Importance of Venous Congestion for Worsening of Renal Function in Advanced Decompensated Heart Failure

The Bezold-Jarisch reflex revisited: Clinical implications of inhibitory reflexes originating in the heart

Role of cardiac vagal C-fibers in cardiovascular control.

The sections in this article are:


1
Techniques
1.1
Carotid Sinus Massage

1.2
Electrical Stimulation of Carotid Sinus Nerves

1.3
Section or Anesthesia of Carotid Sinus Nerves and Vagi

1.4
Occlusion of Common Carotid Arteries

1.5
Neck Chamber

1.6
Vasoactive Drugs

1.7
Nonselective Techniques




2
Arterial Baroreceptor Control of Heart Rate
2.1
Autonomic Mediation

2.2
Other Properties

2.3
Relationship to Base-Line R-R Interval

2.4
Relationship to Respiratory Cycle




3
Arterial Baroreceptor Control of Atrioventricular Conduction and Ventricles

4
Carotid Baroreceptor Control of Blood Pressure

5
Carotid Baroreceptor Influence on Cardiac Output and Total Peripheral Resistance

6
Arterial Baroreceptor Control of Regional Circulations

7
Arterial Baroreceptor Control of Veins

8
Set Point of Carotid Baroreflex

9
Aortic Baroreflexes

10
Factors That Modify Arterial Baroreceptor Control of Circulation
10.1
Age

10.2
Exercise

10.3
Mental Stress

10.4
Sleep

10.5
Anesthesia

10.6
Central Blood Volume and Posture




11
Pathological States
11.1
Hypertension

11.2
Heart Disease

11.3
Carotid Sinus Syndrome

11.4
Other Pathological Conditions




12
Modification of Arterial Baroreflexes by Drugs
12.1
β-Adrenergic Antagonists

12.2
Cardiac Glycosides

12.3
Antihypertensive Drugs

Arterial Baroreflexes in Humans

Cardiac dysfunction in animals has been associated with impairment of arterial and cardiopulmonary baroreflex control of the circulation. Chronic heart failure in human beings is associated with neurohumoral excitation, which could result in part from impairment in the inhibitory influence of baroreflexes. We postulated that (1) patients with left ventricular dysfunction (LVD) have impaired baroreflex modulation of vascular resistance and (2) administration of a digitalis glycoside would immediately restore baroreflex sensitivity. Eleven patients with LVD (NYHA class, 2.8 +/- 0.2, mean +/- SEM; baseline left ventricular ejection fraction, 18 +/- 2%; cardiac index, 2.4 +/- 0.21/min/m2; and pulmonary capillary wedge pressure, 26.0 +/- 3.2 mm Hg) were compared with 17 normal control subjects. We measured forearm vasoconstrictor responses to simulated orthostatic stress with use of lower body negative pressure (LBNP) at -10 and -40 mm Hg to unload cardiopulmonary and arterial baroreceptors. Baseline forearm vascular resistance (FVR) was higher in patients with LVD than in normal subjects: FVRLVD, 68.8 +/- 15.3 U; FVRN, 23.2 +/- 2.1 U (p less than .001). During unloading of baroreceptors with LBNP -10 mm Hg, normal subjects developed vasoconstriction (delta VRN at LBNP -10 mm Hg, +5.7 +/- 1.6 U) but patients with LVD failed to have vasoconstriction and tended to develop vasodilation (delta FVRLVD at LBNP -10 mm Hg, -8.6 +/- 8.5 U) (p = .05, normals vs patients with LVD at LBNP -10 mm Hg). A more marked disparity in response was seen during unloading of baroreceptors of LBNP -40 mm Hg: delta FVRN at LBNP -40 mm Hg, +16.6 +/- 1.5 U; delta FVRLVD at LBNP -40 mm Hg, -10.3 +/- 9.6 U (p less than .001, normals vs patients with LVD). Despite high baseline values for FVR, patients with LVD developed vasoconstriction during intra-arterial infusions of norepinephrine, thereby excluding a nonspecific depression of vascular reactivity as the mechanism for abnormal responses to LBNP in patients with LVD. We also studied the short-term effects of administration of a digitalis glycoside, ouabain 0.0075 mg/kg (seven patients) or lanatoside C (Cedilanid-D) 0.02 mg/kg (three patients), on baroreflex-mediated vasoconstrictor responses to LBNP in the patients with LVD. Digitalis glycoside reduced baseline FVR from 71.8 +/- 16.6 to 48.6 +/- 12.0 U (p less than .02). Responses to LBNP tended to be normalized after administration of digitalis glycoside: delta FVR during LBNP -40 mm Hg, -11.1 +/- 10.5 U before and +7.8 +/- 5.6 U after the drug (p less than .05).(ABSTRACT TRUNCATED AT 400 WORDS)

Selective impairment of baroreflex-mediated vasoconstrictor responses in patients with ventricular dysfunction.

In a study of the effects of heart failure on the responses of cardiac receptors, ten dogs were subjected to tricuspid avulsion and pulmonary artery stenosis. One case of spontaneous heart failure was included in the series, and the electrical spike responses of atrial receptors to progressive changes in atrial stretch induced by infusion and hemorrhage were contrasted with those in normal control dogs. In the control dogs, the number of spikes per cycle increased very sharply with moderate, i.e., 5-10 cm H2O, venous pressure increments before reaching a maximum at 20 cm H2O. In the experimental dogs, the firing rate failed to increase to the same extent despite large increases in pressure. The resulting sets of curves exhibited a sharp dichotomy. This evidence for the impaired response of elements of the subendocardial receptor network is compatible with a decrease in the sensitivity of feedback mechanisms responsible for the regulation of sodium and water metabolism.

Purshotim D. Gupta

Papers

Impaired Atrial Receptor Responses in Dogs with Heart Failure Due to Tricuspid Insufficiency and Pulmonary Artery Stenosis