Biology 2402  AP II      Lecture Notes   Heart
Dr. Weis

Heart Anatomy :

Location......anterior mediastinum in pericardial cavity

Shape : cone-like, has superior broad base and inferior pointed apex

Coverings : Double walled pericardium, to keep heart suspended, anchored and to reduce friction

Wall :  Three layers

Myocardium : three types of cardiac muscle

Cardiac muscle :

Myocardium also has connective tissue (collagen & elastin fibers) that are arranged in bundles to form a fibroskeleton that fxn: links myocardium together, provides reinforcement and anchor, and helps direct electrical conduction pathway.

---

CHAMBERS : #4  --> 2 upper atria (R,L);  2 lower ventricles (R,L)

            The chambers have muscular and connective tissue divisions.

Atria : small, thin walled, separated by interatrial septum that has a depression --> fossa ovalis

Atria have an auricle as an extensable appendage for extra blood storage within its walls

            Within the auricle are ridges of tissue called the pectinate muscle.

            right atria : receives blood from three veins -->

Ventricles : thick walled, muscle ridges formed and consist of trabeculae carnae and papillary muscles

right ventricle : forms anterior surface of heart pumps blood to pulmonary trunk
thin walled structure as compared to the left ventricle

left ventricle  : posterior surface of heart  forms apex and PMI (point of maximal intensity) for auscultation.  It is the thickest of all chambers, pumps blood to aorta -> body.

---

Grooves :

Interventricular sulcus :

---

---

BLOOD PATHWAY : two pump system in series create the Systemic Circuit and Pulmonary Circuit

Systemic Circuit                                                         Pulmonary Circuit

serves many tissues/organs                                                        serves single organ

many controls and requirements by different organs                   passive system, single organ requirement

high resistance (R = P/F)                                                           low resistance

covers long distance                                                                  short distance, lungs @ same level as heart

high pressure due to left ventricle                                               low pressure

BLOOD FLOW :
Arteries carry blood AWAY from the heart, Veins carry blood back to the heart

  Blood from body --> rt atrium --> rt ventricle --> pulmonary trunk / pulmonary arteries -->

 pulmonary capillaries in lungs for gas exchange (CO2, O2) --> pulmonary veins  --> left atria --> left ventricle --> aorta --> body

---

Heart Valves  (#4)

A) Two atrioventricular (AV) at junction of atria/ventricle

These valves are anchored by collagen fibers called the  CORDAE TENDINAE that extend from the papillary muscles to help keep valves in closed postion and prevent bulging of valves too far back into atria.

B) Two semilunar valves at junction of ventricles and vessels

 The semilunar valves have three cusps that are cup-like and normally stay closed to prevent back flow of blood into the ventricles.  They will open with increased pressure in ventricles.

Problems with valves :

incompetent valve..............does not close

valvular stenosis..............stiff, constrict opening

---

CARDIAC CIRCULATION :

Fxn ....blood supply within epicardium, for the heart muscle itself

From base of aorta, first arterial branches of the ascending aorta are the Coronary Arteries.

   The Coronary arteries encircle the heart in the AV groove and has right and left branches.

These arteries interconnect to form an anastomoses and allow continual blood flow to heart m.

The left coronary artery give rise to the:

1) anterior interventricular a.

2) circumflex a.

The right coronary artery gives rise to the :

1) marginal a. 

2) posterior interventricular a.

Blood return from the heart back to the Right Atrium:

Coronary capillaries form the cardiac veins :

Great C.V. from the anterior interventricular a., lies in the Anterior Interventricular sulcus

Middle C.V. from the posterior interventricular a., lies in the Posterior Interventricular sulcus

Small C.V. from the marginal a., lies along the Right Inferior Margin

  These cardiac veins and other anterior and posterior cardiac veins will drain into the cardiac sinus that empties into the right atrium.

In addition to the blood supply, the cardiac muscle requires a constant supply of oxygen, and can store oxygen on the heme units of the myoglobin.  The muscle contains large number of mitochondria and will use energy stores from glycogen and lipids.

---

CARDIAC PHYSIOLOGY

Cardiac Muscle Histological Characteristics:

---

Functional cardiac cells

1) Synctial.......cells that are electrically fused together to create a single unit. 

Created by intercalated discs (gap junctions anchored by desmosomes) and branching of cardiac muscle cells found in the atria and ventricles

2) Specialized Conduction System....... ~ 1 % of cardiac muscle, modified cardiac muscle cells that are autorhymic

may be seen grossly, pale large areas of modified cardiac fibers that contain large amounts of glycogen

parts of this conduction system :

Cardiac Conduction System :

a. sinoatrial node (SA node)...........Pacemaker

b. Atrioventricular node (AV node)

c. AV bundle (Bundle of His) connects atria and ventricular synctia

d. Rt., Left Bundle branches in septal wall

e. Purkinje Fibers and moderator band
located in papillary muscle and ventricular free wall

---

---

Contraction.........Muscle Action Potential Events

Cardiac muscle has

1) ion channels : fast sodium channels for initial depolarization

   slow calcium channels, voltage regulated

   slow potassium channels

2) smaller sarcoplasmic reticulum, stores some Ca++

3) shorter, wider T-tubules, store Ca++

4) no triads

Upon stimulation from the specialized cells of the cardiac conduction system, Cardiac muscle events are as follows:

Na+ channels open, Na+ in, changes membrane potential and causes depolarization. 

