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W. Crone (303 FTZ, 629-7439, cronewil@hvcc.edu, http://www.hvcc.edu/academ/faculty/crone/index.html)

Cormack: Ch. 5; Guyton/Hall: Chs. 9-24, 25 (pp. 308-312), 61; Michael and Rovick: Unit 5; van Wysberghe and Cooley, Cases 12-15

possible web sites: http://sln.fi.edu/biosci/heart.html

(an online heart tutorial--simplistic, but able to click to additional material from there)


(a collection of cardiovascular images and graphs that may assist you to integrate concepts)

other potentially useful web sites for cardiology:

http://homepages.enterprise.net/djenkins/ecghome.html? (EKG samples--practice for the summer!)

http://www.medlib.com/spi/coolstuff2.htm (heart murmurs)

The overall path of conduction leads from the SA node across the atria in general (along with several bundles) to the AV (atrioventricular) node. Set up of the node slows conduction enough to allow contraction and drainage of the atria. From there, conduction in the interventricular septum via the Bundle of His, the left and right bundle branches, and into the Purkinje fibers allow a coordinated contraction of the ventricles. Latent pacemakers in the conducting pathways are usually overriden by the SA node.

Electrocardiogram (EKG) basics: The waves described below represent the composite effects of action potentials on the different parts of the heart:

P wave:

indicates atrial muscle depolarization

P-R interval:

from beginning of P wave to beginning of QRS. Indicates the time it takes for the impulse to make it through the atria, AV node, bundle of His, and bundle branches before ventricular depolarization.

QRS interval:

from the beginning of the Q wave to the end of the S wave, reflecting the depolarization of the ventricular muscle fibers.

S-T segment:

between the end of the QRS interval and the beginning of the T wave, representing a pause between ventricular muscle firing and repolarization.

T wave:

ventricular repolarization

Q-T interval:

between beginning of QRS and end of the T wave, or the duration of ventricular electrical activity.

Leads of an EKG are attached to RUE, LUE, LLE to create three bipolar limb leads:


positive direction

negative direction










Augmented unipolar limb leads help to complete this"circle." The positive pole is at the extremity, the (-) in the center:


positive direction

negative direction










Unipolar chest leads help to"read" the heart's electrical activity in a different plane:

v1---v6, from 4th R intercostal space to 5th L ICS at the midaxillary line

Generally, the overall vector arrow points in the direction of Lead II, which is in the general direction of the major normal activity of the atria and ventricles. The heart is a dipole, with negative and positive poles. Cardiac depolarization towards a positive electrode results in a positive (upward) deflection above the baseline in the EKG. Impulses traveling away from a positive electrode result in a negative (downward) deflection, or below the baseline. Two examples of the types of items that EKGs can tell us (think of how the pattern"reflects" the underlying situation):

1st degree (partial) heart block: occurs when the impulse is delayed more than normal in traversing the AV node, although the impulse does gets through and excites the bundle of His with normal ventricular excitement. So, P-R prolonged, but atrial and ventricular rate normal and a P wave precedes each QRS.

Premature ventricular contraction (PVC): in a non-MI (myocardial infarction) situation, a preventricular premature beat may occur from cells in Purkinje system. During MI or healing afterward, PVCs can occur in muscle too. The PVC produces widening in QRS since the excitation impulse has to propagate from one ventricle to another (as vs. the coordinated bundle branches activating both ventricles at once).

The cardiac cycle:

The atria are thin walled, low pressure, functioning more as reservoir conduits for their ventricles than as important pumping units. The 25% contribution of atrial contraction to vetricular filling is more noticeable during exercise.4 With no valves separating RA from SVC, RA pressures are transmitted to the jugular vein, as described in Bates.

The ventricles are high pressure (particularly the LV), pumping units with systole (contraction) and diastole (relaxation). As the AV valves close and the ventricules contract, initially isovolumic contraction. When ventricular pressure exceeds the great arteries, then ejection phase. As ventricular pressure drops below artery pressure, diastole begins, with isovolumic relaxation, until the AV valves open up and the filling phase occurs.

