1. Function of the heart
Chapter 17

2. Cardiac Cycle Systole- contraction of myocardium
Sequence of events that occurs during one heartbeat
Coordinated contraction and relaxation of the chambers of the heart
Systole- contraction of myocardium
Diastole- relaxation of myocardium

3. Systole & Diastole Systole Diastole
Contraction of heart muscle forces blood out of the chamber
Diastole
Relaxation of heart muscle allows the chamber to fill with blood
Atrial and ventricular activity are closely coordinated: atrial systole = ventricular diastole

4. Three Stages of Cardiac Cycle
Atrial Systole
Atria contract; pump blood into ventricles
AV valves open, ventricles relaxed
Ventricular Systole
Ventricles contract; pushes AV valves closed; pushes semilunar valves open
Blood pumped to pulmonary artery & aorta

5. Three Stages of Cardiac Cycle
Diastole
Brief time when both atria and ventricles are relaxed
Blood flows into atria; some blood flows passively into ventricles
Diastole is a “filling” period
Cycle repeats itself starting with atrial contraction again

7. Position of valves during systole & diastole

8. Which of the following occurs during ventricular diastole?
The ventricles fill with blood.
The atrioventricular valves close.
The ventricles pump blood into the great vessels.
The semilunar valves open.
Answer: a. The ventricles fill with blood.

9. Cardiac Cycle
Cardiac cycle is repeated with every heartbeat; if heart rate is 70 bpm, then cardiac cycle lasts approx. 0.8 sec; diastole lasts approx. 0.4 sec
If heart rate increases, diastole shortens- can impact cardiac function. How?
Decreased filling time reduces the amount of blood that enters the ventricles; and coronary blood flow occurs during diastole

10. Autonomic Control of the Heart
If cardiac cells can initiate cardiac impulses, why are autonomic nerves needed?
Affect the rate at which cardiac impulses are fired
Affects how fast the impulses travel through the heart
Affects how forcefully the heart contracts

11. ANS
The autonomic nervous system allows the heart to respond to increased oxygen demand by increasing the rate and force of cardiac contraction.

12. Autonomic Wiring Sympathetic Parasympathetic
Supply the SA node, AV node and ventricular myocardium
Parasympathetic
Vagus nerve
SA node and AV node (does not innervate the ventricles)

13. Autonomic Firing Sympathetic stimulation
Increases SA node activity ( HR)
Increases speed of impulse (from SA node to His-Purkinje)
Increases strength of contraction

15. Important points to remember
Excessive sympathetic activity leads to “fight or flight” response (panic causes racing and pounding heart)
May be involved in certain illnesses- shock, heart failure (need to treat with drugs that reduce excessive sympathetic firing)

16. Important points to remember
Causes tachydysrhythmias
Nurses often give drugs that mimic or block sympathetic activity
Drugs that mimic sympathetic activity increase HR and force of contraction (epinepherine & dopamine); called sympathomimetic drugs
Drugs that inhibit SNS effects are called sympatholytic drugs (clonidine)

17. Autonomic Firing Paraympathetic stimulation
Decreases SA node activity ( HR)
Decreases the speed of cardiac impulses from SA to AV node
Does not affect strength of myocardial contraction (no innervation of ventricles)

19. Important points to remember
Parasympathetic effects are exerted by the vagus nerve
In the resting heart, the vagus nerves slows the firing of the SA node (SA node wants to fire at 90 bpm, vagus nerve keeps it around 70)
Excessive vagal discharge can be caused by different things, including certain drugs(digoxin) and conditions (MI)

20. Important points to remember
Excessive vagal discharge causes bradycardia (<60 bpm); it also increases the likelyhood of lethal dysrhythmias
Vagal stimulation can also slow conduction through the heart, leading to potentially lethal heart blocks

21. Important points to remember
Drugs that mimic the effects of vagal activity (slow HR or conduction) are called vagomimetic (or, parasympathomimetic) drugs (digoxin)
Drugs that inhibit vagal discharge (like atropine) are called vagolytic (or, parasympatholytic) drugs

22. Cardiac Output
Cardiac output is the amount of blood pumped by each ventricle each minute
Normal cardiac output is 5 liters per minute (an average adults entire blood volume)
Cardiac output is determined by heart rate and stroke volume
CO = HR x SV

23. Heart Rate
The number of times the heart beats in one minute (avg 72 bpm for adult)
Resting HRs differ because of size, age and gender
Larger size- slower HR
Women tend to have faster HR than men
Age- generally, younger hearts beat faster (fetal HR avgerages 140’s)

24. Heart Rate Other factors that affect HR
Exercise- increases HR (response to increased oxygen demand)
Stimulation of ANS (sympathetic stim causes increased HR, parasympathetic (vagus) stim causes decreased HR
Hormone secretion- epi, norepi and thyroid hormones increase HR

25. Heart Rate
Pathology- certain diseases or conditions can affect HR (sick sinus syndrome, MI, fever)
Medications- many drugs can affect the heart rate (digoxin, epi/ norepi, caffeine); important to know effects of drugs and the patients HR before giving them

26. Stroke Volume The amount of blood pumped by the ventricles per beat
Average is ml per beat
Normally, ventricles pump out about 65% of the blood they contain; if force of contraction is increased, more blood will be forced out

27. Changing Stroke Volume
Stroke volume can be changed though Starling’s Law or through an inotropic effect (strength of contraction)

28. Starling’s Law
Depends on the degree of stretch of the myocardial fibers
Greater the stretch, greater the force of contraction
If more blood enters the ventricle, the fibers are stretched more, the ventricle contracts more forcefully (conversely, less blood = less stretch, decreased force of contraction)
So, stroke volume can be increased by increasing venous return to the heart

29. Starling’s Law

30. An increase in end diastolic volume
elicits Starling’s law of the heart.
decreases stroke volume.
decreases cardiac output.
All of the above
Answer: a. elicits Starling’s law of the heart.

31. Inotropic Effect
Increasing the force of myocardial contraction without stretching the myocardial fibers; called (+) inotropic effect
Stimulation of the heart by sympathetic nerves causes +inotropic effect; epi and digoxin are +inotropes
(-)Inotropic effects decrease the force of contraction (excessive depression can lead to heart failure)

32. Cardiac Output
Since cardiac output is determined by heart rate and stroke volume, changing one or both can affect output
Cardiac reserve refers to the capacity to increase cardiac output above normal resting state
Diseased hearts often have little reserve, so the person may become easily tired with minimal exertion

33. Clinical Terminology
Special vocabulary related to the heart

34. End Diastolic Volume
The amount of blood in the ventricle at the end of diastole (resting phase)
Determines the amount of stretch in the muscle fibers; basis for Starling’s Law

35. Preload
Same as EDV; amount of blood in the ventricles after diastole; increased preload stretches the ventricles, causing stronger force of contraction (which increases stroke volume, and therefore cardiac output)
Drugs can affect preload- dilate veins to decrease preload, constrict veins to increase preload

36. Ejection Fraction
Remember ventricles pump about 65-67% of their volume; this is referred to as the ejection fraction
Indicated cardiac health- a healthy heart can increase EF to 90% with exercise; diseased or weakened heart are much lower, may be less than 30%

37. Afterload
Refers to resistance against blood as it is pumped out of the heart
From the LV, blood must push against blood already in the aorta; increased resistance (stenosis, high pressure) causes the heart to work harder
Continued increased resistance (hypertension, especially) can cause LV hypertrophy

38. Afterload
Afterload in the right ventricle is determined by the pulmonary artery; high pressure can be caused by chronic lung diseases (asthma, emphysema)
RV hypertrophy and increased pulmonary artery pressure is referred to as cor pulmonale (often causes RV failure)

39. Afterload
Drugs can alter afterload by relaxing or dilating blood vessels in the periphery; decreases workload of the heart
Drugs that constrict blood vessels will increase afterload and increase the workload of the heart

41. Which of the following is most related to preload?
Blood pH
End-diastolic volume
Cyanosis
Coronary blood flow
Answer: b. End-diastolic volume

42. Inotropic Effect
Refers to change in myocardial contraction not due to stretching of fibers
+ inotrope increases contractile force
- inotrope decreases contractile force
Sympathetic nerve stimulation causes a positive inotropic effect

