CV Lecture 3

To maintain a constant level of arterial pressure and blood volume.

Aortic diastolic pressure minus intraventricular pressure.

To counteract a change in a sensed variable.

Diastole.

Negative feedback loops.

It generally involves a region of atherosclerotic lesion.

Blood pressure and blood volume.

18% MI.

The subendocardium.

Fixed obstruction (plaque) in the coronary artery.

Exercise, cold, and stress.

Carotid sinus (junction of external and internal carotid artery) and aortic arch.

14% MI.

Arterial baroreceptors are responsible for detecting changes in blood pressure and initiating the baroreflex to maintain stable blood pressure.

Degradation exceeds growth, outward remodeling, thinning/erosion of cap, more prone to fissure/rupture, thrombosis, and myocardial infarction.

BP = CO x TPR (Cardiac Output x Total Peripheral Resistance).

Myocardial infarction.

Vasodilator reserve.

Soft or vulnerable plaque.

In individuals with hypertension, the baroreflex is reset to a higher pressure, and the reflex tries to maintain this higher pressure even when antihypertensive drugs are given.

4-6 hours after the infarct.

Evokes a pattern of autonomic nervous system (ANS) and/or hormonal changes that reverse the initial change.

Baroreflex sensitivity can be decreased by stiffening of the arterial wall due to disease (e.g., diabetes, hypertension), arteriosclerosis, and aging.

Baroreceptors sense pressure via changes in stretch (distortion) of the arterial wall.

It releases renin/angiotensin.

Intense vasoconstriction in the skin, intermediate vasoconstriction in the kidney, intestine, and skeletal muscle, and least vasoconstriction in the heart and brain.

It is a type of angina caused by vasospasm of a major coronary artery.

It is predictable and resolves with rest.

Baroreceptors convert mechanical (pressure) to electrical (nerve action potentials).

As pressure increases, baroreceptor firing increases.

Right ventricular flow increases with the onset of contraction.

Changes in the set point (e.g., due to disease) can cause a change in blood pressure.

The diastolic interval decreases as heart rate increases.

Yes, baroreflex sensitivity and set point can be altered by disease, aging, drugs, and physiological factors such as exercise.

Negative feedback in cardiovascular regulation involves mechanisms that counteract changes in the body to maintain homeostasis, such as adjusting heart rate and blood vessel diameter in response to blood pressure changes.

It is unpredictable, can occur at rest, and does not respond to rest.

Adequate flow is maintained at rest.

It releases renin/angiotensin.

It increases salt and water retention, blood volume, and renin release, leading to the synthesis of angiotensin II.

Angina.

The set point is where the reflex is most sensitive and will be most stable.

Deposition of lipid beneath the endothelial lining.

Yes, it can occur in angiographically normal arteries.

Baroreceptors.

Sympathetic nervous system activity is increased.

Total coronary flow is the least during systole.

Stretch or distortion of the arterial wall activates the baroreceptors to increase parasympathetic nervous system activity and decrease sympathetic nervous system activity.

S-T segment elevation or depression, and T wave inversion.

Growth promoting and degradative factors.

Approximately 80% of oxygen is extracted in the myocardium.

Reabsorption of fluid increases, leading to an increase in plasma volume.

Coronary flow can meet a 5-6 fold increase in oxygen demand in a normal heart.

They produce vasodilation.

By dilation of terminal arterioles downstream.

Carotid sinus massage distorts the carotid baroreceptors, increases vagal discharge, decreases sympathetic discharge, slows AV node conduction, and can interrupt arrhythmias.

Myocardial blood vessels are compressed during systole due to pressures in the ventricular chambers.

Diffuse substernal crushing, suffocating feeling, tightness, and pain that may radiate to the left arm, face, or back.

The major components of the arterial reflex pathway include arterial baroreceptors, afferent nerves, the medullary cardiovascular center, efferent nerves, and the heart and blood vessels.

The heart and brain, due to dominant local factors.

