Station 3: Cardiology
Saira Ghafur, Parminder K Judge, Richard Kitchen, Samuel Blows, Fiona Moss in The MRCP PACES Handbook, 2017
This patient has mixed aortic valve disease with a predominant stenotic lesion. There is a slow-rising radial pulse and a normal blood pressure, but there are no stigmata of infective endocarditis. The apex beat is in the fifth intercostal space, midclavicular line. The heart sounds are normal, but there is a harsh ejection systolic murmur radiating to the carotids and an end-diastolic murmur heard loudest at the left sternal edge in forced expiration. When suspecting mixed aortic valve disease, it is crucial to look for and present the above features. Be sure to ask about the patient’s blood pressure. Where possible, decide on the predominant lesion, as the clinical manifestation usually follows that.
Cardiovascular
Ian Mann, Alastair Noyce in The Finalist’s Guide to Passing the OSCE, 2021
An example of your presentation may be: This well-looking, 70-year-old gentleman is sitting comfortably at rest. There are no paraphernalia around the bed indicating why this gentleman may be in hospital. There are no peripheral stigmata of cardiovascular disease. His pulse rate is 68 beats per minute and regular. The pulse is of low volume and appears to be slow rising. The blood pressure of 118/95 indicates a narrow pulse pressure. On inspection of the chest, I can see a well-healed sternotomy scar. There is also a scar on the medial aspect of the right leg, indicating venous harvesting. The apex beat is in the 5th intercostal space, mid-clavicular line. There is a loud ejection systolic murmur best heard in the aortic area in expiration that radiates to the carotids. The lung bases are clear, and there is no peripheral oedema. These findings are consistent with a gentleman who has undergone a coronary artery bypass graft and who also has a murmur of aortic stenosis. There are no signs of heart failure or endocarditis.
The cardiac valves
Swati Gupta, Alexandra Marsh, David Dunleavy, Kevin Channer in Cardiology and the Cardiovascular System on the move, 2015
SignsSigns of pulmonary congestion appear before eventual RV failure.Right heart failure may cause RV heave and elevated JVP.Malar flush is a dusky appearance over the cheeks associated with high pressures in the pulmonary vasculature.An irregular pulse due to atrial fibrillation.Apex beat is not usually displaced but may be tapping in nature.
AL amyloidosis presenting as inflammatory polyarthritis: a case report
Published in Modern Rheumatology Case Reports, 2021
Muhammad Shoaib Momen Majumder, Shamim Ahmed, Md. Nahiduzzamane Shazzad, Mohammad Mamun Khan, Syed Atiqul Haq, Mohammed Kamal, Md. Sohrab Alam, Johannes J. Rasker
On physical examination, the patient was found moderately pale looking, all vital signs were normal. His pulse rate was 80/min, regular with normal volume, blood pressure 120/70 mm of Hg, respiratory rate 18/min, there was no lower limb edoema or lymphadenopathy. There were papules and plaques over the periocular, perinasal, and perioral area, macroglossia with indentation of the tongue, pinch purpura in the oral cavity (Figures 1 and 2). Nail dystrophy was present in some of his fingers. There was no organomegaly, apex beat was situated in the 5th intercostal space along the midclavicular line. Musculoskeletal examination revealed localised, mildly tender, soft tissue swelling of variable size and shape (largest one was 5Х3 cm, Figure 3 over the wrist) over flexor and extensor aspects of wrists and back of knees. Both shoulders were swollen (shoulder pad sign positive, Figure 4), tenderness was present over MCPs, wrists, elbows, and shoulders. He had an antalgic gait. Active and passive movements of wrists and shoulders were painful and restricted. Flexion contracture (30 degrees) was present in the left elbow.
Heart failure in congenital heart disease: management options and clinical challenges
Published in Expert Review of Cardiovascular Therapy, 2020
Elsbeth M. Leusveld, Robert M. Kauling, Laurie W. Geenen, Jolien W. Roos-Hesselink
Congenital conditions with a predominantly right-sided phenotype and heart failure often exhibit signs of systemic venous congestion, such as peripheral edema (ankles, lower legs, and abdomen), raised jugular venous pressure, hepatic and splenic enlargement, and pleural effusion. Conditions associated with right-sided congestion include left-to-right shunts (e.g. atrial septal defects), Ebstein’s anomaly with severe tricuspid valve regurgitation and Tetralogy of Fallot (ToF) with abnormalities of the pulmonary valve, arteries, and the right ventricular outflow tract. Importantly, patients with predominantly right-sided abnormalities such as ToF may also develop left ventricular dysfunction, which may in turn cause symptoms [32]. Signs of left-sided causes of heart failure include crackles on lung auscultation, third heart sound, and a displaced apex beat. It is important to realize that failure of the right ventricle and tricuspid valve in systemic right ventricles (e.g. ccTGA or after atrial switch surgery) leads to symptoms and signs of pulmonary congestion. In patients after Fontan procedure with a univentricular heart systemic congestion often predominates, related to elevated pressures in the Fontan circulation.
Evolution of out-of-hospital emergency cardiac care: Heart attack therapy for a retired president helped modernize American emergency medical services
Published in Baylor University Medical Center Proceedings, 2019
Nathaniel P. Rogers, Richard S. Crampton
Our wee hours, predawn team included C-ARS EMTs Lynwood McCauley and John R. Miles, also a medical student; as well as Dr. Robert Harris; Deaton Smith, a third-year medical student; and myself. We found President Johnson sweating profusely with chest pain radiating to the left shoulder and neck. When chest pain had awakened him at 2:30 am, he took an antacid and six sublingual nitroglycerin tablets without relief. Examination disclosed a blood pressure of 165/90 mm Hg, no jugular vein distention, a regular heart rhythm with premature beats, a forceful apex beat, a loud fourth heart sound, a single second sound, no murmur, no friction rub, and rales at both lung bases. He quickly responded to our intravenous morphine 4 mg injection and oxygen by mask. Next, intravenous lidocaine 100 mg abolished his R on T early coupled ventricular premature beats. His 12-lead ECG showed anterior Q waves with ST segment elevation indicative of acute anterior myocardial infarction (Figure 2). On the spot, LBJ’s wife Lady Bird wisely phoned Dr. J. Willis Hurst of Atlanta so that we could discuss LBJ’s cardiac history. Hurst had cared for LBJ during his 1955 heart attack and recalled it as inferior infarction. Thus, we both realized that LBJ had a new site of acute infarction.