitral valve opens in response to an

Increasing LA pressure (from filling) and low LV pressure -When mitral valve opens, LV begins to fill

The atria contract in response to SA nodal firing; | this represents the later stage of

Ventricular diastole

Only about 20% of ventricular filling is due to

Atrial systole

Filling causes preload on the LV muscle fibers. In other words, preload is caused by blood induced filling that causes

Stretch from L0

What is laplaces law for the left ventricle?

T = P x r Wall tension = Pressure x radius

Therefore, greater chamber wall tensions are experienced with greater filling, and increased wall tension upregulates

Oxygen demand

As the LV muscle fibers are stretched to the optimal length, intracellular Ca2+ is increased and systole begins; this early systolic phase is specifically referred to as

Isovolumetric contraction

The optimal myosin cross-bridge/actin overlap is referred to as the

Optimal length

Contraction of cardiomyocytes depends upon Na+ stimulated AP that in turn activates

Voltage-dependent Ca2+ channels

What happens during isovolumetric contraction?

Mitral and aortic valves are closed and LV pressure (LVP) soars

As isovolumetric contraction proceeds, the resistance of aortic blood pressure against LVP is added, and this opposing aortic pressure is known as

Afterload

What must happen in order for the LV to empty efficiently?

Preload must be greater than afterload

As the force of isovolumetric contraction exceeds afterload, the aortic semilunar valve is pushed open, the LV ejects blood into the aorta, and

Systolic contraction of the LV terminates

When arterial blood pressure is increased, the heart has to work even harder to eject blood from the LV. This is the case often seen with

Hypertension

In cardiac muscle, how do we represent 1. ) Stress 2. ) Length

1. ) Pressure | 2. ) Volume

The relationship between volume and pressure seen in the heart are referred to as the

Frank-Starling Laws

Explains what happens to the stress (pressure) in a cardiac cycle?

Minimum stress exists at L0. Then as the chamber fills (increased LVV during diastole) a slight stretch from L0 is initiated and from the onset of isovolumetric contraction, we see an exponential increase in the rise of stress (pressure). Then, as contraction proceeds (chamber emptying, systole) and blood is ejected, the rate of rise of pressure (stress) slows, peaks, and begins a rapid exponential decline and returns to near zero at the end of systole

The pressure-volume plot shows these relationships during one cardiac cycle and reads sequentially from

Left to right, then bottom to top, then right to left, then top to bottom

Phase 1 of the pressure-volume plot represents

Diastolic filling and generation of preload

The difference between the beginning of isovolumetric relaxation and end diastolic volume (EDV) represents the

Stroke volume (SV)

Phase 2 of the pressure-volume plot represents

The isovolumetric contraction stage of systole

Phase 3 of the pressure-volume plot represents

Systolic ejection

Phase 4 of the pressure-volume plot represents

Isovolumetric relaxation

Represent the maximal ventricular pressure developed at a given inotropic state

The end systolic pressure-volume (ESPVR) plots

What are the effects of an increased end diastolic volume (EDV)?

Increased preload, increased systolic intraventricular pressure (IVP), and slightly increased end systolic volume (ESV)

Will increase both systolic IVP and ESV and result in a greater ESV than increased preload

Increased afterload

How does positive inotropy change the pressure-volume relationship?

Reduced ESV (from greater systolic ejection) and increased stroke volume

What is phase 1 of a velocity of fiber shortening vs LVV?

Muscle fiber velocity is 0, ventricular myocardium is relaxing

What is phase 2 of a velocity of fiber shortening vs LVV?

Isovolumetric contraction that terminates upon aortic valce opening

Myocyte tension rises dramatically during

Isovolumetric contraction

Myocyte tension rises dramatically during isovolumetric contraction. This provides the generation of force that is required to

Overcome afterload and push open aortic valve

The rapid decline in muscle fiber shortening during phase 3 represents

Systole

The velocity of muscle fibers shortening precipitously declines during

Systole

Increased afterload is translated as an opposing force that results in a

Robust decrease in contractile velocity and increase in ESV

Abnormally increased preload causes a

Slight decrease in contractile velocity and a concomitant increase in ESV

Why does an abnormally increased preload cause a slight decrease in contractile velocity?

Because the fibers are stretched beyond optimal length for myosin-actin overlap

Naturally occurring and pharmacologic factors that can alter the force of cardiac muscle contractility

Inotropic compounds

What 4 things do positive inotropins increase?

1. ) Ventricular contractile force 2. ) EDV 3. ) Contractile velocity 4. ) May or may not alter time between excitation episodes

Thus, a positive inotropin such as adrenergics or digitalis may increase -as long as HR does not increase such that the time required for ventricular filling is compromised

Cardiac output

The goal of positive inotropic compounds is to increase

Cardiac pumping efficiency

Contraction of cardiac muscle is dependent upon APs induced by

Na+ influx

Contraction of cardiac muscle is dependent upon APs induced by Na+ influx, and contraction results from (and depends upon)

Increased sacoplasmic Ca2+

Prolongs the duration of contraction, thus lengthening the QT interval within the electrocardiogram (ECG)

Hypocalcemia

Reduces the duration of contraction, and thereby shortens the QT interval

Hypercalcemia

The effects of abnormally high or low calcium on QT involve allosteric modulation by calcium on the voltage-gated Na+ channels which control

Ventricular myocyte depolarization

Abnormally low extracellular calcium (hypocalcemia) tends to cause a rapid

Activation-inactivation of these Na+ channels

A cardiac glycoside; this drug that inhibits the Na+/K+ ATPase within the cardiomyocytes, this results in increased intracellular Na+

Digoxin

Elevated intracellular Na+ impedes the

Na+/Ca2+ exchanger (NCX)

Trades Na+ import for Ca2+ export from cardiomycetes

NCX

What are the effects of impeding the NCX?

Intracellular Ca2+ increaes, thus enhancing contraction

Thus, Digoxin exerts what type of inotropic effect?

Positive inotropic effect

Digoxin is also a vagomimetic agent, meaning it

Slows SA and AV conduction and sensitizes broreceptors

Increases afferent inhibitory activity which reduces activation of the sympathetic nervous system (SNS) afferents which up-regulate heart rate and vasoconstriction

Digoxins effect on baroreceptors