A & P 2 - Cardiac Output

Front 1

What are Cardiac Output?

Back 1

volume of blood pumped per minute by each ventricle

COP = SV x HR

N value (rest) = 5 L/min, maximum 20 (35 for athletes)

Cardiac Reserve:
-COPmax - COPrest

Front 2

What are the different regulations of SV?

Back 2

SV of LV = SV of RV

Preload:
-EDV (veintricular filling) - degree of stretch of heart during systole
factors affecting EDV:
-filling pressure - The pressure in the atria depends on the venous return to RA, factors that increase VR increase SV
-filling time - duration of ventricular diastole but is inadequate when HR exceeds 180 beats/min
-the more the heart is filled during diastole, the greater the contraction during systole
-increase EDV and SV automatically increases COP

Myocardial Contractility:
-determines strength of contraction of EDV
-Ejection fraction = SV/EDV (60-70 %)
-positive ionotropic agents = Adr, NAdr, glucagon, thyroid hormone, cadiac glycosides, caffeine, INCREASE contractility
-negative ionotropic agents = Ca++ channel blockers, acidosis, hyperkalemia, DECREASE contractility

Afterload:
-Tension-afterload relationship = to eject blood, ventricular pump must overcome resistance (BP) across blood vessels
-energy required affects SV
-increase afterload (increase blood pressure) = decrease SV

Front 3

What is the mechanism of the Frank Starling Law?

Back 3

degree of stretching of myocardium depends on EDV

as EDV increases:
-actin filaments overlap with myosin at edges of A band giving more forceful contractions

Front 4

What are characteristics of HR?

Back 4

increase HR = increase COP

HR = rate of discharege of physiological pacemaker; modified by ANS

controls:
sympathetic:
-postgang, fibers innervate atria and ventricles
-impt under special conditions, release NAdr = Beta-1 receptors
effects:
+ ionotropic = increase contractility
+ chronotropic = increase HR, automaticity; increase permeability of SA node for Ca++ and Na+, decrease electronegativity, increase spontaneous depolarization
+ dromotropic = increase conductivity (decrease AV delay)

parasympathetic:
-mainly in atria
-continuous tension on heart
-releases Ach --> muscarinic receptors
effects:
- ionotropic = decrease contractility (small effect due to little innervation on ventricles
- chronotropic = decrease HR and automaticity; increase K+ efflux, lower Na+ and Ca2+ influx, increase RMP
- dromotropic = decrease conductivity

Front 5

What are the Cardiac Reflexes?

Back 5

Sensory Receptors:
Baroreceptors:
-monitor BP (stretch of vascular wall)
-located in aortic arch and carotid sinus
reflex: increase arterial BP --> increase vagal tone --> decrease HR, conductivity, and contractility)
Chemoreceptors:
-in aortic arch and carotid bodies
-monitor blood tension of CO2, O2, and H+
reflex = increase blood PCO2, H+ and PO2 --> increase sympathetic discharge of heart --> increase HR, contractility, and conductivity
Proprioceptors:
-monitor joint movement

Cardiomotor (vasomotor) center:
-in reticular formation of medulla

efferent innervation of heart:
sympathetic = cardiac acceleratory nerves
parasympathetic = vagus

Front 6

What are the Humoral controls HR?

Back 6

Electrolytes
Calcium:
-hypercalcemia = increase contractilty and HR
Sodium:
-Hypernatremia: decrease in calcium influx into cells leading to decrease force of contraction and HR
Potassium:
-Hyperkalemia = block AP generation and decrease HR and contractility

Hormones:
-Adr - positive effect on heart
-thyroxin = increase metabolic rate, oxygen consumption --> increase HR

Local factors:
-hypoxia, acidosis, hypercapnia = iincrease HR

Drugs:
-beta blockers decrease HR

Front 7

What is Ischemic Heart Disease (IHD) or Coronary Heart Disease (CAD)?

Back 7

IHD:
-due to insufficient supply of oxygenated blood to the heart ("ischemic")

-most frequent cause is CHD

Risk factors:
-family history
-obesity
-hyperlipidemia
-smoking
-hypertension
-diabetes

Front 8

What is Atherosclerosis?

Back 8

-formation of atherosclerotic plaque

-thickening and loss of elasticity of aterial walls, hardening of arteries

-high blood cholesterol is associated with risk of atherosclerosis

LDL:
-carry cholesterol to arteries
-bind to specific plasma membrane receptors

HDL:
-remove excess cholesterol from cells; anti-atherosclerotic effect

Front 9

What is the Pathogenesis behind Atherosclerosis?

Back 9

1. starts as inflammation and damage to endothelial cell wall (ex. diabetes, cholesterol, smoking)

2. Accumulation and oxidation of LDL

3. Secretion of cytokines

4. Attraction of monocytes and lymphocytes

5. endocytosis of LDL by macrophages --> foam cell (macrophages filled up with LDL)

6. T lymphocytes intensify inflammatory response

7. accumulation of foam cells, macrophages, and T cells leads to beginning of plaque formation

8. Smooth muscle cells migrate to tunica interna and synthesize CT proteins called fibrous plaques

9. Precipiation of calcium ions

10. arterial stenosis

12. activation of enxtrinsic pathway --> thrombosis

Front 10

What are the roles of some chemical factors in the pathogenesis of atherosclerosis?

Back 10

C creative proteins:
-promote uptake of LDL by macrophages activated by inflammation otherwise remain inactive after produced by liver

Lipoprotein A:
-promotes proliferation of smooth muscle fibers; inhibits fibrinolysis

Fibrinogen:
-regulates cellular proliferation, vasoconstriction, and platelet aggregation

Homocysteine:
-promotes platelet aggregation and smooth muscle fiber proliferation