TPR is increased.

The volume reflex responds to a change in blood volume by adjusting heart rate, blood vessel diameter, and kidney function to counteract the change and maintain stable blood volume.

Metabolic autoregulation is the dominant factor controlling coronary resistance vessels and coronary blood flow.

It may be due to destruction of endothelium and enhanced vasoconstrictor reactivity.

The brain.

A phenomenon where blood flow is diverted away from the ischemic area, worsening the condition.

Venous constriction increases mean circulatory filling pressure (MCFP) and venous return.

It controls venous return, cardiac filling, cardiac function, and cardiac output.

Atrial and venous baroreceptors detect changes in blood volume and send signals to the brain to adjust heart rate, blood vessel diameter, and kidney function to maintain stable blood volume.

Capillary hydrostatic pressure decreases.

It contributes to endothelial cell damage and enhanced constriction/vasospasm.

Growth exceeds degradation, inward remodeling, thick fibrous cap, less prone to fissure/rupture, greater lumen occlusion, and angina.

Baroreflex resetting is the adaptation of baroreceptors to a new pressure, where the baroreceptor reflex will defend pressure around the new set point value.

Arterial baroreceptors detect changes in arterial pressure and send signals to the brain to adjust heart rate and blood vessel diameter to maintain stable blood pressure.

Ischemia of sufficient duration and severity to result in tissue damage.

They are not present in other tissues (high specificity), not normally found in plasma (high sensitivity), released 4-6 hours after infarct, and remain elevated for up to 7-14 days after the initial infarct.

Lactate from glycolysis acts as a vasodilator.

There is a decrease in parasympathetic activity and an increase in sympathetic nervous system activity, leading to an increase in heart rate and cardiac contractility.

Total coronary flow is the greatest during diastole.

Epigastric burning, sweating, dizziness, fatigue, nausea, and dyspnea.

Increased vascular resistance, endothelial cell damage, increased oxidative stress, loss of nitric oxide, and enhanced constriction/vasospasm.

Adenosine acts as a vasodilator.

It can detect multiple infarcts.

Left ventricular flow decreases with the onset of contraction and has a slight rebound during systole.

Left ventricular flow peaks during diastole.

68% MI.

Myocardial ischemia without angina.

The capillary density in the heart is approximately three times that of skeletal muscle.

Baroreceptor activation decreases heart rate, cardiac output, vascular resistance, and blood pressure.

Back pain, jaw pain, dyspnea, nausea, and fatigue.

To critical tissues such as the brain and heart.

Sympathetic nervous system activity is increased.

A local inflammatory response involving inflammatory cells.

They occur around a central lipid core.

The major components of the volume reflex pathway include atrial and venous baroreceptors, afferent nerves, the medullary cardiovascular center, efferent nerves, and the kidneys.

Myocardial oxygen consumption (MVO2) is very high even at rest.

Up to 7-14 days after the initial infarct.

The arterial baroreflex responds to a change in arterial pressure by adjusting heart rate and blood vessel diameter to counteract the change and maintain stable blood pressure.

There is a tight coupling between coronary oxygen demand and coronary blood flow via metabolic autoregulation of terminal arteriole resistance vessels.

A coronary flow reserve (CFR) of less than 2 indicates that the heart is prone to ischemia.

A soft central core overlaid with a stiff fibrous cap.

About 48 hours.

The main mediators are decreased oxygen (pO2), increased CO2 (pCO2), opening of K channels, and adenosine.

BP = CO x TPR (Blood Pressure = Cardiac Output x Total Peripheral Resistance).

CO2 acts as a vasodilator.

There is a loss of nitric oxide.

The pain/feeling is similar to severe angina but the duration is much longer and does not resolve with rest.

They are an index of tissue damage.

4-6 hours after the infarct.

Oxygen acts as a vasoconstrictor everywhere but the lungs.

CPK-MB is more specific for cardiac muscle, released 4-6 hours after infarct, and returns to normal in about 48 hours.