Test 2 Cardio Flashcards

1
Q

Parietal pericardium

A

Outer later
Surface layer of mesothelium over a thin layer of connective tissue

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2
Q

Visceral pericardium (pericardium)

A

Inner layer
Folds back and is continuous with the parietal pericardium to allow large vessels to enter/exit the heart without breaching the layers

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3
Q

Pericardial cavity

A

Fluid containing space between visceral and parietal pericardium

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4
Q

Pericardial fluid

A

Secreted by cells of the mesothelium to lubricate membranes and minimize friction as the heart beats

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5
Q

Phase 1 - isovolumetrics contraction

A

Ventricular volume is constant
Increase in ventricular pressure closes AV valves

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6
Q

Phase 2 of cardiac cycle

A

Increase in ventricular pressure opens semilunar valves and blood is ejected to the circulation
Intraventricular volume and pressure decrease

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7
Q

Phase 3 - isovolumetric relaxation

A

Decrease in ventricular pressure closes semilunar valves
Ventricle continue to relax

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8
Q

Phase 4

A

Decrease in ventricular pressure opens AV valves
Permits ventricular filling from the atria

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9
Q

1st heart sound

A

AV valves shut at beginning of systole due to increasing pressure in the ventricles
Valves shit > surrounding tissue vibrates & blood flow becomes turbulent -> heart sound

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10
Q

2nd heart sound

A

Semilunar valves shut at end of systole due to falling pressure in the ventricles
“Physiologic split” - aortic valve closure by .02-.04 sec during expiration and to .04-.06 sec during inspiration

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11
Q

Third heart sound

A

May be heard if ventricular wall compliance is decreased and structures in ventricular wall vibrate
Can occur in conditions such as congestive heart failure or valvular regurgitation
May be normal finding in individuals younger than 30 yrs of age

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12
Q

4th heart sound

A

May be heard on atrial systole if resistance to ventricular filling is present
NOT a normal finding
Causes include: cardiac hypertrophy, disease, or injury to ventricular wall

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13
Q

Coronary vessels

A

Blood within the chambers does NOT supply oxygen and nutrients to heart cells
Heart cells are nourished by vessels of the systemic circulation
Branch that supplies heart is called the coronary circulation

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14
Q

Right coronary artery

A

Conus - supplies blood to the upper right ventricle
Right marginal branch - transversely right ventricle to apex
Posterior descending - supplies smarter branches to both ventricles

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15
Q

Left coronary artery

A

Left anterior descending artery (LAD) aka anterior interventricular artery - blood to portions of the left and right ventricles and much if the interventricular septum
Circumflex artery - supplies blood to the left atrium and lateral wall of the left ventricle

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16
Q

Collateral arteries

A

Connections or anastomoses between two branches of the same coronary artery or connections of branches of the right coronary artery with branches of the left
Particularly common within the interventricular and interatrial septa, apex, anterior surface of RV, and around the sinus node
More in epicardium than endocardium
Collateral circ protects heart

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17
Q

Coronary capillaries

A

3300 capillaries per square millimeter
One per muscle cell
Where exchange of O2 and nutrients take place

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18
Q

Coronary veins

A

Most venous drainage occurs through veins in the visceral pericardium
Smaller veins feed into the great cardiac vein > empties into RA through the coronary sinus

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19
Q

Coronary lymphatic vessels

A

With cardiac contraction, lymphatic vessels drain fluid to lymph nodes in the anterior mediastinum that eventually employ into the superior vena cava
Important for protecting myocardium against injury

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20
Q

Conduction system

A

Cardiac cycle depends on transmission of electrical impulses
Muscle fibers uniquely joined so that action potentials pass very quickly from cell to cell
Heart contains own conduction system - no stim from NS
Specialized cells are concentrated in areas called nodes
ANS provides regulation via SNS and PSNS nerve fibers that affect heart rate and diameter of the coronary vessels

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21
Q

Cardiac action potentials

A
  • Electrical impulse > fibers shorten > muscular contraction > systole
  • After action potential > fibers relax > return to resting length > diastole
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22
Q