43. Chronotropic Effect Refers to a change in heart rate
+ chronotropic effect increases HR
- chronotropic effect decreases HR
Sympathetic nerve stimulation causes a + chronotropic effect
Parasympathetic (vagal) stimulation causes a – chronotropic effect

44. Dromotropic Effect
Refers to a change in the speed at which the cardiac impulse travels through the conduction system
+ dromotropic effect increases speed of conduction
- dromotropic effect decreases speed of conduction
Pronounced (-) dromotropic effects may lead to heart block

45. A (+) inotropic effect increases cardiac output because it
decreases afterload.
increases stroke volume.
intensifies vagal discharge.
expands blood volume.
Answer: b. increases stroke volume.

46. Autonomic Receptors

47. Beta1 adrenergic receptors
The adrenergic neurotransmitter is norepinepherine (NE)
The cardiac receptors for NE are beta1-adrenergic receptors
Activation of beta1 receptors cause
+chronotropic effects
+dromotropic effects
+inotropic effects

48. Beta1 adrenergic receptors
Drugs that activate beta1-adrenergic receptors increase HR, stroke volume and overall cardiac output
These drugs are called beta1-adrenergic agonists (or simply “beta agonists”)
Include dopamine and epinephrine
Note: beta1 receptor activation is the same as a sympathomimetic effect

49. Beta1 Receptor Blockade
Blockade of the beta1-adrenergic receptors prevents receptor activation
People taking beta1-adrenergic blockers (or, “beta blockers”) will not increase their heart rate when sympathetic nerves fire (stress or exercise)

50. Beta1 Receptor Blockade
May be administered to tachycardic patients or patients having an MI; reduces HR and force of contraction… reduces workload of heart and therefore oxygen demand of the heart
Beta1-adrenergic blockade is the same as a sympatholytic effect

51. Cholinergic (muscarinic) Receptors
The cholinergic neurotransmitter is acetylcholine (ACh) (vagus nerve)
The cardiac cholinergic receptors are called muscarinic receptors
Activation of muscarinic receptors causes
(-)chronotropic effect
(-) dromotropic effect
No inotropic effect (vagus does not innervate ventricles)
Same as parasympathomimetic effect

52. Cholinergic (muscarinic) Blockade
Muscarinic/ cholinergic blockers act by blocking the effects of ACh at the muscarinic receptors
Therefore, HR and speed of conduction is increased (atropine)
Muscarinic (cholinergic)-receptor blockade is the same as parasympatholytic effect

53. Tricky terminology… Muscarinic agonist = cholinergic agonist
Muscarinic blocker = antimuscarinic agent = cholinergic blocker = anticholinergic agent
Beta1 receptor activation = sympathomimetic effect
Beta1-adrenergic blockade = sympatholytic effect

54. Tricky terminology…
Muscarinic (cholinergic) receptor activation = parasympathomimetic effect
Muscarinic (cholinergic) receptor blockade = parasympatholytic effect

55. Which of the following is least apt to slow heart rate?
Activation of the muscarinic receptors
Firing of the vagus nerve
A sympathomimetic effect
Binding of ACh to its receptor on the SA node
Answer: c. A sympathomimetic effect

56. The Failing Heart
When the heart can’t pump

57. The heart as a double pump…
Remember the heart functions as two pumps
The right side of the heart pumps blood to the lungs for oxygenation
The left side of the heart pumps blood to the aorta and to the systemic circulation

58. Left-Heart Failure Two main components
Blood backs up in the lungs
Insufficient amount of blood is pumped out to the systemic circulation
Can be described in terms of forward failure of backward failure

59. Backward Failure
Blood backs up in structures behind the left ventricle- left atrium, pulmonary veins and pulmonary capillaries
Increased pressure in the pulmonary capillaries forces fluid into the lungs
Called pulmonary edema
Fluid in the lungs impairs the lungs’ ability to oxygenate blood

60. Backward Failure Pulmonary Edema
Signs & symptoms (S&S) include: exertional dyspnea (-pnea means breathing)
Cyanosis
Blood tinged sputum and cough
Orthopnea (pillows?)
Tachycardia and restlessness

