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CARDIOVASCULAR PHYSIOLOGY

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ELECTRICAL CONDUCTION OF THE HEART

MYOCARDIUM DEPOLARIZATION:

SA-NODE DEPOLARIZATION: It is similar to depolarization in the myocardium, except for the following differences:

REFRACTORY PERIOD: Cardiac muscle cells have prolonged refractory periods, to prevent tetany of cardiac muscle.

AUTONOMIC REGULATION of HEARTBEAT:

PROPAGATION of ACTION POTENTIAL:

EKG LIMB LEADS:

ELECTROCARDIOGRAM:

READING THE ECG:

At standard speed:

PRECORDIAL LEADS: V1 thru V6 are placed to specific places on the chest, for advanced ECG diagnostics. V1 is right-most, near the SA-Node, while V6 is leftmost, past the apex of the heart.

MEAN ELECTRICAL AXIS OF THE HEART:

ECG ABNORMALITIES:

CLINICAL LECTURE: WOLF-PARKINSON-WHITE SYNDROME


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THE CARDIAC CYCLE

VENTRICULAR DIASTOLE:

VENTRICULAR SYSTOLE: QRS-Complex occurs and ventricles start contracting.

HEART SOUNDS: Left Side -vs- Right Side:

SPLIT SECOND HEART SOUND: During inspiration, You should be able to hear the pulmonic and aortic valves close separately during the second heart sound (i.e. a "split" sound).


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HEMODYNAMICS

NORMAL RANGE OF VALUES

P-Wave ~ 80 msec
QRS-Wave 30 - 100 msec
P-R Interval 180 - 220 msec
S-T Interval 230 - 460 msec
Q-T Interval 260 - 490 msec
Mean Electrical Axis -30 to +110
End Diastolic Volume (LVEDV) 120 - 140 mL
End Systolic Volume (LVESV) 40 - 60 mL
Stroke Volume (SV) 60 - 100 mL
Ejection Fraction 0.50 - 0.70
Cardiac Output (CO) 5.0 - 6.0 L / min
Cardiac Index 2.6 - 4.2 L / min / m2
Systolic Pressure 100 - 140 mm Hg
Diastolic Pressure 60 - 90 mm Hg
Systemic Resistance (TPR) 0.9 PRU, or mm Hg / mL / sec
Pulmonary Blood Distribution ~ 10% total; 500 mL
Heart Blood Distribution ~ 10% total; 500 mL
Systemic Arterial Blood Distribution ~ 10% total; 500 mL
Arteriolar Blood Distribution ~ 5% total; 250 mL
Venous Blood Distribution ~ 65% total; 3250 mL
Capillary Hydrostatic Pressure, Pc ~ 30 mm Hg
Capillary Oncotic Pressure, PIp ~ 25 mm Hg
Interstitial Hydrostatic Pressure, Pi ~ 0 mm Hg
Interstitial Oncotic Pressure, PIi 1 - 10 mm Hg
Arterial Compliance 1 mL / mm Hg
Venous Compliance 20 mL / mm Hg

STROKE VOLUME = (END DIASTOLIC VOLUME) - (END SYSTOLIC VOLUME)

CARDIAC OUTPUT = (STROKE VOLUME) x (HEART RATE)

PULSE PRESSURE = (SYSTOLIC PRESSURE) - (DIASTOLIC PRESSURE)

MEAN ARTERIAL PRESSURE = (CO) x (TPR) = (HR) x (SV) x (TPR)

RESISTANCE alpha VISCOSITY


General Trends in Circulation:

MEASURING BLOOD PRESSURE / SPHYGMOMANOMETER:

FLOW, VISCOSITY, TURBULENCE, RESISTANCE:

BRUIT: Turbulent flow is detected as a bruit which can be heard by the stethoscope.

STANDING BLOOD PRESSURE: Mean Arterial Pressure goes down when standing, because of lower venous return.

BLOOD PRESSURE AND THE RESPIRATORY CYCLE:

CENTRAL VENOUS PRESSURE: The pressure going into the right atrium.

PRESSURES IN PERIPHERY -vs- AORTA:

COMPLIANCE: The degree to which a pressure change leads to a corresponding change in volume. Or, Compliance = DeltaV / DeltaP, or the slope of a pressure-volume curve.