Cardiac conduction

A

Pacemaker rates
- sinus node about 70-170 bpm
- AV node about 50 bpm
- bundle for His
- bundle branches
- purkinje fibers about 15-30 bpm

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23
Q

Propagation of cardiac action potential

A

Depolarization = activation
- inside of cell becomes less negatively charged
Repolarization = deactivation
Membrane potential = electrical difference across the cell membrane
- r/t changes in permeability of cell membranes
Threshold = point at which the cell membranes selective per ability to Na and K is team disrupted -> depolarization

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24
Q

Hyperpolarization

A

Ex: hypokalmeia (low potassium)
Resting membrane potential becomes more negative

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25
Pacemaker cells (cardiac action potential)
More permeable to Na and start off more + charged -> reach threshold and fire sooner
26
Depolarization (cardiac action potentials)
Voltage-sensitive Na channels open and allow rapid influx of Na then rapidly close K channels close then reopens slowly Voltage-sensitive Ca channels have delayed and slowed opening relative to Na Normal circumstances < max amt of Ca released which permits modulation of contractile strength
27
Repolarization (cardiac action potentials)
Return to resting membrane potential is delayed Makes it impossible to fire a second action potential before the first is complete Prevents summation and tetany
28
Sympathetic stimulation
Releases neurotransmitter norepinephrine -> increased HR, ^ conduction spreed through AV node, ^ atrial and ventricular contractility and peripheral vasoconstriction, stimulation occurs when a decrease in pressure is detected
29
Parasympathetic stimulation
Releases neurotransmitter acetylcholine > decreases HR and lessens atrial and ventricular contractility and conductivity, stimulation occurs when an ^ in pressure is detected
30
Electrocardiogram (ECG) EKG
A common non-invasive diagnostic test that evaluates the heart’s function by recording electrical activity
31
Implementation of ECG/EKG
Determine ability to lie still Advise lie still, breathe normally and refrain from talking during the tests Reassure client that an electrical shock will not occur Document any cardiac medications the client is taking
32
ECG/EKG tracing
P wave: contraction of the atrial muscles - SA node depolarizing QRS complex: contraction of the ventricles - atria repolarizes here but cant see on EKG T wave: electrical changes during relaxation phase of the ventricles - ventricles repolarizing
33
Echocardiogram
Noninvasive procedure that uses sound waves (ultrasound) Evaluates how well the heart is moving, how well the valves are working, the size of the heart and its pumping chambers (ventricles)
34
Implementation of echocardiogram
Determine ability to lie still Advise lying still, breathe normally and refrain from talking Gel applied to the chest and a transducer (wand-like apparatus) moved over the chest area to produce an image of the internal structures of the heart 30-90 minutes
35
Exercise ECG “stress test”
Exercise on a treadmill or bike until ischemic ECG changes, angina or dyspnea occurs Should NOT be performed when significant aortic stenosis, untreated hypertension, CHF, unstable angina Radionuclide studies may be added
36
Persantine
Used in exercise ECG for patients unable to exercise -> produces dilation of coronary arteries
37
Exercise testing (stress)
Noninvasive test that studies the heart during activity and detects and evaluates coronary artery disease Treadmill testing most common May be used in conjunction with myocardial radionuclide testing, at which point the procedure becomes invasive becomes invasive Consent form required
38
Exercise testing pre procedure
Ensure informed consent Ensure the client has adequate rest the night before the procedure Instructions client to eat a light meal 1-2 hours before Avoid smoking, alcohol and caffeine prior to Ask dr about taking meds day of Wear nonconstrictive , comfortable clothing and supportive shoes
39
Holster monitoring
Noninvasive test in which the client wears a holster monitors and an ECG tracing is recorded continuously over a period of 24 hours Identifies dysrhythmias if they occur and evaluates the effectiveness of anti dysrhythmics or pacemaker therapy
