CHP 19 HEART

The two divisions of the circulatory system

1) Pulmonary Circuit

• right side of heart, smaller

• carries blood TO the LUNGS

2) Systemic Circuit

• left side of heart

• oxygenated blood TO the TISSUES of the body

Simplistic flow of blood w/ left and right sides:

RIGHT SIDE

-oxygen poor blood arrives from inferior + superior venue cavae

-blood sent to lungs via pulmonary trunk

LEFT SIDE

-full oxygenated blood arrives from lungs via pulmonary veins (the one exception to vein/artery rule)

-blood sent to all organs via aorta

Blood Flow Through the Chambers (PROCESS)

1) Deoxygenated blood enters right atrium from superior + inferior venae cavae

2) through right atrioventricular valve into right ventricle

3) right ventricle contracts = pulmonary valve open

4) blood flows through pulmonary valve into pulmonary trunk

5) distributed by right + left pulmonary arteries to the lungs (LOAD UP O2)

6) blood returns from lungs via pulmonary veins to the left atrium

7) flows through left atrioventricular valve into left ventricle

8) left ventricle contracts (NOTE: same time as step 3) = aortic valve opens

9) blood flows through aortic valve into aorta

10) goes to every organ in the body (unload O2 LOAD UP CO2)

11) blood returns to right atrium via superior + inferior venae cavae

Ventricles contracting vs relaxing

relaxing = pressure drops, semilunar valves close, blood tries to back up into the ventricles, AV valves open, blood flows from atria to ventricles

Contract = blood tries to flow back into atria but AV valves close, pressure rises in ventricles, semilunar valves open and blood flows into ventricles

*Remember: blood wants to flow from high pressure to low pressure

Angina Pectoris

chest pain from partial obstruction of coronary (heart) blood flow

Myocardial infarction (MI)

sudden death of a patch of myocardium from long term obstruction of coronary circulation

HEART ATTACK

parts of a cardiac muscle

1) Cardiomyocytes = “branching tissue”

2) Intercalated disc = joins cardiomyocytes through junctions (allows for FAST electrical signals)

• mechanical junctions = connecting cells through transmembrane proteins

• Desmosomes = mechanical linkages that keep cardiomyocytes from being pulled apart from each other

• electrical junctions (gap junctions) = allow ion flow between cells

Metabolism of Cardiac Muscle

-dependent on aerobic respiration to make ATP

-fatigue resistant; makes little use of anaerobic fermentation or oxygen debt mechanisms

what is the conduction system

coordinates the heartbeat

internal pacemaker

conduction system (PROCESS)

1) Sinoatrial (SA) node fires; initiates heartbeat and determines heart rate

2) signal spreads throughout atria

3) Atrioventricular (AV) node fires; electrical gateway to ventricles

• Fibrous Skeleton; insulator that SLOWS DOWN the signal allowing for ventricles to have low pressure

4) signal spreads down Atrioventricular (AV) bundle (Bundle of His); right + left branches through interventricular septum toward apex

5) Subendothelial conducting networks (purkinje fibers) send signal through ventricular myocardium, then passing from cell to cell through gap junctions

systole

contraction

diastole

relaxation

sinus rhythm

normal heartbeat triggered by the SA node

typically 70-80 bpm

what nerves to what to heart rate

sympathetic nerves increase heart rate

parasympathetic nerves slow heart rate

Pacemaker Physiology (PROCESS)

SETTING OFF HEARTBEAT

1) SA node starts negative, slow Na+ inflow = gradual depolarization = pacemaker potential

2)reaches threshold, BOOM, Ca2+ and Na+ channels open, cont. depolarization until 0mv reached

3) K+ channels open, K+ leaves = repolarization, pacemaker potential starts over

Typical Electrical Behavior of Myocardium (PROCESS)

1) Voltage gated Na+ channels open

2) Na+ inflow = depolarization, positive feedback cycle (RAPID)

3) Na+ channels close and positive voltage peaks

4) Ca2+ entering very slowly through channels creating a plateau, it is slightly down curved due to K+ leakage out

5) Ca2+ channels close, K+ channels open, rapid outflow = polarization back to resting potential

electrocardiogram (ECG or EKG)

composite of ALL action potentials

detected, amplified, and recorded by electrodes

Electrocardiogram (PROCESS)

1) P wave = SA node fires, atria depolarizes and contract cardiomyocytes

2) QRS complex = ventricular depolarization (contraction), spike!

