pharm cardiac ch 42

2 jobs of the heart

deliver oxygen and nutrients to every body cell. •

pick up waste products so they can be excreted.

blood going AWAY from the heart

artery

blood coming BACK to the heart

vein

carries oxygen-rich blood from the lungs back to the heart

pulmonary vein

carries deoxygenated blood (it goes away from the heart, to the lungs)

pulmonary artery

the signal starting in the SA node and spreading through the atria

P wave

upper part of each side of heart that is receiving

atrium

lower part of each side of the heart that is pumping

ventricle

small ear-like pouches on the atria.

auricles

the wall dividing right from left.

septum

valve that is (right atrium to right ventricle),

tricuspid

valve that is (right ventricle to pulmonary artery

pulmonic

valve that is (left atrium to left ventricle

mitral

valve that is (left ventricle to aorta)

aortic

right half of the heart

receives deoxygenated blood from the whole body through veins (superior and inferior vena cava, and the great cardiac vein)

right heart of the heart sends blood to

lungs via the pulmonary artery.

left side of heart.

receives oxygenated blood (from the lungs via pulmonary veins) and sends it into the aorta

delivers blood to the body through arteries (systemic circulation).• .

• The aorta

order of blood through heart

: Body, vena cavae, right atrium, tricuspid valve, right ventricle, pulmonic valve, pulmonary artery, lungs (drop off CO2, pick up O2), pulmonary veins, left atrium, mitral valve, left ventricle, aortic valve, aorta, body

relaxation. Blood returns to the heart.

diastole

contraction. Blood is pushed out

systole

the more the heart muscle is stretched (filled), the stronger it springs back, until it is stretched so far that it will not respond at all.

Starling's law of the heart

Order of the signal heart

SA node: the pacemaker cells. Starts every beat.

2 Atrial bundles: carry the impulse through the atrial muscle.

3 AV node: slows the impulse on purpose (so the atria finish squeezing before the ventricles start).

4 Bundle of His: carries the impulse into the ventricles.

5 Right and left bundle branches.

6 Purkinje fibers: spread it through the ventricle muscle

the pacemaker cells. Starts every beat

SA node

carry the impulse through the atrial muscle.

Atrial bundles:

slows the impulse on purpose (so the atria finish squeezing before the ventricles start).

AV node

carries the impulse into the ventricles.

bundle of his

Right and left bundle branches. and spread it through the ventricle muscle

Purkinje fibers:

conduction is slowest in

AV node

conduction is fastest in

Purkinje fibers.

cells in the electrical system can generate an electrical impulse (action potential) without being excited by an outside stimulus.

Automaticity

they pass the impulse rapidly so all the muscle cells are stimulated at about the same time

Conductivity

the muscle's ability to squeeze (Starling's law, calcium).

Contractility

) makes the heart beat faster, speeds conduction through the AV node, and makes the muscle contract hard

The sympathetic nervous system (SNS

changes heart rate, rhythm and strength.

: the ANS

is the electrical change in a cell when it fires. There are phases 0 to 4.

An action potential

SA node cell (the pacemaker):phase 4

slowly drifts upward on its own (this drift is automaticity).

SA node cell (the pacemaker):phase 4 starts at

-60 mV

SA node cell (the pacemaker): phase order

phase 4

phase 0

phase 3

SA node cell (the pacemaker):phase 0

upstroke (fires, goes positive

SA node cell (the pacemaker):phase 3

repolarization (comes back down

SA node cell (the pacemaker):phase 0 starts at

peaks around +15 to +20 mV)

SA node cell (the pacemaker):phase 3 starts at

-65 mV)

Ventricular muscle cell: phase order

phase 0-4

Ventricular muscle cell:

• Resting membrane potential (RMP) about -85 mV and flat in phase 4. Stimulation triggers it.

• Phase 0: very fast upstroke (depolarization).

• Phase 1: quick small drop (early repolarization).

• Phase 2: plateau (stays up, around 0 mV; calcium is entering).

• Phase 3: repolarization (falls back down).

• Phase 4: back to resting potential.

the working unit of cardiac muscle

sarcomere

sarcomere contains

actin filaments, myosin filaments, troponin, Ca2+ channels, and Z bands at each end.

when cardiac muscle is stimulated

, calcium enters through channels in the cell membrane and storage sites inside the cell

inactivates troponin',

removes troponin's brake so actin and myosin can connect).

calcium

what happens after calcium removes troponin's brake so actin and myosin can connect).

Actomyosin bridges form and break quickly.

The proteins slide together, which .

shortens the sarcomere

whats the (the syncytium effect).

5 When one cardiac muscle cell is stimulated, they all are stimulated to contract

how does muscle contract through sarcomere

When cardiac muscle is stimulated, calcium enters through channels in the cell membrane and from storage sites

inside the cell.

2 Calcium acts on troponin (the slide words it 'calcium inactivates troponin', meaning calcium removes troponin's brake

so actin and myosin can connect).

3 Actomyosin bridges form and break quickly.

4 The proteins slide together, shortening the sarcomere.

5 When one cardiac muscle cell is stimulated, they all are stimulated to contract (the syncytium effect).

6 Result: the pumping action of the hear

More calcium coming in =

stronger contraction.

impulse from the SA node (pacemaker) passing through the atria (atrial depolarization).

p wave

depolarization of the bundle of His (Q wave) and the ventricles (R and S waves).

qrs complex

repolarization of the ventricles.

t wave

happens at the same time as the QRS, so it is hidden by it.

