Fatal Pressure Over Neck by Hanging
Sudhir K. Gupta in Forensic Pathology of Asphyxial Deaths, 2022
Stage of terminal agonal respiration: These are irregular and disorganized movements of respiration seen in the agonal period. There are respiratory movements during this phase, but these are not synchronized. The duration of this stage is variable and lasts for approximately 1–4 minutes in most cases. The muscles of neck become rigid during this phase.
Pathophysiology and Management of Shock
Anthony R. Mundy, John M. Fitzpatrick, David E. Neal, Nicholas J. R. George in The Scientific Basis of Urology, 2010
The assessment begins with an evaluation of respiratory function and, in particular, the quality of the airway and breathing. Four broad situations can usually be recognized by (i) respiratory arrest, (ii) agonal respiration, (iii) abnormal breathing, and (iv) normal breathing. Tachypnea is an early and useful sign of clinical deterioration (21) and, in patients with shock, may reflect acidosis (tissue hypoperfusion, renal dysfunction) or increased carbon dioxide production associated with the hypermetabolism of sepsis. More recently, it has been shown that sepsis (22) induces early contractile failure in the diaphragm, a fact that may explain ventilatory failure in patients with an extrapulmonary source of sepsis. In adults, respiratory arrest is almost always secondary to cardiac arrest, the management of which is beyond the scope of this chapter. Agonal respiration is usually easily recognized as intermittent stertorous and labored respiration accompanied by marked impairment of neurological function. Assessment using the Glasgow scale is likely to reveal a patient whose eyes open to pain (2) or not at all (1), who is able to make incomprehensible sounds (2), and who either localizes (5) or withdraws from a painful stimulus. This peri-arrest situation requires immediate attention, with urgent tracheal intubation and mechanical ventilation by members of the ICU team. In the meantime, having established vascular access and initiated fluid resuscitation, further examination of the patient is likely to provide clues as to the underlying problem. Warm peripheries with a brisk capillary refill are typical of systemic inflammation, and in some patients gentle pressure on the nail-bed elicits the capillary pulsation of Quincke’s sign. Otherwise, cool peripheries with a prolonged capillary would be expected. Most patients in shock are likely to have a tachycardia up to 150/min, with a bounding pulse being typical of systemic inflammation, and a weak thready pulse indicating other types of shock.
Brugada syndrome and the story of Dave
Published in Neuropsychological Rehabilitation, 2018
Samira Kashinath Dhamapurkar, Barbara A Wilson, Anita Rose, Gerhard Florschutz
There are several abnormal ECG patterns that identify BrS including a heart block affecting the right ventricle so that it is not directly activated by impulses travelling through the right bundle branch (known as the right bundle branch block). ST-segment elevations noted in leads v1–v3, prolonged PR and negative T wave may also indicate BrS (Brugada, 2016). This segment is part of the ECG. An ST segment elevation myocardial infarction (STEMI) is the name for one type of heart attack that arises from an acute interruption of blood supply to a part of the heart. Initially, it was believed that people with BrS had a structurally normal heart but this has been challenged (Frustaci et al., 2005) and the syndrome can also occur as a consequence of subtle structural changes in the right ventricular outflow tract (Antzelevitch, Brugada, Brugada, & Brugada, 2005; Nademanee et al., 2011). Other terms for this syndrome include sudden unexplained death syndrome; sudden unexplained nocturnal death syndrome and sudden arrhythmic death syndrome (Nademanee et al., 1997; Vatta et al., 2002). Symptoms vary from palpitations and giddiness to recurrent fainting, nocturnal agonal respiration (breathing with short, sporadic gasps) and sudden cardiac death (Antzelevitch & Patocskai, 2016; Wilde et al., 2002). The condition is accountable for 4% of all sudden deaths and 20% of sudden deaths reported to be in those without structural heart disease (Vohra & Rajagopalan, 2015). A family history is present in about 20 to 30% of patients.
Recent advances in the treatment of Brugada syndrome
Published in Expert Review of Cardiovascular Therapy, 2018
Mariana Argenziano, Charles Antzelevitch
Spontaneous Type 1 BrS ECGHistory of cardiac events or syncope likely due to VT/VF [25,31]Aborted sudden cardiac deathDocumented VT/VFNocturnal agonal respirationLate potentials on epicardial bipolar electrogram or SAECG [55,56]T wave amplitude variability [57]Short ventricular refractory period (VRP < 200 ms) [58]Fragmented QRS [58,59]Prolonged QRS duration [60]ER pattern in the inferolateral leads [47,48].High daily fluctuation of ECG and SAECG parameters [61]
Brugada syndrome
Published in Acta Cardiologica, 2021
Haarika Korlipara, Giridhar Korlipara, Srinivas Pentyala
The 2013 diagnostic criteria for BrS states that BrS is exclusively diagnosed in patients with a spontaneous or drug-induced Type-1 ECG Brugada pattern, which is a coved-type ST-segment elevation in one or more of the right precordial leads. It can also be diagnosed in patients with a Type-2 or Type-3 ST-segment elevation in 20]. Prior to 2013, guidelines also required at least one of six additional clinical features (Table 2) to make a definitive diagnosis including documented VF or VT, family history of SCD at <45 years, coved-type ECG in family members, inducibility of VT with programmed electrical stimulation, syncope, or nocturnal agonal respiration [7,20]. Despite these clinical features not being included in current diagnostic criteria, several experts have suggested that either symptoms (documented VT/VF, syncope, cardiac arrest, agonal nocturnal respiration) or a positive family history be included for a more definitive diagnosis [1,10].