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Cardiology > Cardio Physiology > Flashcards

Cardio Physiology Flashcards

1
Q

How are cardiac muscle cells connected in order to allow AP to travel freely btwn cells?

A

Intercalated discs

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2
Q

What is the term that describes individual cells connected in series or parallel and how many are there in the heart?

A

Syncytium (2 = Atrial and ventricular)

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3
Q

Why is cardiac AP duration longer than skeletal muscle, and why does plateau exist?

A

• (1) AP of skeletal muscle is fast Na+ channels only; in cardiac muscle, it is fast Na+ channels AND slow Ca channels (that allow both Ca and Na to enter cell)
o Compared to fast Na+ channels, the slow Ca channels are slower to open and remain open for longer (0.2-0.3 sec)
• (2) After onset of cardiac AP, membrane becomes LESS permeable to K+ = major K+ efflux (repolarization) does not occur until after slow Ca channels close

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4
Q

What is unique regarding Ca2+ in cardiac cells?

A

• (2) Unique to cardiac muscle: AP opens voltage-gated Ca channels on T tubule membrane  Ca enters cell → activates ryanodine receptor channels (Ca-release channels) in SR membrane → additional release of Ca into sarcoplasm
o The major source of calcium for contraction comes from the T tubules

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5
Q

What happens to Ca2+ in cardiac muscle after plateau?

A

Relaxation = Ca pumped out of sarcoplasm into SR (Ca-ATPase) or out of cell (Na/Ca exchanger; Na then pumped out via Na-K ATPase)

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6
Q

What is the role of papillary muscles on AV valves?

A

Prevent too much backward movement of valves into atria during systole

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7
Q

What are the semilunar valves?

A

Prevent backflow from aorta or pulmonary artery in diastole (shut due to pressure changes)

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8
Q

Name 4 heart sounds that you may hear.

A

1st: Closure of AV values
2nd: Closure of semilunar valves
3rd: Rapid ventricular filling (during first 1/3 of diastole)
4th: Atrial contraction (prior to systole as atria pump blood into noncompliant ventricle)

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9
Q

What is the dicrotic notch?

A

Defect in the aortic pressure wave that is caused by closure of aortic valve

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10
Q

When does the mitral valve open?

A

When that atrial pressure> ventricular pressure

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11
Q

What is preload?

A

Degress of tension/stretch on cardiac muscle when contraction begins = LVEDP

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12
Q

What is afterload?

A

Load against which cardiac muscle exerts contractile force = systolic Ao pressure (systolic PA pressure for RV)
Determines amount of work needed to eject blood

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13
Q

What determines cardiac output?

A

CO = HR x SV

SV depends on PRELOAD> afterload, contractility

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14
Q

Where do the vagal fibers (parasympathetic) get distributed?

A

R vagus = SA node

L vagus = AV node

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15
Q

How can hyperkalemia affect the heart function?

A

Makes RMP less negative by partially depolarizing cell membrane - decreased intensity of AP = decreased contractility
Can lead to dilated flaccid heart, slow HR, AV block

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16
Q

How can hypercalcemia affect the heart function?

A

Initiates depolarization = Spastic contraction

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17
Q

Does increased systolic BP affect CO?

A

Co determined by venous return NOT arterial resistance (CO not affected until pathologic level = 160 mmHg)

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18
Q

What is the resting membrane potential of the sinus node and why is it different from the ventricles?

A

RMP: -60mV vs ventricular myocytes -90mV
Lower RMP b/c cell membranes leaky to Na+ and Ca2+ (means that fast Na+ channels always inactivated (gate closed) = Major determinant of AP is the slow Ca channels

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19
Q

What causes the self excitation of the sinus node?

A

The inherent leakiness of sinus nodal fibers to Na+ and Ca2+

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20
Q

What is the basic cycle in the sinus node?