• Atrial repolarization

the normal delay of conduction at the AV node; from the start of atrial excitation to the start of ventricular excitation

p-r interval

the critical timing of depolarization AND repolarization of the ventricles.

q-t interval

important information about repolarization of the ventricles.

s-t segment

Each vertical square =

0.1 mv

. Each horizontal square =

0.04 seconds.

normal PQ (PR) is

0.16 s,

normal QT is

0.3 s

normal QRS ia

0.08 s

normal p wave is

0.08 s

normal st is

0.1 s

Causes of changes in rate/rhythm:

drugs, acidosis, decreased oxygen level, electrolyte changes, buildup of waste products

artyhtmias • can arise from changes in

automaticity or conductivity.

types of Arrhythmias

Sinus arrhythmias

• Supraventricular: premature atrial contractions (PACs), paroxysmal atrial tachycardia, atrial flutter, atrial fibrillation

• Atrioventricular (AV) block

• Ventricular arrhythmias

PAC = a change in focus of the SA node: an ectopic focus (the pacemaker shifts from the SA node to another spot in the atria) fires an impulse out of the normal rhythm.

Pulmonary (heart-lung) circulation

• Right side of the heart sends blood to the lungs. Low-pressure, distensible thin-walled vessels.

• CO2 and some waste are removed; oxygen is picked up by red blood cells.

• Steps: deoxygenated blood enters the right atrium (superior and inferior vena cavae + great cardiac vein). Pressure

rises. When atrial pressure beats right ventricle pressure, most blood flows in passively. The atrium contracts to

push in the remaining blood. The ventricle contracts, pressure opens the pulmonic valve, blood goes into the

pulmonary artery, around the alveoli (O2 in, CO2 out), through pulmonary capillaries into veins, and back to the left

atrium.

Systemic circulation

• Left side sends oxygenated blood to every cell. High-pressure system.

• When left atrial pressure is greater than left ventricle pressure, blood flows in. Atrium contracts to push in the rest.

Ventricle contracts and blood is pushed through the aorta.

• The resistance system responds to the body's needs.

• Blood flows from arterioles into the capillaries. Oxygen, fluid and nutrients pass through the arterial end of the

capillaries into the spaces between tissue cells.

• Vessel traits: arteries are elastic with thick walls; veins are distensible with thin walls (pulmonary vessels too).

Fluid shift at the capillary (why fluid leaves, then comes back)

the heart's driving force, pushes fluid OUT of the capillary

hydrostatic pressure

pull from plasma proteins, pulls fluid IN.

Oncotic pressure

= net force = HP minus OP.

Filtration pressure

HP 36, OP 28, filtration +8 mmHg: HP > OP, fluid leaves the capillary.

arterial end

HP 21, OP 28, filtration -7 mmHg: HP < OP, fluid enters the capillary.

venous end

Coronary circulation (the heart feeding itself)

• Heart muscle needs a constant supply of oxygenated blood.

• Coronary arteries receive blood during diastole. The body is fed during systole, but the heart feeds itself only while

resting.

• Pulse pressure denotes the filling pressure of the coronary arteries.

• Oxygenated blood reaches every cardiac muscle fiber. This pattern is called end artery circulation (a blocked branch

means the muscle past it is starved).

• Main vessels: right coronary artery (with a posterior descending branch), left coronary artery (with the anterior

descending branch and the circumflex branch), and the coronary sinus collecting venous blood.

What makes the heart need more oxygen (4 forces):

1 Heart rate: the more it pumps, the more oxygen it needs.

2 Preload: more blood returned to the heart = harder work.

3 Afterload: higher resistance in the system = harder contraction.

4 Contractility: increased with more calcium influx.

1.12 Pressures

• Systemic arterial pressure: systolic and diastolic readings show the pumping pressure of the ventricle and the

generalized pressure in the system. Topics: hypotension, hypertension, humoral mechanisms (hormone-based

control), natriuretic peptides.

• Venous pressure: blood in veins can exert pressure above normal, causing backup/congestion of blood waiting to

enter the heart.

• Heart failure: the muscle cannot pump effectively, so congestion occurs.

• Left side fails: pulmonary edema (fluid in lungs).

• Right side fails: peripheral, abdominal and liver edema.

• Two systems to think about: the mechanical pump (clinical targets: diuretics and inotropes) and the electrical grid

(clinical target: antiarrhythmics).

1.13 RAAS as shown in Ch 42 (also see Part 2)

• Low blood flow/low oxygenation reaches the juxtaglomerular (JG) cells in the nephron.

• Two things happen: erythropoietin is released (bone marrow makes more RBCs, so oxygenation of the nephron

improves) AND renin is released.

• Renin activates angiotensinogen, giving angiotensin I, which goes to the lungs. ACE converts it to angiotensin II.

• Angiotensin II acts on angiotensin receptors (vasoconstriction, so BP and blood flow to the nephron go up) and on

the adrenal gland (angiotensin III, then more aldosterone, so sodium and water are retained, raising volume, BP

and blood flow to the nephron).

• Angiotensin III and sodium/water retention also stimulate hypothalamic osmoreceptors, which release ADH, so

water is retained, raising volume, BP and nephron blood flow.