What is orthopnea and pnd
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orthopnea paroxysmal nocturnal dyspnea PND pathophysiology heart failure
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Here is a comprehensive explanation of both symptoms:
Orthopnea
Definition: Dyspnea (breathlessness) that occurs when the patient lies in the recumbent (flat) position, relieved by sitting up or elevating the head and chest with pillows.
Clinical assessment: Graded by the number of pillows needed — e.g., "two-pillow orthopnea." In severe cases, patients cannot sleep in a bed at all and instead sleep in a recliner or chair.
Timing: Occurs within 1–2 minutes of lying down.
Pathophysiology:
- Lying flat causes redistribution of fluid from the abdomen, lower extremities, and splanchnic circulation into the central (thoracic) circulation
- This raises ventricular preload → increases pulmonary venous and pulmonary capillary hydrostatic pressure → fluid transudation into the interstitium/alveoli
- Additional factors: reduced gravitational assistance for diaphragm effort, and in patients with ascites or hepatomegaly, elevation of the diaphragm further impairs breathing
- Orthopnea correlates well with severity of pulmonary congestion and is a fairly specific symptom of heart failure
Paroxysmal Nocturnal Dyspnea (PND)
Definition: Acute, severe shortness of breath that suddenly awakens a patient from sleep, associated with anxiety and a sensation of suffocation, requiring the patient to sit upright for relief.
Timing: Typically occurs 1–2 hours after lying down (after prolonged recumbency, unlike orthopnea which is almost immediate). Relief may take 30 minutes or longer of sitting upright.
Pathophysiology:
- Similar mechanism to orthopnea: prolonged recumbency allows gradual reabsorption and mobilization of interstitial fluid from the splanchnic circulation and lower extremities into the central circulation
- This builds up over time → acute alveolar edema develops → patient wakes gasping
- Episodes are often accompanied by coughing and wheezing ("cardiac asthma") — caused by increased bronchial arterial pressure → airway compression + interstitial pulmonary edema → increased airway resistance
- Cheyne-Stokes respiration and central sleep apnea can also precipitate PND, due to increased sensitivity of the respiratory center to PCO₂ and prolonged circulatory time in heart failure
Significance: PND is relatively uncommon but almost always represents severe heart failure, and is associated with increased mortality.
Key Differences
| Feature | Orthopnea | PND |
|---|---|---|
| Onset after lying down | Immediate (1–2 min) | Delayed (1–2 hrs into sleep) |
| Predictability | Predictable, consistent | Less predictable |
| Relief | Quick with sitting up | Takes 30+ min upright |
| Severity indicator | Moderate-severe HF | Usually severe HF |
| Associated features | Nocturnal cough | Wheezing, "cardiac asthma" |
Clinical Context
Both are classic symptoms of left-sided heart failure and are listed as cardinal signs of congestion alongside jugular venous distension, rales, edema, and hepatomegaly. They also occur in group 2 pulmonary hypertension (due to left heart disease) and — in a different mechanism — in neuromuscular disorders, where the diaphragm is placed at a mechanical disadvantage in the recumbent position.
Sources: Goldman-Cecil Medicine, p. 1084 (signs of congestion); Harrison's Principles of Internal Medicine 22E, pp. 2289–2296; Goldman-Cecil Medicine, Heart Failure chapter, pp. 2319–2323
Features of a patient with temporal lobe stroke
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temporal lobe stroke clinical features symptoms signs neurology
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I now have comprehensive information to give a thorough answer. Let me compile it.
Temporal Lobe Stroke — Clinical Features
The temporal lobe is supplied primarily by the middle cerebral artery (MCA) — specifically its inferior division — and partly by the posterior cerebral artery (PCA). Features depend on which hemisphere is affected.
1. Visual Field Defect — "Pie in the Sky"
Contralateral superior homonymous quadrantanopia is the hallmark visual defect of temporal lobe lesions.