A

When RMP reaches threshold voltage ~ -40 mV, slow calcium channels (ICa) open, causing depolarization
• Slow Ca channels then inactivate and K+ channels open = inward Na/Ca current stops, outward K+ current starts
 Repolarization: K+ outflow brings the resting potential back to –55 mV
→ After RMP restored, Na channels begin to leak again → AP generated when threshold reached

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21
Q

What causes the delay in transmission of the impulse through the AV node?

A

Fewer gap junctions = Increased resistance btwn muscle cells, high RMP - Slow conduction through AV node to slow the atria to empty and ventricles to fill

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22
Q

What is the Purkinje system?

A

Purkinje fibers conduct from AV node to AV bundle, bundle branches, to ventricles
VERY Rapid conduction = Ventricles contract at SAME time

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23
Q

Why is the SA node the heart’s pacemarker?

A

The SA node has the highest rate of spontaneous discharge and thus it is the pacemarker

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24
Q

How does parasympathetic stimulation affect the heart?

A

Ach→ increases permeability of the SA and AV fibers to K+ → hyperpolarization (RMP -65 to -75mV)
Decreases SA rate and AV conduction; can cause complete sinus arrest or AV block
(SA node, AV node, some atria, little ventricles)

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25
Q

How does sympathetic stimulation affect the heart?

A

NE → B1 receptors → increases permeability of membranes to Na+ and Ca++
Increases SA rate and AV conduction (more positive RMP and faster drift upwards)
Increases conduction velocity and excitability in all areas (easier for AP to excite surrounding areas)
Increases force of contraction (more Ca++ influx)
(All parts of the heart)

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26
Q

What are the depolarization waves on ECG?

A

P and QRS

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27
Q

What are the repolarization waves on ECG?

A

T and atrial T wave buried in QRS

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28
Q

What is one of the earliest signs of digitalis toxicity?

A

Inversion of T wave

Digitalis causes prolongation of depolarization in ventricular muscle

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29
Q

What is the mean electrical axis?

A

Predominant direction of vectors of ventricles during depolarization

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30
Q

What is first degree AV block?

A

Prolonged PR interval

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31
Q

What is second degree AV block?

A

Occasional dropped beats

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32
Q

What are the 1 types of second degree AV block?

A

Mobitz Type I: Prolonged PR before dropped beat

Mobitz Type II: Random dropped beats (BAD, can progress to 3rd degree)

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33
Q

What is third degree AV block?

A

P waves are disassociated from QRS complexes

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34
Q

What is unique about the cardiac AP?

A

Its plateau (phase 2) = Inward Ca2+ current from ECF to ICF = Known as trigger Ca

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35
Q

What is another word for contractility?

A

Inotropism - Intrinsic ability of myocardial cells to develop force

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36
Q

What does contractility correlate directly with?

A

Intracellular Ca2+ (which depends on amount of Ca2+ in sarcoplasmic reticulum)

37
Q

What will result in greater contractility?

A

Larger Ca2+ current (or trigger Ca2+ from AP) and larger intraceullar stores of Ca2+

38
Q

What is stroke volume?

A

Volume of blood ejected by ventricles on each beat

39
Q

What is ejection fraction?

A

Fraction of end-diastolic volume ejected in each stroke volume = Measure of ventricular efficiency

40
Q

What is cardiac output?

A

Total volume ejected by ventricle per unit time

41
Q

What is the Frank Starling relationship?

A

Volume of blood ejected by ventricle depends on volume present in ventricule at end of diastole

42
Q

What is the width of the ventricular pressure-volume loop?

A

The stroke volume

43
Q

What happens to stroke volume when you increase preload?

A

Increasing preload = Increased venous return = increased end-diastolic volume
= = Increased SV

44
Q

What happens to stroke volume when you increase afterload?

A

Increased afterload = Increased aortic pressure
Need greater pressure during isovolumetric contraction
== Decreased SV, end-systolic volume increased

45
Q

What happens to stroke volume when you increase contractiliy?

