416
Y. A. Abdulhameed et al.
As demonstrated in earlier studies on malarial microvascular function
[18, 19, 45], it was observed that febrile malaria resulted in a significantly increased
respiratory rate and instantaneous heart frequency, compared to healthy subjects.
Skin temperature was significantly higher in malaria. Skin temperature is believed
to be a determining factor of respiratory rate, and of heart rate [10]. This increase in
instantaneous heart frequency alongside skin temperature in malarial subjects may
perhaps result in a mixture of vasodilation, resulting in hypovolaemia, and high
metabolic rate due to pyrexia. It is worth noting that a significant increase in skin
temperature also leads to more vasodilation, and lowers diastolic and systolic blood
pressure as observed in the malaria patients. This decrease in blood pressures of
malarial patients demonstrates significant effects of the disease on both the heart’s
pumping function and the systemic resistance. The striking reduction in the diastolic
pressure may perhaps be associated with the tachycardia observed in malaria.
Hematological examination showed a decrease of PCV in malaria. This is probably
due to the compromised red blood cell deformation, and ineffective erythropoiesis
within malarial vasculature [2, 42]. In terms of cardiovascular dynamics, malaria
resulted in significantly reduced blood flow spectral power in the frequency interval
associated with cardiac and myogenic activity. This effect is probably associated
with the compromised delivery of oxygen and nutrients observed in malaria [4, 7].
Furthermore, the lactic acidosis in the malarial state is exacerbated by inadequate
removal of metabolic waste products, resulting from increased production of lactic
acid by the parasites as well as reduced clearance by the liver [11].
It has also been reported that many treatments fail due to the reduced oxygen delivery in malaria, resulting in metabolic acidosis (through stimulation by cytokines),
leading in turn to respiratory distress [40]. Significantly higher normalised spectral
power was observed in the blood flow frequency intervals related to neurogenic (IV)
and NO-dependent endothelial (V) activity in febrile malaria, compared to healthy
non-malaria (Fig. 26.1a, b). However, no such effects were found in the same frequency intervals for non-febrile malaria. This might imply that these physiological
processes are not markedly affected in non-febrile malaria due the absence of fever.
Coherence provides additional insight into the changes that occur with malaria
in the modulation of the heart rate by the respiratory frequency. The significant
attenuation of cardiac interval coherence between IHF (derived from the ECG) and
breathing in malaria implies an impairment in respiratory sinus arrhythmia (RSA),
given that the high frequency component in IHF reflects the influence of breathing
on the heart rate [12, 21, 44], an inference that is supported by an additional finding:
significantly decreased blood flow coherence in the frequency interval associated
with cardiac activity. In addition, the results may also signify destruction of both the
sympathetic and parasympathetic modulations that critically influence the oscillations in heart beat intervals. These modulations are widely known to contribute to
the oscillatory components manifesting in IHF [6, 25, 27, 35]. Hence this finding
may perhaps explain the alteration we observed in the power spectra of skin blood
flow cardiac oscillations.
As mentioned above in the introduction, there are drawbacks associated with
existing methods for assessing and diagnosing malaria. These have made the quest
Y. A. Abdulhameed et al.
As demonstrated in earlier studies on malarial microvascular function
[18, 19, 45], it was observed that febrile malaria resulted in a significantly increased
respiratory rate and instantaneous heart frequency, compared to healthy subjects.
Skin temperature was significantly higher in malaria. Skin temperature is believed
to be a determining factor of respiratory rate, and of heart rate [10]. This increase in
instantaneous heart frequency alongside skin temperature in malarial subjects may
perhaps result in a mixture of vasodilation, resulting in hypovolaemia, and high
metabolic rate due to pyrexia. It is worth noting that a significant increase in skin
temperature also leads to more vasodilation, and lowers diastolic and systolic blood
pressure as observed in the malaria patients. This decrease in blood pressures of
malarial patients demonstrates significant effects of the disease on both the heart’s
pumping function and the systemic resistance. The striking reduction in the diastolic
pressure may perhaps be associated with the tachycardia observed in malaria.
Hematological examination showed a decrease of PCV in malaria. This is probably
due to the compromised red blood cell deformation, and ineffective erythropoiesis
within malarial vasculature [2, 42]. In terms of cardiovascular dynamics, malaria
resulted in significantly reduced blood flow spectral power in the frequency interval
associated with cardiac and myogenic activity. This effect is probably associated
with the compromised delivery of oxygen and nutrients observed in malaria [4, 7].
Furthermore, the lactic acidosis in the malarial state is exacerbated by inadequate
removal of metabolic waste products, resulting from increased production of lactic
acid by the parasites as well as reduced clearance by the liver [11].
It has also been reported that many treatments fail due to the reduced oxygen delivery in malaria, resulting in metabolic acidosis (through stimulation by cytokines),
leading in turn to respiratory distress [40]. Significantly higher normalised spectral
power was observed in the blood flow frequency intervals related to neurogenic (IV)
and NO-dependent endothelial (V) activity in febrile malaria, compared to healthy
non-malaria (Fig. 26.1a, b). However, no such effects were found in the same frequency intervals for non-febrile malaria. This might imply that these physiological
processes are not markedly affected in non-febrile malaria due the absence of fever.
Coherence provides additional insight into the changes that occur with malaria
in the modulation of the heart rate by the respiratory frequency. The significant
attenuation of cardiac interval coherence between IHF (derived from the ECG) and
breathing in malaria implies an impairment in respiratory sinus arrhythmia (RSA),
given that the high frequency component in IHF reflects the influence of breathing
on the heart rate [12, 21, 44], an inference that is supported by an additional finding:
significantly decreased blood flow coherence in the frequency interval associated
with cardiac activity. In addition, the results may also signify destruction of both the
sympathetic and parasympathetic modulations that critically influence the oscillations in heart beat intervals. These modulations are widely known to contribute to
the oscillatory components manifesting in IHF [6, 25, 27, 35]. Hence this finding
may perhaps explain the alteration we observed in the power spectra of skin blood
flow cardiac oscillations.
As mentioned above in the introduction, there are drawbacks associated with
existing methods for assessing and diagnosing malaria. These have made the quest