Na+ channels will close rapidly.  Voltage regulated Ca++ open, 20% Ca++ flows in and triggers the T-tubules to cause a releases some of its stored Ca++ in the SR and allow Ca++ in extra cellular fluid (ECF) to go down the tubules which prolongs the depolarization via the slow Ca++ channels.

SR completes the release the rest of its stores of Ca++ into the myocardial cells. The SR will contribute 80% of the calcium need for contraction.

Ca++ binds to troponin & allows myosin to interact with actin to cause cross bridge formation and movement of Sarcomeres to create a contraction.   Contraction is graded, variable and is proportional to the number of cross bridges formed (myosin binding to actin)

 The contraction stops when the AP ceases and Ca++ is then taken up by SR and T-tubules

---

Heart (cardiac muscle) contraction has ::

a) prolonged depolarization and increased strength of contraction due to slow Ca++ channels

b) K+ slow channels are delayed in opening until all Na + and Ca++ channels close.

 This will delay the return of membrane potential toward resting which affects prolonged depolarization. 
When K+ channels open, K+ out to repolarize membrane

c) Refractory period also longer to prevent wave summation and tetany

1) The resting membrane potential is @ -60mV (vs -90mV) due to the leaking of Na+ in. 
(K+ is kept out due to decreased permeability)

2) Na+ in will allow for a change membrane potential toward threshold (-40mV)

3) At threshold, Na+ and fast Ca++ channels open generating AP

4) Ca++/Na+ channels close

5) K+ channels open, K+ out, repolarize and overshoot to hyperpolarize membrane

6) K+ channels close, Na+ leaks back in via leak channels to cause Na+ gated channels to open and start the cycle again.

Sequence for conduction system and resulting events:

SA node.........spontaneously depolarizes, determines fastest heart rate ==> sinus rhythm at 75-100 bpm

            then

atria..........contract to empty final contents of blood into ventricles

            then

AV node (inferior to interatrial septum).........delays AP to ventricle due to the delay in the node itself due to decreased number of gap junctions and therefore decreased ion transport and smaller more resistant fibers.
This delay allows the atria to finish their contraction (systole) phase.

            then

AV bundle (Bundle of HIS at the superior interventricular septum)..... will divide into

the right and left Bundle branches.... in intra-ventricular septum

            then

Purkinje fibers... large fibers, velocity of AP --> FAST gap junctions @ intercalated discs
Start from base of septum --> apex --> ventricles  (papillary muscles then ventricular free walls)

Since ventricular muscle spirals, the impulse angles and contraction occurs at the same time due to the sequencing of Purkinje fibers and so an  ejection wave is created.

If conduction too slow, one part may contract before another.

---

Summary of conduction :

*Ion effect......

Ca++          

K+              

 

*Link between atria and ventricles

AV node ==> AV Bundle (AVB)

must be functional to transmit SA node impulses to the ventricles

*Spontaneous depolarization of autorhythmic cells

SA...........70-80 beats per minute (bpm) = sinus rhythm

AV............40-60  approx. 50 bpm = junctional rhythm

AVB............35 bpm

Purkinje........15-40   approx. 30 bpm

---

*Defects/Problems

1. irregular cardiac rhythm.........arrhythmia

2. uncoordinated contraction...atrial or ventricular

3. fibrillation.........irregular, out of phase

4. ectopic focus........abnormal pacemaker

5. premature contractions......PVCs, extra systole

Other control ........

* ANS to modify the activity of the intrinsic system

* Drugs

---

ECG

electrical currents recorded by electrocardiography to produce a tracing --> Electrocardiogram (ECG)

Standard Leads :  Lead I, II, III are called bipolar limb leads that use the right leg as ground and records same event from different perspective

These leads form an equilateral triangle around the heart known as Einthoven's triangle

If the voltage in two leads is known, the other lead can be calculated since :      

voltage of II = I + III, known as Einthoven's Law

If the heart is placed in the center, these voltage lines will allow for vector analysis to determine which direction the heart is depolarizing.

Other leads involve chest leads and augmented unipolar leads.

The current flows from base to apex, from endocardium outward  through the ventricular muscle.

 The ECG tracing will detect the electrical events and depict the event as a deflection wave:

ECG can be divided into Segments and Intervals ::

Segment/Interval                                               Bioelectrical Event

P - Q interval                            conduction from SA node TO ventricular muscle

P - Q segment                          His/Purkinje impulse conduction

QRS interval                             impulse conduction through ventricular myocardium

Q - T interval                            depolarization of ventricular myocardium, repolarization of ventricular myocardium

S - T segment                           depolarized state, no current,  should be at baseline if deviates......myocardial damage/ ischemia

T - P segment               no Bioelectrical activity, variable length : depends on heart rate if fast may not see, since P wave will overlap t wave

---

ECG tracings are calibrated using lined paper

10 vertical lines = 1mV

1" horizontal  = 1 second

---

Arrhythmias :: can be detected on ECG

causes...............

