Wednesday, 19 September 2007

Hyperdynamic Circulation

The following case has been supplied by a colleague at another hospital and has been anonymised.

A patient was admitted into hospital with a three week history of intermittent malaena.

The malaena had started gradually and there was on average one stool produced per day of the typical 'tarry' black consistency.

The patient had no abdominal pain / no diarrhoea / no back pain. She was complaining of fatigue but no postural dizziness / collapse / palpitations / breathlessness.

There was no history of any use of non-steroidal anti-inflammatory drugs / steroids.

However, she was a long term alcoholic and she was drinking 3 cans of beer per day at that time and had done so for 20 years.

She had known chronic liver disease for which she was taking medication but despite this, she was still drinking regularly.

Medications included furosemide 40mg daily, spironolactone 25mg daily, and multivitamins.

There was no family history of note and the patient lived with her husband in the locality to the hospital.

She was an ex-smoker having smoked 20 pieces per day for 20 years although she stopped 5 years previously.

On examination, she appeared confused and had a poor nutritional state. Blood pressure was 100 / 40, heart rate regular at 90 beats per minute. Respiratory rate was 18 / minute, Sats 95% on room air. Temp 38.4 degrees C.

Hands: Palmar erythema, Dupytrens Contracture and Hepatic Flap.

Head and Neck: JVP was not raised. Eyes showed mild anaemia and there was scleral discolouration of jaundice. No Lymph nodes were palpable. Temporal muscles were severally wasted. Oral mucosa appeared dry. There was a smell of 'fetor' from the patient's mouth.

CVS: Pulse quality felt Bounding and Collapsing. Heart sounds were normal with No Diastolic murmur. Quinke's sign was negative but Corrigan's Sign (neck pulsations) and Waterhammer Pulse (palpation of the brachial pulse lifting the arm into the air producing bounding pulse which collapses) were positive. There was mild leg oedema.

RESP: The was diffuse wasting of the intercostal muscles and muscles around the neck. Her chest was hyperinflated. Chest percussion was resonant, and there was no evidence of wheeze or crackles.

ABDO: Soft and distended. There was dilatation of the superficial veins on the abdominal wall (caput medusae) with the blood flowing away from the umbilicus (a sign of increased portal pressure). The liver and spleen were not palpable. The abdomen was stony dull to percussion consistent with accumulation of ascites. It was not possible to perform shifting dullness as there was no evidence of bowel gas and fluid thrill test was negative. Bowel sounds were absent.
Rectal examination revealed malaena but no rectal masses.

CNS: pupils were equal and reactive to light and accommodation and the consensual reflexes were normal. Other cranial nerves appeared intact.

PNS: The patient was moving all 4 limbs, with equal power throughout. Tone was normal. Reflexes were generally depressed. Sensation was difficult to ascertain due to the patient's confusion. Babinski sign was negative.

Clinical Impression

  • Decompensated Liver Disease
  • Upper Gastrointestinal Bleed
  • Hepatic Encephalopathy
  • Spontaneous Bacterial Peritonitis
  • Hyperdynamic Circulation from High Output Heart Failure
This is therefore quite a complicated case and to go into the depths of investigating and treating each problem here goes beyond the scope of this blog. However, the final diagnosis on the list is somewhat obscure and often missed.

The signs of Bounding and Collapsing Pulses can either be due to Aortic Regurgitation (although in this case there was no diastolic murmur) or due to a Hyperdynamic Circulation from High Output Heart Failure.

When we think of heart failure normally we consider systolic or diastolic heart dysfunction. However, in high output heart failure, the heart fails to supply the metabolically active tissues with blood and oxygen because of Shunting of Blood.

Shunting is where this is a connection or multiple connections between artery and vein thereby bypassing the capillary beds. Hence, the Cardiac Output must increase to compensate for the Shunt of blood. These patients typically have a wide pulse pressure, bounding arterial pulses that sudden collapse beneath the examining fingers which denotes the shunting of blood into the venous circulation.

There are a vast number of conditions that cause shunting to a greater or lesser degree which include:

  • AV fistulae e.g. iatrogenic in renal dialysis / complication of cardiac angiography
  • Acromegally
  • Anaemia
  • Anxiety
  • Beri-beri
  • Carcinoid syndrome
  • Cor pulmonale
  • Erythroderma
  • Hepatic failure
  • Hypercapnia
  • Morbid obesity
  • Multiple Myeloma
  • Paget's Disease
  • Polycythaemia rubra vera
  • Pregnancy
  • Pyrexia
  • Thyrotoxicosis
  • Vasodilator Drugs
In liver disease the shunting of blood occurs via the Portosystemic Anastomoses as a result of raised portal blood pressure. The raised portal pressure is as a result of damaged liver architecture. However, the splanchnic vascular bed become dilated and engorged with blood. As a result, the systemic blood pressure drops and there is an increase in peripheral vascular tone although, overall there is a total reduction in systemic vascular resistance as a consequence of the dilated splanchnic bed.

As a consequence, there is release of mediators from the kidney to increase Na+ and water retention via the Renin-Angiotensin-Aldosterone axis. This avid reabsorption of water and Na+ precipitates the ascites that is seen in decompensated liver disease.

Eventually, the increased peripheral vascular tone results in worsening renal failure and hence, hepatorenal failure can ensue. Hepatorenal failure can be precipitated by bleeding and infection, particularly spontaneous bacterial peritonitis, and portends an unfavourable outcome.

Hence, patients with Hepatic Failure develop Splanchic Steal of blood from the systemic circulation and have an increased cardiac output to try and compensate. The blood from the portal system is shunted into the venous circulation due to portosystemic anastomoses. The ascites occurs due to low systemic blood pressure despite signs of a bounding hyperdynamic circulation!

It is a very complicated process indeed !!!

Because these patients have secondary hyperaldosteronaemia, they usually require high doses of spironolactone (Aldactone). The usual starting dose is 100mg up to 400mg daily. Blocking the action of aldosterone reduces ascites but can result in hypotension becoming worse which is not unsurprising. Hence, a balance needs to be established between appropriate dose of spironolactone, renal function and blood pressure. Patients unresponsive to medication and fluid restriction require paracentesis to remove the ascitic fluid.

For an excellent description of the Splanchnic Steal in Liver Failure, please go to the following link.

So, the next time you feel a bounding and collapsing pulse think possible Aortic Regurgitation, but in the absence of an audible murmur think High Output Heart Failure causing a Hyperdynamic Circulation and refer to the above list of causes !!!

Please Consider...

No comments: