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39 Cards in this Set

  • Front
  • Back

1. Cardiac output is

2. formula for cardiac output

3. volume of blood flowing through pulmonary circulation

4. volume of blood flowing through systemic circulation

5. at rest total blood volume averages

1. volume of blood pumped by each ventricle per minute (CO from each vent is identical)

2. 5L from RV

3. 5L from LV

4. heart rate x stroke volume (at rest) = CO

5. 5- 5.5L/min

Heart Rate regulation and contractibility by ANS:

heart -> SA Node -> deopl -> action pot-> ...

1. decrease in K permeability

2. constant Na permeability

3. increase in Ca permeability

- > action pot. spread throughout the heart (70 beats/min)

Innvervation of the heart and contractibility by ANS

1. parasympathetic NS innervates what parts of heart with what nerve

2. sympathetic nervous system innervares what parts of heart with waht nerve

3. both para and symp alter the activity of

1. VAGUS NERVE: atria (SA and AV nodes) and sparsely vent.

2. SYMPATHETIC NERVE: atria (SA and AV) and richly vent.

3. alters activity of cAMP in innervated cardiac cells of heart to modify HR

Heart regulation by parasympathetic nervous system (11)

(relaxed situation)

1. vagus nerve

2. ACh

3. muscarinic receptor

4. inhibitory G-protein

5. decrease activity of cAMP pathway

6. decreases SA Node

7. increase K permeability

8. more K leaves cell

9. slow inward movement of Ca

10. hyperpolarizes SA node

11. decreases HR

Heart regulation by sympathetic NS(12)


1. sympathetic nerve

2. N.E

3. B1 - adrenergic receptor

4. stimulatory G-protien

5. increas cAMP activity

6. increase SA node

7. decrease K permeability

8. increase inactivation ofK channels

9. increase Ca permeability

10 mem becomes less -

11. mem. depoarizes

12. increase HR


1. PS - NS

2. S - NS

1. decreases rate of depolarization to threshold

2. increases rate of depolarization to threshold


1. ps - ns

2. s - ns

1. decreases excitability - increase AV nodal delay

2. increase excitability - decreases AV nodal delay

Ventricular conduction pathway

1. ps - ns

2. s - ns

1. no effect

2. increases excitability thru His and purkinje

Atrial muscle

1. ps - ns

2. s - ns

1. decreases contractility weakens contraction

2. increase contractility strengthens contractoin

Ventricular muscle

1. ps - ns

2. s - ns

1. no effect

2. increase contractility

Adrenal medulla

1. ps - ns

2. s- ns

1. no effect

2. promotes adrenomedullary secretion of epinephrine (augments SNS actions on heart)


1. ps - ns

2. s -ns

1. no effect

2. increase venous return

The parasympathetic NS decreases HR by (2)

1. decreasing K efflux

2. decreasing AV nodal excitability

1. What is stroke volume?

2. 4 factors that affect SV

1. amount of blood pumped by each ventricle/beat (70ml/beat)

2. - intrinsic control

- extrinsic control

- increased EDV

- frank-startling law of heart

1, Intrinsic control on SV

2. Extrinsic control on SV

3. both factors ..

1. extend of venous return

2. sympathetic stimulation

3. increases SV by increasing contractile strength

1. EDV is directly correlated to

2. How does EDV affect SV

1. intrinsic control of SV

2. increase (intrinsic control) venous return = increase EDV -> moves cardiac muscle closer to optimal length -> increases contractily tension of fibers on next systole -> squeeze out more blood -> increaseSV

What is theFrank-Startling Law of the heart

1. increased length results in greater force on cardiac contraction and thus greater stroke volume

(intrinsic relationship between EDV and SV)

Length-tension relationship in cardiac muscle depends on (2)

1. muscle fiber length

2. lateral spacing b/w myosin and actin fil

1. Sympathetic nervous system increases contractility by

2. it shifts F-S curve to the

1. increase Ca by triggering NE and Epine.

2. shifts frank-starling law more to the left

Sympathetic stimulation on heart contractility (3)

1. increase SV by increasing contractility

2. increase venous return

3. increase EDv

1. Afterload is

2. how might the heart compensate for sustained increased afterload?