3) ST segment = ventricular systole, the platue in myocardial action potential

4) T Wave = ventricular repolarization (relaxation)

Cardiac cycle

one complete contraction and relaxation of all four chambers of the heart

-only can happen w a pressure gradient (flow from high to low) and resistance

-pressure changes allow for opening and closing of valves

How do we measure blood pressure

sphygmomanometer (blood pressure cuff)

Auscultation

listening to sounds made by the body

The Heart Sounds

S1 = “lubb” louder and longer = closure of AV valves

S2 =”dupp” softer and shaper = closure of semilunar valves

S3 = rarely heard in people over 30 = opening of left AV valve and filling of left ventricle (blood whooshing)

Cardiac Cycle (PHASES)

1) Ventricular filling (during diastole/relaxation) = AV valves open, pressure drops, filling of ventricles from atrias

• End-diastolic volume (EDV) = EQUAL blood filling

2) Isovolumetric Contraction (during systole/contraction) = ventricles contract but BLOOD STAYS

3) Ventricular ejection (during systole/contraction) = ventricles contract AND EJECT BLOOD

• Stroke Volume (SV) = total amount after ejection (70 ml)

• Ejection Fraction = ratio of blood ejected to blood leftover (54%)

• End-Systolic Volume (ESV) = blood left over after ejection (EDV - SV)

4) Isovolumetric Relaxation (during diastole/relaxation) = tension goes down and the volume remains the same

Quiescent Period

when all four chambers are in distal (“quite time”)

Congestive Heart Failure

failure of either ventricle to eject blood effectively

Pulmonary Edema

left ventricle failure

fluid accumulates in pulmonary tissue

Systemic Edema

right ventricle failure

fluid accumulates in systemic tissue

Cardiac Output and how to calculate

amount ejected by each ventricle in one minuye

= heart rate * stroke volume (total amount after ejection)

about 4-6 L/min

cardiac reserve

the difference between a persons maximum and resting CO

Pulse

surge of pressure produced by heart beat that can be felt by palpating a superficial artery

smaller organisms have faster bpm

Tachycardia

resting heart rate above 100 bpm

bradycardia

rest heart rate less than 60 bpm

positive vs negative chronotropic agents

positive = raise heart rate

negative = lower heart rate

Cardiostimulatory effect vs cardio inhibitory effect

stim =some neurons in cardiac center transmit signals to the heart by sympathetic pathways 

inhib = transmit parasympathetic signals by vagus nerve

Chronotopic effects of the atomic nervous system (PROCESS)

(lowering and rising heart rate)

SYMPATHETIC

1) postganglionic fibers are adrenergic and release norepinephrines

2) bind to B(beta)-adrenergic fibers in the heart

3) activate cAMP second messenger in cardiomyocytes

4) opening of Ca2+ channels in plasma membrane

5) inc Ca2+ inflow accelerates depolarization of SA node

6_ cAMP accelerates uptake of Ca2+, cardiomyocytes relax quicker

7) accelerating contraction and relaxation, heart rate increases as high as 230 bpm

PARASYMPATHETIC

1) vagus nerve has cholinergic inhibitory effects on SA and AV nodes

2_ acetylcholine binds to muscarinic receptors

3) opens K+ gates, inside is more negative = harder to initiate action potential

Vagal Tone

holds heart rate at 70-80 bpm at rest

Proprioceptors

in muscles and joints

sense changes in activity so HR increases before metabolic demands arise

Baroreceptors

sense changes in blood pressure

“lightheadedness” + correcting it

-BP dec = signal rate drops = inc heart rate

-BP inc = signal rate rises = dec heart rate

Chemoreceptors

sense blood pH, CO2, and O2 levels

Hypercapnia = high CO2 levels = inc heart rate for respiratory control

Hypoxemia = oxygen deficiency = slow down heart

Chemicals that affect heart rate

• Autonomic neurotransmitters (NE and Ach)

• Adrenal hormones (NE and epinephrine)

• Nicotine

• Thyroid hormone

• Caffeine

impacts of electrolytes on heart rate

-K+ greatest chonotropic effect

• Hyperkalemia = excess K+, heart rate slows + irregular

• Hypokalemia = deficient in K+, needs stimulation

hyper vs hypo calcemia

hyper = excess of Ca+2, decreases heart rate

hypo = deficiency of Ca+2, increases heart rate

Preload

amount of tension in ventricular myocardium before it begins to contract

Frank-starling law of the heart

stroke volume is proportional to end diastolic volume

-more stretch (more blood in there) = harder contraction

Positive Inotropic Agents

-increase contractility

• hypercalcemia

• catecholamines (inc calcium levels)

• glucagon 

• digitalis

negative inotropic agents

reduce contractility

• hypocalcemia

• hyperkalemia

• vagus nerves (not too significant)

afterload

sum od all forces opposing ejection of blood from ventricle

-blood pressure in the aorta and pulmonary trunk

hypertension

increases afterload and opposes ventricular ejection

cor pulmonale

right ventricular failure due to obstructed pulmonary circulation

inc and dec cardiac output

-exercises increases cardiac output

-proprioceptors signal cardiac center, sympathetic output increases cardiac output

-increasing muscular activity increases preload and cardiac output

Ventricular hypertrophy effects

increases stroke volume, allows heart to beat more slowly at rest

Coronary Artery disease (CAD)

-a constriction of the coronary arteries

-Cause: usually from the degradation of material wall that obstructs the lumen (hole of artery)

-the the degradation becomes atherosclerotic plaques that build up and block the lumen

-risks: cholesterol, neutral fats, LIPIDS IN DA BLOOD

-unavoidable risks: heredity, aging, being male

-avoidable risks: obesity, smoke, lack of excesses

-impacts: angina pectoris, inflammation, artery spasms, artiniosclerrosis (hardening of blood vessel)

-fix it: coronary bypass surgery