Cheyne-Stokes respiration in congestive heart failure.

Cheyne-Stokes respiration is an abnormal breathing pattern which commonly occurs in patients with decompensated congestive heart failure and neurologic diseases, in whom periods of tachypnea and hyperpnea alternate with periods of apnea. In the majority of these patients, the ventilatory patterns may not be recognized, and the clinical features are generally dominated by the underlying disease process. Cheyne-Stokes respiration may, however, have profound effects on the cardiopulmonary system, causing oxygen desaturation, cardiac arrhythmias, and changes in mental status. Treatment of Cheyne-Stokes respiration in congestive heart failure with supplemental oxygen or nasal continuous positive airway pressure, in addition to conventional therapy, may improve the overall cardiac function and perhaps the patient's prognosis.     

Influence of Cheyne-Stokes respiration on ventricular response to atrial fibrillation in heart failure.

In subjects with sinus rhythm, respiration has a profound effect on heart rate variability (HRV) at high frequencies (HF). Because this HF respiratory arrhythmia is lost in atrial fibrillation (AF), it has been assumed that respiration does not influence the ventricular response. However, previous investigations have not considered the possibility that respiration might influence HRV at lower frequencies. We hypothesized that Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) would entrain HRV at very low frequency (VLF) in AF by modulating atrioventricular (AV) nodal refractory period and concealed conduction. Power spectral analysis of R-wave-to-R-wave (R-R) intervals and respiration during sleep were performed in 13 subjects with AF and CSR-CSA. As anticipated, no modulation of HRV was detected at HF during regular breathing. In contrast, VLF HRV was entrained by CSR-CSA [coherence between respiration and HRV of 0.69 (SD 0.22) at VLF during CSR-CSA vs. 0.20 (SD 0.19) at HF during regular breathing, P < 0.001]. Comparison of R-R intervals during CSR-CSA demonstrated a shorter AV node refractory period during hyperpnea than apnea [minimum R-R of 684 (SD 126) vs. 735 ms (SD 147), P < 0.001] and a lesser degree of concealed conduction [scatter of 178 (SD 56) vs. 246 ms (SD 72), P = 0.001]. We conclude that CSR-CSA entrains the ventricular response to AF, even in the absence of HF respiratory arrhythmia, by inducing rhythmic oscillations in AV node refractoriness and the degree of concealed conduction that may be a function of autonomic modulation of the AV node.     

Models of Cheyne-Stokes respiration with cardiovascular pathologies

Cheyne-Stokes respiration (CSR) is a periodic breathing pattern, characterized by short intervals of very little or no breathing (apnea), each followed by an interval of very heavy breathing (hyperpnea). This work presents a new compartmental model of the human cardio-respiratory system, simulating the factors that determine the concentrations of carbon dioxide in the compartments of the cardiovascular system and the lungs. The parameter set on which a Hopf bifurcation gives birth to stable CSR oscillations has been determined. The model predicts that the onset of CSR oscillations may result from an increase in any of: ventilation-perfusion ratio, feedback control gain, transport delay, left heart volume, lung congestion, or cardiovascular efficiency. The model is employed to investigate the relationship between CSR and serious cardiovascular pathologies, such as congestive heart failure and encephalitis, as well as the effects of acclimatization to higher altitudes. In all cases, the model is consistent with medical observations.     

Hemodynamics, cerebral circulation, and oxygen saturation in Cheyne-Stokes respiration

Franklin, Karl A., Erik Sandström, GöranJohansson, and Eva M. Bålfors. Hemodynamics, cerebralcirculation, and oxygen saturation in Cheyne-Stokes respiration.J. Appl. Physiol. 83(4): 1184-1191, 1997.Because cardiovascular disorders and stroke may induceCheyne-Stokes respiration, our purpose was to study the interactionamong cerebral activity, cerebral circulation, blood pressure, andblood gases during Cheyne-Stokes respiration. Ten patients with heartfailure or a previous stroke were investigated during Cheyne-Stokesrespiration with recordings of daytime polysomnography, cerebral bloodflow velocity, intra-arterial blood pressure, and intra-arterial oxygensaturation with and without oxygen administration. There weresimultaneous changes in wakefulness, cerebral blood flow velocity, andrespiration with accompanying changes in blood pressure and heart rate~10 s later. Cerebral blood flow velocity, blood pressure, and heartrate had a minimum occurrence in apnea and a maximum occurrence duringhyperpnea. The apnea-induced oxygen desaturations were diminishedduring oxygen administration, but the hemodynamic alterationspersisted. Oxygen desaturations were more severe and occurred earlieraccording to intra-arterial measurements than with finger oximetry. Itis not possible to explain Cheyne-Stokes respiration by alterations inblood gases and circulatory time alone. Cheyne-Stokes respiration maybe characterized as a state of phase-linked cyclic changes in cerebral,respiratory, and cardiovascular functions probably generated byvariations in central nervous activity.