** abnormal sinus rhythm :

** impulse conduction :

vagus nerve excessive stimulation

1) first degree AV block

2) second degree AV block

3) Complete or third degree AV block

other arrhythmias ::

* premature contractions (ectopic beats)

result of ectopic foci that emit abnormal impulses at odd times.

                        Caused by ischemia, calcification, toxins

types.........

* paroxysmal tachycardia

* fibrillation : ventricular and atrial

* cardiac arrest

---

Cardiac Physiology Continued:

CARDIAC CYCLE.....all the events that happen with blood flow through the heart in the period from one heart beat to the next

   > 1 sec.

Cardiac Cycle Events::  

contraction and relaxation change the pressure and blood volume within the heart

            Mechanical phases:

            cycle occurs for all chambers, so that we have

---

Cardiac cycle ----->

1) DIASTOLE (atrial and ventricular)

2) Ventricular SYSTOLE

AV valves closed, increase in ventricular pressure during isovolumetric contraction that finally exceeds arterial side and forces open the semilunar valves and creates the ventricular ejection phase to move blood to aorta or pulmonary trunk

3) Ventricular Diastole (t - wave)

Therefore.........blood flow controlled by pressure changes due to contraction and relaxation phases

   flow from higher pressure to lower heart valves keep blood flow in one direction

AV (tricuspid, mitral)  --> prevent back flow of blood from ventricles to atria during systole

Semilunar (aortic, pulmonary) --> prevent back flow of blood from aorta and pulmonary artery during diastole

---

NOTE:

Valves passively close and open due to pressure gradients created by myocardial contraction

Heart sounds :: associated with closing of the heart valves

Auscultation of individual valve sounds at various intercostal spaces

Murmur.....abnormal heart sound due to the turbulence of blood flow

1) incompetent valve, blood flows backward

2) stenotic valve, restricts blood flow

---

CARDIAC OUTPUT..............measured in ml/min

Defined as: the amount of blood pumped out by each ventricle in one minute

Formula is based on the product of heart rate (HR) and stroke volume (SV)

Heart rate is given in beats per minute

Stroke volume or ejection fraction is the amount of blood pumped by a ventricle with each beat and is calculated by EDV-ESV

If the heart rate is 75 beats per minute and the normal stroke volume is 70 ml per beat, then the cardiac output would be :

CO = 75 bpm X 70 ml/beat = 5250 ml/min  = 5.25 l/min

    (remember that normal blood volume is 5 liters)

---

Factors that affect CO

Cardiac Output can be increased or decreased depending on the demand, and can be affected by volume or rate
The difference between cardiac output at rest and cardiac output at maximum is known as the cardiac reserve.

The amount of volume that the heart can pump is regulated by :

I. Venous return : The primary control for CO

the greater the heart is filled during diastole, the greater the quantity of blood that is pumped into the aorta.

This degree of stretching before cardiac contraction is called the PRELOAD

Increased stretching ==> causes a change in the orientation of actin and myosin, and will increase the # of cross-bridges, therefore increasing the force of contraction.  Preload will also stretch nodes in atria and therefore increase HR

So, the enlargement or the degree of stretch of ventricles is the preload and affects its control over::

 AFTERLOAD : is the load against which the muscle exerts its  contractile force.

for the ventricle --> the pressure in artery against which the ventricle must contract

Increase in resistance will decrease CO and is measured during the diastolic phase and indicated by the diastolic pressure.

---

II. ANS....the medulla contains cardiac centers controlled by the hypothalamus and monitored by baroreceptors for pressure and chemoreceptors for O2 and CO2

Sympathetic : distributed to all parts of the heart

Norepinephrine (beta 1) -->> increases Na+/Ca++ perm.

 Parasympathetic effects via the Vagus Nerve:

ACH from postganglionic parasympathetic neurons will decrease rate of rhythm of SA node due to:

---

HEART RATE factors that affect Cardiac Output

Regulation via:

1) ANS......Symp/Parasymp

      Vagal tone on SA node

2) Pressure -- Baroreceptors to detect Blood pressure

3) Chemical .........

4) Other.......Exercise, Drugs, age, gender, exercise tolerance, temperature

Increased cardiac rate ---> pump more blood will occur up to a certain limit

Excessive rate --> decreased strength due to decreased ventricular filling since diastolic time is reduced

---

HOMEOSTASIS ::

Balance between Venous return and Cardiac Output

Disease............Congestive Heart Failure (CHF)

---

EMBRYOLOGY ::

     the heart      develops from mesoderm in the region of the neck

two tubes fuse into one chamber, fold and change into a 4 chamber structure.

Begins beating by three weeks

Fetal circulation : bypass lungs, due to certain structures

Congenital defects : 

---

AGE changes in the heart.........

Valve :: sclerosis, thickening primarily occurs in the mitral valve since the left ventricle,  has increased stress due to increased pressure and blood flow.

Cardiac muscle :