Physio Memory: Cardiovascular

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11.

Atrial Fibrillation

2.

Cardiac action potential of a ventricular myocyte

Well tolerated and common in the elderly. Complications: bloodpools in parts of atriaforms clots. Normal but irregular QRS complexes; no P waves but the baseline may show irregular fibrillation waves. AF may be paroxymal, persistent or permanent. May be asymptomatic or may cause palpitations, breathlessness and fatigue. Digitalis is used for A-Fib, increases contractility.
106. 108.

Phase 4: REsting- stable pot at -85mV Phase 0: Rapid depolarization- inward Na current ina Phase 1: Initial Rapid Repolarization- Na inactivation and outward K current ito Phase 2: Plateau Phase- Inward flow of Ca- ica Phase 3: Rapid repolarization- Outward K current ik through the delayed rectifier channels Phase 4: Resting phase- Voltage gated Na channels and Ca channels are closed- ib and iK1 are counterbalanced by the Na/K pump. NO HYPERPOLARIZATION!!!

Decompensated shock

Body's response to hemorrhage (flow chart)

31.

10.

Bundle Branch Block

55.

Definition of stroke work and kinetic work

Stroke work is the work done to eject a volume of blood into the aorta against a resistance Kinetic work is the work done to accelerate blood to its velocity of ejection through the aorta and pulmonary valves.

A block in both bundles will cause 3rd degree block, but an interruption of the right or left bundle of his will delay conduction to the appropriate ventricle. Ventricular depolarization is then asynchronous and the QRS complex is prolonged. Left bundle branch block generally a serious condition often underlying significant heart disease.

Describe metabolic and reactive hyperemia

77.

Draw a cardiac performance curve

78.

Draw a vascular function curve. What alters VR curve?

69.

Draw the baroreceptor reflex when there is a fall in BP

MSFP = pressure at +7 = pressure that would be measured throughout the CVS if the heart stopped beating. There would be no pressure gradient to drive the blood around the circulation. Blood volume, venomotor tone and arteriolar resistance (TPR) affect VR. Increased BV and venomotor tone increase VR. Increased TPR DECREASES VR because the blood is 'held' in the arterial side.
13.

26.

Draw the cardiac myocyte action potential and the SA node action potential Draw the effect of changing blood volume on the Guyton Cross Plot

see special sheets

82.

Draw a wigger diagram of the ventricular phase.

79.

Draw the effect of different blood volumes/venoconstriction/venodilation on the vascular function curve.

Venoconstriction = increased blood volume Venodilation = decreased blood volume

80. 3.

Draw the absolute and relative refractory periods of a cardiac action potential Draw the baroreceptor reflex (intervention)

Draw the effects of changing TPR on the vascular fxn curve

67.

83.

Draw the effects of increased and decreased TPR on the Guyton Cross Plot

4.

Draw the relationship between muscle action potential and muscle twitch in skeletal vs. cardiac m.

81.

Draw the effects of increasing or decreasing contractility on the guyton cross plot.

71.

Draw the renin angiotensin system in terms of organs

72.

Draw the reninangiotensin system in terms of a flow chart

57.

Draw the epinephrine MOA as far as nerve endings, NT, receptors, etc.

58.

Draw the time vs. blood flow/blood pressure graphs of coronary circulation

32.

Draw the pressure volume loop and indicate diastole, systole, EDV, ESV, Isovolumetric contraction/relaxation and where the valves open and close

63.

Effect of exercise on skeletal muscle blood flow

75.

Factors that affect CVP

1. Blood volume (increased, causes increased CVP) 2. Venomotor tone (Venoconstriction increases CVP) 3. Arteriolar tone (arteriolar vasoconstriction decreases venus return, whereas vasodilation increases venous return. Increased TPR > decreased VR and vice versa. ***Arteriolar tone is the major determinant of TPR!!!

59.

Effects of exercise on coronary blood flow

6.

First degree heart block

Slowed conduction through the AV node. PR interval prolonged. Not life threatening.
50.

Explain metabolic control of blood flow- metabolic hyperemia and reactive hyperemia

30.

How do hyper and hypokalemia look on an ECG?

27.

How do parasympathetics affect the heart?

52.

Explain MOA of Nitroglycerin

34.

Explain the effect of changes in contractility on force-velocity relationship. In which does Vmax stay the same? Explain the effects of hyperkalemia and hypokalemia on the heart.

Decreases heart rate, causes bradycardia. ACh causes a slower rate of rise for the pacemaker potential = decreased heart rate. Slower depolarization. Opening of the K channels is fast which explains why the vagus quickly slows down the heart. Ex include: Slowing of heart during expiration (sinus arrhythmia) low heart rate of a trained athlete slowing of heart during a dive (dive reflex) transient arrest of the heart at the onset of fainting (vasovagal attack)

29.

28.

How do sympathetics affect the heart?

15.

How does decreased arterial compliance affect pulse pressure? How does the cerebral ischemic response work?

