RELATO DE CASO. Angina de Prinzmetal. Eduardo Contreras Zuniga; Juan Esteban Gomez Mesa; Sandra Ximena Zuluaga Martinez; Vanesa Ocampo;. A angina de Prinzmetal (AP) carac- teriza-se por: 1) a dor med Prinzmetal's variant angina or simply va- riant angina or FISIOPATOLOGIA. Foi demonstrado. Download PDF. More article options. ePub. Statistics. Outline. Introducción; Fisiopatología; Clínica y características de los pacientes; Diagnóstico; Tratamiento Vasospastic or Prinzmetal's variant angina as it is also known is a special type of.
|Language:||English, Portuguese, German|
|ePub File Size:||29.39 MB|
|PDF File Size:||14.68 MB|
|Distribution:||Free* [*Registration Required]|
(ANGINA INESTABLE E INFARTO AGUDO DEL MIOCARDIO .. Fisiopatología del síndrome coronario agudo . Definición focal, como ocurre con la angina de Prinzmetal (espas-. fisiopatologia observada na HbSC, que apesar de pouco estudada, apresenta Mutation, a Reversible Etiology of Prinzmetal's Angina Pectoris. Am J Cardiol . angina could not be attributed to increasedmyocardial demands. In postulated by Prinzmetal et al.7 8 .. Condorelli L: Fisiopatologia clinica della stenocardia.
When she stopped calcium antagonists for 2 days only, the episode of angina occurred. Usually angina was relieved in a few minutes by sublingual nitroglycerin. Because of repeated episodes of angina at rest, despite medical treatment, the patient was referred to our Department. Troponin test was negative. During arteriography a transient spasm of the right coronary artery was observed.
Preliminary Observations on Cavodil in Treatment of Angina Pectoris
Cardiopulmonary resuscitation was successful. After cardiac arrest the doses of calcium antagonists were increased. The echocardiography showed akinesis of inferior wall and hipokinesis of posterior wall. Figure 5 ECG changes during pain episode a and a few minutes later b , without pain.
Discussion We have presented three patients with diagnosed Prinzmetal's angina who developed cardiac arrest in a mechanism of ventricular fibrillation or electromechanical dissociation.
The final diagnosis was confirmed by visualization of coronary spasm at arteriography Fig. According to the literature, coronary arteriography is recommended in all patients with Prinzmetal's angina [ 2 , 3 , 7 ]. Provocative tests can cause refractory coronary spasm requiring intracoronary nitroglycerin for relief or sometimes there is also need for an intracoronary calcium antagonist or emergency percutaneous transluminal coronary angioplasty, so the tests should be conducted in a catheterization laboratory [ 13 ].
Hyperventilation [ 14 , 15 ], exercise [ 16 ], or exposure to cold [ 17 ] are other provocative tests [ 2 , 3 , 14 ]. These patients are at high risk for lethal arrhythmias and multivessel spasm [ 14 ].
According to the literature [ 5 , 6 , 18 - 21 ] calcium antagonists and nitrates are very effective in preventing coronary artery spasm in patients with variant angina. They act in different mechanisms and that is why the vasodilatory effect of these two classes of drugs is additive.
Usually, a calcium antagonist at a high dose e. It is preferred to combining diltiazem or verapamil with dihydropyridines nifedipine, amlodipine or nicardipine.
Diltiazem and verapamil are more potent negative inotropes than dihydropyridines, which in return are more potent peripheral vasodilators [ 6 ]. The most dangerous complication in patients with Prinzmetal's angina is cardiac arrest.
Most authors believe that this treatment can reduce the risk of sudden death if it prevents angina attacks [ 18 , 22 , 23 ]. Our observations are in agreement with this opinion.
In our patients cardiac arrest occurred despite the treatment with calcium antagonists, but all of them suffered from severe chest pain before the event. Therefore, we think that doses of calcium antagonists in the first and second patient were not high enough. Two induced beats are shown. We can observe the progressive reproduction of antero-septal myocardial infarction signs ap- pearance of Q wave in V2-V4 and on the horizontal VCG an absence of anteriorly directed forces, clockwise efferent limb, 20 msec vector directed posteriorly.
AI QRS d. O t h e r electro- pacing. Recordings from a year-old man who had a myocardial infarction five years later and who was admitted for unstable angina. The VCG was registered simultaneously with the induced beat last complex to the right. The basal ECG is indicative of antero-septal myocardial infarction.
The VCG shows an absence of initial anteriorly directed QRS forces: little R wave in V1 can probably be explained by the direction to the right and posteriorly of the first vectors. The duration of QRS is 96 msec.
Tratamiento inicial prehospitalario del infarto agudo de miocardio
The first induced VCG panel B, to the left is indicative of antero- lateral myocardial infarction duration initial rightward QRS forces 24 msec, clockwise efferent limb. A slight decrease in the duration of QRS 88 msec can be observed.
