The Heart LECTURE A&P II

Located in the mediastinum

about the size of a fist

• covered in a 2 layer pericardium
• -fibrous layer
• -visceral layer (epicardium)

2 Layers

Superficial fibrous pericardium: protects, anchors, and prevents over filling

• Deep two layered serous pericardium: 
• Parietal layer lines the interal surface of the fibrous pericardium
• Visceral layer (epicardium) on the external area of the heart
• *they are separated by a serous fluid filled pericardial cavity that decreases friction

• Epicardium
• -visceral layer of the serous pericardium

• Myocardium
• -forms the bulk of the heart  muscle
• -spiral bundles of cardiac muscle
• -anchors cardiac muscle fibers
• -supports great vessels and valves
• -limits spread of APs to specific paths

• Endocardium
• -continuous with endotheial lining of the blood vessels

***equal volumes of bloof are pumped thru both the systemic and the pulmonary circuits***

Left side has much more pressure to pump to the entire body (systemic)

Right side has much less pressure as it is only pumping to the lungs (pulmonary)

Thoracic pain cased by a fleeting deficiency in blood delivey to the myocardium (coronary circulation)

Cells are weakened

HEART ATTACK!

Prolonged coronary blockage

Areas of cell death are repaued with noncontractile scar tissue (damage to LV is most serious)

Cardiac muscle cells are short, fat, branched, and interconnected

They have a central Nuclei

Connective tissue matrix (endomysium) connects to the fobrous skeleton for both the origin and the insertion

T Tubukes are wide but less numerous than in skeletal muscle and SR is much simpler

Numerous large mitochondria create resistance to fatigue (25-30% of cell volume)

Intercalated discs: Junctions between cells that anchor cardiac cells

desmosomes prevent cells from separating during contraction

Gap junctions allow ions to pass; electrially couple adjacent cells

**Heart muscle behaves as a functional syncytium**

Depolarization of the heart is rhythmic and spontaneous

about 1% of cardiac cells have automaticity (are self excitable)

Gap junctions ensure the heart contracts as a unit

long absolute refractory period (250ms) prevents tetanic contractions

Depolarization opens the voltage-gates fast Na⁺ channels in the sarcolemma

Reversal of membrane potential from -90 mV to +30 mV

Depolarization wave in T tubules causes the SR to release Ca²⁺

Depolarization wave also opens slow Ca²⁺ channels to the sarcolemma (allows Ca²⁺ to come in from extracellular space)

Ca2+ surge prolongs depolarization phase (plateu)

Ca²⁺ influz triggers the opening of Ca²⁺ sensitive channels in SR, which liberates bursts of Ca²⁺ (calcium triggered calcium release)

E-C coupling occurs as Ca²⁺ binds to troponin and sliding filaments begins

Duration of the AP and the contractile phase is much greater in cardiac muscle than in skeletal muscle

Repolarization results from inactivation of Ca²⁺ channels and opening of voltage gated K⁺ channels

A network of noncontractile (autorythmic) cells that initiate and distribute impulses to coordinate the depolarization and contraction of the heart

They have automaticity or are self-excitable

Have unstable resting potentials (pacemaker potentials or prepotentials) due to open sloe Na+ channels

At threshold, Ca²⁺ channels open

Explosive Ca²⁺ influx produces the rising phase of an AP

Repolarization results from inactivation od Ca²⁺ channels and opening of voltage-gated K+ channels

• 1. Sinoatrial Node (SA Node): The pacemaker
• -generates impulses about 75x/min (sinus rhythm)
• -depolarizes faster than any other part of the myocardium

• 2. Atrioventricular Node (AV Node):
• -smaller diameter fibers; fewer gap junctions
• -slows down or delays impulses by .1 seconds
• -depolarizes 50x/min in absence of SA node input

• 3. Atrioventricular Bundles (AV Bundle) (Bundle of His)
• -only electrical connection between atria and ventricles

• 4. Right and left bundle branches
• -two pathways in the interventricular septum carry impulses towards the apex

• 5. Perkinje Fibers (from wall to wall)
• -complete the pathway to the apex and ventricular walls
• -AV bundle and Purkinje Fibers depolarize only 30x/min in absence of AV node input

• 1. Arrythmias: irregular heart rhythms
• 2. Uncoordinated atrial and ventricular contractions
• 3. Fibrillation: rapid, irregular contractions; useless for pumping blood (like a squirming worm)

• Ectopic Focus: abnnormal pacemaker takes over
• -if the AV node takes over, there will be a junctional rhythm (40-60bpm)

Partial or total heart block

few oe no impulses from SA node reach the ventricles

Heart is modified by the Automic Nervous System

Cardiac centers located in the medulla oblongata

-Cardioacceleratory center innervates the SA and NA nodes, heart muscle, and coronary arteries through sympathetic neurons

-Cardioinhibitory center inhibits SA and AV nodes through the parasympathetic fibers in the vagus nerves

EKG: a composite of all the action potentials generated by nodal and contractile cells at a given time (not tracing a single AP!)

• 3 Waves:
• 1. P wave: Atrial Depolarization
• 2. QRS complex: Ventricular Depolarization
• 3. T wave: Ventricular Repolarization

Two sounds LUB-DUP associated with closing of the heart valves

First sound occurs as AV valves close and signifies the beginning of systole

Second Sound occurs when SL valves close at the beginning of ventricular diastole

Heart murmurs: abnormal heart sounds most often indicative of valve problems. Either an incompetant valve which leaks or a stenotic valve which doesn't open. The sound is caused by a turbulent flow

All events associated with blood flow through the heart during one complete heartbeat

• Systole: contraction
• Diastole: Relaxation

• 1. Ventricular Filling
• 2. Ventricular Systole
• 3. Isovolumetric Relacation

• Ventricular Filling: takes place in mid-to-late diastole
• -AV Valves are open
• -80% of blood passively flows into ventricles
• -Atrial Systole occurs delivering the remaining 20%

End Diastolic Volume (EDV): volume of blood in each ventricle at the end of ventricular diastole

• Ventricular Systole
• -Atrial diastole and ventricles begin to contract
• -Rising Ventricular pressure closes the AV valves
• -Isovolumetric contraction phase (all valves closed)
• -In ejection phase, ventricular pressure exceeds pressure in largr arteries and the SL valves open

End systolic volume (ESV): volume of blood remaining in each ventricle at the end of systole

• Isovolumetric Relaxation: occurs during early ventricular diastole
• -ventricles relax
• -backflow of blood in aorta and PAT close the SL valves and causes dicrotic notch (brief rise in aortic pressure)

CO: volume of blood pumped by each ventricle in ONE MINUTE. measure as ml/min



Heartrate (HR)- number of beats per minute

Stroke Volume (SV)- volume of blood pumped out by one ventricle each beat

The difference between resting and maximum CO

• At rest: (average)
• CO ml/min = HR (75bpm) x SV (70ml/beat)= 5.25L/min
• *thats about all your blood in one minute!

Maximum CO is 4-5 resting CO in nonathletic people

COMax may reach 35/min in trained atheletes

• The three main factors affecting SV:
• 1. Preload
• 2. Contractility
• 3. Afterload

Preload: degree of stretch of cardiac muscle cells before the contract (Frank-Starling law of the heart)

• -Cardiac muscles exhibits a length tension relationship
• -At rest, cardiac muscle cells are shortal than optimal length (more contractile force)
• -Slow heartbeat and exercise increase venous return
• -increased venous return distends or stretches the ventricles nad increases contraction force 
• *increases EDV*

Contractility: contractile strength at a given muscle length, independent of muscle stretch and EDV

• Positive inotropic agents increase contractility (lowers ESV heightens SV)
• -increased Ca2+ influx due to sympathetic stimulation
• -hormones (thyroxine, glucagon, and epinephrine)

• Negative inotropic agents decrease contractility
• -Acidosis
• -increased extracellular K+
• -calcium channel blockers

Afterload: pressure that must be overcome for ventricles to eject blood

Hypertension increases afterload, resulting in increased ESV and lower SV

Positive chronotropic factors increase heart rate

Negative chronotropic factors decrease heart rate

• Sympathetic nervous system is activated by emotional or physical stressors
• -norepinephrine causes the pacemaker to fire more rapidly (and at the same time increases contractility)

• Parasympathetic nervous system opposes sympathetic effects
• -Acetylcholine hyperpolarizes pacemaker cells by opening K+ channels

The heart at rest exhibits vagal tone (dominant influence due to vagal nerve is inhibitory)

• The Atrial (Bainbridge reflex): a sympathetic reflec initiated by increased venous return
• -stretch of atrial walls stimulates SA node
• -also stimulates atrial stretch receptors activating aympathetic reflexes

• 1. Hormones
• -Epinephrine from adrenal medulla enhances heart rate and contractility
• -thyroxine increases heart rate and enhances the effects of norephinephrine and epinephrine

• 2. Intracellular and Extracellular Ion concetrations (such as Ca²⁺ and K+)
• -these must be maintained for normal heart function

• -Age (declines throughout life)
• Gender (faster in females)
• -Exercise
• -Body Temperature

• Abnormally fast heart rate (above 100bpm)
• -could be from fever, stress, drugs, or heart disease
• -if persistent, could lead to fibrillation

• Heart rate slower than 60bpm
• -could be from low body temp, drugs, or parasympathetic activation
• -could be a sign of brain edema after head injury
• -may result in grossly inadequate blood circulation
• -may be a desireable result of endurance training

Progressive condition where the CO is so low that blood circulation is inadequate to meet tissue needs (resulting in a weakening of the myocardium)

• Caused by:
• -coronary atherosclerosis
• -persistent high bp
• -multiple myocardial infarcts (myocardium replaced with scar tissue)
• -dilated cardiomyopathy (DCM): ventricles stretch and become flabby

• 1. Sinous Venous
• 2. Atrium
• 3. Ventricle
• 4. Bulbus cordis

Foramen Ovale connects the two atria

Ductus Arteriosus connects the pulmonary trunk and the aorta

1. septal defects-mixing of systemic and pulmoary blood

2. Involving narrowed valves or vessels that increase heart workload

Schlerosis and thickening of valve flaps (more common in the mitral valve, murmurs common in elderly)

Decline in Cardiac Reserve

Fibrosis of cardiac muscle (Scarring of heart and nodes)

Atherosclerosis (fat/hardening of arteries)