Increases pulse pressure

70.

1. increases HR (+chronotropic effect) -increases rate of pacemaker depolarization- threshold is reached sooner - increased conduction through av node -reduced duration of atrial and ventricular myocyte action potentials 2. Increases force of contraction (+inotropic effect)
68.

51.

How is Nitric Oxide made?

How do the cardiovascular centers in the CNS work?

41.

Synthesized in endothelial cells L-Arginine > NO (by iNOS) Stimulates guanylyl cyclase > increases cGMP > vasodilation Continually modulates basal vascular tone Responsible for -flow-induced vasodilation of exercise -vasodilation of erection -vasodilation of inflammation Increased stroke volume increases pulse pressure Decreased arterial compliance increases pulse pressure (as in aging)

40.

How does a graph of the Aorta differ from the Vena Cava in terms of compliance?

How is Pulse pressure related to: Stroke Volume Arterial Stiffness Hypovolemic shock- effects

113.

56.

Compliance = Volume/Pressure
14.

How does an increase of stroke volume affect pulse pressure?

Pulse pressure increases

In general what are the consequences of vasoconstriction in response to sympathetic stimulation Management of shock Ensure adequate lung ventilation and provide extra oxygen Restore blood volume by infusion of blood or other fluids Use interventions that improve cardiac performance

114.

33.

Mechanism by which NE and E increase the force of contraction

45.

Pathways of Right ventricular failure and Left Ventricular failure?

1.

Pumps and Exchangers

In general, factors or drugs which increase contractility do so by increasing [Ca]i. Increased iCa increased rate of uptake of Ca into the SR > increased stored Ca in SR Inhibiting the Na-Ca exchanger
103.

Na/K-atpase. Na out, K in Na-H exchanger- Na in, H out Na/Ca exchanger- 3Na in, 1 Ca out Ca ATPase: pumps Ca back into the sarcoplasmic reticulum.

107.

Renin Angiotensin System in hemorrhage

Neurogenic or stress hypothesis for essential hypertension

104.

Salt Imbalance/Renal hypothesis of essential hypertension

61.

Pathway of angina

7.

Second Degree Heart BlockMobitz Type I

60.

The pathway of atheromatous plaque to cardiac problems

PR interval gets progressively longer until you miss an R. Conduction block is seen in kids and athletes with increased vagal tone. Benign, due to conduction block in AV node.

8.

Second Degree Heart Block- Mobitz Type II

105.

Vascular hypertrophy

Every nth QRS is missing. PR is constant. 2:1 heart block (every 2nd R is missing) Dangerous and needs a pacemaker. Loss of conduction is BEYOND AV node
5.

12.

Ventricular Fibrillation

Sinoatrial Node action potential

Phase 4. Pacemaker potential- slow diastolic potential due to Inward Na current if, then Inward Ca current ICa Phase 0. Rapid depolarization- L-type Ca channels open. if are closing. Phase 3. Repolariation- due to closing of Ca channels and opening of K channels- ik Phase 4. Pacemaker potential, Na if channels open and membrane starts to spontaneously depolarize again.

Medical emergency- life-threatening. Electrical chaos. No coordinated ventricular contraction and cardiac output and blood pressure falls with lethal consequences. Treatment is DC cardioversion. Not useful force
111.

9.

Third Degree Heart Block

What are characteristics of shock

Fairly constant P-P intervals and relatively constant R-R intervals but there is no relationship between the P waves and QRS complexes.
94. 62.

Treatment of Angina

What are differences between static and dynamic exercise?

110.

Treatment strategies for hypertension

17.

What are factors that decrease venous return? What are factors that increase CVP?

Hemorrhage Venodilation

16.

1. Increased blood volume 2. Venomotor tone

42.

What are some factors that increase CVP and what are some factors that decrease CVP? Increase VR: Increased blood volume Increased venomotor tone.

98.

What are the effects of age on blood pressure in terms of a graph?

97.

Decrease VR: Hemorrhage Venodilation

112.

What are the effects of age on the CVS?

What are the categories of shock? What are the effects of dynamic exercise on BP? Flow chart

93.

109.

What are the consequences of Hypertension?

39.

64.

What are the different types of exercise, and which hyperemia is dominant? What are the different ways Angiotensin II effects the circulating volume?

Phasic, Dynamic exercise: eg running -Active hyperemia is predominant Isometric exercise: eg weight lifting -blood flow to exercising muscle impaired -on termination of exercise > Reactive hyperemia.

What are the effects of exercise on the pressure-volume loop?

20.

73.

What are the heart sounds made by? Splitting of which is pathological vs. physiological?

Splitting of 1 is pathological- occurs in conduction defects on 1 side of the heart Splitting of 2 is physiological and is enhanced in inspiration

19.

What are the mean pressures during the cardiac cycle

54.

What are the metabolic vasodilators

48.

What controls vascular tone? Intrinsic and extrinsic mechanisms

66.