MODULATION OF MEAN ARTERIAL PRESSURE: Under a lot of circumstances, it doesn't change, even when stroke volume and/or pulse pressures do change.


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MYOCARDIAL PERFORMANCE

General Effects of Autonomic Control on Heart:

PRELOAD: The diastolic filling pressure, or end-diastolic volume.

AFTERLOAD: Ventricular systolic pressure, which is equal to arterial systolic pressure under normal circumstances.

LAPLACE'S LAW: The stress on the ventricular wall is proportional to the Ventricular Pressure x Ventricular Radius, where the size of the ventricle is determined by stretching, i.e. by ventricular volume.

STARLING'S LAW OF THE HEART: Within limits, increases in end-diastolic volume result in a corresponding increase in stroke volume. Most simplified, within limits, the volume that comes into the heart goes back out.

PRESSURE-VOLUME LOOP: P/V graph, with both diastolic and systolic lines plotted on it. You use this graph to plot the pressure and volume at all points in the cardiac cycle.

VENTRICULAR FUNCTION CURVE: A comparison of End-Diastolic Volume (or Pressure or Fiber Length) and Stroke Volume (or Stroke Work). The curve is essentially a line that levels off at high values. It is a way of expressing Starling's Law.

EFFECT OF PRELOAD ON STROKE-WORK:

EFFECT OF AFTERLOAD ON STROKE VOLUME: A higher afterload ------> Higher systolic pressure must be developed ------> Higher end-systolic volume to achieve that pressure, but the end-diastolic volume remains the same ------> lower stroke volume.

AUTOREGULATION OF AFTERLOAD: Due to heterometric autoregulation, within limits, stroke volume will be maintained even in face of a higher blood pressure, but it takes a few beats for the mechanism to kick in.

TOTAL RESERVE: The total stored capacity the heart has to do extra stroke work. It is equal to Starling Reserve + Inotropic Reserve + Heart-Rate Reserve.

INOTROPIC STATE: It's the contractile force in the muscle, at any particular fiber-length. That is the same as the Ca+2 concentration in the sarcomeres.

HEART-RATE AND STROKE VOLUME: Heart rate extremes lead to lower stroke volume.


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VALVULAR DYSFUNCTION

MITRAL INSUFFICIENCY: Insufficiency means the valve can't stay completely closed, so it is leaky. Mitral Insufficiency causes fluid to reflux into the Left Atrium with each systole, leading to a chronically high end-diastolic volume ------> left-ventricular hypertrophy.

MITRAL STENOSIS: Leads to lower filling of the left atrium, as the system backs up. This leads to overload of blood in the pulmonary system.

AORTIC INSUFFICIENCY: Regurgitation back into left-ventricle, on each systole, leads to severe left-ventricular hypertrophy (when the insufficiency is severe).

AORTIC STENOSIS: Very common in old people.

THE RIGHT HEART: Tricuspid and Pulmonic Valve problems are similar to those found in the left heart.

MEASUREMENT OF CARDIAC OUTPUT (Last few pages of handout):


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THE MICROCIRCULATION

CAPILLARY FILTRATION AND RESORPTION: STARLING PRINCIPLE FOR CAPILLARY EXCHANGE:

CAPILLARY PERMEABILITY:

EDEMA: It can occur from a lot of sources, such as no resorption. Consequences of edema:

LYMPHATIC BLOCKAGE: If you block lymphatics, then interstitial fluid along with interstitial proteins will rise ------> increase interstitial oncotic pressure ------> more filtration ------> massive edema.

VASCULAR SMOOTH MUSCLE: Anything that increases intracellular Ca+2 concentration will increase contractility of vascular muscle.

ENDOTHELIAL-DERIVED FACTORS: Nitric Oxide

ENDOTHELIN-1: Vasoconstrictive agent produced by endothelial cells.

LOCAL REGULATION OF BLOOD FLOW:

AUTOREGULATION:

MYOGENIC RESPONSE: Sudden stretch of vascular wall can lead to vasoconstriction to counteract the higher blood-volume. Works in conjunction with the metabolic response to maintain blood flow.

METABOLIC RESPONSES: Works in conjunction with the Myogenic Response to maintain blood flow.

ACTIVE HYPEREMIA: Blood flow changes in proportion to changes in metabolic activity of the organ. Occurs in Skeletal Muscle.