The second induced VCG panel B, to the right shows signs of extensive-anterior myocardial infarction absence of anteriorly directed forces, transverse plane inscribed clockwise , and left anterior hemiblock. Note the initial slowing down and the increase in the duration of QRS up to I00 msec.
The third induced VCG Panel C shows right bundle branch block and signs of antero-septal and inferior myocardial infarction posteriorly and leftward directed initial forces; clockwise efferent limb on the frontal plane, and superiorly directed initial forces 28 msec.
Recordings from a year-old man with an old myocardial infarction. In fact this patient The MI-QRS were induced only in patients with showed both the appearance of MI-QRS and an coronary heart disease or hypertensive heart initial delayed QRS like the "intrainfarction disease and never in normal cases or in patients block" It is known that an in- We did not find any increase in the duration of crease of myocardial refractoriness can be found QRS in our patients.
This was probably due to an in the myocardial tissue surrounding a gross or involvement of only the first part of the ven- microscopic scars.
Since the MI-QRS which we tricular activation as demonstrated by the impor- observed appeared only in patients with coronary t a n t changes of the initial forces with slight heart disease or hypertensive heart disease and changes in the middle and terminal forces.
In none of these cases did we prolonged refractoriness. Only in patient no. Many experimental electrophysiological VCG morphologically similar to an incomplete data have shown that premature aberrant beats left bundle branch block, but the simultaneous are generally the result of a delay or block of the reduction of the duration of QRS is in contrast stimulus in the specific pathways.
Nevertheless it with this interpretation. Two other possible ex- cannot be excluded that in some conditions the planations are more likely. Firstly, the induction site of the block can be in the common myocar- of a conduction disturbance generating electrical dium. Recordings from a year-old man 9The basal VCG to the left is indicative of posterior, inferior and lateral myocardial infarction horizontal plane: initial rightward forces 30 msec and 0.
This anterior MI patterns. In fact, there are m a n y clinical observa- changes of the QRS duration. Some changes in some nonischemic heart disease. Histological myocitolisis unrecognized at autop- However, it has never been shown that conduc- sy47, cellular edema 4s, cellular metabolic stress 1, J. QRs a. Silvan0 szyr.
I I Fig. Our work sug- A client with angina complains that the anginal pain is prolonged and severe and occurs at the same time each day, most often at rest in the absence of precipitating factors.
How would the nurse best describe this type of anginal pain?
Stable angina 3. Unstable angina 4. Nonanginal pain Variant angina, or Prinzmetal's angina, is prolonged and severe and occurs at the same time each day, most often at rest.
Tratamiento inicial prehospitalario del infarto agudo de miocardio
Stable angina is induced by exercise and relieved by rest or nitroglycerin tablets. Unstable angina occurs at lower levels of activity or at rest, is less predictable, and is often a precursor of myocardial infarction. The nurse in the medical unit is assigned to provide discharge teaching to a client with a diagnosis of angina pectoris. The nurse is discussing lifestyle changes that are needed to minimize the effects of the disease process.
The client continually changes the subject during the teaching session. The nurse interprets that this client's behavior is most likely related to which problem? Anxiety related to the need to make lifestyle changes 2.
Boredom resulting from having already learned the material 3.
An attempt to ignore or deny the need to make lifestyle changes 4. Lack of understanding of the material provided at the teaching session and embarrassment about asking questions Denial is a defense mechanism that allows the client to minimize a threat that may be manifested by refusal to discuss what has happened.
Denial is a common early reaction associated with chest discomfort, angina, or myocardial infarction MI. Anxiety usually is manifested by symptoms of sympathetic nervous system arousal. No data are provided in the question that would lead the nurse to interpret the client's behavior as boredom or as either understanding or not understanding the material provided at the teaching session.
The nurse is caring for a client who has been hospitalized with a diagnosis of angina pectoris.
The client asks why the oxygen is necessary. The nurse should provide which information to the client? Oxygen has a calming effect. Oxygen will prevent the development of any thrombus. Oxygen dilates the blood vessels so that they can supply more nutrients to the heart muscle.
The pain of angina pectoris occurs because of a decreased oxygen supply to heart cells. The pain associated with angina results from ischemia of myocardial cells. The pain often is precipitated by activity that places more oxygen demand on heart muscle.Prinzmetal's variant form of angina as a manifestation of alpha-adrenergic receptor-mediated coronary artery spasm: documentation by coronary arteriography.
The nurse should provide which information to the client?
Guidelines for the diagnosis and treatment of non-ST-segment elevation acute coronary syndromes. All of them were successfully defibrillated. The third pa- In all cases the HV interval was normal in basal tient was a y o u n g man with atypical angina and conditions and did not decrease either during ECG-VCG pattern of inferior, posterior and P R A S or during atrial pacing.