Chapter 15 - Cardiovascular Physiology

Cardiovascular system is a closed or open system?

Closed system

Cardiovascular system function

transport of material (gases, nutrients, waste, communication, defense against pathogens, temperature homeostasis)

Artia

receives blood returning to heart

Ventricles

pump blood out to system

Septum

divides left and right halves

Left contains

Oxygenated blood

Right contains

Deoxygenated blood

Blood vessels include

veins, arteries, capillaries

blood include

cells and plasma

Portal system

joins two capillary beds in series

heart composed of mostly

myocardium

Pericardium

membranous fluid-filled sac that cases the heart

systole

ventricular contraction

diastole

ventricular relaxation

Internodal pathway from SA to atriventricular node

routes direction of electrical signals (contraction from apex to base)

AV node delay is accomplished by

conductional signals through nodal cells
—> allows efficient contraction of the heart

Purkinje fibers

transmit electric signals down the atriventricular bunde (bundle of his) to left and right bundle branches

what are the primary pacemakes in the heart?

SA Node

Characteristic of SA node

has no true resting potential
- generates spontaneous, regular action potential

What type of ion primarily carries the depolarizaing current in SA nodal cells?

Slow Ca2+ currents (and lacks fast Na+ currents)

two major circulatory systems in the body

pulmonary and systemic circulation

what ensures one way flow of blood in the heart?

atrioventricular and semilunar values

myocardium

muscle tissue responsible for contraction and pumping blood

AV valves separate the

atria from ventricles

semilunar valves separate

ventricles from major arteries

what happens during ventricular contraction?

- pushes blood out of heart into aorta
- AV valves remain closed to prevent blood flow backward into atria

what happens during ventricular relaxation?

- receives deoxygenated blood through arteries through AV valve
- semilunar valves close to prevent blood from flowing back into ventricles (aorta로 이미 보냈으니까)

Sinoatrial (SA) node

Sets the pace of the heartbeat at 70bpm

What are the secondary pacemakers of the heart (when SA node fails)

AV node and Purkinje fibers

bundle of His

transmits signals from AV node to left and right bundle branches

Order of electrical impulse through heart’s conduction system

Sa node —> internodal pathways —> AV node —> AV bundle (bundle of His) —> left and right bundle branches —> purkinje fibers —> ventricles contract

role of AV node

delays electrical signal (by being slow) to allow atria to contract before ventricles —> efficient blood flow

why do SA nodal cells have slower action potentials compared to non-pacemaker cells?

lack fast Na+ channels —> slower depolarization phase

How does the heart propagate electrical signals?

through cardiac muscle tissue

Myocardial contractile cells function

responsible for heart muscle contraction

Myocardial autorhythmic cells function

unstable membrane potential called pacemaker

Two main types of miocardial cells

Myocardial contractile cells and myocardial authorhythmic (pacemaker) cells

which ion is responsible for depolarization in myocardial CONTRACTILE cells?

Na+ through fast channels

what ion is responsible for depolarization in myocardial AUTORHYTHMIC cells?

Ca2+ through slow channels

Tetanus

sustained muscle contraction caused by repeated rapid stimulation without allowing the muscle to relax between contractions

how are contractile cells different from neurons in action potential?

Contractile cells are depolarized for longer (through Ca2+ influx) while neurons dont have a plateau

Why do contractile cells have to be contracted for longer than normal conduction cells?

full blood ejection + extension of absolute refractory period —> prevents tetanus

Three types of waves in ECG

P, QRS compex, T

P wave in ECG represents

depolarization of atria —> atrial contraction near end of P wave

QRS complex in ECG represents

wave of atrial repolarization + ventricular depolarization
—> atrial repolarization begins with R wave
—> ventricular contraction begins at end of QRS complex

T wave in ECG represents

repolarization of ventricle (occurs at peak)

P-R segment in ECG

conduction through AV node and AV bundle (bundle of his)

ECG helps

diagnose heart function by looking at waves and intervals

Heart rate

time between two P waves or two Q waves

Rhythm

regular pattern

waves analysis

looks at presence and shape

Segment length constant

length of each segments should remain constant

Visual features of contractile cardiac muscle cells

- Striated fibers as sarcomeres
- branched
- single nucleated
- attached through intercalated disks (w/ desmosomes and gap junctions)

Visual features of autorhythmic cells (pacemaker)

- Smaller and fewer contractile fibers
- NO sarcomere

desmosomes function

transfer force form cell to cell

gap junction function

allows electrical signals to pass rapidly from cell to cell

Cardiac muscle cell VS skeletal muscle

Cardiac: smaller, single nucleus, larger and branched t tubles, SR smaller, A LOT OF MITOCHONDRIA
Skeletal: larger, multinucleated, smaller t tubles, larger SR, adequate mitochondria

force generated proportional to

number of active crossbridges —> determined by how much Ca bound to troponin

Determinants for force generated

- number of active crossbridges
- sarcomere length

Ca2+ spark

local release of Ca2+

First heart sound

Lub - caused by closure of AV valves

Second hear sound

Dup - caused by closing of semilunar valve

Ausculation

listening to heart through chest through stethoscope

Isovolumic ventricular relaxation

when volume of blood in ventricles does not change

End diastolic volume (EDV)

total volume of blood in a ventricle at the end of diastole (just before contraction)

End systolic volume (ESV)

amount of blood remaining in ventricle after contraction

Stroke volume

amount of blood pumped by one ventricle during single contraction

how to calculate stroke volume

SV = EDV - ESV

average stroke volume

70mL

Cardiac output (CO)

volume of blood pumped by one ventricle in given period of time

how to calculate CO

CO = heart rate x SV

Average cardiac output

5L/min

preload

degree of myocardial stretch before contraction

determinants for force of contraction

- length of muscle fiber (determined by EDV since more volume = more stretching = more force generated)
- Contractility of heart

Stretch on ventricular wall proportional to

stroke volume

what nervous system controls heart rate?

autonomic nervous system (sympathetic and parasympathetic)

Sympathetic activity of heart

speeds heart rate (through NE on B1 adrenergic receptors)

Parasympathetic activity of heart

slows heart rate (ACh on M receptor)

Contractility

ability of heart to generate force during contraction

Inotropic agent

chemical that affects contractility

Chemicals with positive inotropic effects

Epinephrine, norepinephrine, digitalis

Positive inotropic effect

increases contractility

Negative inotropic effect

decreases contractility

Chemicals with negative inotropic effects

beta-blockers

Diastolic heart failure (Hypertrophic)

heart muscle stiff and thick —> difficult for ventricles to relax and fill with blood

Systolic heart failure (Dialated)

Heart chambers become stretched and thin, weakening heart’s ability to contract and pump blood efficiently

Type 1 Myocardial infarction Heart Attack

caused by atherosclerosis (plaque buildup)

Type 2 Myocardial infarction Heart Attack

blocked artery BUT with a mismatch b/w oxygen supply and demand