Pulmonary artery pressure Vs. Pulmonary artery wedge pressure

DC cardioversion is the best treatment for Atrial Fibrillation patients who are hemodynamically unstable !

A 76-year-old woman is evaluated in the emergency department for dizziness, shortness of breath, and palpitations that began acutely one hour ago. She has a history of hypertension and heart failure with preserved ejection fraction. Medications are hydrochlorothiazide, lisinopril, and aspirin.
On physical examination, she is afebrile, blood pressure is 80/60 mm Hg, pulse rate is 165/min, and respiration rate is 30/min. Oxygen saturation is 80% with 40% oxygen by face mask. Cardiac auscultation reveals an irregularly irregular rhythm, tachycardia, and some variability in S1 intensity. Crackles are heard bilaterally one-third up in the lower lung fields.

Electrocardiogram demonstrates atrial fibrillation with a rapid ventricular rate.
Q: Which of the following is the most appropriate acute treatment?
A. Adenosine
B. Amiodarone
C. Cardioversion
D. Diltiazem
E. Metoprolol

This patient with atrial fibrillation is hemodynamically unstable and should undergo immediate cardioversion. Hypotension and pulmonary edema in the setting of rapid atrial fibrillation requires DC cardioversion . In patients with heart failure with preserved systolic function, usually due to hypertension, the loss of the atrial “kick” with atrial fibrillation can sometimes lead to severe symptoms. The best treatment in this situation is immediate cardioversion to convert the patient to normal sinus rhythm. Although there is a risk of a thromboembolic event in patients who are  not anticoagulated, she is currently in extremis and is at risk of imminent demise if not aggressively treated. In addition, but in patients who  acutely became symptomatic, and while this is not proof that she developed atrial fibrillation very recently, her risk of thromboembolism is low if the atrial fibrillation developed within the previous 48 hours.

Adenosine can be useful for diagnosing a supraventricular tachycardia and can treat atrioventricular node-dependent tachycardias such as atrioventricular nodal reentrant tachycardia, but it is not useful in the treatment of atrial fibrillation.
Amiodarone can convert atrial fibrillation to normal sinus rhythm as well as provide rate control, but immediate treatment is needed and amiodarone may take several hours to work. Oral amiodarone may be a reasonable option for long-term atrial fibrillation prevention in this patient given the severity of her symptoms, especially if she has significant left ventricular hypertrophy.
Metoprolol or diltiazem would slow her heart rate; however, in patients who are  hypotensive and these medications could make their blood pressure lower. In addition, in patients who are  in active heart failure, and metoprolol or diltiazem could worsen the pulmonary edema.

Two dangerous late appearing signs of retroperitoneal hemorrhage following cardiac catheterization !

Cardiac catheterization is one of the most commonly performed procedures in medical practice and has low overall complication rates. However, numerous potential life- and limb-threatening complications are possible.

The bleeding is typically from arterial puncture above the inguinal ligament or inadequate hemostasis after the procedure but may also occur spontaneously from the anticoagulation used for PCI. Diagnostic catheterizations in the past were typically performed after administration of variable amounts of heparin. In current practice, many of these diagnostic catheterizations are performed without administration of anticoagulant therapy. Anticoagulant therapy used during PCI varies depending on the operator and the clinical situation but can include high doses of unfractionated heparin, enoxaparin, the direct thrombin inhibitor bivalirudin (Angiomax), and platelet glycoprotein IIb/IIIa inhibitors (potent antiplatelet agents). The half-life of these agents varies from between 20 minutes to 12 hours or more. The major determinant of successful ultimate hemostasis is the quality of the initial puncture, which depends primarily on operator skill and experience. Typically, at the end of cardiac catheterization, the sheath in the femoral artery is removed, and hemostasis is achieved from one of several methods. Manual compression of the artery is the traditional method and is easy to perform, but it is associated with the longest period of bed rest, considerable patient discomfort, and a low but definite complication rate. Vascular closure devices (mechanical and biochemical devices that help “seal” the artery) were developed in an attempt to reduce bed rest time, improve patient comfort, and perhaps lower the complication rate associated with manual compression. However, their use may actually increase the risk of local vascular complications with diagnostic catheterization and PCI or the severity of such complications. These depend upon the specific device used and whether the procedure is a diagnostic catheterization or a PCI, as well as upon operator expertise. Closure devices may also increase the risk of local infection or endarteritis. Decisions regarding whether to use manual compression or a vascular closure device, as well as which vascular closure device, are complex and must weigh the location of the groin stick, patient body habitus, anticoagulants used, and local expertise with a particular closure device.