Systolic pressure: peak aortic pressure during systolic injection

Diastolic pressure: lowest aortic pressure during diastole

Pulse pressure: the difference between the two, wider than normal in arteriosclerosis--why?

Therefore, with cardiac valves, the movement of the leaflet valves is essentially passive and dependent on pressure differences across them. The closure of the AV valves coincides with the first heart sound S1, the beginning of systole just after the beginning of ventricular excitation, which is signalled by the QRS deflection. The semilunar valves: at the end of the ejection phase of ventricular systole, there is a brief reversal of blood flow toward the ventricles that snaps the cusps together and prevents regurgitation of blood into the ventricles. The second heart sound S2 is therefore the closure of the semilunar valves, marking the end of ventricular systole and the beginning of diastole.

Variation in heart sounds:2

S2 can be split especially in children with two rapid components heard during inspiration and single sound during expiration. Inspiration causes increased blood flow of blood to the right heart and decrease to the left heart, so that there is a slight prolongation of the ejection phase of the RV during inspiration.

S3 ("Ken-tuc-ky") (S1, S2, S3) is low in pitch, representing a rapid passive filling of the ventricles as they expand during diastole. A prominent S3 in nonathletic adult >40 YO suggests LV volume overload with"stretching" of LV wall.

S4 ("Ten-nes-see") (S4, S1, S2) is caused by atrial contraction, or rapidly active ventricular filling. Not usually heard, but important in those conditions restricting LV filling, such as those with low LV wall compliance, e.g. severe LV hypertrophy with AS (aortic stenosis).

The Frank-Starling relationship:

There are optimum amounts of overlap of the actin and myosin in cardiac muscle to allow for forceful contraction. Generally speaking, increases in fiber length create an increase in developed tension. On a normal basis, the Frank-Starling curve allows the matchup of cardiac output to venous return, e.g., so that the pulmonic and systemic circulations do not get out synch from each other. But when sarcomeres are stretched beyond the optimum, the developed force is less than maximum due to the Frank-Starling curve. Hence, in acute fluid overload (e.g., too much IV fluid), the volume overload of the ventricle reduces the pumping efficiency of the heart, and one needs to shift the ventricle to a lower volume so that we will be back on the ascending portion of the Frank-Starling curve. Chronically, we will see the Frank-Starling effects on congestive heart failure (CHF), where cardiac output is decreased.

Cardiac output (CO) = stroke volume (SV) x heart rate (HR)

stroke volume: volume of blood pumped out per beat

preload of LV is the end-diastolic volume (EDV)

afterload of LV is the total peripheral resistance (TPR)

TPR is made of two components, with the LV afterload from the SVR (systemic vascular resistance) and the RV afterload from the PVR (pulmonary vascular resistance).

MAP = mean arterial pressure; calculated by diastolic pressure + 1/3 pulse pressure


ejection fraction: SV/EDV. The ejection fraction is increased during exercise. Values: normal 60%, below 50% abnormal, 20-25% severe depression of ventricular function.

congestive heart failure (CHF): vicious cycle of low CO and low tissue perfusion, so that increased EDV and increased TPR to compensate, which makes a failing heart needing to work that much harder. CHF will be further understood after coverage of blood pressure maintenance mechanisms.

Another way to apply this: stroke work: SV x TPR; the work of the heart. By the LaPlace equation, tension = pressure X radius. The principal determinant of oxygen consumption is active tension in the myocardial wall, e.g., aortic stenosis (AS): LV hypertrophy and failure, from increased work needed to raise pressure to force blood through the small valve. Therefore, onset of angina is a poor prognostic sign.

compliance (capacitance): C=dV/dP, or in words, capacitance is the increment in volume per unit change in pressure. Cv is much greater than Ca, so that veins can hold much more blood than arteries.

The pressure gradient across the peripheral resistance is the most important factor responsible for the venous return to the heart and this pressure gradient is due to the pumping action of the heart itself. For example: acute myocardial infarction from coronary artery occlusion: substantial reduction in cardiac output, fall in arterial pressure and a rise in CVP (central venous pressure, pressure in the large veins).

Mean circulatory pressure is increased during hypervolemia and decreased during hypovolemia. Value of CO at a given venous pressure is dependent on blood volume. So the ability for the heart to maintain a maximum cardiac output becomes progressively more limited as the total blood volume is reduced. Increasing blood volume increases circulatory pressure by increasing CO. Blood volume changes with body levels of sodium, the most common of the plasma electrolytes:"water follows the sodium."

Posieuille's Law:

F (flow) = P D Pr4/8h L applies to flow in a single blood vessel during laminar flow. In other words, radius is the major determinant. Flow is usually laminar (streamline) up to a critical velocity, when flow is turbulent (and hence sound making, e.g., bruits). The biggest drop in pressure and hence the control point is the arterioles with smooth muscle in their walls. Hence you can see why the blood vessels are under chronic sympathetic tone--a slight change in radius has a large effect.

From our formulas, we know that the pressure drop through any vascular level is proportional to the resistance to blood flow through that level, since the same cardiac output must go through each level. Hence, if arterioles dilate, the flow through them increases and so the pressure drop through the arteries, capillaries, and veins must increase. Higher capillary pressure will tend to push fluid out of the blood vessels, with more fluid filtration into tissue.

Another factor to consider, F = V (velocity) x A (cross-sectional area), so that blood flow is highest at the aorta and slowest at the capillaries, even though only a few seconds are spent at the capillary level.

Hydrostatic pressure = height x density x gravity, for a continuous vertical column of fluid. Valves in veins break up the fluid column so that the effective"height" is that between valves. In venous insufficiency, the whole fluid column is continuous so that there are high venous pressures and varicosities as a result.


osmosis: passive flow of water down an osmotic pressure gradient across a selectively permeable membrane. This gradient is created by different solute concentrations on either side of the membrane.

As stated earlier, osmotic pressure is a colligative property, so we are interested in the difference in particle concentrations, not molar concentrations per se.

Overall fluid balance across capillaries is described by the Starling-Landis equation, that the relative magnitude of the hydrostatic forces and the oncotic forces will determine whether water moves in or out of the vasculature. Generally speaking, the balance of these forces favors filtration at the arterial end and reabsorption on the venous end of the capillary, with the slight overall excess from filtration picked up by the lymphatic system.4

(Pc + P if) - (Pif + P p)

out of capillary pressures: capillary hydrostatic and interstitial osmotic

into capillary pressure: interstitial hydrostatic and plasma osmotic

In light of the above factors, possible causes of edema should make sense:1,4

increased blood pressure:

a) high arterial blood pressure increasing capillary filtration

b) venous obstruction causing increased capillary filtration by congestion

changes in oncotic factors:

c) leakage of plasma proteins into issue fluid, e.g., inflammatory response

d) myxedema (hypothyroidism) leads to overproduction of interstitial mucin

e) decreased plasma protein concentrations, e.g., liver failure

decreased drainage of interstitial regions:

f) obstruction of lymphatic vessels: elephantiasis, anyone?


As discussed above, the overall control point of blood pressure is accomplished at the precapillary sphincters of the arterioles. The arteriolar smooth muscle of arterioles can be influenced by local (metabolic, paracrine, myogenic), hormonal, and neural factors.


Metabolites are produced and washed out continously, so that increase in production (or decrease in washout) will lead to higher [metabolite] and vasodilation. Paracrine compounds give smooth muscle feedback to the status of surrounding tissue, e.g., nitric oxide produced by the endothelium relaxes the smooth muscle of the tunica media. Also, myogenic factors are direct responses by vascular smooth muscle due to changes in pressure, as seen in cerebral circulation. These local factors can override more global control aspects.


