1 / 19

Case report no . 1 , Department P athological Physiology

Case report no . 1 , Department P athological Physiology. V. Danzig, MD, PhD, 2 nd Dept. Internal Medicine C ardiolog y a nd A ngiolog y Division 1 st Med. F C U NI. Patient history. 78 yr. old male, retiree, worked as mechanical engineer

suzy
Download Presentation

Case report no . 1 , Department P athological Physiology

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Casereport no. 1,Department Pathological Physiology V. Danzig, MD, PhD,2nd Dept. Internal MedicineCardiology andAngiologyDivision 1st Med.F CUNI

  2. Patient history • 78 yr. old male, retiree, worked as mechanical engineer • Family history: longevity, cardiovascular complications, yet no early deaths • (Ab)usus: quitted smoking 15 yrs ago, 10-15 cigarettes daily before, alcohol drinking denies • Patient history: repeated herniotomy, benign prostatic hypetrophy, diabetes mellitus last 6 years – on diet

  3. Patient history- questions • What is the risk (high/ medium/ low) of cardiovascular disease in this 78 year old former smoker? • When is the onset of cardiovascular disorder considered early and when timely? • What are the effects of smoking on the cardiovascular system and on the respiratory system (related to malignant tumors), what are the differences?

  4. Current disorder • Last 3 years progression ofexertional dyspnea and chest pain projecting to medium and lower sternum • Progressive worsening last 2 weeks, pains in rest • Once a pain attack in walking, loss of consciousness, awakened lying on ground • Admitted to hospital after a nigh long lasting retro-sternal pains, dyspnea, felt forced to sit, first time felt as well irregular and fast heardbeats

  5. Current disorder- questions • Give clinical definition of dyspnea. What is its origin in (left) heart disorder? Other causes besides cardiomyopathy? • Name/ description: ischemic myocardial pain, its mechanism/ cause? • Name/ description: of a short time loss of consciousness • What is the prime cause of myocardial ischemia in Czech population? What is differential diagnostics? • Synonyms for palpitations? They are signs of what diseases? What does it mean when patient complains that they are irregular?

  6. What investigation methods to use in this patient • ECG: - what are signs of acutemyocardial infarction?Elevations of the ST segment? - cardiac rhythm ? • Biochemical markers – in this patient were not elevated – no myocardial necrosis • X-ray of heart and lungs – venostasis (oedema)

  7. ECG at admission

  8. Next: atrial fibrillation w. wide QRS complexes

  9. Definition of atrial fibrillation • Atrial fibrillation isan irregular atrial activity. ECG record shows no P waves. Instead there are fast oscillations, also denoted as “F” waves. Ventricular response are typically QRS complexes with RR intervals of different length.

  10. Investigation methods - questions • How many leads are in standard ECG? Names and groups of leads? How we record continuous ECG and how many leads in it we use? • Name biochemical cardiac markers, describe them, what is their use? • What are signs of atrial fibrillation? What are the risks?

  11. Further investigations • echokardiography, ECHO: - Findings: calcified aortal valve with limited cusp excursions, Doppler – tight stenosis w. gradients 65/ 34 mm Hg, mouth area 0.4 cm2/m2 (per body surface) - Ascendent aorta dilation - dilatace ascendentní aorty - EF (ejection fraction) LV 0,45 – 0,49 (= 45-49%) • selectivecoronarography: no pathology/ normal findings

  12. ECHO – morphological investigation

  13. ECHO – continuous Doppler

  14. Cathetrisation record – aortal stenosis

  15. Further investigations - questions • What gradient is important here (related to aortal valve and its stenosis) • What are two basic approaches to measure the gradient? Compare the two? Can we always use both of them? • What can be the complications? • Why we calculate the area? Explain cases when area is significantly reduced yet the high gradient is not present. • What is left ventricle ejection fraction, its units and normal values?

  16. Therapy • Temporary therapy: aim to compensate – therapy of heart failure and control of ventricular response to atrial fibrillation • Definitive therapy: replacement of aortal valve by bio-prosthesis, eventually a plastic surgery of ascendent aorta

  17. Therapy - questions • What is the relation of atrial fibrillation to the principal heart disorder (aortal stenosis)? • Why as a first step in the therapy of atrial fibrillation we need a slow down of the ventricular frequency? • Why and when a plastic surgery of aorta is needed as well?

  18. Conclusions I • Aortal stenosis: is frequent and becoming yet more frequent acquired valve disorder, as the population is ageing. • This condition is followed up by a pressure overload of left ventricle. This propagates backwards and leads to atrial dilation (closing a vicious circle this way) and back to pulmonary circulation. • Typical compensatory mechanism is left ventricle hypertrophy. This is followed up by development of ventricle dilation, deterioration of systolic function and failure.

  19. Conclusions II • Symptomes and their patho-physiological explanations (Q/+A): • dyspnoe • by back-propagationof elevatedintra-ventricular pressure • stenocardia • loweredthroughput in coronary arteries, esp. in tachycardia • exertional syncope • inability to elevatecardiac outputwhen valve mouth area is reduced • low pressure amplitude • slower onsetof systolic pressure in aorta • Therapy: aortal valve replacement (bio-prosthesis) by cardio-surgery. Transcatheter Aortic Valve Implantation in selected high risk patients.

More Related