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Why does the patient of acute pulmonary edema has tachypnea, tachycardia, hypertensive crisis

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"acute pulmonary edema" AND hypertension

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acute pulmonary edema tachypnea tachycardia hypertension pathophysiology

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In acute pulmonary edema, fluid rapidly accumulates in the lung interstitium and alveoli, most often because left-sided heart failure raises pulmonary venous and capillary pressure. The resulting hypoxemia and respiratory distress trigger powerful compensatory responses:
  • Tachypnea: Fluid-filled, stiff lungs have reduced compliance, and gas exchange is impaired by ventilation-perfusion mismatch and intrapulmonary shunt. Hypoxemia stimulates peripheral chemoreceptors, while pulmonary J-receptors and increased work of breathing stimulate rapid, shallow breathing. The patient breathes faster to improve oxygen uptake and reduce CO₂ retention.
  • Tachycardia: Hypoxemia, anxiety, and falling effective forward cardiac output activate the sympathetic nervous system. Catecholamines increase heart rate to preserve cardiac output: [ CO = HR \times SV ] Since stroke volume may be reduced in acute left-ventricular failure, heart rate rises as compensation. However, excessive tachycardia can worsen ischemia and shorten diastolic filling time.
  • Hypertensive crisis: In many cases, severe hypertension is a precipitating cause of acute pulmonary edema. A sudden marked rise in systemic vascular resistance increases left-ventricular afterload. The LV, especially if stiff from diastolic dysfunction, cannot eject adequately, so LV end-diastolic pressure rises and is transmitted backward to the left atrium and pulmonary veins, forcing fluid into the lungs. In addition, the severe dyspnea and hypoxemia cause an endogenous catecholamine surge, which can further raise blood pressure, heart rate, and afterload.
So the cycle is:
[ \text{Hypertension / LV dysfunction} \rightarrow \uparrow \text{LV filling pressure} \rightarrow \uparrow \text{pulmonary capillary pressure} \rightarrow \text{alveolar edema and hypoxemia} \rightarrow \text{sympathetic activation} \rightarrow \text{tachypnea, tachycardia, and often worse hypertension} ]
Acute pulmonary edema typically presents with rapid-onset dyspnea, tachypnea, tachycardia, severe hypoxemia, crackles, and sometimes wheeze. Endogenous catecholamine release often contributes to hypertension. Harrison’s Principles of Internal Medicine, 22e, pulmonary edema section, lines 617-620.

In heart failure with preserved ejection fraction the left ventricle isn't able to relax adequately. What affect does that have on ventricle, does the ventricle stiffens?

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"heart failure preserved ejection fraction" AND diastolic dysfunction

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HFpEF diastolic dysfunction ventricular stiffness impaired relaxation pathophysiology

Yes. In HFpEF, the left ventricle usually becomes less compliant, meaning stiffer during diastole.
Two related abnormalities may occur:
  1. Impaired relaxation
    • Normally, after systole the LV muscle actively relaxes and its pressure falls quickly, allowing blood to flow easily from the left atrium into the LV.
    • In HFpEF, relaxation is slower or incomplete. Early diastolic filling is therefore reduced.
  2. Increased ventricular stiffness
    • The LV wall and chamber resist stretching during filling.
    • Thus, a small increase in LV volume produces a disproportionately large increase in LV diastolic pressure.
[ \text{Compliance} = \frac{\Delta V}{\Delta P} ]
In HFpEF, compliance falls. So for the same filling volume, LV filling pressure is higher.
Common structural contributors are LV hypertrophy from long-standing hypertension, interstitial fibrosis, aging-related changes, and increased stiffness of individual cardiac muscle cells. The ventricular cavity may be normal sized or even smaller, while the ejection fraction remains normal because the fraction of the smaller end-diastolic volume ejected can still be normal.
The consequence is:
[ \text{stiff LV} \rightarrow \uparrow \text{LV end-diastolic pressure} \rightarrow \uparrow \text{left atrial pressure} \rightarrow \uparrow \text{pulmonary venous pressure} \rightarrow \text{dyspnea / pulmonary edema} ]
So HFpEF is not primarily a weak pumping problem. It is mainly a filling problem: the LV may contract adequately, but it cannot relax and expand enough to receive blood without a high pressure. Tintinalli’s Emergency Medicine, systolic and diastolic heart failure section, pp. 792-794.

So cardiac output can be less in HFpEF?

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"heart failure preserved ejection fraction" AND "cardiac output"

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HFpEF cardiac output stroke volume limited exercise preserved ejection fraction

Yes. Cardiac output can be reduced in HFpEF, despite a normal or preserved ejection fraction.
The key distinction is:
[ \text{Ejection fraction (EF)} = \frac{\text{Stroke volume}}{\text{End-diastolic volume}} \times 100 ]
A normal EF tells you that the ventricle ejects a normal percentage of the blood it receives. It does not guarantee that the actual amount ejected, the stroke volume, or cardiac output is normal.
[ \text{Cardiac output} = \text{Heart rate} \times \text{Stroke volume} ]
In HFpEF, the stiff LV fills poorly. Its end-diastolic volume may be low or unable to rise appropriately, especially during exertion. Therefore:
[ \downarrow \text{LV filling} \rightarrow \downarrow \text{stroke volume} \rightarrow \downarrow \text{cardiac output} ]
even if EF remains, for example, 60%.
Example
  • Normal LV: EDV 120 mL, SV 72 mL
    [ EF = 72/120 = 60% ]
  • Stiff LV in HFpEF: EDV 70 mL, SV 42 mL
    [ EF = 42/70 = 60% ]
Both have an EF of 60%, but the second ventricle ejects far less blood per beat.
At rest, many patients with HFpEF maintain a near-normal cardiac output through higher filling pressures and sometimes a higher heart rate. During exercise, however, they often cannot increase filling volume or stroke volume adequately, so their cardiac output reserve is reduced. This contributes to fatigue and exercise intolerance.
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