Heart Review

inotropic

Heart myofibers don't receive potential from individual nerves, and there are no neuromuscular junctinos

• Spontaneous depolarization causes channels to open at -60, Na+ rushes in, goes to threshshold at -40V, this voltage triggers Ca2+ channels in the plasma of the pacemaker cells to open
• -Inward flux of calcium results in the spike and thereafter contractions

Occurs during diastole, when the spontaneous depolarization occurs as Na+ comes in

Na+ is responsible in other cells for depolarization, Unlike other cells, Ca+ is reponsible for the depolarizat

Rhythm set by a pacemaker other than the SA node

• AV node gives potential to a ventricular myocyte
• This myocyte will now produce it's own potential
• -Resting potential: -85V (so it's more stable)
• -Upon being stimulated, they reach threshold, and the Na+ gates open
• -Na inwardly diffuse through rapid Na+ channels

Long action potential results in longer refractory period

• P wave: spread of depolarization thru atria (when half mass depolarized, v reaches max, when all polarized, it reaches 0 since no dif in polarity in atria)
• QRS wave: Depolarization into the ventricle
• T wave Repolarization of the ventricle

Depolarization goes from endocardium to epicardium, while repolarization occurs from epicardium to endocardium

Depolarization goes from endocardium to epicardium, while repolarization occurs from epicardium to endocardium

• 1. Falls through
• 2. Squeezed through by tricuspid and bicspic (or atriaventricular valves) because of the contraction

• QRS is seen at the beginning of systole (contraction)
• 1st heart sound (lub) produced by the contraction of the ventricle right after the QRS wave, when the intraventricular pressure is high and the atrioventricular valve is shut
• 2nd sound (dub) is after the T wave begins, when the ventricle is relaxed (beginning of diastole, decrease pressure, causing the semilunar aorta valve to shut

Infarctd heart causes slower waves because action potential can't travel through

This issue is called Ischemic, you can detect a depression of the S-T segment as a result of myocardial ischemia

• A strong beta agonist, causing the heart rate to sky-rocket;
• a heart attack may happen- causing an inversion of the T wave

A cardiac rate slower than 60 beats per minute

A cardiac rate faster than 100 beats per minute

While it's good at tell you what's going on with your heart at the moment, but it doesn't tell you what happens when your heart is under stress, under workload, therefore, stress tests are important

• (atrial contraction)
• pressure low, P wave comes, atrial pressure goes up a little to squeeze 30 percent of the blood into the ventricle

Ventricular contraction: comes about from the ventricular contraction-ventricular pressure goes up really high

• Due to this, the ventricles bulge into the atrial chamber, less
• Since there is less area in the atria, it causes a higher prssure in the atria as well

Slow pressure buildup in the atria: ventrical contraction but atrial relaxation and blood is returning to the atria from venus return, so the slow buildup of pressure in the atria is the V wave

The AV valve opens, 70% blood falls back

Isometric, because as the AV nod shuts (lub), the blood is trapped in the ventricle but ventricle is contracting against it

The semilunar valve, it snaps shut in order to trap the blood in the aorta, otherwise there would be back flow into the venetricles

Then blood drops from the atria, next contraction happens, valve opens

120mmHg/80mmHg

• When pressure in the ventricle goes above aortic, the aortic valve opens up, now increased pressure from the continued systole of the ventricles squeezse the blood into aorta to 120mmHg
• -Ventricle at this point, starts to relax (T wave), pressure drops
• -When the pressure in ventricle is dropped to lower than prssure in atria, the AV valves passively open

Since the ventricular pressure dropped, the AV valve closes, blood starts to flow back from the aorta into the ventricle, that's when the aortic valve snaps shut (dub)

• Now we are going from the HIGH pressure in the aorta to the systemic circulation, and immediately before the next systole
• (Diastolic pressure (80 mmHg)

That's when you know the aortic valve shut

25/8 mmHg

Cardiac output (amount pushed out of left ventricle into aorta and circulation)

QRS wave

T wave

• QRS happens at the beginning of systole
• T waves happens at the beginning of diastole

• Sympathetic nerve stimulation: increase the rate of spontaneous depolarization
• Parasympathetic: Decrease

It will go up, because you're removing the parasympathetic tone which dominates under resting conditions

Chronotropic effect, when sym and parasym acts in antagonistically

• Ach promotes opening of K channels, which affects action potentials in pacemaker region
• Increase K permeability, results in lower and longer hypopolarization threshold whichslows heart rate

• Parasympathetic predominates on the SA node,
• It doesn't decrease the force,
• -Slower rate--->weaker contractions

Sympathetic, sends fiber directly to the ventricular muscle mass--> affects force of contraction

• 1. Norepi and Epi stimuate opneing of HCN channels (hyperpolarization channels)
• Opens the HCN (Na and Ca channels more, causing sharter slope (meaning more cardiac cycles per minute)

• 1. Neurally controlled
• 2. Major center in CNS is located in medulla
• 3. Endocrine
• 4. Frank Starling Law

• On x-axis, ventricular end-diastolic volume (ml)
• On y-axis, stroke volume (ml)

Frank-Starling: increased contractibility caused by sympathetic nerve stimulation (the steeper curve)

• =End-diastolic volume-systolic volume
• 135ml-65ml=70ml

• Volume of blood in ventricle at the end of diastole, before the next ventricular contraction
• -135 ml
• Increase diastolic volume with a higher venus return

• 1. Lay on the floor, no more gravity to fight, this also allows the stroke volume to go up
• 2

• After contraction volume
• 65ml in heart after contraction
• -This blood is left because when the ventricle starts to relax, even if it squeezed out all the blood from it into the aorta, the aortic pressure is higher than the ventricle and some of the blood flow back in before the semilunar valve snaps shut

The PERCENT you actually pump out

Start with 135ml and pump out 70 you get about 55% ejection fraction

• If you increase end diastolic volume, you stretch th cradaic muscle myofibers, and they reach a more optimum overlap, by doing so, contract more forcefully
• Although we don't have resting length in cardiac muscle, but we have some length where there is an optimum OVERLAP

• Increases contractility which shifts curve to th left in the Frank-Starling law effect graph
• Causing it to be hypereffective
• It INCREASES the stroke volume
• but end-diastolic volume STAYS the same

• 1. Blood volume (Urine volume and tissue-fluid volume both contribute indirectly)
• 2. Negative intrathoracic pressure (Caused by breathing)
• 3. Venous pressure (Venoconstriction, caused by sympathetic nerve stimulation, and skeletal muscle pump)