Thanks go to Alex Walker for the article. 

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​OK, I’ve read several posts lately in different Emu groups about the hatching process of Emu, it’s probably the only time that we humans think we can interfere to "help", either by drilling small holes in the air cell end of the shell or breaking away parts of the shell to “assist" the baby chick get out. Therefore, I thought I’d go through the actual process of a baby Emu (or other chick) hatching.

Depending on the species, the chick will orientate itself in the hatching position a few days before hatching. To do this the chick wriggles around inside the shell and gets its head under its left wing. At the same time this is happening the egg shell which is made up of three layers of crystalline calcium with minerals in a Nano structure is being dissolved, from the inside out by a protein called 'osteopontin' which takes this calcium into the membrane surrounding the chick and through that, into the chicks bloodstream. The calcium is then absorbed into the chicks skeleton strengthening the chicks bones, like you taking calcium tablets! This process weakens the shell layers from the inside out making pipping and hatching easier.

The membrane called the chorioallantois has been allowing the chick to inhale oxygen from outside, and exhale carbon dioxide from the chick through the shell pores (the lighter coloured specs on the eggs). This membrane is full of tiny blood vessels that transport the oxygen through the shell and into the chick. A couple of days before hatching (in Emu), the chick breaks through the internal wall into the air cell end of the egg (internally pips), and starts breathing air through its lungs, as well as still being attached to the membrane via an umbilicus.

At the same time a muscle on the back of the chicks neck enlarges several times it original size to form a 'pipping muscle'. The chick then continues to breathe the air in the air cell whilst getting ready for the big push. At the same time the movements inside the shell are helping the yolk sac to be absorbed into the abdomen, sometimes this is only complete right before hatching.

As the air in the air cell gets used up the chick starts to 'suffocate', oxygen is running out and carbon dioxide levels in its blood increase dramatically, this TRIGGERS the pipping muscle which will involuntary to go into spasm, it starts to flex causing the beak to strike the weakened shell from the inside. When the spasms become strong enough the chick breaks through the three layers of shell into the big wide world and can take a breath of fresh air and recover from a very traumatic (near death) experience. After resting, sometimes for several hours, it continues to enlarge the hole, and it’s struggles help the last remaining yolk sac to be absorbed, also, the stress and exhaustion of hatching strengthens the lungs and blood system. Only towards the end of hatching does it detach itself from the membrane that is full of blood vessels, If the membrane and blood vessels are dried from premature drilling it can be fatal at the time of releasing from the membrane, 

For the above reasons you can see why - 1) You shouldn’t interfere by drilling holes in the shell. 2) You shouldn’t start breaking bits of shell away to make the hole bigger as you risk breaking a blood vessel and causing the chick to bleed to death. 

The Science, with Research Papers

“Circulatory changes associated with the closure of the ductus arteriosus in hatching emu (Dromaius novaehollandiae)”
https://sites.biology.unt.edu/.../181_Shell%20et%20al%20...

Summary:
The ductus arteriosus is a blood vessel that lets blood bypass the lungs while the chick is inside the egg (because it’s not breathing air yet).

In emu embryos, this vessel doesn’t begin to close until after the chick externally pips (starts breathing air).

Closure is gradual in emus and involves both functional closure (the vessel constricting due to smooth muscle action) and anatomical closure (remodelling of the blood vessel walls).

This transition allows more blood to flow to the lungs as the chick switches from getting oxygen through the shell to breathing on its own.

“Embryonic control of heart rate in emu and chicken embryos”
https://sites.biology.unt.edu/.../%28149%29Tazawa...
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Summary:
This study looks at how heart rate is controlled in emu and chicken embryos as they develop.
As chicks approach hatching, their bodies begin to respond more strongly to oxygen, preparing them for the demands of hatching.
Oxygen levels and cardiovascular function are closely tied to metabolic activity, which includes powering the muscles used for pipping.