REACTIVE HYPEREMIA: The short-term increase in flow following temporary ischemia to a region.

REGIONAL CIRCULATIONS:


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CARDIOVASCULAR CONTROL MECHANISMS

PARASYMPATHETIC DILATORS: They cause local vascular relaxation. Parasympathetics do not have an important effect on systemic blood pressure.

NOCICEPTORS: Sensory receptors to noxious chemicals or toxins. They also cause local vasodilation.

SYMPATHETIC CONTROL OF VASCULAR MUSCLE: This is the primary short-term mediator of TPR and hence arterial blood pressure.

MODULATION OF SYMPATHETIC NEUROTRANSMITTERS: Cotransmission principles are based on increased likelihood that a dense-core vesicle will fuse with the pre-synaptic membrane. The higher the impulse frequency, the more likely that is to occur.

AUTONOMIC TONE: Heart rate and vascular tone is determined by the relative amounts of sympathetic and parasympathetic continual stimulation.

VASCULAR BEDS: There are six main vascular beds in the body. Going from supine to upright lowers blood pressure, so blood is conserved for the organs that really need it.
VASCULAR BED SNS DENSITY TONE (SUPINE) TONE (UPRIGHT) NOTES
Cerebral Moderate Low Low High metabolic requirements; no change
Coronary Low Low Low No Change
Cutaneous High High High Skin doesn't get much blood either way (not much change)
Skeletal Muscle Moderate Low Moderate +
Splanchnic (Mesenteric) High Low HIGH +++ Blood is pulled away from the GI-System
Renal High Low HIGH +++ Renal blood flow (urine prod.) is cut down.

BARORECEPTOR REFLEX: Short-term modulation of blood-pressure.

Bainbridge Reflex: An exception to baroreceptor regulation, where increased stretching actually increases the inotropic state of the heart, i.e. turns on sympathetics.

CHEMORECEPTORS: They have the exact opposite effect as Baroreceptors.

THE SYMPATHO-ADRENAL SYSTEM: Intermediate and long-term modulation of blood pressure.

ANTI-DIURETIC HORMONE (ADH): It increases Na+-retention in the kidney ------> more water retention ------> high blood volume. It is a "long-term," slow-responding effect.

RENIN-ANGIOTENSIN SYSTEM:

ATRIAL NATRIURETIC PEPTIDE (ANP): It causes increased Na+-Excretion (opposite effect as ADH) in the kidney.

Carotid Sinus Syndrome: Hypersensitivity of the Carotid Sinus, in some old people. Turning their head to the right stimulates parasympathetics and makes them pass out.


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HYPOTENSION AND HYPERTENSION

Classifications of Shock: Shock means low blood volume.

HYPERTENSION: Defined as worse than 140 / 90.

CONGESTIVE HEART FAILURE: From chronic hypertension.

DOG BLOOD PRESSURE DEMO

PROCEDURE MABP HEART RATE TPR SV CO
Acetylcholine DOWN DOWN DOWN UP

Higher preload from longer diastolic filling

UP
Phenylephrine (alpha-agonist) UP

No effect on pulse pressure

DOWN

Baroreceptors compensate for higher TPR

UP

This is the primary effect

SAME

Increased afterload but also preload

DOWN

Because of lower heart rate

Isoproterenol (beta-Agonist) DOWN

From lower TPR

UP

beta1-Receptors

DOWN

Vasodilation beta2-Receptors

UP UP
Epinephrine (beta+alpha Agonist) UP

Systolic increases but not diastolic:

UP

beta1-Receptors on heart

DOWN

beta2 at low doses; maybe some alpha1 at high doses

UP UP
Carotid Massage DOWN

Baroreceptors

DOWN

Baroreceptors

DOWN DOWN DOWN
Carotid Occlusion UP

Inhibition of Baroreceptors

No change in pulse pressure

UP

Inhibition of Baroreceptors

UP

Because Diastolic Pressure went up

SAME UP
Nitroglycerin (NO) DOWN SAME

Or slightly up

DOWN UP

From higher EDV

UP

RIGHT VAGAL STIMULATION: Acts primarily on the SA-Node, hence it will cause a decrease (or arrest) of heart-beat.

LEFT VAGAL STIMULATION: Acts primarily on the AV-Node, causing an atrioventricular heart-block when stimulated.


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Copyright 1999, Scott Goodman, all rights reserved