40
Implementation of holter monitoring
Instruct client the resume normal daily activities and to maintain a diary documenting activities and any symptoms that may develop
41
Coronary angiography
GOLD STANDARD = patient w/ symptoms suggesting CVD should be evaluated Invasive test that requires iodine contrast dye injected into venous circulation via a large bore IV catheter to coincide with cardiac output, timing appropriately
42
Implementation of coronary angiography
Must lay flat on CT table Assessed for allergies MUST be monitored for post dye injection allergies ‘ HR and BP must be maintained within certain parameters to allow visualization of the coronary arteries when CT contrast dye is injected HR <60 BP<120-110
43
Factors influencing providers decision to perform coronary angiography includes
Finding of history and physical Risk score Calc - variety of cardiovascular risk scoresm not one is optimal Athlete status, public safety concerns, high risk avocation (scuba diving)
44
Coronary Arteriography
GOLD STANDARD = cardiac catheterization Most precise means to document presence of CAD, also gives measures of left ventral function - LV end diastolic pressure - LV end diastolic volume - ejection fraction Indicated in patients w/ severe angina, recurrent chest pain of uncertain etiology, survivors of cardiac arrest
45
Tunica Adventitia
Outermost later of blood vessels Connective tissue
46
Tunica media
Middle layer of blood vessels Composed of vascular smooth muscle Maintains basal tone -Increased tone - vasoconstriction -Decreased tone - vasodilation
47
Tunica intima
Innermost layer of vessels Smooth single layer of cells permits laminar blood flow
48
Resistance vessels
Arteries Arterioles No valves Think muscular walls High capacity to change resistance Ay anytime: 25% of blood volume is in the arterial system
49
Capacitance vessels
Veins Venules Contains valves Elastic and distensible High capacity to “hold” blood At all times 75% of blood volume is in the venous system
50
Pulse pressure
Difference between systolic and diastolic pressures
51
Mean arterial blood pressure (estimate)
Add 1/3 pulse pressure to diastolic pressure Reflects average pressure during contraction and relaxation Good indicator of tissue perfusion in critically ill
52
Cardiac output
Measured in L/min CO = stroke volume x HR
53
Stroke volume
Amount of blood ejected with each ventricular contraction
54
End diastolic volume
Total volume of blood in LV at end of filling just prior to contraction
55
Ejection fraction
Prevent of volume of blood ejected w/ each ventricular contraction 55-75% of total ventricular volume
56
Total peripheral resistance (TPR)
Aka systemic vascular resistance or peripheral vascular resistance Reflects the tone (degree of vasoconstriction) of resistance vessels (arteries and arterioles) as well as viscosity of the blood
57
Aortic impedance
Loss of elasticity of aortic wall ^ w/ aging and functioning of aortic valves Aortic narrowing > L ventricle must generate higher pressure to get blood through Can lead to left sides heart failure and hypertension
58
Starling’s law
Strength of contraction is directly proportional to initial length of cardiac muscle fiber at onset of contraction Degree to which heart muscle is stretched corresponds to EDV Myocardial fiver stretch has an upper optimal limit, when exceeded, contraction strength is decreased (Slinky) if stretch beyond limit cannot return to normal size
59
Preload
Degree of myocardial muscle strength Determined by blood volume ^ preload ^ stretch ^ force of ventricular contraction Related to the degree of compliance of the ventricular wall - ischemic heart muscle > ^ compliance - hypertrophied heart muscle > decreased compliance Heart failure > ^ stretch w/out ^ force of ventricular contraction
60
Afterload
Determined by: Resistance offered by aortic and pulmonic valves (aortic impedance) - aortic stenosis > ^ afterload Condition and tone of aorta and resistance offered by systemic and pulmonary arterioles (TPR) - hypertension > ^ afterload ^ afterload > ^ cardiac workload and ^ O2 consumption
61