A

Increased SV, end systolic volume decreases

46
Q

Name the 7 phases of the cardiac cycle.

A
  1. Atrial Sysole = Atrial contraction (p wave)
  2. Isovolumetric Ventricular Contraction = Mitral Valve closes, ventricules contract (QRS)
  3. Rapid Ventricular Ejection = Aortic Valves open, ejection
  4. Reduced Ventricular Ejection = Slower rate of ejection (T wave)
  5. Isovolumetric Ventricular Relaxation = Aortic values close, ventricular relaxation
  6. Rapid Ventricular FIlling = Mitral valve opens, filling of ventricules
  7. Reduced Ventricular Filling or Diastasis = Ventricules relaxed (longest phase)
47
Q

What is autoregulation?

A

Tissues adjust vascular resistance to maintain normal blood flow during changes in arterial BP

48
Q

What is vascular compliance?

A

Extra amount of blood that can be stores in vascular bed with a given rise in pressure

49
Q

What is pulse pressure?

A

Difference btwn systolic and diastolic pressure

Impacted by: Increased stroke volume and decreased compliance = Increased pulse pressure

50
Q

What is the mean arterial pressure?

A

Average arterial pressure over period of time, NOT average, but rather 60% diastole (heart spends more time in diastole) and 40% systolic

51
Q

What is the central venous pressure?

A

Also know as RA pressure, close to 0mmHg (can be negative if hypovolemia)

52
Q

What serves as blood reservoir for circulatory system?

A

Venous system (liver sinues, large abdominal veins, venous plexus under skin, spleen)

53
Q

What is the capillary wall made up of?

A

Single layer of endothelial cells surrounded by basement membrane

54
Q

What is the caveolae in capillaries?

A

Invaginations on luminal surface of endothelial cells (formed by cholesterol and sphinolipids) - Role in Endocytosis
Also called plasmalemmal

55
Q

What is considered the pore of endothelial cells?

A

Intercellular clefs

56
Q

What are the Starling’s forces?

A

Determine the net filtration rate in capillaries

  1. Capillary pressure
  2. Interstitial fluid pressure (negative from lymphatics)
  3. Plasma colloid osmotic pressure (COP about 28 mmHg - Donnan Effect)
  4. Interstitial Fluid colloid osmotic pressure
57
Q

What is the Donnan Effect?

A

Retention of cations (esp Na+) by negatively charged proteins in capillaries (albumin, globulins, fibrinogen) that results in a pull in of water
Affects plasma colloid osmotic pressure within capillaries (Starlings forces)

58
Q

How does lymph flow?

A

From interstital fluid = 10% net filitered fluid that is not resorbed at venous end of capillaries
Allows for high MW proteins to return to circulation
Proteins leak from the capillary into the interstitium → interstitial osmotic pressure rises →draws fluid out of capillaries → interstitial hydrostatic pressure rises → opening of the lymphatic channels and removal of the proteins and accumulated fluid (steady state)

59
Q

What does NO cause in capillaries?

A

Vasodilation

O2 + L-Arginine (endothelial nitric oxide synthease) = NO that results in increased CGMP = Relaxation/vasodilation

60
Q

What is the MOA of sildenafil?

A

Inhibits cGM specific PDE-5 = Increased cGMP that results in vasodilation in lungs

61
Q

What does endothelin cause in capillaries?

A

Vasoconstriction (can be potent) - released from damaged endothelial cells

62
Q

Name 3 hormal regulators of vasoconstriction.

A

Norepinephrine and epinephrine
Angiotensin II
Vasopressin (ADH)

63
Q

Name 2 hormal regulators of vasodilation.

A

Bradykinin (from alpha 2 macroglobulin that is cleaved by protease (kallikrein)
Histamine

64
Q

What does the SNS do in muscles for blood flow?

A

Results in vasoldilation (vasovagal syncope)

65
Q

How can the SNS increase arterial pressure?