The inferior optic radiations (Meyer's loop) sweep anteriorly through the temporal lobe around the tip of the temporal horn of the lateral ventricle before traveling to the occipital cortex. Damage here causes loss of the upper contralateral visual quadrant in both eyes — classically described as the "pie in the sky" defect. Larger lesions may produce a full contralateral homonymous hemianopia.
2. Dominant (Usually Left) Temporal Lobe
Wernicke's Aphasia (Receptive/Fluent Aphasia)
The most characteristic feature. Caused by damage to Wernicke's area in the posterior superior temporal gyrus.
| Feature | Finding |
|---|---|
| Spontaneous speech | Fluent, but filled with paraphasic errors; may be logorrhoeic |
| Comprehension | Severely impaired (cannot understand spoken or written words) |
| Repetition | Impaired |
| Naming | Impaired (paraphasias) |
| Reading | Impaired (alexia often accompanies) |
The patient speaks in jargon ("word salad") — sentences flow easily but make no sense — and crucially does not recognize their own errors.
Dysnomia / Anomic Aphasia
Difficulty retrieving words (naming), even when comprehension is relatively preserved — seen with lesions of the posterior temporal-occipital junction.
Amusia
Inability to recognise or produce music (dominant temporal lobe).
Visual Agnosia
Failure to recognize objects by sight alone, despite intact vision — due to disconnection of visual association cortex in the temporal lobe from meaning.
Amnesic (Korsakoff-like) Syndrome
Occasionally, if the hippocampal-parahippocampal regions are involved.
3. Non-dominant (Usually Right) Temporal Lobe
- Contralateral superior quadrantanopia (same visual defect as dominant side)
- Impaired processing of visually presented non-verbal material (faces, spatial patterns)
- Agnosia for sounds and musical qualities — difficulty recognizing environmental sounds or tone/melody
- Impaired spatial judgment in some cases
4. Either Temporal Lobe (Regardless of Dominance)
- Auditory, visual, olfactory, and gustatory hallucinations — due to involvement of primary/association sensory cortices and limbic connections
- "Dreamy" states and focal temporal lobe seizures — déjà vu, jamais vu, complex automatisms, micropsia/macropsia
- Emotional and behavioral changes — irritability, aggression, or mood disturbance (limbic system involvement)
- Agitated delirium — particularly with right temporal lesions or hemorrhage
- Disturbances of time perception
- Déjà vu / Jamais vu phenomena (temporal-limbic involvement)
5. Bilateral Temporal Lobe Involvement
| Feature | Mechanism |
|---|---|
| Korsakoff amnesic syndrome | Bilateral hippocampal damage → anterograde amnesia, confabulation |
| Apathy and placidity | Bilateral limbic disruption |
| Klüver-Bucy syndrome | Bilateral temporal-limbic lesions: hyperorality, hypersexuality, compulsion to attend all visual stimuli, blunted emotion — rare in humans |
Summary Table
| Feature | Side |
|---|---|
| Contralateral superior quadrantanopia ("pie in sky") | Either |
| Wernicke's aphasia (fluent, poor comprehension) | Dominant (L) |
| Dysnomia, amusia, visual agnosia | Dominant (L) |
| Impaired non-verbal/spatial processing | Non-dominant (R) |
| Hallucinations (auditory/visual/olfactory/gustatory) | Either |
| Focal seizures with "dreamy" states, déjà vu | Either |
| Behavioral/emotional changes | Either |
| Agitated delirium | Either (esp. R) |
| Bilateral: amnesia, Klüver-Bucy | Bilateral |
Note: Pure motor weakness is not a feature of isolated temporal lobe strokes (the motor cortex lies in the frontal lobe). However, large MCA territory strokes involving the temporal lobe often also involve frontal/parietal regions, producing hemiparesis.
Sources: Adams and Victor's Principles of Neurology 12E, pp. 3078–3120; Localization in Clinical Neurology 8E, pp. 71–75; Neuroanatomy through Clinical Cases 3E, pp. 1592–1861; Bradley and Daroff's Neurology, Wernicke Aphasia section
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