Normal or Innocent Murmurs

Cardiology Online Case-discussion Chapter - Idiopathic Dilated Cardiomyopathy and role of defibrillator biventricular pacemaker

Case Scenario:  Sixty-seven year- old female who presented to the outpatient department with a several week history of exertional shortness of breath, more so when she takes the stairs or goes up a hill. She had undergone a nuclear cardiac stress test 1 year previously and this was normal. ECG was done and presented below. She has otherwise no cardiac history and has continued to remain healthy with a reasonably active life style.

Examination and Investigations - Patient was resting comfortably speaking in full sentences. Blood pressure 110/72mmHg and pulse 74/min. estimated jugular venous pressure was felt to be normal. Cardiac examination was normal with the exception of a pradoxically split second heart sound. Her lungs sere clear. Her extremities demonstrated no edema. - A transthoracic echocardiogram was performed and this confirmed a mildly dilated left ventricle with a global reducation in left ventricular systolic function with an estimated left ventrcular ejection fraction of 25%. The left atrium was moderately enlarged. The right atrium was normal. The mitral valve demonstrated mild to moderate central mitral regurgitation. No other findings of abnormal significance were seen.

A 12-lead ECG was performed and this demonstrated a normal sinus rhythm rate of 74/min. A widened QRS complex is demonstrated greater than 120 msec in duration. There is complete LBBB pattern. Additionally, a terminally negative P wave is seen in lead V1 supporting left atrial abnormality.

The patient subsequently underwent a left heart catheterization confirming a global moderately severe reduction of left ventricular systolic function and normal epicardial coronary arteries.

Discussion/Treatment/Outcome

The Patient presented with subacute shortness of breath in the setting of unexplained left ventricular systolic dysfunction and an antecedent history of complete LBBB. She was deemed to have non-ischemic left ventricular systolic dysfunction base on her diagnostic left heart catheterization. Treatment with oral beta blockade, an ACE inhibitor, and a low dose diuretic was instituted with prompt improvement of her symptomatology.

After an appropriate interval, follow-up transthoracic echocardiography was performed, which failed to demonstrate improved left ventricular systolic function. She next underwent placement of a biventricular pacemaker defibrillator. Follow-up transthoracic echocardiography at 3 months post defibrillator placement demonstrated near normalization of her left ventricular systolic function that has persisted since her defibrillator biventricular pacemaker placement over the past 2 years.

In the interim, the patient did present with several defibrillator shocks, and upon device interrogation she was noted to be in paroxysmal atrial fibrillation with a rapid ventricular response. She was started on an anti-arrhythmic medication and has done well since without further episodes of atrial fibrillation or defibrillator discharge. She remains in a functional class I performance status.

 

Why was the case Chosen?

Patients with a complete LBBB and symptomatic CHF can benefit from Biventricular cardiac pacing with a significant improvement in left ventricular systolic function. Generally, the wider the QRS complex with a left bundle branch QRS complex morphology, the greater the likelihood of being a positive responder to biventricular pacing.

Learning points from the case/how the case altered the treatment pattern

This patient with a functional class II performance status in the setting of a complete left bundle branch block of uncertain etiology. After further evaluation, non-ischemic left ventricular systolic dysfunction was highly suspected. After appropriate placement on oral medications, a follow-up of her left ventricular systolic function failed to demonstrate an improvement, and thus she was deemed to be an excellent candidate for an implantable biventricular pacemaker defibrillator. While not all patients respond favorably to biventricular pacing, she has demonstrated a remarkable response not only in the objective improvement with regard to her left ventricular ejection fraction, but also her complete resolution of any cardiovascular symptomatology. A complete LBBB is not a normal finding a merits further investigation. Often times , it can precede the development of subsequent left ventricular systolic dysfunction and if upon initial evaluation the left ventricular systolic function is deemed to be normal , follow-up evaluation both clinically and with cardiac imaging is suggested to ensure that left ventricular systolic dysfunction has not transpired . A additionally , depending on the patient’s function status and symptom , an evaluation of the patient’s coronary artery status is often indicated either in the form of cardiac stress imaging or a diagnostic left heart catheterization depending on the clinical situation .