     

Respiratory modulation of the autonomic nervous system during Cheyne-Stokes respiration

Cheyne-Stokes respiration (CSR) is associated with increased mortality among patients with heart failure. However, the specific link between CSR and mortality remains unclear. One possibility is that CSR results in excitation of the sympathetic nervous system. This review relates evidence that CSR exerts acute effects on the autonomic nervous system during sleep, and thereby influences a number of cardiovascular phenomena, including heart rate, blood pressure, atrioventricular conduction, and ventricular ectopy. In patients in sinus rhythm, heart rate and blood pressure oscillate during CSR in association with respiratory oscillations, such that both peak heart rate and blood pressure occur during the hyperpneic phase. Inhalation of CO2 abolishes both CSR and the associated oscillations in heart rate and blood pressure. In contrast, O2 inhalation sufficient to eliminate hypoxic dips has no significant effect on CSR, heart rate, or blood pressure. In patients with atrial fibrillation, ventricular rate oscillates in association with CSR despite the absence of within-breath respiratory arrhythmia. The comparison of RR intervals between the apneic and hyperpneic phases of CSR indicates that this breathing disorder exerts its effect on ventricular rate by inducing cyclical changes in atrioventricular node conduction properties. In patients with frequent ventricular premature beats (VPBs), VPBs occur more frequently during the hyperpneic phase than the apneic phase of CSR. VPB frequency is also higher during periods of CSR than during periods of regular breathing, with or without correction of hypoxia. In summary, CSR exerts multiple effects on the cardiovascular system that are likely manifestations of respiratory modulation of autonomic activity. It is speculated that the rhythmic oscillations in autonomic tone brought about by CSR may ultimately contribute to the sympatho-excitation and increased mortality long observed in patients with heart failure and CSR.     

Real-world heart failure management in 10,910 patients with chronic heart failure in the Netherlands

Aims

Data from patient registries give insight into the management of patients with heart failure (HF), but actual data from unselected real-world HF patients are scarce. Therefore, we performed a cross sectional study of current HF care in the period 2013–2016 among more than 10,000 unselected HF patients at HF outpatient clinics in the Netherlands.

Methods

In 34 participating centres, all 10,910 patients with chronic HF treated at cardiology centres were included in the CHECK-HF registry. Of these, most (96%) were managed at a specific HF outpatient clinic. Heart failure was typically diagnosed according to the ESC guidelines 2012, based on signs, symptoms and structural and/or functional cardiac abnormalities. Information on diagnostics, treatment and co-morbidities were recorded, with specific focus on drug therapy and devices. In our cohort, the mean age was 73 years (SD 12) and 60% were male. Frequent co-morbidities reported in the patient records were diabetes mellitus 30%, hypertension 43%, COPD 19%, and renal insufficiency 58%. In 47% of the patients, ischaemia was the origin of HF. In our registry, the prevalence of HF with preserved ejection fraction was 21%.

Conclusion

The CHECK-HF registry will provide insight into the current, real world management of patient with chronic HF, including HF with reduced ejection fraction, preserved ejection fraction and mid-range ejection fraction, that will help define ways to improve quality of care. Drug and device therapy and guideline adherence as well as interactions with age, gender and co-morbidities will receive specific attention.

     

Protein kinetics in stable heart failure patients.

Heart failure (HF) is a slow progressive syndrome characterized by low cardiac output and peripheral metabolic, biochemical, and histological alterations. Protein loss and reduced protein turnover occur with aging, but the consequences of congestive HF (CHF) superimposed on the normal aging response are unknown. This study has two objectives: 1) to determine whether there was a difference between older age-matched controls and those with stable HF (i.e., ischemic pathology) in whole body protein turnover and 2) to determine whether protein metabolism in liver and skeletal muscle protein turnover is impacted by CHF. We measured the whole body protein synthesis rate with a U-(15)N-labeled algal protein hydrolysate in 10 patients with CHF and in 10 age-matched controls. Muscle fractional synthesis rate of lateral vastus muscle was determined with [U-(13)C]alanine on muscle biopsies obtained by a standard percutaneous needle biopsy technique. Fractional synthesis rates of five plasma proteins of hepatic origin (fibrinogen, complement C-3, ceruloplasmin, transferrin, and very low-density lipoprotein apoliprotein B-100) were determined by using (2)H(5)-labeled l-phenylalanine as tracer. Results showed that whole body protein synthesis rate was reduced in CHF patients (3.09 +/- 0.19 vs. 2.25 +/- 0.71 g protein x kg(-1) x day(-1), P < 0.05) as was muscle fractional synthesis rate (3.02 +/- 0.58 vs. 1.33 +/- 0.71%/day, P < 0.05) and very low-density lipoprotein apoliprotein B-100 (265 +/- 25 vs. 197 +/- 16%/day, P < 0.05). CHF patients were hyperinsulinemic (9.6 +/- 3.1 vs. 47.0 +/- 7.8 microU/ml, P < 0.01). The results were compared with those found with bed rest patients. In conclusion, protein turnover is depressed in CHF patients, and both skeletal muscle and liver are impacted. These results are similar to those found with bed rest, which suggests that inactivity is a factor in depressed protein metabolism.     

