1. Circulatory system
Pressure gradients move blood through the heart and vessels. Pulmonary circulation vs. systemic circulation

2. Higher resistance through the systemic circuit
head
and arms
aorta
(to pulmonary
circuit)
(from
pulmonary
circuit)
“Double pump” both ventricles pump an equal volume of blood into systemic and pulmonary circuits
Higher resistance through the systemic circuit
heart
other organs
diaphragm
liver
intestines
legs

3. Pressure - force exerted by pumped blood on a vessel wall Resistance - opposition to blood flow from friction

4. vena
cava
Right atrium
Tricuspid
valve
Right ventricle
vena cava

5. Right ventricle Pulmonary semilunar valve Right atrium Tricuspid valve
Right pulmonary
artery
Left pulmonary
artery
Pulmonary
semilunar
valve
Right atrium
Tricuspid
valve
Right ventricle

6. Bicuspid valve Left atrium Left ventricle Aorta Left pulmonary vein
Right
pulmonary
vein
Left atrium
Bicuspid
valve
Left ventricle

7. Aortic semilunar valve Left atrium Left ventricle Aorta Bicuspid valve
Left pulmonary
vein
Aortic
semilunar
valve
Right
pulmonary
vein
Left atrium
Bicuspid
valve
Left ventricle

8. Valves ensure one-way flow
When pressure is
greater behind the
valve, it opens.
When pressure is greater in front of the valve, it closes
Leakproof
“seams”
semilunar valve

9. Shape of the AV valves is maintained by chordae tendineae
Right atrium
Tricuspid valve
Chordae tendineae
Septum
Papillary muscle
contracts with ventricle
Right ventricle

10. Ventricular Ventricular
Systole Diastole

11. Blood pressure variation

12. Heart myocardium Cardiac muscle fibers
are interconnected by intercalated discs.

13. Junctions between cardiac muscle cells
Desmosome
Gap junction
Action
potential
Intercalated disc

14. These cells do not contract
Pacemaker activity
Slow depolarizations set off action potentials in a cycle
Pacemaker cells only!
These cells do not contract
Summarize – the action pots don’t utilize fast opening sodium gates. black line due to sodium channels opening and slow amounts of na go in…then rest of black line is really calium gates opening..more depolarization..reaches threshold and then different fast acting calcium gates open…then potassium gates allow it to enter..these gates take a while to close allowing for hyperpolarzization..they continue to stop closing in black line phase.
Cells within the sinoatrial (SA) node are the primary pacemaker site within the heart. These cells are characterized as having no true resting potential, but instead generate regular, spontaneous action potentials. Unlike non-pacemaker action potentials in the heart, and most other cells that elicit action potentials (e.g., nerve cells, muscle cells), the depolarizing current is carried into the cell primarily by relatively slow Ca++ currents instead of by fast Na+ currents. There are, in fact, no fast Na+ channels and currents operating in SA nodal cells. This results in slower action potentials in terms of how rapidly they depolarize. Therefore, these pacemaker action potentials are sometimes referred to as "slow response" action potentials.
Phase 4 (black part on graph above) is the spontaneous depolarization (pacemaker potential) that triggers the action potential once the membrane potential reaches threshold between -40 and -30 mV). Phase 0 is the depolarization phase of the action potential. This is followed by phase 3 repolarization. Once the cell is completely repolarized at about -60 mV, the cycle is spontaneously repeated.
More about phase 4 At the end of repolarization, when the membrane potential is very negative (about -60 mV), ion channels open that conduct slow, inward (depolarizing) Na+ currents. These currents are called "funny" currents and abbreviated as "If". These depolarizing currents cause the membrane potential to begin to spontaneously depolarize, thereby initiating Phase 4. As the membrane potential reaches about -50 mV, another type of channel opens. This channel is called transient or T-type Ca++ channel. As Ca++ enters the cell through these channels down its electrochemical gradient, the inward directed Ca++ currents further depolarize the cell. When the membrane depolarizes to about -40 mV, a second type of Ca++ channel opens. These are the so-called long-lasting, or L-type Ca++ channels. Opening of these channels causes more Ca++ to enter the cell and to further depolarize the cell until an action potential threshold is reached (usually between -40 and -30 mV).

