We performed a systematic review to determine whether the physical examination can reliably assist in the diagnostic approach for patients suspected of having pulmonary hypertension (PH). Using dual extraction, two investigators independently searched PubMed, Ovid MEDLINE, Cochrane Library, and Embase for studies that compared physical examination findings with a right heart catheterization, from inception until July 10, 2021. We obtained data from four studies that evaluated physical examination findings in patients receiving a right heart catheterization to diagnose PH. Pooled diagnostic odds ratios (DOR) were calculated for right ventricular heave, a loud pulmonic component of the second heart sound (P2), jugular venous pressure (JVP) 3 cm above sternal angle, and a palpable P2. Three physical examination findings had DOR that supports the diagnosis of PH: the JVP > 3 cm above the sternal angle (5.90, 95% CI 2.57, 13.57), a loud P2 (2.91, 95% CI 1.38, 6.10), and a right ventricular heave (2.78, 95% CI 1.12, 6.89). The palpable P2 had a DOR less than one and was not able to be conclusive in diagnosing PH. Our systematic review found a small body of evidence supporting the use of physical examination tests in the diagnostic evaluation of pulmonary hypertension. The JVP > 3 cm above the sternal angle was the most accurate physical examination sign for the diagnosis of PH. Larger cohort studies using a combination of tests may shed more light on the role of the physical examination in the diagnosis and early detection of pulmonary hypertension.

A 24-year-old female patient presented to us with progressive dyspnea on exertion for last three year. She was not a known case of rheumatic heart disease. Her physical examination showed regular pulse and her blood pressure was 100/76 mm Hg. Cardiac palpation showed grade 3 parasternal heave and auscultation revelled an accentuated first heart sound, loud P2 and mid-diastolic long rumbling murmur at apex and pansystolic murmur of tricuspid regurgitation at lower left sterna border. Chest X-ray showed evidence of grade 3 pulmonary venous congestion. Transthoracic and transesophageal two-dimensional echocardiography revealed a double-orifice mitral valve of complete bridge type at the leaflet level. Both orifice sizes were unequal, with the anterolateral orifice being smaller than its counterpart. There was moderate subvalvular fusion and both commisures were fused. Color doppler examination showed two separate mitral diastolic flows with mean gradients of 22 mm and 20 mm of Hg, respectively. There was no mitral regurgitation and no left atrial or appendage clot was seen by transesophageal echocardiography. Transseptal puncture was done by the modified fluoroscopic method. Posteromedial orifice was crossed with a 24 mm Inoue balloon and dilated using the stepwise dilation technique. Anterolateral orifice was not crossed by Inuoe balloon after multiple attempts. A TYSHAK (NuMAD Canada Inc.) balloon (16 × 40mm) was taken over the wire and inflated successfully across the anterolateral orifice with the help of transthoracic echocardiography guidance. Mean gradient become 9 and 8 mm across the medial and lateral orifice. Patient was discharged in stable condition after two day. © 2015 Wiley Periodicals, Inc.

Mitral stenosis(MS) detected below the age of 20 years is called juvenile mitral stenosis (JMS). JMS constitute 25-40 % of all cases of isolated mitral stenosis, though overall incidence of rheumatic fever and rheumatic heart disease (RHD) within mixed population is 7.5- 7.8 per thousand. The patient was 5 years old girl hailing from Modhupur, Tangail got herself admitted into CCU Mymensingh Medical College Hospital with the complaints of low grade fever, shortness of breath and also associated with failure to thrive. She was ill looking, mildly anaemic. Precordial examination revealed apex beat was in the left 5th intercostals space, tapping in nature, palpable P(2). There was left parasternal heave. 1st heart sound loud, pulmonary component of the 2nd heart sound was accentuated, opening snap with mid diastolic murmur with pre systolic accentuation. Routine blood examination reveals leucocytosis with raised ESR. C-reactive protein (CRP) and ASO titre were significantly raised. X-ray chest P/A view showing the features of mitral stenosis. Echocardiography showing MS (moderate) with pulmonary hypertension. She was treated with antibiotics and other relevant drugs and discharge with an advice for follow up and take preparation for cardiac intervention.

Contraction of the orbicularis oculi muscle in response to a sudden loud sound (acoustic startle response) and the N1/P2 component of the auditory evoked potential are both attenuated when a brief low-intensity stimulus is presented 30-500 ms before the 'startle-eliciting' stimulus (PPI). Here, we report the effects of the 'atypical' antipsychotic drug quetiapine and the 'conventional' antipsychotic haloperidol on these responses. Sixteen males (aged 19-38 years) participated in four sessions at 7-day intervals, in which they received quetiapine 12.5 mg, quetiapine 25 mg, haloperidol 3 mg and placebo, according to a balanced double-blind design. Electromyographic (EMG) responses of the orbicularis oculi muscle and N1/P2 auditory evoked potentials were recorded in a 20-min session, 2 h after treatment. Subjects received 40 trials in which 1-kHz sounds were presented: (i) 40 ms, 115 dB ('pulse alone' trials) and (ii) 40 ms, 85 dB, followed after 120 ms by 40 ms, 115 dB ('prepulse/pulse' trials). Mean amplitudes of the EMG response and the N1/P2 potential were derived from the pulse-alone trials and, in each case, percentage PPI was calculated. Serum prolactin was measured after each treatment, and autonomic (heart rate, blood pressure, salivation) and psychological (visual analogue self-ratings of mood and alertness, critical flicker fusion frequency) measures were taken before and after each treatment. Quetiapine 12.5 mg and 25 mg significantly reduced the amplitude of the EMG response without altering its inhibition by prepulses; haloperidol had no effect on EMG response amplitude or PPI. Neither drug affected N1/P2 amplitude or PPI of this response. Quetiapine, but not haloperidol, reduced subjective alertness and critical flicker fusion frequency. Haloperidol, but not quetiapine, elevated serum prolactin level. The ability of quetiapine to attenuate the startle response may reflect its sedative action.

