Internal Environment- Cardiac Function

Draw, in correct temporal relationship, the pressure, volume, heart sounds, and ECG changes in the cardiac cycle. Identify the intervals of isovolumetric contraction, rapid ejection, reduced ejection, isovolumetric relaxation, rapid ventricle filling, reduced ventricular filling and atrial contraction

Wigger’s diagram → tied to CO

• how much blood leaves the heart every minute (HR * SV = CO)

  • SV is how much blood leaves during a single contraction

  • when talking about CO, talking about left sided CO

    • right sides CO is going to the lungs, still the same (not lower)

• if right side of heart didn’t pump as much blood out as left…

  • get more blood to body than lungs (bad things happen)

  • right sides gets more…

    • blood goes to lungs, not body

  • left-sided heart failure

    • end up with fluid in the lungs → pneumonia

    • left-side isn’t taking blood from lungs and transitioning it to body

• right and left side balanced in a healthy individual

Describe the role of Starling’s Law of the Heart in keeping the output of the left and right ventricles equal

What keeps the right and left side balanced

Define ejection fraction and be able to calculate it from end diastolic volume, end systolic volume, and/or stroke volume

• commonly used by cardiologists to do prognostication of how healthy a person is

• ours is ~55%

  • every time heart contracts, ~55% of the blood in that ventricle goes out

    • when a person goes into heart failure, that ejection fraction begins to go down

  • right when you get at ~20% ejection fraction is the break point → heart can’t maintain flow (decompensation)

    • patient goes downhill, intervene medically and pharmacologically

Which of the following would not increase cardiac output? CO = HR * SV

• Increased heart rate

• Increased stroke volume

• Increased resistance

• Increased blood volume in the ventricle

• Increased venous return

ICQ1 explanation

• if either HR or SV go up, CO will go up

  • B1 stimulation inc. both HR & SV

• inc. resistance → dec. CO

  • how much pressure is required to send blood into circulation

    • value we use is diastolic BP

      • point that blood begins to leave the heart & go into circulation

      • pressure required to open aortic valve

    • if that pressure goes up, the aortic valve doesn’t open at low pressure, it takes a higher pressure… the amount of time for blood to leave the heart gets cut down, less blood leaves the heart & CO drops

      • one of problems with hypertension with a high diastolic pressure

        • don’t get as much blood out of the heart for every beat

        • heart has to inc. rate to maintain CO… only choice is to beat faster

  • inc. venous return → inc. blood in the ventricles

    • the more blood we have in the ventricles, the harder the strength of contraction → Starling’s Law (mechanical example)

    • right now, most of blood is in our veins & lower extremities… when we stand up, blood is going to fall down bc of gravity… if our system doesn’t compensate, going to lay there… EMS/pass out

      • as you stand, the muscles squeeze the blood & more blood goes to the heart

    • the heart expands, physically stretches larger & contracts harder → Starling’s Law (automatic. adjustment based on varying the load)

    • 50 mL of IV fluids directly into heart → heart would expand even more & pump out more than 50 mL

      • adjusts automatically

        • patient in heart failure → Starling’s Law is not working

The mitral or left AV valve opens when:

• The atria contract

• The ventricles contract

• Ventricular pressure exceeds atrial pressure

• Atrial pressure exceeds ventricular pressure

• None of these are correct

ICQ2 explanation

• the atria contract: valve was already open during atrial systole/contraction

• the ventricles contract: closes valve → pressure is going to jump

• ventricular pressure exceeds atrial pressure: valve closes

• valve is sitting on the left side of the heart b/w the atria and ventricle

  • opens when pressure in the ventricle is lower than pressure in the atria

Inputs

• Endocrine

  • Epinephrine

    • Stimulates B1 & B2 receptors of the heart

  • T3/T4 (excess thyroid hormone → higher rate & higher strength of contraction & higher BP)

    • Induces B1 receptor expression on the heart

  • GH/IGF-1

    • Required for normal cardiac function

  • High insulin

    • Disrupts B1 activity (type 2 diabetics that are high in insulin have impaired cardiac function/cardiac response)

• CNS

  • Sympathetic

    • Increase rate & strength

  • Parasympathetic

    • Decrease rate

• Inflammatory mediators

  • IL-5

  • TNF-a

  • when we look at coronary circulation, we have inflammation

  • damage coronary arteries & cause endothelial cell dysfunction

    • blame for everything

    • cause coronary arteries to not respond correctly

      • instead of relaxing, they constrict sometimes → can cause impaired blood flow

Cardiac Cycle

Pressure, volume, electrical activity, mechanical activity

Wigger’s Diagram

• Independent variable

  • ECG

    • pacer → independent variable

    • causing everything else, are dependent on ECC

      • P wave, precedes atrial contraction

      • QRS, precedes ventricular contraction

• Dependent variables

  • Aortic pressure

  • Ventricular pressure

  • Atrial pressure

  • Ventricular volume

  • Heart sounds (confirms what’s going on)