15. Cardiac muscle Self-excitable muscles - action potential gradually
depolarizes, then repolarizes
Spontaneous action potential
Action potential spread
to other cells
Pacemaker cell
Gap junctions
Gap junctions

16. No gap junctions between atria and ventricles Fibrous insulating tissue prevents AP from directly spreading from atria to ventricles

17. Conduction of contraction
Pacemaker locations:
SA node
AV node
Bundle of His
Purkinje fibers
Sinoatrial
(SA) node
Atrioventricular
(AV) node
Bundle of His
Purkinje
fibers

18. Problems with heart rhythm
AV node rhythm is slower - bradycardia

19. Problems with heart rhythm
Heart block – a type of bradycardia. Ventricles pump slowly and out of rhythm of atria

20. Ventricular fibrillation
quivering of ventricles..like having a soaked sponge you try to wring out but you just quiver your hand rapidly to squeeze it
Ventricular fibrillation

21. Problems with heart rhythm
Ventricular fibrillation
Atrial fibrillation

22. Action potential in cardiac muscle
These are contractile cells
not pacemaker cells
Plateau
phase
Threshold
potential

23. Long refractory
period ensures no
summation of twitches
Relaxation of cardiac muscles is essential

24. Electrocardiogram
Currents from heart spread to body tissues and fluid Sum of all electrical activity spread to electrodes and recorded R T P P Q S PR ST
TP interval

27. Cardiac cycle
Ventricular and atrial diastole

28. Cardiac cycle
Atrial contraction

29. Cardiac cycle Isovolumetric ventricular contraction “Lub”
End diastolic volume
is in the ventricles

30. Cardiac cycle
Ventricular ejection

31. Cardiac cycle Isovolumetric ventricular relaxation “Dub”
End systolic volume
is in ventricles

33. Diastolic patent ductus arteriosus
Heart murmurs
Systolic or diastolic murmurs Often due to stenosis or regurgitation at a valve (“whistle” vs. “swish”)
Normal heart
“lub-dup”
Systolic aortic stenosis
“lub-whistle-dup”
Mention that stiff valve causes congestion, high pressure behind it.
Innocent heart murmurs aren't caused by heart problems. These murmurs are common in healthy children. Many children will have heart murmurs heard by their doctors at some point in their lives.
People who have abnormal heart murmurs may have signs or symptoms of heart problems. Most abnormal murmurs in children are caused by congenital (kon-JEN-ih-tal) heart defects. These defects are problems with the heart's structure that are present at birth.
In adults, abnormal heart murmurs most often are caused by acquired heart valve disease. This is heart valve disease that develops as the result of another condition. Infections, diseases, and aging can cause heart valve disease.
Mitral valve prolapse: Normally, your mitral valve closes completely when your left ventricle contracts, preventing blood from flowing back into your left atrium. If part of the valve balloons out so that the valve does not close properly, you have mitral valve prolapse. This causes a clicking sound as your heart beats. Often, this common condition is not serious. However, it can lead to regurgitation (backward blood flow through the valve).
Mitral valve or aortic stenosis: Your mitral or aortic valves, both on the left side of your heart, can become narrowed by scarring from infections, such as rheumatic fever, or may be narrow at birth. Such narrowing or constriction is called stenosis. In mitral valve or aortic stenosis, the heart has to work harder to pump enough blood to satisfy your body's oxygen needs. If untreated, stenosis can wear out your heart and can lead to heart failure. Mitral and aortic stenosis can both occur as calcium is deposited on the valves as people age.
Aortic sclerosis: One in three elderly people have a heart murmur due to the scarring, thickening, or stiffening (sclerosis) of the aortic valve, without evidence of narrowing, or stenosis. This condition is generally not dangerous; typically, the valve can function for years after the murmur is detected. Aortic sclerosis is usually seen in people with atherosclerosis, or hardening of the arteries.
Mitral or aortic regurgitation: Regurgitation (backward flow) of blood can occur with mitral valve prolapse or mitral valve or aortic stenosis. To counteract this back flow, the heart must work harder to force blood through the damaged valve. Over time, this can weaken and/or enlarge the heart and can lead to heart failure.
Diastolic mitral stenosis
“lub-dup-whistle”
Systolic tricuspid regurgitation
“lub-swish-dup”
Diastolic aortic regurgitation
“lub-dup-swish”
Diastolic patent ductus arteriosus

35. Sympathetic signals increase stroke volume
Extrinsically:
conduction speed
contraction strength

36. Recall: muscle length and force

37. Frank Starling law (intrinsic increase in stroke volume)
Optimal length
Stroke volume (SV) (ml)
(Cardiac muscle does
not normally operate
within the descending
limb of the length–
tension curve.)
Increase
in SV B1 A1
Normal resting length
Increase
in EDV
End-diastolic volume (EDV) (ml)