A
  1. Constriction of arterioles = Increased SVR
  2. Constriction f large capacitance veins = Increased preload and CO
  3. Increased HR and contractility
66
Q

What is the Bainbridge reflex?

A

Increased atrial stretch caused increased HR and increased contractility

67
Q

What is the Cushing response?

A

Increased ICP = Increased systemic blood pressure in order to maintain cerebral blood flow - thus leads to reflex bradycardia

68
Q

What is pressure diuresis and pressure natriuresis?

A

As BP increased, kidney excreted more water and more sodium

69
Q

How does increased fluid volume lead to increased in arterial blood pressure?

A

Increased EC fluid volume → increased blood volume → increased venous return → increased cardiac output → increased ABP

70
Q

In what cell is renin stored in the kidney?

A

Juxtaglomerular cells (prorenin)

71
Q

When is renin released from the kidney?

A

When there is decreased BP (sensed by change in stretch on juxtaglomerular cells) or decreased Na+ (sensces by macula densa)

72
Q

What does renin do?

A

When released due to decreased BP or decreased Na+ results in conversion of angiotensinogen (liver) to angiotensin I

73
Q

What does angiotensin I do?

A

Once angiotensin I is in lungs it is converted to angiotensin II by ACE

74
Q

What are the 3 major roles of angiotensin II?

A
  1. Vasconstriction (a>v) = Increased PVR, increased BP, increased venous return
  2. Resorption of Na+ and water from kidneys (constricts efferent arteriole - more resorption, directly stimulates resoprtion of water/Na+ in tubular cells, adrenals to secrete aldosterone (increased Na+ resoprtion)
  3. Release of ADH = Water absoprtion in collecting ducts in kidneys
    All will increased blood pressure!!
75
Q

Name 3 mechanisms that occur within sec-mins to control arterial pressure.

A
  1. Baroreceptor reflex
  2. Chemoreceptor reflex
  3. Central ischemic response
76
Q

Name 3 mechanisms that occur within mins to hours to control arterial pressure.

A
  1. RAAS
  2. Stress-relaxation of vasculature
  3. Capillary fluid shifts
77
Q

Name main mechanism that occurs over hours to days to control arterial pressure.

A
  1. Renal Blood Volume Pressure Controls (diuresis and natriuresis)
  2. Interaction with RAAS, aldosterone, SNS
78
Q

What is the Frank-Starling Law for CO?

A

→Increased venous return → increases stretch of the heart chambers →increases the force of contraction → increases CO

79
Q

When resting the muscle mainly uses this for energy?

A

Fatty acids (about 70%)

80
Q

What is the main mechanism for changing blood flow in cardiovascular system?

A

Changing resistance of blood vessels (esp in arterioles)

81
Q

What is compliance in blood vessels?

A

High compliance of vessels = more volume it can hold at a given pressure

82
Q

What are latent pacemarkers?

A

AV node, bundle of His, Purkinje fibers

Have capcity for spontaneous Phase 4 depolarization

83
Q

How is the SA node action potential different than classic AP in heart?

A
  1. Automaticity - Determined by inward Na+ by funny channels = that are turned on by repolarization from previous AP
  2. Unstable resting membrane potential
  3. No plateau
84
Q

What is different about the pward stroke of the AP in the SA node?

A

Inward Ca2+ from T -type channels (instead of rapid Na+ entry into cell)

85
Q

What is overdrive suppression?

A

When the SA node drives the HR (based on rate of Phase 4 of AP) and this suppresses latent pacemarkers

86
Q

Where are the baroreceptors located?

A

Carotid sinus and aortic arch

87
Q

What are baroreceptors sensitive to?

A

Stretch (mechanoreceptors)

88
Q

What two nerves are important for sensory input for the baroreceptor reflex?

A

Glossopharyngeal nerve (CN IX) and Vagal nerve (CN X)

Cardiology (3 decks)

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