When myocardial contractility is increased
More blood is ejected Decrease systolic volume Increase systolic ejection fraction
62
When myocardial contractility is decreased
Less blood ejected Increased end systolic volume Decreased ejection franction
63
Most important factor in ventricular performance
Myocardial contractility
64
Pericardium functions
Prevent displacement of heart during gravitational acceleration/deceleration Physical barrier against infection and inflammation from the lungs and pleural space Contains pain and mechanoreceptors that elicit reflex changes in blood pressure and heart rate
65
Myocardium function
Cardiac muscle Anchored to hearts fibrous skeleton Thickness varies and is r/t amount of resistance needed to overcome to pump (left ventricle is thickest)
66
Myocardium function
Cardiac muscle Anchored to hearts fibrous skeleton Thickness varies and is r/t amount of resistance needed to overcome to pump (left ventricle is thickest)
67
Endocardium
Internal lining composed of connective tissue and squamous cells Continuous with the endothelium the lines arteries, capillaries and veins Creates a continuous closed circuit
68
Atrioventricular valves
Open at the beginning of diastole and allow blood to fill the ventricles Close at the beginning of ventricular contraction to prevent backflow of blood into the atria
69
Semilunar valves
Open at the end of ventricular contraction when the pressure in the ventricles exceed the pressure in the pulmonary artery and aorta Close at the beginning of ventricular relaxation as the pressure in the chambers drops below the pressure in the pulmonary artery and aorta to prevent back flow into ventricles
70
Right coronary arteries
Conus - supplies blood to the upper RV Right marginal branch - traverses right ventricle to apex Posterior descending - supplies small branches to both ventricles
71
Why myocardial contractility is important to ventricular performance
Dependent on concentration of catecholamines in heart muscle Epinephrine and norepinephrine directly stimulate beta adrenergic receptors in myocardium to ^ force of contraction
72
Influences of myocardial contractility
Preload After load SNS stimulation
73
Beta 1 receptors
Sympathetic NS for Affect heart ^ HR + chronotropic ^ force of contraction + inotropic
74
Beta 2 receptors
SNS Lungs Broncodilation
75
Alpha 1 receptor
^ vasoconstriction
76
Adrenergic
Released by SNS ^ BP
77
Cholinergic
Released by PNS Decrease BP Dominant neural control decreased HR - chronotropic Slight decrease in force of contraction - inotropic
78
Carotid sinus
Baroreceptor that monitors BP to brain
79
Aortic arch
Baroreceptor that monitors BP to heart Makes sure heart has adequate blood flow to get blood to brain
80
Baroreceptors
Most important function is to modify BP when there is postural change or valsalva maneuver - decrease BP : decreased stim of vasodepressor (^ PVR) center and cardio inhibitory center (^ HR) > ^ in CO and BP - increase BP : stimulate vasodepressor center (decrease PVR) and cardio inhibitory center (decrease HR) > decrease CO and BP
81
Chemoreceptors
Primary function is regulation of ventilation Stimulated when arterial pressure drops below a critical level Located in carotid bodies
82
Norepinephrine and Epinephrine
Adrenal medulla secretes into the blood Travel to heart Produce + chronotropic (^HR) and + inotropic (^ contractility) responses Similar response produced by stress
83
R-A-A
Juxtaglomerular cells secrete renin Renin changes angiotensinogen to angiotensin 1 Angiotensin 1 is converted to angiotensin II in the lungs by ACE
84
Effects of R-R-A
Angiotensin II is a potent vasoconstrictor ^ BP and ^ aldosterone secretion from adrenals ^ BP and ^ aldosterone secretion for adrenals - ^ Na and H2O retention by kidneys - ^ ECF volume > ^ BP
85
Antidiuretic hormone (ADH)
Aka vasopressin Problem: ^ plasma osmolarity or ^ BP posterior pituitary secretes ADH - potent vasoconstrictor - controls reabsorption of water in collecting ducts of kidneys ^ plasma volume and BP and CO
86
Problems of R-A-A
Decreased Pressure in renal arteries Decreased Na in renal tubules SNS stimulation
87
Atrial stretch receptors
Respond to degree of dissension of L atrial walls during diastole Problem: ^ venous return