Cardiovascular Physiology

Daniel H Williams

• performed the first open heat surgery in 1893

• one of few black cardiologist at the time

Cardiomyocytes

contractile but do not initiate their own AP

Fibroblasts

• most abundant cells in heart

• non excitable

Auto rhythmic cells

• non-contractile

• initiate and conduct APs

nodal cells

• capable of spontaneously depolarizing

• set “pace” for the whole heart

Sinoatrial node

• neural tissue/modified myocytes

• can stimulate only atria

• usually the fastest to spontaneously depolarize

Atrioventricular node

• usually slowest to depolarize to allow atria time to contract before the ventricles do

Bundle of His

continuation of the specialized tissue of the AV node and serves to transmit the electrical impulse to the bundle branches

rule of autorhythmic cells

faster APs override slower ones

If channels

• unique channels in nodal cells capable of causing a drifting membrane potential

• open upon hyperpolarization

• allow sodium to flow into the cell and potassium to flow out of the cell

• inward flow of sodium predominates

-60 mV

resting membrane potential of autorhythmic cells

intrinsic potential

• drifting potential that is unstable

• keeps heart contracting at a pace

• no voltage gated sodium channels involved

T-type channels

transient(fast) calcium channels

L-type channels

calcium channel along t tubule that opens in response to an action potential

tricuspid valve

separates the right atrium and right ventricle

bicuspid valve

valve between the left atrium and left ventricle

coronary arteries

artery supplying blood to the heart muscle and runs along shallow grooves in the heart

right coronary artery

• runs from aorta around right side of heart in coronary sulcus

• feeds the right atrium, most of right ventricle, and some of the left ventricle

left coronary artery

• branches into circumflex branch and anterior interventricular branch

intercalated discs

specialized cell junctions that contain gap junctions and desmosomes

gap junction

• electrically connect cardiac cell

• allow waves of depolarization to spread rapidly from cell to cell

E-C coupling in cardiac muscle

1. action potential enters and voltage gated calcium channels open

2. opens RyR channels

3. summed calcium spark starts calcium signal

4. contraction

5. relaxation - calcium is pumped back into SR and into excellular space

NCX antiporter

exchange calcium with extracellular sodium

the number of cross bridges that are active

force generated by cardiac muscles is proportional to:

steps of action potential in cardiac muscle

1. resting membrane potential of about -90 mV

2. depolarization - voltage gated sodium channels open

3. na channels close at 20 mV and K efflux channels open

4. voltage gate calcium channels open and ca enters the cell

5. repolarization: calcium channels close and potassium channels open

steps of action potential in autorhythmic cells

• If channels open at negative potential, sodium influx exceeds potassium efflux

• membrane slowly depolarizes until If channels close and calcium channels open

• rapid depolarization as calcium flows in

• Ca channels close at peak of AP and potassium channels open

internodal pathway

conduction pathway from the SA node to the AV node

AV node delay

• delay between atria and ventricular contraction

• accomplished by slower conduction signals through nodal cells

complete heart block

condition where the conduction of electrical signals from the atria to the ventricles through the AV node is disrupted

fibrous skeleton

• composed of dense connective tissue

• lies in the plane between the atria and the ventricles

• non excitable

AV node

lowest conduction velocity is in the:

cardiac muscle

• small fibers

• highly vascular

• fatigue resistance

• amitotic

hypertrophy

enlargement of heart muscle due to increased work demand

acorn device

• electric net placed around heart

• reduces LV failure

syncytium

• network of heart cells that contract as a unit

• due to intercalated disc connections

components of intercalated disc

• fascia adherens junction

• gap junction

• desmosome

calcium induced calcium release

• extracellular calcium enters through L-type channels due to action potential

• opens RyR calcium channels on SR and starts contraction

junctophilin-2

• determines the distance that the influx of calcium must travel before reaching the calcium binding sites on RyR-2

• ensures RyR-2 is in close proximity to L-types DHPR

sympatheic fibers

• innervate SA and AV nodes as well as ventricles

• release norepinphrine

norepinphrine

increases sodium and calcium conductance via beta-1 adrenergic receptors

parasympathetic fibers

• from vagus nerve

• innervate SA and AV nodes

• release acetylcholine

acetylcholine

increases potassium conductance via M2 muscarinic receptors and decreases calcium conductance

tachycardia

• abnormally fast heart rate

• caused by body temp, stress, drugs, heart disease

bradycardia

• abnormally slow heart rate

• endurance athletes

• hypertrophy

• pathologic (inadequate blood supply)

• edema from head trauma

• hypothermia

electrocardiogram

a recording of the summed electrical events of the cardiac cycle

einthoven’s triangle

a hypothetical triangle created around the heart when electrodes are placed on both arms and the left leg

waves

parts of ECG trace that go above or below the baseline

segments

sections of ECG baseline between two waves

intervals

combinations of waves and segments

P wave

wave of ECG that represents atrial depolarization

QRS complex

wave complex that represents ventricular depolarization and atrial repolarization