3. diseased heart

1. the pressure that the LV musrt generate in order to eject blood from the chamber (arterial bp - workload imposed on heart after ventricle contraction begins

2. hypertrophy OR enlargment of cardiac muscle fibers

3. diseased heart w/ age may not be able to compensate completely -> can result in heart failure

Chronically elevated afterload is one of the major factors that causes

heart failure

1. backward failure

2. forward failure

3. what is congestive heart failur

1. veins behind heart become congested with blood

2. failure of heart to pump blood forward into arteries

3. inability of CO of heart to keep up with body's needs for blood delivery - with blood damming up in veins behind the heart

1. backward failure (CHF) causes

1. pulmonary edema (due to accumulation of fluid)

- fluid accumulation in lungs:

> reduces O2/Co2 exchange (blood/lungs)

> leads to reduced arterial oxygenation

> elevate acid forming CO2 in body

Treatment for congestive heart failure (3)

measures/drugs that will

1. reduce salt and water retention (diuretic drugs)

2. increase urinary output

3. enhance contractile ability of weakend heart

Cardiac cells are nourished by(2)

1. abundant mitochondria

2. abundant myoglobin which stores O2 for immediate energy use

1. blood is supplied to the heart by

2. why can't the heart receive blood from the heart

1. coronary circulation

2. watertight endocardial lining (doesn't permit blood to pass from heart chamber to myocardium)

- thickened heart wall (doesn't permit the diffusion of O2 and other suppliesto ind. cells)

1. how much blood supply does heart muscles receiv during diastole?

2. systole?

1. 70% of coronary blood flow

2. 30% or coronary blood flow

Reduced blood flow to heart is due to 2 reasons:

1. Major coronary arteries compressed by contractions of myocardium

2. entrance to the coronary vessel partial blocked by open aortic valve

How is oxygen made available to heart (2)

1. increasing coronary blood flow

2. conversion of adenosine from ATP in cardiac cells

Increased formation and realease of adenosine from cardiac cells occurs when (2)

1. there is cardiac O2 deficit

2. when cardiac activity increased and heart requires more O2

1. increased formation and release of adenosine forms major _______ supply to heart

2. released adenosine induces _____ of coronary vessels

1. O2

2. vasodilation of coronary vessels - increasing more O2 rich blood flow to cardiac cells to meet O2 demand

What is atherosclerosis?

a progressive degenerative arterial disease that leads to gradual blockage (occlusion) of affected vessel reducing blood flow

1. Atherosclerotic plaques consist of

2. where do they form

1. lipid-rich core covered by abnormal overgrowth of smooth muscle cells, topped off by collagen-rich connective tissue cap

2. plaque forms beneath vessel lining and forms bulge that protrudes into vessel lumen

Angina pectoris:

1. gradual enlargement of plaque narrow bl. vessel lumen ->causes reduced coronary bllod flow to heart -> limits O2 supply -> pain beneath sternum and lef shoulder/arm -> heart attack characterized by anginal attack

Is anginal attack permanent/

no, it's temporary - can be reversed by rest or administration of a drug (nitroglycerine)

- nitroglycerine converts into nitric oxide (NO) which relaxes smooth muscles lining arteries


- enlarged atherosclerotic plaque break through weakened endothelial lining -> exposes collagen and collagen rich connective tissue -> foam cells release chem -> chem break down connective tiss in fibrous cap -> plaque within is weak and unstable -> likely to rupture and loose -> rupture of fibrous cap can trigger clot formation -> platelets+foam cells form clot -> attachment of abnormal to bl vess (thrombus) -> thrombus enlarges

1. IF thrombus breaks loos it is called

2. if embolus blocks coronary arteries

3. if embolus blocks cardiac arteries

1. embolus

2. stroke

3. heart attack

Complex series of events leading to atherosclerosis

injury to bl. vess. wall -> inflammartory resp. -> low grade inflammatory resp. over time lead to arterial plaque formation -> oxidized cholesterol triggers atherosclerosis -> LDL in arterial wall oxidizes -> chemicals attracts monocytes from blood -> monocytes becomes macrophages -> macrophages phagocytoze oxidized LDL and becomes packed with fatty acid droplets called foam cells -> foamy macrophages accumulates beneath vessel lining and forms plaque -> atheromas (smooth muscle over top) -> oxidized LDL inhibit release of NO -> thickening of plaque interfere with nutrient exchange -> damaged area called fibroblast -> fibrous connective tissue (sclerosis) over plaque -> Ca precipitate plaque