Central role of left atrial dynamics in limiting exercise cardiac output increase and oxygen uptake in heart failure: insights by cardiopulmonary imaging

2020 ◽  
Vol 22 (7) ◽  
pp. 1186-1198 ◽  
Author(s):  
Tadafumi Sugimoto ◽  
Marta Barletta ◽  
Francesco Bandera ◽  
Greta Generati ◽  
Eleonora Alfonzetti ◽  
...  
Author(s):  
Alessandro Malagoli ◽  
Luca Rossi ◽  
Alessia Zanni ◽  
Concetta Sticozzi ◽  
Massimo Francesco Piepoli ◽  
...  

1999 ◽  
Vol 83 (11) ◽  
pp. 1573-1576 ◽  
Author(s):  
Akihiro Matsumoto ◽  
Haruki Itoh ◽  
Ikuo Yokoyama ◽  
Teruhiko Aoyagi ◽  
Seiryo Sugiura ◽  
...  

1958 ◽  
Vol 192 (2) ◽  
pp. 331-334 ◽  
Author(s):  
Henry Badeer ◽  
Avedis Khachadurian

The relative influence of bradycardia and of cold per se on the oxygen consumption and mechanical efficiency of the dog heart was investigated in the modified heart-lung preparation (11 experiments). Myocardial oxygen uptake was determined under constant arterial pressure and cardiac output in a) normothermia, b) normothermia with bradycardia induced by a cold thermode on the pacemaker, and c) hypothermia producing the same bradycardia as in ( b). At 36.8°C with a rate of 153 beats/min. the efficiency was 8.5% ± 0.3(S.E.), whereas with a rate of 110/min. efficiency was 9.1% ± 0.4(S.E.), a change that is statistically not significant. In hypothermia of 31.5°C with a rate of 110/min. the efficiency was 10.8% ± 0.3(S.E.), an increase that is statistically significant. Performing the same stroke work the hypothermic myocardium consumed less oxygen than the normothermic. It is concluded that the metabolic effect of cold per se is the chief factor responsible for increasing the mechanical efficiency of the hypothermic heart when pressure-volume work is kept constant.


Heart ◽  
2019 ◽  
Vol 105 (20) ◽  
pp. 1552-1558 ◽  
Author(s):  
Christopher M Hearon Jr ◽  
Satyam Sarma ◽  
Katrin A Dias ◽  
Michinari Hieda ◽  
Benjamin D Levine

ObjectiveThe time needed to increase oxygen utilisation to meet metabolic demand (V̇O2 kinetics) is impaired in heart failure (HF) with reduced ejection fraction and is an independent risk factor for HF mortality. It is not known if V̇O2 kinetics are slowed in HF with preserved ejection fraction (HFpEF). We tested the hypothesis that V̇O2 kinetics are slowed during submaximal exercise in HFpEF and that slower V̇O2 kinetics are related to impaired peripheral oxygen extraction.MethodsEighteen HFpEF patients (68±7 years, 10 women) and 18 healthy controls (69±6 years, 10 women) completed submaximal and peak exercise testing. Cardiac output (acetylene rebreathing, Q̇c), ventilatory oxygen uptake (V̇O2, Douglas bags) and arterial-venous O2 difference (a-vO2 difference) derived from Q̇c and V̇O2 were assessed during exercise. Breath-by-breath O2 uptake was measured continuously throughout submaximal exercise, and V̇O2 kinetics was quantified as mean response time (MRT).ResultsHFpEF patients had markedly slowed V̇O2 kinetics during submaximal exercise (MRT: control: 40.1±14.2, HFpEF: 65.4±27.7 s; p<0.002), despite no relative impairment in submaximal cardiac output (Q̇c: control: 8.6±1.7, HFpEF: 9.7±2.2 L/min; p=0.79). When stratified by MRT, HFpEF with an MRT ≥60 s demonstrated elevated Q̇c, and impaired peripheral oxygen extraction that was apparent during submaximal exercise compared with HFpEF with a MRT <60 s (submaximal a-vO2 difference: MRT <60 s: 9.7±2.1, MRT ≥60 s: 7.9±1.1 mL/100 mL; p=0.03).ConclusionHFpEF patients have slowed V̇O2 kinetics that are related to impaired peripheral oxygen utilisation. MRT can identify HFpEF patients with peripheral limitations to submaximal exercise capacity and may be a target for therapeutic intervention.


1997 ◽  
Vol 82 (3) ◽  
pp. 908-912 ◽  
Author(s):  
William W. Stringer ◽  
James E. Hansen ◽  
K. Wasserman

Stringer, William W., James E. Hansen, and K. Wasserman.Cardiac output estimated noninvasively from oxygen uptake during exercise. J. Appl. Physiol. 82(3): 908–912, 1997.—Because gas-exchange measurements during cardiopulmonary exercise testing allow noninvasive measurement of oxygen uptake (V˙o 2), which is equal to cardiac output (CO) × arteriovenous oxygen content difference [C(a-[Formula: see text])], CO and stroke volume could theoretically be estimated if the C(a-[Formula: see text]) increased in a predictable fashion as a function of %maximumV˙o 2(V˙o 2 max) during exercise. To investigate the behavior of C(a-[Formula: see text]) during progressively increasing ramp pattern cycle ergometry exercise, 5 healthy subjects performed 10 studies to exhaustion while arterial and mixed venous blood were sampled. Samples were analyzed for blood gases (pH, [Formula: see text],[Formula: see text]) and oxyhemoglobin and hemoglobin concentration with a CO-oximeter. The C(a-[Formula: see text]) (ml/100 ml) could be estimated with a linear regression [C(a-[Formula: see text]) = 5.72 + 0.105 × %V˙o 2 max; r = 0.94]. The CO estimated from the C(a-[Formula: see text]) by using the above linear regression was well correlated with the CO determined by the direct Fick method ( r = 0.96). The coefficient of variation of the estimated CO was small (7–9%) between the lactic acidosis threshold and peakV˙o 2. The behavior of C(a-[Formula: see text]), as related to peakV˙o 2, was similar regardless of cardiac function compared with similar measurements from studies in the literature performed in normal and congestive heart failure patients. In summary, CO and stroke volume can be estimated during progressive work rate exercise testing from measuredV˙o 2 (in normal subjects and patients with congestive heart failure), and the resultant linear regression equation provides a good estimate of C(a-[Formula: see text]).


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