First, finish the material from last week…

In skeletal muscle, a higher frequency of action potentials leads to a greater amount

of tension

Figure 2. Graphs showing muscle summation, demonstrating the relationship between stimulus frequency and muscle tension.

http://slidingfilament.webnode.com/applications/nervous-system-control/

http://www.wellsphere.com/heart-health-article/some-of-the-best-illustrations-in-basic-cardiac-electrophysiology/921006

Children with Kwashiorkor

http://www.cs.stedwards.edu/chem/Chemistry/CHEM43/CHEM43/Leukotr/Kwashiorkor.GIF

Blood Pressure, Hypertension and Atherosclerosis

Heart Disease Death Rates2002-2007, Adults Ages 35+, by County

Source: US CDC

Obesity Trends* Among U.S. AdultsBRFSS, 2009

(*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person)

No Data <10% 10%–14% 15%–19% 20%–24% 25%–29% ≥30%

Arterial Blood Pressure

• One of the primary regulated variables of the cardiovascular system

• Sensed by arterial baroreceptors

• Regulated in the short term (sec. to min.)

• Blood volume, the other primary regulated variable, is regulated over the longer term (min. to hrs.)

Determinants of Blood Pressure

MAP = CO x TPR

CO = HR x SV

• MAP is mean arterial pressure (normal ~100 mmHg)• CO is cardiac output (normal ~ 5 L/min)• HR is heart rate (normal ~ 72 BPM)• SR is stroke volume (normal ~ 70 L)• TPR is total peripheral resistance

Determinants of Heart Rate

• Activation of the sympathetic NS increases HR

• Activation of the parasympathetic NS decreases HR

• At rest, parasympathetic neural activity predominates, so normal HR is slower than intrinsic rate of SA node depolarization.

Determinants of Stroke Volume

• Increased end diastolic volume (EDV) stretches cardiac muscle fibers, which causes heart to contract more forcefully, leading to an increase in SV.

• Increased sympathetic NS activity increases SV by increasing the influx of calcium into the cardiac muscle cells.

• These two mechanisms are additive.

Preload

• Preload is the amount that a muscle is stretched before it contracts.

• In the case of the heart, the end diastolic volume, which stretches the cardiac muscles, is the preload

Afterload

• Afterload is the force that a muscle contracts against.

• The afterload on cardiac muscle is the arterial blood pressure.

• High blood pressure (hypertension) increases the afterload, so the heart has to work harder.

Blood volume

• Most important long-term determinant of blood pressure

• Sensed by venous, atrial and arterial baroreceptors

• Regulated largely by the kidneys

The Role of the Vasculature in Arterial Blood Pressure

• Recall that arteries are elastic tubes with low resistance

• Serve as a “pressure reservoir”. They are stretched during systole, and their recoil during diastole maintains blood flow.

• The ease with which a structure can be stretched is called compliance

• Compliance = volume / pressure

MAP = DP + 1/3 (SP-DP)

• Systolic blood pressure (SP) is the maximum arterial pressure reached during peak ventricular ejection.

• Diastolic blood pressure (DP) is the minimum blood pressure that occurs just before ventricular ejection.

• Mean Arterial Pressure (MAP) is the average blood pressure over the course of the cardiac cycle. It is calculated to account for the fact that diastole lasts about twice as long as systole.

Arterioles regulate blood flow

• Determine relative blood flow to each organ

• Collectively the arterioles act as the major determinant in determining the TPR, and thereby influence the MAP

F = ∆P Where: Flow = pressure gradientR resistance

R = L8 =fluid viscosity r4 p L=tube length

r=inside radius of tube8/p = a proportionality constant

From these equations, we can derive Poiseuille’s equation:

F = ∆P r4 p hL8

Factors influencing flow

Significance for blood pressure

• The radius of a blood vessel is the most important determinant of resistance

• A 2-fold decrease in radius will lead to a 16-fold increase in resistance

• Blood viscosity is proportionate to hematocrit – excess RBC’s increase TPR and therefore MAP

Local Control of Arteriolar Tone• Increased metabolic

– Local increases in CO2, H+, K+– Local decreases in O2

• Endothelial factors that cause vasodilation:– Nitric Oxide– Prostaglandins– Endothelium-derived Hyperpolarizing Factor

• Endothelial factor that causes vasoconstriction:– Endothelin 1

Systemic Control of Arteriolar Tone

• Increased sympathetic NS activity causes general vasoconstriction

• The following hormones also cause vasoconstriction:– Epinephrine and norepinephrine– Vasopressin– Angiotensin II

Hypertension

Distribution of hypertension

Blood pressure generally increases with age.

Cardiac HypertrophyConsequence of increased afterload

http://www.moondragon.org/health/graphics/cardiomegaly.jpg

Atherosclerosis

www-ermm.cbcu.cam.ac.uk/nfig003jal.gif

The Arterial Wall

Yellow Streak

http://www.surrey.ac.uk/SBMS/MicrobialSciences/research/immunology.html

Development of Fibrous Plaque

1. Abdominal obesity (waist circumference >40 inches for men, 35 inches for women)

2. Triglyceride levels >150 mg/dL

3. HDL cholesterol <40 mg/dL for men, <50 mg/dl for women

4. Blood pressure >130>85 mmHg (normal is about 120/80)

5. Fasting blood glucose >110 mg/dL (normal is 100 mg/dL)

The Metabolic Syndrome

Vulnerable plaques are most likely to rupture, causing a myocardial infarction or a stroke