Heart rate and blood oxygen levels increase sharply around the time of external pipping — showing that the embryo is preparing for an intense physical effort.

So what happens to the emu chick at hatch — especially concerning pipping muscles?
Pre-pipping (inside the egg):
The emu chick gets oxygen by diffusion through the eggshell.
Oxygen levels are limited, so the chick’s metabolic rate is relatively low.
It’s not yet using the pipping muscles much at this stage.
Internal pipping (into the air cell):
The chick breaks into the air space in the egg and begins to breathe a small amount of air.
This causes a big rise in blood oxygen, stimulating the ductus arteriosus to start closing and signalling the chick’s body to gear up for external pipping.
The pipping muscles begin to activate more seriously now.
External pipping (breaking the shell):
Oxygen intake increases significantly.
The increased oxygen supports high-energy demands, including sustained contractions of the complexus (pipping) muscle, which is the main muscle used to drive the beak into the shell.
At the same time, cardiovascular changes occur: the ductus arteriosus begins closing, and more blood goes to the lungs to support breathing.
After pipping and hatching:
The pipping muscle reaches peak development at hatch and then atrophies (shrinks) quickly, as it’s no longer needed.
The cardiovascular system finishes transitioning to a post-hatch setup, with full reliance on lung breathing.

Summary:
At hatch, the emu chick transitions from a low-oxygen environment inside the egg to high oxygen after external pipping. This oxygen boost:
Powers the pipping muscles so the chick can break out of the shell.
Triggers cardiovascular changes, especially the closure of the ductus arteriosus.
Supports high metabolic demands needed to complete hatching.

In brief... 

Before hatch: The emu embryo relies on gas exchange through the chorioallantoic membrane (via the eggshell). But as it grows, oxygen becomes limited, and hypoxia (low oxygen) develops — this is a physiological trigger.

Internal pip (into the air cell): The chick breaks into the air cell and starts pulmonary respiration — breathing a small amount of air with its lungs for the first time. But this air pocket is limited, so oxygen is quickly depleted. The resulting acute hypoxia stimulates:

- Increased metabolic activity
- Activation of the complexus muscle (used for external pipping)
- Rising heart rate and preparation for major circulatory changes

External pip: Once the chick breaches the shell and accesses atmospheric air, oxygen saturation rises rapidly. This initiates:

- Functional and anatomical closure of the ductus arteriosus (the vessel that bypassed the lungs during development)
- A shift from embryonic to neonatal circulation
- Full activation of pulmonary gas exchange

Another critical part of the natural hatching process is the physiological stress the chick experiences as it works to emerge from the egg. This stress plays a vital role in triggering essential developmental processes. Firstly, it helps draw the yolk sac fully into the abdominal cavity, which is crucial for nutrient absorption and healing. More importantly, this natural stress response also stimulates the release of biologically active compounds—possibly through the bone marrow, such as enzymes or endorphins—into the bloodstream. These compounds are believed to play a key role in boosting the chick’s immune system at a critical stage, laying the foundation for a healthier start to life. In cases where a chick is assisted and does not undergo this natural exertion, this immune-priming process may be disrupted or absent altogether, which could explain the higher juvenile mortality rates often observed in assisted hatches.

Helping a chick to hatch can disrupt cardiovascular transition, leave the ductus arteriosus open, and result in a chick that isn’t physiologically ready for the outside world.

Recommended further reading. 
This is a very interesting article explaining the same emu hatch process... 
​https://www.patreon.com/posts/emu-eggs-part-2-35048141​

Also, 
Circulatory changes associated with the closure of the ductus arteriosus in hatching emu (Dromaius novaehollandiae)

Dynamics of Structural Barriers and Innate Immune Components during Incubation of the Avian Egg: Critical Interplay between Autonomous Embryonic Development and Maternal Anticipation
The Unique Features of Proteins Depicting the Chicken Amniotic Fluid

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