Cephalization of pulmonary blood flow- mechanism

In normal chest xrays, the lower zone pulmonary vessels are more prominent than the upper zone vessels. This is due to the effect of gravity resulting in a pressure difference in the pulmonary vasculature of upto 20mmHg between the apex and base of lung, with increased flow to the lower lobe vessels.
In patients with LV failure, the development of post-capillary pulmonary hypertension results in exudation of fluid into the interstitial space resulting in interstitial edema. This fluid compresses the pulmonary blood vessels, decreasing their compliance and interfering with gas exchange. The resultant alveolar hypoxia is a potent stimulator of pulmonary vasoconstriction. Due to dependent position and increased compression by edema fluid, alveolar hypoxia is more in basal regions compared to thex. This results in more vasoconstriction in the basal regions. So, redistribution of pulmonary blood flow occurs towards the apical region.This is called "Cephalization" of pulmonary blood flow.

Aborted Myocardial Infarction

"Aborted myocardial infarction" is a term first coined by Weaver when reporting the MITI trial of prehospital fibrinolysis.

Aborted MI is characterised by:

1. Resolution of ST elevation by > 50% from the initial levels in presentation ECG after 90 minutes post-fibrinolysis, and

2. Absence of cardiac enzyme elevation, or an increase less than twice the upper limits of normal

Early fibrinolysis results in lesser degrees of myocardial injury and necrosis thereby preventing significant enzyme release. An increased incidence of aborted infarction has been reported with prehospital fibrinolysis, patients with prior angina and well developed coronary collaterals, and with lesser degrees of ST elevation in the initial ECG.

The therapeutic significance of an aborted infarction lies in the fact that the extent of myocardial necrosis is less along with the presence of potentially viable myocardium thereby necessitating early coronary angiography and revascularisation procedures.

Lead aVR in ACS- neglected but informative!!

The lead aVR is usually not taken into consideration while interpreting ECGs, even complicated ones. This is because of the fact that aVR displays reciprocal information covered by II, aVL, V5 & V6. But it has been shown recently by various authors that careful evaluation of lead aVR can give a lot of valuable information in patients with ACS that can help in therapeutic decision making.

In patients with STEMI:

Presence of ST elevation in aVR in patients with acute AWMI strongly predicts proximal LAD occlusion proximal to the first septal perforator.

Also, in the presence of evolved IWMI, presence of an initial 'r' wave > 1.5 mm in aVR suggests additional infaction of the apical lateral wall, either due to occlusion of LCX or larger RCA involving a large posterolateral branch of LV.

In patients with NSTE-ACS:

Presence of ST elevation in aVR in the presence of ST depression in 7 or more leads indicates incomplete occlusion of the LMCA or its equivalent (very proximal LAD plus LCX)

Thus, careful evaluation of lead aVR in the ECG of patients with ACS may provide additional information regarding the artery involved, site of occlusion and its extent and help plan interventions.

Third heart sound- theories behind its genesis

The Third Heart Sound was first described by Obrastzow in l905. Since then, various theories have been proposed to explain the genesis of S3. Three major theories that are used these days include:

1. Valvular theory

2. Ventricular theory

3. Impact theory

Valvular theory:

Earliest theory proposed regarding the origin of S3 is the valvular theory according to which S3 is produced by the diastolic tenting of the atrioventricular valves at the end of rapid ventricular filling phase. This theory was rejected by various investigators after it was demonstrated that S3 continued to occur in patients who had their valves replaced by mechanical prostheses.

Ventricular theory:

The most accepted theory explaining the origin of S3 is the ventricular theory. According to this theory, these sounds originate within the left or right ventricle or their walls. S3 occurs when the ventricle suddenly reaches its elastic limit and abruptly decelerates early diastolic blood flow, thereby setting the entire cardiohemic system into vibration.

The major factor here is the dynamic interplay between the force of delivery of blood into the ventricle and the ability of the ventricle to accept this flow.

This theory also partly explains the 'low frequency' nature of the S3 because the the vibrating structure (ventricle) producing S3 has a great mass in proportion to its small elasticity.

Impact theory:

According to this theory proposed by Reddy and associates, S3 is produced by the dynamic impact of the heart against the chest wall. The intensity of S3 is dependent on the force of impact which in turn is decided by the size of the heart, its movement within the thorax and, the chest wall configuration. This theory explains the occurrence of S3 in hyperdynamic states.

Theories apart, presence of S3,especially if persistent, in a patient with cardiomyopathy or an MI is an ominous sign associated with high mortality needs aggressive treatment of the underlying disease state!!

Roentgenology of cardiac diseases- alive or dead?

The discovery of X-rays by W.C.Roentgen in 1985, was a major landmark in the field of medicine.X-rays were used a lot in earlier days in the diagnosis of cardiac diseases. In the present day cardiology, with the latest & sophisticated imaging modalities available for use,where do cardiac x-rays stand?
Even today, chest x-rays give a lot of clues in diagnosing cardiac diseases, especially:
1. rough assessment of chamber enlargements
2. status of pulmonary vasculature
3. signs of cardiac failure
4. pericardial effusion
5. cardiac calcifications
The classic "straightening of the left heart border" in mitral stenosis or 'boot-shaped heart" in TOF or "water-bottle appearance" of pericardial effusion are beauties of chest x-ray to appreciate.
All these said, the concept of reading and using cardiac x-rays ends at the level of teaching institutions itself & the slow death of cardiac roentgenology is evident by the sheer lack of available textbooks in cardiac roentgenology

Hi!!

Hi to all! Iam trying out something way out of my usual being and entering into blogging. Through this, I will try to post something useful points in Cardiology and updates as far as possible. Hoping to get all your support!