Contraction of the orbicularis oculi muscle in response to a sudden loud sound (acoustic startle response) and the N1/P2 component of the auditory evoked potential are both attenuated when a brief low-intensity stimulus is presented 30-500 ms before the 'startle-eliciting' stimulus (prepulse inhibition). Here, we report the effects of the serotonin (5-HT)2 receptor antagonist ketanserin and the D2 dopamine receptor blocking antipsychotic drug haloperidol on these responses. Fifteen males (aged 18-35 years) participated in four sessions at 7-day intervals, in which they received ketanserin 20 mg, ketanserin 40 mg, haloperidol 3 mg and placebo, according to a balanced double-blind design. Electromyographic (EMG) responses of the orbicularis oculi muscle and N1/P2 auditory evoked potentials were recorded in a 20-min session, 3 h after ingestion of haloperidol or 1 h after ingestion of ketanserin. Subjects received 40 trials in which 1-kHz sounds were presented: (i) 40 ms, 115 dB ('pulse alone' trials), and (ii) 40 ms, 85 dB, followed after 120 ms by 40 ms, 115 dB ('prepulse/pulse' trials). Mean amplitudes of the EMG response and the N1/P2 potential were derived from the pulse-alone trials and, in each case, percentage prepulse inhibition was calculated. Serum prolactin was measured after each treatment, and autonomic (heart rate, blood pressure, salivation) and psychological (visual analogue self-ratings of mood and alertness, critical flicker fusion frequency) measures were taken before and after each treatment. Ketanserin 40 mg significantly reduced the amplitude of the EMG response and both doses of ketanserin significantly suppressed prepulse inhibition of the response; haloperidol had no effect on EMG response amplitude or prepulse inhibition. Neither drug affected N1/P2 amplitude or prepulse inhibition of this response. Ketanserin, but not haloperidol, reduced subjective alertness and critical flicker fusion frequency. Haloperidol, but not ketanserin, elevated serum prolactin level. These results confirm that prepulse inhibition of the startle response and of the N1/P2 complex have different pharmacological sensitivities. The ability of ketanserin to attenuate the startle response may reflect its sedative action, as other drugs with sedative properties have also been found to attenuate the startle response in man. The ability of ketanserin to suppress prepulse inhibition of the startle response is consistent with previous evidence for the involvement of 5-HTergic mechanisms in the regulation of prepulse inhibition in man.

Contraction of the orbicularis oculi muscle in response to a sudden loud sound (acoustic startle response) and the N1/P2 component of the auditory evoked potential are both attenuated when a brief low-intensity stimulus is presented 30-500 ms before the 'startle-eliciting' stimulus (prepulse inhibition). Here, we report the effects of the 'conventional' antipsychotic drug haloperidol and the 'atypical' antipsychotic clozapine on these responses. Fifteen males (aged 19-54 years) participated in four sessions at 7-day intervals, in which they received clozapine 3 mg, clozapine 6 mg, haloperidol 3 mg and placebo, according to a balanced double-blind design. Electromyographic (EMG) responses of the orbicularis oculi muscle and N1/P2 auditory evoked potentials were recorded in a 20-min session, 3 h after treatment. Subjects received 40 trials in which 1-kHz sounds were presented: (i) 40 ms, 115 dB ('pulse alone' trials) and (ii) 40 ms, 85 dB, followed after 120 ms by 40 ms, 115 dB ('prepulse/pulse' trials). Mean amplitudes of the EMG response and the N1/P2 potential were derived from the pulse-alone trials and, in each case, percentage prepulse inhibition was calculated. Serum prolactin was measured after each treatment, and autonomic (heart rate, blood pressure, salivation) and psychological (visual analogue self-ratings of mood and alertness, critical flicker fusion frequency) measures were taken before and after each treatment. Clozapine 6 mg significantly reduced the amplitude of the EMG response without altering its inhibition by prepulses. Clozapine 6 mg did not affect the amplitude of the N1/P2 potential, but significantly attenuated prepulse inhibition of that response. Clozapine 3 mg and haloperidol had no significant effect on either response. Clozapine 3 mg and 6 mg, but not haloperidol, reduced subjective alertness and critical flicker fusion frequency. Clozapine 6 mg reduced salivation. Haloperidol, but not clozapine, elevated serum prolactin levels. These results confirm that prepulse inhibition of the startle response and of the N1/P2 complex have different pharmacological sensitivities. The abililty of clozapine to attenuate the startle response may reflect its sedative action. The basis of the abililty of clozapine to suppress prepulse inhibition of the N1/P2 potential remains uncertain.