Left ventricular pacing in patients with congestive heart failure

Cardiac resynchronisation therapy (CRT) using biventricular (BIV) pacing has proved its effectiveness to correct myocardial asynchrony and improve clinical status of patients with severe congestive heart failure (CHF) and widened QRS. Despite a different effect on left ventricular electrical dispersion, left univentricular (LV) pacing is able to achieve the same mechanical synchronisation as BIV pacing in experimental studies and in humans. This results in clinical benefits of LV pacing at mid-term follow-up, with significant improvement in functional class, quality of life and exercise tolerance at the same extent as those observed with BIV stimulation in non randomised studies. Furthermore these benefits are obtained at lesser costs and with conventional dual-chamber devices. However, LV pacing has to be compared to BIV pacing in randomised trials before being definitely considered as a cost-effective alternative to BIV pacing.     

Renal blood flow in heart failure patients during exercise

During exercise, reflex renal vasoconstriction maintains blood pressure and helps in redistributing blood flow to the contracting muscle. Exercise intolerance in heart failure (HF) is thought to involve diminished perfusion in active muscle. We studied the temporal relationship between static handgrip (HG) and renal blood flow velocity (RBV; duplex ultrasound) in 10 HF and in 9 matched controls during 3 muscle contraction paradigms. Fatiguing HG (protocol 1) at 40% of maximum voluntary contraction led to a greater reduction in RBV in HF compared with controls (group main effect: P <0.05). The reduction in RBV early in HG tended to be more prominent during the early phases of protocol 1. Similar RBV was observed in the two groups during post-HG circulatory arrest (isolating muscle metaboreflex). Short bouts (15 s) of HG at graded intensities (protocol 2; engages muscle mechanoreflex and/or central command) led to greater reductions in RBV in HF than controls (P <0.03). Protocol 3, voluntary and involuntary biceps contraction (eliminates central command), led to similar increases in renal vasoconstriction in HF (n=4). Greater reductions in RBV were found in HF than in controls during the early phases of exercise. This effect was not likely due to a metaboreflex or central command. Thus our data suggest that muscle mechanoreflex activity is enhanced in HF and serves to vigorously vasoconstrict the kidney. We believe this compensatory mechanism helps preserve blood flow to exercising muscle in HF.     

Nocturnal oxygen desaturation in patients with congestive heart failure

The aim of our study was to evaluate the modifications of the respiratory pattern during sleeping in patients with congestive heart failure (CHF) by a simple pulse-oxymetry. We studied 10 subjects (8M/2F), mean age 71.4 +/- 12.4 yrs, admitted to sub-intensive cardiological therapy unit, with diagnosis of CHF due to left ventricular insufficiency by ischemic, hypertensive or idiopathic cardiopathy, when in a stable clinical condition. All patients presented arterial blood gas values within normal limits. The ejection fraction of left ventricle showed a mean value of 30.4 +/- 8.2% (range 20%-45%). Nocturnal pulse-oxymetry was performed by pulse-oxymeter (PULSOX 7 Minolta) provided with a digital probe at a sliding speed 24 cm/h. Our data showed that all patients presented nocturnal desaturation episodes (mean oxygen desaturation index 15.7 +/- 18.4). In two patients, we found an "Overlap Syndrome" (obstructive sleep apnoea in presence of cardiopathy). In other patients pulse-oxymetry showed a typical sequence of "fall-rise" basal O2 saturation lasting from 36 to 72 seconds, collected in "wave trains" which were present from 14% to 70% of total sleep time compatible with periodic breathing. In conclusion, our study shows that patients affected by CHF, even if in stable condition and with a PaO2, within normal values, present more or less severe disturbances of nocturnal SaO2, with periodic and regular sequences of SaO2 fall-rise that may be referred to ventilatory troubles such as periodic breathing or Cheyne-Stokes breathing. In these patients the pulse-oxymetry may be considered an efficacious, simple, cheap and well tolerated method.