61. Backward Failure Most symptoms are respiratory Treatment includes:
+inotropic agent (increase force of myocardial contraction to push excess blood out)
Nitroglycerine (NTG) (decreases preload)
Oxygen (increase oxygenation)
Morphine (decrease workload, anxiety)
Upright position (ease work of breathing)
Diuretic (relieve edema)

63. Left-sided heart failure

64. Forward Failure
The damaged ventricle cannot pump adequate blood to the systemic circulation
S&S include:
kidneys filter less water and reabsorb excess salt and water, increases blood volume and edema
Decreased cardiac output stimulates sympathetic activity- temporarily improves C.O. but eventually the heart wears out

65. Left-Heart Failure
Commonly caused by myocardial infarction and chronic, uncontrolled hypertension (HTN)
In MI, if the damaged tissue is in the left ventricle, the heart may fail as a pump (LAD- the “widow maker”)
In HTN, the LV has to continuously pump against resistance- LV hypertrophies and eventually fails

66. Right-Heart Failure
Blood backs up in the veins that return blood to the heart
Superior vena cava receives blood from the jugular veins; congestion in the jugular veins is known as jugular vein distention (JVD)
Blood also backs up into major viscera, causing enlargement- hepatomegaly and splenomegaly (-megaly means enlargement)

67. Right-Heart Failure
Edema also found in the feet and ankles- pedal edema; pitting edema is severe edema that will indent when pressed
Right-heart failure is usually a result of left heart failure; can also be caused by chronic lung disease (emphysema)

68. From Crowley
Marked pitting edema of leg (arrow) as a result of chronic heart failure.

70. Right-sided heart failure

71. Treatment of Heart Failure
Goals of treatment
Strengthen myocardial contraction
Remove excess edema
Decrease workload of heart
Protect the heart from excess sympathetic activity

72. NCLEX Question
After an anterior wall myocardial infarction (MI), which problem is indicated by auscultation of crackles in the lungs?
left sided heart failure
right sided heart failure
pulmonic valve dysfunction
tricuspid valve malformation

73. Rationale
1. Anterior wall MIs usually cause extensive damage to the left ventricle, resulting in left sided heart failure. The symptoms of left sided failure are predominantly pulmonary in nature- usually resulting in pulmonary edema

74. NCLEX Question
Which drug class protects the ischemic myocardium by decreasing catecholamines and sympathetic nerve stimulation?
opiods
beta-adrenergic blockers
nitrates
calcium channel blockers

75. Rationale
2. Beta-adrenergic blockers work by blocking receptors activated by norepinepherine, thereby decreasing the sympathetic stimulation to the heart

76. NCLEX Question
With which disorder is jugular vein distention (JVD) most prominent?
abdominal aortic aneurysm
anterior wall myocardial infarction
right sided heart failure
pneumothorax

77. Rationale
3. Right sided heart failure results in congestion of the superior vena cava, which drains the jugular veins

78. NCLEX Question
Stool softeners would be given to a client after a myocardial infarction for which reason?
to stimulate the bowel because of loss of nerve innervation
to prevent the Valsalva maneuver, which may lead to bradycardia
to prevent straining, which increases intracranial pressure (ICP)
to prevent constipation when osmotic diuretics are used

79. Rationale
2. Straining to have a bowel movement may stimulate the vagus nerve, resulting in bradycardia. This can be potentially life-threatening in a patient with damage to the myocardium

80. NCLEX Question
A nurse is collecting data from a client with left-sided heart failure. The client states that it is necessary to use three pillows under the head and chest at night to be able to breathe comfortably while sleeping. The nurse documents that the patient is experiencing:
orthopnea
dyspnea on exertion
dyspnea at rest
paroxysmal nocturnal dyspnea

81. Rationale
1. Left sided heart failure results in pulmonary edema. This is exacerbated by lying flat. The patient will find it easier to breath while sitting up, called orthopnea

82. NCLEX Question
A nurse is performing a cardiovascular assessment on a client. Which of the following items should the nurse check to obtain the best information about the client’s left-sided heart function.
status of breath sounds
presence of hepatojugular reflex
presence of peripheral edema
presence of jugular vein distention

83. Rationale
Left sided heart failure will result in pulmonary edema, so a client’s lung sounds need to be assessed frequently

84. THE END