Wigger’s Diagram (cont’d)

Cardiac Output

• Defined: the volume of blood pumped to the body per minute

  • Focuses on left side

  • Right-sided is equal to left

    • look at right side when looking at someone with pulmonary hypertension

  • total CO ≠ left + right

    • CO determines BP and blood flow to body

• Determinants

  • Heart rate

  • Stroke volume

  • CO = HR x SV

Heart rate

• Influences on pacing

  • Parasympathetic (muscarinic receptors → hyperpolarize pacemaker cells, action potential of the pacemaker cells, further from threshold takes them longer to reach it & get an AP)

    • Increases K+ permeability

      • makes cell more (-) → review

    • Decreases Na+f & Ca++t slope

      • positive, upward movement is slowed

  • Sympathetic

    • Increases Na+f & Ca++t slope

      • makes it happen quicker, B1 effect

        • put a patient on a B1 blocker → slowing that effect

Stroke Volume (all about sympathetic, parasympathetic doesn’t impact directly)

• Determinants

  • Sympathetic stimulation

    • Increased Ca++L influx

  • Venous return

    • Blood from the body to the heart

    • Greater volume of return = greater stroke volume

Stroke Volume (cont’d)

• Determinants

  • Sympathetic stimulation

    • Increased Ca++L influx

  • Venous return

    • Blood from the body to the heart

    • Greater volume of return = greater stroke volume

Stroke Volume (cont’d 2)

• Determinants

  • Sympathetic stimulation

    • Increased Ca++L influx

  • Venous return

    • Blood from the body to the heart

    • Greater volume of return = greater stroke volume

Stroke Volume (cont’d 3)

• Determinants

  • Sympathetic stimulation

    • Increased Ca++L influx

  • Venous return

    • Blood from the body to the heart

    • Greater volume of return = greater stroke volume

    • Also known as Frank-Starling Law

    • Also known as preload

  • Afterload

    • Arterial pressure

  • occurs in striated muscle (cardiac & skeletal)

    • has a point where you get optimal alignment of the sarcomeres (A&I bands)

    • get muscle at right length, have a stronger contraction → everything is lined up

  • optimal alignment for heart is when it’s at its maximum fill of blood, going to contract its hardest

  • faint → elevate legs → more venous return → more blood goes back to the heart → heart stretches & contracts → brings BP up naturally bc of S.L.

    • problem with high BP is a lifetime of pushing harder at a faster rate causes S.L. to fail, goes past optimum

Stroke Volume (cont’d 4)

• Determinants

  • Sympathetic stimulation

    • Increased Ca++L influx

  • Venous return

    • Blood from the body to the heart

    • Greater volume of return = greater stroke volume

    • Also known as Frank-Starling Law

    • Also known as preload

  • Afterload (pressure required to open aortic valve)

    • Arterial pressure

  • heart can handle a high preload, but not a high afterload

    • diastolic BP is high → isovolumetric ventricular contraction time got longer

      • ejection ends when T wave says it’s done

      • if we have less time to eject, we have less SV

    • someone who has hypertension has a higher HR bc they’re trying to maintain CO

figure 9-16, p. 322

Ejection Fraction

• Percentage of End-diastolic volume that leaves the heart

  • Normal is roughly 55%

• Formula

  • Ef= SV/EDV

    • SV → how much blood came out, EDV → how full was the heart

• Ef declines in heart failure

  • SV & SL begin to fail

  • sympathetic will try to compensate

Overall Sympathetic Impact of Cardiac Output

• Increased sympathetic activity in heart failure

  • Compensation

  • Failure of sympathetic to correct

    • Decompensation

      • dec. CO, pushing will cause more damage

Coronary Blood Flow

Coronary Artery Disease

Myocardial Perfusion

• Myocardium is highly aerobic

• Not constant

  • Greatest flow during diastole

    • want low HR

    • resting HR of 50 → diastole is long

      • muscle is happy bc it’s spending most of its time at rest instead of working (systole)

    • resting HR of 120 → diastole period is short, myocardium is not well perfused

• Increased flow

  • Adenosine

    • healthy heart releases breakdown product of ATP, will cause coronary artery dilation in a healthy heart

  • B2 stimulation

  • both want to inc. blood flow to the heart

• Decreased flow

  • Platelet activating factor

    • Endothelial cell dysfunction (causes vascular constriction of coronary arteries → bad)

  • Coronary artery disease

Coronary Artery Disease (blockage → flow drops)

• Any impingement on a vessel negatively impacts flow

  • Poiseuille’s Law

Coronary Artery Disease (cont’d)

• Blockage of a coronary artery is referred to as a Myocardial Infarct (MI)

  • usually due to a clot

  • get triangle shape piece of damage

• Outcomes

• Re-establishment

Coronary Artery Disease (cont’d 2)

• Blockage of a coronary artery is referred to as a Myocardial Infarct (MI)

• Outcomes

• Re-establishment