T wave

ECG wave that represents ventricular repolarization

cardiac cycle

period of time from the end of one heartbeat through the end of the next beat

arrhythmia

irregular rhythm of the heartbeat

premature ventricular contractions (PVCs)

type of arrhythmia where extra beats occur when an autorhythmic cell other than the SA nodes fires an action potential out of sequence

long QT syndrome (LQTS)

• a heart rhythm disorder characterized by a prolonged QT interval on an ECG

• has several forms including defective channels and proteins

diastole

the time during which cardiac muscle relaxes

systole

the time during which the muscle contracts

end-diastolic volume (EDV)

maximum volume at the end of ventricular relaxation

first heart sound (S1)

sounds created by vibrations from closure of AV valves

isovolumic ventricular contraction

phase of the cardiac cycle when the ventricles are contracting but all valves are closed and the volume of blood in them is not changing

end-systolic volume (ESV)

the amount of blood left in the ventricle at the end of contraction

sound heart sound (S2)

vibrations created by the closing of the semilunar valves

isovolumic ventricular relaxation

phase of the cardiac cycle when the ventricles are relaxing but the volume of blood is not changing

muscarinic cholinergic receptors

• activated by Ach and influence K and Ca channels in pacemaker cells

• lowers pacemaker potential and slows rate at which the pacemaker potential depolarizes

beta 1 -adrenergic receptors

• located on autorhythmic cells

• activated by norepinephrine and epinephrine

• uses cAMP second messenger system

• increase ion flow through If and calcium channels

inotropic agent

any chemical that affects cardiac contractility

positive inotropic effect

chemical effects that increases the force of contraction

PQ segment

AV node delay

ST segment

time during which ventricles are contracting and emptying or “systole”

TP interval

time during which ventricles are relaxing and filling or diastole

cardiac output

• measures the volume of blood the heart/ventricles pumps per minute

• HR x SV

• measure of heart efficiency

5 liters

rough total blood volume

increasing stroke volume and heart rate

Can increase cardiac output by:

increasing preload, contractility and decreasing afterload

Can increase stroke volume by:

preload, contractility, afterload

Factors affecting stroke volume:

cardiac contractility (iontropism)

the intrinsic ability of the myocardium to pump in the absence of changes in preload or afterload

myocardial contractility is depressed by

• anoxia

• acidosis

• depletion of catecholamines

• loss of muscle mass

afterload

• force needed to eject blood from ventricles

• determines by back pressure from arterial blood

proprioceptors

• major stimulus for quick rise in heart rate

• monitor limb position and send impulses to cardio center in medulla

bainbridge reflex

• sympathetic reflex

• activated by stretching of atrial wall

• increases heart rate (SA node firing)

baroreceptors

• sense pressure

• help control blood pressure and heart rate by communicating with medulla

thyroxine

hormone produced by thyroid that increases heart rate

hypocalcemia

• impairs cardiac contractility

• SR is unable to maintain sufficient amount of calcium content to initiate myocardial contraction

Hyperkalemia

• most commonly seen in patient with end-stage renal disease

• flattened P waves and prolonged PR interval, widened QRS, deep S wave, merging of S and T waves

• earliest sign is peaked T wave

heart failure

decreased cardiac output and venous return

compensated heart failure

• early heart failure

• often goes unnoticed due to homeostatic mechanisms

decompensated heart failure

late heart failure when compensation mechanisms aren’t enough anymore

counter measures to compensate heart failure

1. frank starling

2. myocardial hypertrophy

3. increased sympathetic stimulation

4. renin angiotensin Aldosterone mech.

Renin Angiotensin Aldosterone Mechanism

involves the kidneys retaining water to increase blood volume

ejection fraction

• percent of EDV ejected with 1 contraction

• = SV/EDV

length of muscle fiber, contractility, and venous return

Force generated by cardiac muscle is affected by:

venous return

• amount of blood entering the heart from venous circulation

• impacted by compression of veins, pressure changes in abdomen, and sympathetic effect on veins

preload

degree of myocardial stretch before contraction

frank-starling law of the heart

the principle that within physiological limits, the heart will pump all the blood that returns to it

skeletal muscle pump

the skeletal muscle contractions that squeeze veins and push blood toward the heart

respiratory pump

• created by thoracic movements of breathing

• low pressure in chest during inspiration draws more blood into the vena cava

• high pressure in abdomen during inspiration pushing blood into vena cava

vasoconstriction

• achieved by sympathetic activity

• squeezes more blood into the heart

• causes larger EDV and more forceful ventricular contraction

phospholamban

• regulatory protein

• phosphorylated by catecholamine activity

• enhances Ca2+-ATPase activity in SR