What are the principal determinants of blood pressure? What are the short term and long term controllers of blood pressure?

Cardiac output and Venous return Baroreceptor reflex- short term -immediate responses to a change in BP -minimizes normal daily fluctuation in BP -returns BP to survival levels in the event of a catastrophic change eg hemorrhage Renin/Angiotensin system- long term -maintain the effective circulating blood volume over days or weeks -involved in the long term control of MAP

Intrinsic- local factors. -Myogenic Control --autoregulation -Metabolic control --Endothelial secretions --Metabolic vasodilators --Autacoids Intrinsic mechanisms mediate Autoregulation and active and reactive hyperemia. Extrinsic Mechanisms -ANS- Sympath/parasym -Circulating hormones- Epinephrine, angiotensin and vasopressin Extrinsic mechanisms support the needs of the whole organism. Involved in teh control of MAP and TPR.

23.

46.

What are the starling forces in relation to capillary pressures?

What does a tricuspid or mitral incompetence sound like?

Mitral incompetence- pan systolicventricular systole causes blood to regurgitate thru the mitral valve back into the LA resulting in a murmur that extends throughout the ventricular contraction = pansystolic murmur.

22. 21.

What are the types of heart murmers?

1. Incompetent- failure of the valve to seal properly such that it becomes leaky allowing blood to regurgitate through it 2. Stenosis- the open valve is narrowed so that a higher pressure gradient is needed to drive blood through.

What does an aortic valve stenosis sound like

100.

What are the types of primary hypertension?

When the aortic valve is narrowed, flow during the ejection phase becomes turbulent. The murmur is heard during the ejection phase of the ventricular cycle. The 1st heart sound is normal, but during the ejection a murmur is heard (systolic murmur) which rises and falls as the ejection waxes and wanes, loudest over the aortic area. S2 which is the closure of the aortic valve should be heard.

"silent killer"
18.

What are the valve positions during the cardiac cycle? Ventricular filling, isovolumetric contraction, ejection, isovolumetric relaxation

24.

What does aortic valve incompetence sound like?

87.

What happens in phase 1 and phase 2 of the valsalva maneuver?

If the aortic valve does not close completely, blood will regurg back into the ventricle during diastole. Actual turbulence is upstream of the aortic valve. Murmur begins at time of S2 and lasts through the early part of diastole. S2 may be affected. Pulse pressure is increased in this abnormality.
53.

88.

What does Endothelin do?

Vasoconstrictor. High Endothelin levels found in: -hypoxia -pre-eclampsia of pregnancy -cardiac failure -cerebrovascular accidents Diastolic murmurblood is forced through the narrowest mitral valve during the phase of ventricular fillingventricular diastole.

What happens in phase 3 and phase 4 of a valsalva maneuver

96.

25.

What does mitral stenosis sound like? What factors regulate CO?

What happens in the diving response?

76.

90.

91.

What happens during exercise in terms of CNS and Local components? Flow chart

What happens to exercise as far as requirements and cardiovascular changes?

92.

What happens during exercise with the sympathetic discharge? Flow chart

47.

What happens to Oncotic pressure and Hydrostatic pressure across a capillary?

37.

What happens to the pressure volume loop if you increase contractility?

35.

Oncotic pressure pretty much stays the same because the plasma protein levels don't change and fluid volume in the capillary changes are negligible. Hydrostatic pressure changes because as the fluid moves through the capillary it encounters resistance, so the pressure drops.
84.

What happens to the pressure volume loop when you increase EDV/Preload?

99.

What happens to the Guyton cross plot when cardiac failure occurs?

What happens to your cvs when you sleep?

85.

Cardiac contractility is reduced. Fluid retention > increased blood volume. Venoconstriction > vascular fxn curve is shifted upwards and MSFP increases. Overall effect: Slight decrease in CO but an increase in RAP. Such CV changes are observed moderate cardiac failure.
36.

What happens upon standing from a supine position in a flow chart format?

What happens to the pressure volume loop if you increase afterload?

74.

What happens when blood volume increases (use bainbridge reflex, ANF)

43.

What happens with the Respiratory pump?

44.

What is the equation for net filtration pressure, and what is the mechanism for fluid transport?

89.

What is a clinical use of the valsalva maneuver? What does a graph look like MAP and HR during the manoeuvre? What happens to BP and HR in each phase? What is secondary hypertension due to?

Osmosis. Positive # favors filtration, Negative # favors absorption.

38.

What is the ESPVR and in what cases does it change?

101.

Changes with contractility

49.

What is the myogenic response

3. PHeochromocytoma: increased release of EPI, NE 4. Pre-eclampsia Toxema: increased BP of pregnancy- they think it has to do with endothelin but no one knows why
95.

What is the alerting response?

86.

What is the overall effect of standing from a supine position?

102.

What is the pathology of hypertension

65.

What keeps blood flow to the brain relatively constant?