I have been reading several articles explaining dizziness after eating (see here and here), and both articles gloss over something that I found pretty remarkable.

Both articles claim that "heart disease" can cause one to experience dizziness after eating. For instance, as one article merely generalizes:

A healthy heart is needed to pump blood faster during digestion. Certain heart conditions can lead to its inability to send enough blood to the abdominal organs, which may lead to a drop in blood pressure, resulting in dizziness and sometimes, nausea.

To me, this is pretty vague and uninformative. Making a blanket statement like "certain heart conditions can...lead to a drop in blood pressure" is like saying "not eating or drinking water can cause death."

I'm interested in are the hows and the whats: How does/can heart disease cause dizziness after eating, what are the reasons why this happens, and what are some examples of heart disease ("certain conditions") that cause this (as I'm sure there are many similarly-related diseases)?


Dizziness after eating, which can lead to falls and passing out, is called postprandial hypotension, and as the heart is indeed responsible for responding to hypotension by increasing it's rate - which can be seen in any number of clinical scenarios from blood loss to standing up too suddenly - failure to do so, for any reason including heart disease, can result in continued hypotension, which is experienced by most of us as dizziness.

Postprandial hypotension (PhTN) is defined as a fall in systolic blood pressure (SBP) of ≥ 20 mmHg occurring within 2 hours of a meal. This hypotension (hTN) can result not only in dizziness, but may also cause syncope, falls, weakness, angina pectoris, and stroke.

Because PhTN is particularly common in older hypertensive patients, and older patients tend to have higher incidences of heart disease, it was initially thought heart disease was the cause. However, that didn't explain why some young people without heart disease have PhTN.

In truth, the mechanism of PhTN is not fully understood.

Normally after a meal, blood supply to the gastrointestinal (GI) tract increases, starting with increased flow through the left gastric and celiac arteries, followed by the mesenteric artery, which is more prolonged. Observations indicate that the postprandial hyperemia progresses along the GI tract in association with the movement of ingested food. The magnitude (25–200%) and the duration (3–7 h) of the hyperemia appear to depend somewhat on the composition of the meal. The increase in GI blood flow means there's less blood to circulate in the rest of the body (relative hTN). Normally this is corrected for in various ways.

Baroreceptors (nerve cells within arteries near the heart and in the kidney) are sensitive to rises, falls, and the rates of change in BP, but are especially sensitive to sudden falls in BP, which results in decreased baroreceptor firing. Autonomic Nervous System responds by increasing sympathetic outflow and decreasing parasympathetic (vagal) outflow. Sympathetic outflow leads to vasoconstriction (increased systemic vascular resistance, or SVR), increased HR (tachycardia) and increased force of contraction on the heart (positive inotropy). This leads to a partial restoration of arterial pressure. In people with PhTN, any abnormality at any point in the system will result in an insufficient rise in SBP to overcome the fall.

Therefore possible contributors to PhTN include inadequate sympathetic nervous system compensation for meal-induced GI blood pooling; impairments in baroreflex function; inadequate postprandial increases in cardiac output; impaired peripheral vasoconstriction, as well as abnormal responses to GI hormones released during digestion.

Dysautonomic patients with postprandial hypotension fail to maintain systemic vascular resistance after a meal. This impairment in vascular response to meal ingestion may underlie the development of PhTN. Power spectral analysis suggests an impairment in the postprandial autonomic modulation of HR in healthy elderly and dysautonomic subjects, possibly predisposing to hTN when vascular compensation is inadequate.

Heart conditions that might result in an inadequate response to PhTN include low heart rate (bradycardia), heart valve problems (decreases cardiac output), heart failure (decreased ejection fraction equals cardiac output), patients with atrial fibrillation (decreases cardiac output because of inadequate filling of ventricles), heart attack (decreased ejection fraction), heart muscle disease (cardiomyopathy), severe left ventricular hypertrophy, people with HTN on medications which cause a lowered heart rate, etc.

Therefore, Postprandial Hypotension is an important hemodynamic abnormality in patients with cardiac diseases as well as autonomic nervous system abnormalities such as can be seen in Parkinson's Disease, diabetes mellitus, and others.

Postprandial Hypotension: Epidemiology, Pathophysiology, and Clinical Management
Association of postprandial hypotension with incidence of falls, syncope, coronary events, stroke, and total mortality at 29-month follow-up in 499 older nursing home residents.
Postprandial hypotension. Pathophysiological mechanisms and clinical implications in different disorders.
Postprandial hypotension in response to duodenal glucose delivery in healthy older subjects
Postprandial Hyperemia
Arterial Baroreceptors

  • $\begingroup$ Vasoconstriction from sympathetic outflow is not generalized. It causes selective vasoconstriction, where skeletal muscles are excluded. I believe the viscera are also spared as sympathetic activation of viscera would inhibit digestion itself? Can you please clarify @anongoodnurse? $\endgroup$
    – One Face
    Feb 5 '15 at 1:49
  • $\begingroup$ What I am asking is if sympathetic system will cause only peripheral vasoconstriction and not general vasoconstriction? Very nice answer BTW... $\endgroup$
    – One Face
    Feb 5 '15 at 1:56
  • 2
    $\begingroup$ @CRags - the effect of sympathetic output is complex, involving not only norepinephrine acting on alpha receptors, but epinephrine, angiotensin II and vasopressin, among other vasoconstrictors. And, no, it does not have the same effect everywhere. The question was not about the sympathetic nervous system, but about PhTN. It's long enough! ;) $\endgroup$ Feb 5 '15 at 3:14

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