Hormones such as epinephrine can influence vascular tone. Norepinephrine and epinephrine activate a 1 receptors, causing vasoconstriction. In addition, epinephrine activates b 2 receptors and cause vasodilation, particularly in skeletal and cardiac muscle, so that the total effect depends on local concentration of the different receptors. Sympathetic activity is important in maintaining orthostatic blood pressure, e.g., HR and vasoconstriction to prevent dropoff when standing up. These orthostatic changes would initially be sensed by...


Baroreceptors in the aortic arch and carotid sinuses sense the stretch of the arterial walls which result from the arterial pressure. The baroreceptors feed into a medullary cardiovascular center. These respond to rapidly changing pressures, but reset after a few days to the pressure level they're exposed to.4 As a result, the kidney is going to be more important for long-term regulation of blood pressure.

In addition, the hypothalamus secretes ADH (antidiuretic hormone or vasopressin), which increases water reabsorption, if osmoreceptors sense too high a plasma osmolality.


Several aspects: if blood pressure is raised, there is more filtration through the kidney, which lessens blood volume and so should lower pressure (or if less blood pressure and less filtration, then relatively more blood volume kept). Renin is produced by granular cells of the juxtaglomerular complex in kidney, which converts angiotensinogen (from liver) into angiotensin I. ACE (angiotensin converting enzyme) in pulmonary capillaries converts angiotensin I to angiotensin II. Angiotensin II has a potent affect on the thirst center of the hypothalamus, a direct vasoconstrictive effect, and particularly stimulates the production of aldosterone from the adrenal cortex. Aldosterone promotes renal tubule reabsorption of sodium, so more blood volume and fluid.

In addition, the macula densa region of the renal tubule can sense if blood volume is low and little sodium coming by, and hence stimulate renin secretion also.4

additional cardiovascular aspect:

Receptors in the atrial wall respond to stretch (increased fluid volume) by the release of atrial natriuretic peptide ANP. As the name implies, it acts to increase sodium excretion, and so reduce plasma volume.


A major example where the above factors come into play is CHF. Decreased cardiac output leads to activation of these compensatory mechanisms:3

sympathetic activity, so vasocontriction, TPR ( afterload, right?)

renin stimulation from renal flow, so blood volume ( preload, right?)

Both of these would make that failing heart work harder, which could mean that:

Left-sided CHF:

backup into pulmonary circulation

Right-sided CHF:

backup into systemic circulation



coronary circulation:

The coronary artery circulation is different than most because blood flow decreases during systole (because of contracting heart tissue). In fact, this systolic compression will most affect subendocardial vessels, particularly in the LV, so that myocardial infarction can be seen there first.4 Given these constant, high energy demands, local autoregulatory affects of the increased oxygen demand will help to dilate vessels.4

cerebral circulation:

A hard skull means that increased intercranial pressure can occlude vessels and stop flow. Flow is under primarily local (pH and pCO2) control, because of the blood-brain barrier prevents hormonal action on vascular smooth muscle. Myogenic autoregulation keeps cerebral blood flow consistent in the face of different MAP, and metabolic autoregulation maintains a constant O2 supply to parts of the brain depending on activity. In this way, we see autoregulation of blood flow so that brain flow maintained in face of varying conditions.4

splanchnic circulation:

Most of liver perfusion is with venous drainage from the intestine/stomach and about one third is from arterial blood via the hepatic artery. Intestinal capillary permeability is higher than many other tissues and liver capillary permeability is very high. After a meal, flow to the splanchnic areas increases rapidly, but with sympathetic nerve stimulation, the splanchnic flow can be drastically decreased. Flow is under largely neural control.

skin circulation:

Most important moment to moment function of this circulation is temperature regulation. The subcutaneous plexus gives rise to capillaries delivering substrates to the dermis and basal layer of the epidermis and also to AV (arteriovenous) shunts which can vary their flow greatly. Since temperature equilibrates quickly, high shunt flow unloads body heat. This flow is under largely neural control.

skeletal muscle circulation:

Flow can vary by a large factor from rest to exercise, usually under the control of local metabolism, but the flow can be altered by neural and humoral factors. For example, sympathetic a 1 receptor activation vasoconstricts and b 2 receptor activation vasodilates, so that muscle can barely perfused in a shock-type crisis, or highly perfused in a"fight or flight" situation.

As a separate issue, muscle pumping also helps venous return, e.g., from the lower extremities.

pulmonary circulation:

In contrast to other tissues, the pulmonary circulation constricts with low pO2 and dilates with high pO2. There are large differences in perfusion between the top and the bottom of the lung. Overall, in the pulmonary circulation, there is very low resistance to flow, with 1/10 the pressure gradient of the systemic circulation.

lymphatic circulation:

Lymphatic vessels are interconnected simple endothelial tubes within tissues. These vessels collect excess tissue water and plasma proteins into a liquid lymph. Lymph is a means of travel of such items as immune system cells and long-chain fatty acids absorbed from the intestine. The two main factors that determine lymph flow are interstitial fluid pressure and activity of lymphatic pumping action.4



The ultimate goal in chronic hypertension is to lower the total peripheral resistance. Three general pharmacologic strategies for control of blood pressure:2

1) reduction of plasma volume.

diuretics to promote water excretion (e.g., thiazide or loop diuretics) or aldosterone antagonists (e.g., spironolactone, which spares potassium)

2) promotion of vasodilation.

  1. central vasodilation from inhibition of sympathetic nervous system centrally. a 2 agonists stimulate a 2 receptors to inhibit sympathetic firing in CNS, and hence lower blood pressure. (drug examples of clonidine, alpha-methyldopa).
  2. alpha-1 antagonists that antagonize the a 1 receptors in the blood vessel smooth muscle walls, allowing for vasodilation (prazosin).
  3. calcium channel blockers, since calcium flux is necessary for smooth muscle contraction, and so these channel blockers are vasodilatory (verapamil, diltiazem).
  4. direct vasodilators of smooth muscle (hydralazine, minoxidil, sodium nitroprusside).
  5. ACE inhibitors (angiotensin-converting enzyme) inhibits the production of the vasoconstrictor angiotensin II (captopril, benazepril) [losartan blocks the angiotensin II receptor].

3) reduction of cardiac output.

b 1 antagonists block sympathetic stimulation of b 1 receptors, and so slower heart and less forceful contractions, as well as less sympathetic stimulation of renin production (atenolol is"cardioselective" compared to more general beta blockers such as propanolol).


Shock: general failure of the circulation to critical organs.

Examples of cardiac shock, hemorrhage, vascular obstruction shock (e.g., massive pulmonary embolus), anaphylatic shock (histamine-like chemicals leading to vasodilation and flow of fluid into interstitial tissue), septic shock with bacterial toxins leading to vasodilation as well.

If blood pressure dropped suddenly, wouldn't the tissues not be perfused and with vasoconstriction to raise blood pressure, wouldn't the tissue perfusion become even worse? True, but initial body responses include the following:4

  1. Vasoconstriction response frees up blood pooled in veins, so"getting" more blood into circulation.
  2. Sympathetic innervation has little to do with coronary and cerebral arterioles. Heart and brain are basically under local autoregulatory control, so that their blood flow is more likely to be maintained during shock.


  1. Fox, SI, Human Physiology, 6th ed. (WCB McGraw-Hill, Boston, 199), p. 414.
  2. Goldberg, S. Clinical Physiology Made Ridiculously Simple (MedMaster, Miami, 1995), pp. 15-16, 49-50.
  3. Gould, BE Pathophysiology for the Health-Related Professions (WB Saunders, Philadelphia, 1997), pp. 191-192.
  4. AC Guyton and JE Hall, Textbook of Medical Physiology, 9th ed. (WB Saunders, Philadelphia, 1996), pp. 111, 187, 196, 214, 218, 258, 260, 286-288, 309, 328, 784.


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